[Federal Register Volume 75, Number 11 (Tuesday, January 19, 2010)]
[Proposed Rules]
[Pages 2938-3052]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2010-340]
Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 /
Proposed Rules
[[Page 2938]]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Parts 50 and 58
[EPA-HQ-OAR-2005-0172; FRL-9102-1]
RIN 2060-AP98
National Ambient Air Quality Standards for Ozone
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
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SUMMARY: Based on its reconsideration of the primary and secondary
national ambient air quality standards (NAAQS) for ozone
(O3) set in March 2008, EPA proposes to set different
primary and secondary standards than those set in 2008 to provide
requisite protection of public health and welfare, respectively. With
regard to the primary standard for O3, EPA proposes that the
level of the 8-hour primary standard, which was set at 0.075 ppm in the
2008 final rule, should instead be set at a lower level within the
range of 0.060 to 0.070 parts per million (ppm), to provide increased
protection for children and other ``at risk'' populations against an
array of O3-related adverse health effects that range from
decreased lung function and increased respiratory symptoms to serious
indicators of respiratory morbidity including emergency department
visits and hospital admissions for respiratory causes, and possibly
cardiovascular-related morbidity as well as total non-accidental and
cardiopulmonary mortality. With regard to the secondary standard for
O3, EPA proposes that the secondary O3 standard,
which was set identical to the revised primary standard in the 2008
final rule, should instead be a new cumulative, seasonal standard
expressed as an annual index of the sum of weighted hourly
concentrations, cumulated over 12 hours per day (8 am to 8 pm) during
the consecutive 3-month period within the O3 season with the
maximum index value, set at a level within the range of 7 to 15 ppm-
hours, to provide increased protection against O3-related
adverse impacts on vegetation and forested ecosystems.
DATES: Written comments on this proposed rule must be received by March
22, 2010.
Public Hearings: Three public hearings are scheduled for this
proposed rule. Two of the public hearings will be held on February 2,
2010 in Arlington, Virginia, and Houston, Texas. The third public
hearing will be held on February 4, 2010 in Sacramento, California.
ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2005-0172, by one of the following methods:
http://www.regulations.gov: Follow the on-line
instructions for submitting comments.
E-mail: [email protected].
Fax: 202-566-9744.
Mail: Docket No. EPA-HQ-OAR-2005-0172, Environmental
Protection Agency, Mail code 6102T, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460. Please include a total of two copies.
Hand Delivery: Docket No. EPA-HQ-OAR-2005-0172,
Environmental Protection Agency, EPA West, Room 3334, 1301 Constitution
Ave., NW., Washington, DC. Such deliveries are only accepted during the
Docket's normal hours of operation, and special arrangements should be
made for deliveries of boxed information.
Public Hearings: Three public hearings are scheduled for this
proposed rule. Two of the public hearings will be held on February 2,
2010 in Arlington, Virginia and Houston, Texas. The third public
hearing will be held on February 4, 2010 in Sacramento, California. The
hearings will be held at the following locations:
Arlington, Virginia--February 2, 2010
Hyatt Regency Crystal City @ Reagan National Airport, Washington Room
(located on the Ballroom Level), 2799 Jefferson Davis Highway,
Arlington, Virginia 22202, Telephone: 703-418-1234.
Houston, Texas--February 2, 2010
Hilton Houston Hobby Airport, Moody Ballroom (located on the ground
floor), 8181 Airport Boulevard, Houston, Texas 77061, Telephone: 713-
645-3000.
Sacramento, California--February 4, 2010
Four Points by Sheraton Sacramento International Airport, Natomas
Ballroom, 4900 Duckhorn Drive, Sacramento, California 95834, Telephone:
916-263-9000.
See the SUPPLEMENTARY INFORMATION under ``Public Hearings'' for
further information.
Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2005-0172. The EPA's policy is that all comments received will be
included in the public docket without change and may be made available
online at www.regulations.gov, including any personal information
provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through www.regulations.gov
or e-mail. The www.regulations.gov Web site is an ``anonymous access''
system, which means EPA will not know your identity or contact
information unless you provide it in the body of your comment. If you
send an e-mail comment directly to EPA without going through
www.regulations.gov, your e-mail address will be automatically captured
and included as part of the comment that is placed in the public docket
and made available on the Internet. If you submit an electronic
comment, EPA recommends that you include your name and other contact
information in the body of your comment and with any disk or CD-ROM you
submit. If EPA cannot read your comment due to technical difficulties
and cannot contact you for clarification, EPA may not be able to
consider your comment. Electronic files should avoid the use of special
characters, any form of encryption, and be free of any defects or
viruses.
Docket: All documents in the docket are listed in the
www.regulations.gov index. Although listed in the index, some
information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in www.regulations.gov or in hard copy at the Air and Radiation Docket
and Information Center, EPA/DC, EPA West, Room 3334, 1301 Constitution
Ave., NW., Washington, DC. The Public Reading Room is open from 8:30
a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The
telephone number for the Public Reading Room is (202) 566-1744 and the
telephone number for the Air and Radiation Docket and Information
Center is (202) 566-1742.
FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Mail Code C504-06,
Research Triangle Park, NC 27711; telephone: 919-541-1146; fax: 919-
541-0237; e-mail: [email protected].
SUPPLEMENTARY INFORMATION:
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General Information
What Should I Consider as I Prepare My Comments for EPA?
1. Submitting CBI. Do not submit this information to EPA through
http://www.regulations.gov or e-mail. Clearly mark the part or all of
the information that you claim to be CBI. For CBI information in a disk
or CD-ROM that you mail to EPA, mark the outside of the disk or CD-ROM
as CBI and then identify electronically within the disk or CD-ROM the
specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2.
2. Tips for Preparing Your Comments. When submitting comments,
remember to:
Identify the rulemaking by docket number and other
identifying information (subject heading, Federal Register date and
page number).
Follow directions--The Agency may ask you to respond to
specific questions or organize comments by referencing a Code of
Federal Regulations (CFR) part or section number.
Explain why you agree or disagree, suggest alternatives,
and substitute language for your requested changes.
Describe any assumptions and provide any technical
information and/or data that you used.
Provide specific examples to illustrate your concerns, and
suggest alternatives.
Explain your views as clearly as possible, avoiding the
use of profanity or personal threats.
Make sure to submit your comments by the comment period
deadline identified.
Availability of Related Information
A number of documents relevant to this rulemaking are available on
EPA web sites. The Air Quality Criteria for Ozone and Related
Photochemical Oxidants (2006 Criteria Document) (two volumes, EPA/and
EPA/, date) is available on EPA's National Center for Environmental
Assessment Web site. To obtain this document, go to http://www.epa.gov/ncea, and click on Ozone in the Quick Finder section. This will open a
page with a link to the March 2006 Air Quality Criteria Document. The
2007 Staff Paper, human exposure and health risk assessments,
vegetation exposure and impact assessment, and other related technical
documents are available on EPA's Office of Air Quality Planning and
Standards (OAQPS) Technology Transfer Network (TTN) web site. The
updated final 2007 Staff Paper is available at: http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html and the exposure and risk
assessments and other related technical documents are available at
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. The
Response to Significant Comments Document is available at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html. These and
other related documents are also available for inspection and copying
in the EPA docket identified above.
Public Hearings
The public hearings on February 2, 2010 and February 4, 2010 will
provide interested parties the opportunity to present data, views, or
arguments concerning the proposed rule. The EPA may ask clarifying
questions during the oral presentations, but will not respond to the
presentations at that time. Written statements and supporting
information submitted during the comment period will be considered with
the same weight as any oral comments and supporting information
presented at the public hearing. Written comments must be received by
the last day of the comment period, as specified in this proposed
rulemaking.
The public hearings will begin at 9:30 a.m. and continue until 7:30
p.m. (local time) or later, if necessary, depending on the number of
speakers wishing to participate. The EPA will make every effort to
accommodate all speakers that arrive and register before 7:30 p.m. A
lunch break is scheduled from 12:30 p.m. until 2 p.m.
If you would like to present oral testimony at the hearings, please
notify Ms. Tricia Crabtree (C504-02), U.S. EPA, Research Triangle Park,
NC 27711. The preferred method for registering is by e-mail
([email protected]). Ms. Crabtree may be reached by telephone at
(919) 541-5688. She will arrange a general time slot for you to speak.
The EPA will make every effort to follow the schedule as closely as
possible on the day of the hearing.
Oral testimony will be limited to five (5) minutes for each
commenter to address the proposal. We will not be providing equipment
for commenters to show overhead slides or make computerized slide
presentations unless we receive special requests in advance. Commenters
should notify Ms. Crabtree if they will need specific audiovisual (AV)
equipment. Commenters should also notify Ms. Crabtree if they need
specific translation services for non-English speaking commenters. The
EPA encourages commenters to provide written versions of their oral
testimonies either electronically on computer disk, CD-ROM, or in paper
copy.
The hearing schedules, including lists of speakers, will be posted
on EPA's Web site for the proposal at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_fr.html prior to the hearing. Verbatim
transcripts of the hearings and written statements will be included in
the rulemaking docket.
Children's Environmental Health
Consideration of children's environmental health plays a central
role in the reconsideration of the 2008 final decision on the
O3 NAAQS and EPA's decision to propose to set the 8-hour
primary O3 standard at a level within the range of 0.060 to
0.070 ppm. Technical information that pertains to children, including
the evaluation of scientific evidence, policy considerations, and
exposure and risk assessments, is discussed in all of the documents
listed above in the section on the availability of related information.
These documents include: the Air Quality Criteria for Ozone and Other
Related Photochemical Oxidants; the 2007 Staff Paper; exposure and risk
assessments and other related documents; and the Response to
Significant Comments. All of these documents are available on the Web,
as described above, and are in the public docket for this rulemaking.
The public is invited to submit comments or identify peer-reviewed
studies and data that assess effects of early life exposure to
O3.
Table of Contents
The following topics are discussed in this preamble:
I. Background
A. Legislative Requirements
B. Related Control Requirements
C. Review of Air Quality Criteria and Standards for
O3
D. Reconsideration of the 2008 O3 NAAQS Final Rule
1. Decision to Initiate a Rulemaking to Reconsider
2. Ongoing Litigation
II. Rationale for Proposed Decision on the Level of the Primary
Standard
A. Health Effects Information
1. Overview of Mechanisms
2. Nature of Effects
3. Interpretation and Integration of Health Evidence
4. O3-Related Impacts on Public Health
B. Human Exposure and Health Risk Assessments
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1. Exposure Analyses
2. Quantitative Health Risk Assessment
C. Reconsideration of the Level of the Primary Standard
1. Evidence and Exposure/Risk-Based Considerations
2. CASAC Views Prior to 2008 Decision
3. Basis for 2008 Decision on the Primary Standard
4. CASAC Advice Following 2008 Decision
5. Administrator's Proposed Conclusions
D. Proposed Decision on the Level of the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
A. Vegetation Effects Information
1. Mechanisms
2. Nature of Effects
3. Adversity of Effects
B. Biologically Relevant Exposure Indices
C. Vegetation Exposure and Impact Assessment
1. Exposure Characterization
2. Assessment of Risks to Vegetation
D. Reconsideration of Secondary Standard
1. Considerations Regarding 2007 Proposed Cumulative Seasonal
Standard
2. Considerations Regarding 2007 Proposed 8-Hour Standard
3. Basis for 2008 Decision on the Secondary Standard
4. CASAC Views Following 2008 Decision
5. Administrator's Proposed Conclusions
E. Proposed Decision on the Secondary O3 Standard
V. Revision of Appendix P--Interpretation of the NAAQS for
O3 and Proposed Revisions to the Exceptional Events Rule
A. Background
B. Interpretation of the Secondary O3 Standard
C. Clarifications Related to the Primary Standard
D. Revisions to Exceptions From Standard Data Completeness
Requirements for the Primary Standard
E. Elimination of the Requirement for 90 Percent Completeness of
Daily Data Across Three Years
F. Administrator Discretion To Use Incomplete Data
G. Truncation Versus Rounding
H. Data Selection
I. Exceptional Events Information Submission Schedule
VI. Ambient Monitoring Related to Proposed O3 Standards
A. Background
B. Urban Monitoring Requirements
C. Non-Urban Monitoring Requirements
D. Revisions to the Length of the Required O3
Monitoring Season
VII. Implementation of Proposed O3 Standards
A. Designations
B. State Implementation Plans
C. Trans-boundary Emissions
VIII. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
B. Paperwork Reduction Act
C. Regulatory Flexibility Act
D. Unfunded Mandates Reform Act
E. Executive Order 13132: Federalism
F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
G. Executive Order 13045: Protection of Children From
Environmental Health and Safety Risks
H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution or Use
I. National Technology Transfer and Advancement Act
J. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
References
I. Background
The proposed decisions presented in this notice are based on a
reconsideration of the 2008 O3 NAAQS final rule (73 FR
16436, March 27, 2008), which revised the level of the 8-hour primary
O3 standard to 0.075 ppm and revised the secondary
O3 standard by making it identical to the revised primary
standard. This reconsideration is based on the scientific and technical
information and analyses on which the March 2008 O3 NAAQS
rulemaking was based. Therefore, much of the information included in
this notice is drawn directly from information included in the 2007
proposed rule (72 FR 37818, July 11, 2007) and the 2008 final rule (73
FR 16436).
A. Legislative Requirements
Two sections of the Clean Air Act (CAA) govern the establishment
and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the
Administrator to identify and list ``air pollutants'' that in her
``judgment, cause or contribute to air pollution which may reasonably
be anticipated to endanger public health or welfare'' and satisfy two
other criteria, including ``whose presence * * * in the ambient air
results from numerous or diverse mobile or stationary sources'' and to
issue air quality criteria for those that are listed. Air quality
criteria are intended to ``accurately reflect the latest scientific
knowledge useful in indicating the kind and extent of all identifiable
effects on public health or welfare which may be expected from the
presence of [a] pollutant in the ambient air. * * *''
Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants for
which air quality criteria are issued. Section 109(b)(1) defines a
primary standard as one ``the attainment and maintenance of which in
the judgment of the Administrator, based on such criteria and allowing
an adequate margin of safety, are requisite to protect the public
health.'' \1\ A secondary standard, as defined in section 109(b)(2),
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on such criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of such air pollutant in
the ambient air.'' \2\
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\1\ The legislative history of section 109 indicates that a
primary standard is to be set at ``the maximum permissible ambient
air level * * * which will protect the health of any [sensitive]
group of the population,'' and that for this purpose ``reference
should be made to a representative sample of persons comprising the
sensitive group rather than to a single person in such a group'' [S.
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970)].
\2\ Welfare effects as defined in section 302(h) (42 U.S.C.
7602(h)) include, but are not limited to, ``effects on soils, water,
crops, vegetation, man-made materials, animals, wildlife, weather,
visibility, and climate, damage to and deterioration of property,
and hazards to transportation, as well as effects on economic values
and on personal comfort and well-being.''
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The requirement that primary standards include an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (DC
Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176, 1186 (DC Cir. 1981), cert. denied,
455 U.S. 1034 (1982). Both kinds of uncertainties are components of the
risk associated with pollution at levels below those at which human
health effects can be said to occur with reasonable scientific
certainty. Thus, in selecting primary standards that include an
adequate margin of safety, the Administrator is seeking not only to
prevent pollution levels that have been demonstrated to be harmful but
also to prevent lower pollutant levels that may pose an unacceptable
risk of harm, even if the risk is not precisely identified as to nature
or degree. The CAA does not require the Administrator to establish a
primary NAAQS at a zero-risk level or at background concentration
levels, see Lead Industries Association v. EPA, 647 F.2d at 1156 n. 51,
but rather at a level that reduces risk sufficiently so as to protect
public health with an adequate margin of safety.
In addressing the requirement for an adequate margin of safety, EPA
considers such factors as the nature and severity of the health effects
involved, the size of the population(s) at risk, and the kind and
degree of the uncertainties
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that must be addressed. The selection of any particular approach to
providing an adequate margin of safety is a policy choice left
specifically to the Administrator's judgment. Lead Industries
Association v. EPA, 647 F.2d at 1161-62; Whitman v. American Trucking
Associations, 531 U.S. 457, 495 (2001).
In setting standards that are ``requisite'' to protect public
health and welfare, as provided in section 109(b), EPA's task is to
establish standards that are neither more nor less stringent than
necessary for these purposes. Whitman v. America Trucking Associations,
531 U.S. 457, 473. In establishing ``requisite'' primary and secondary
standards, EPA may not consider the costs of implementing the
standards. Id. at 471.
Section 109(d)(1) of the CAA requires that ``not later than
December 31, 1980, and at 5-year intervals thereafter, the
Administrator shall complete a thorough review of the criteria
published under section 108 and the national ambient air quality
standards * * * and shall make such revisions in such criteria and
standards and promulgate such new standards as may be appropriate. * *
*'' Section 109(d)(2) requires that an independent scientific review
committee ``shall complete a review of the criteria * * * and the
national primary and secondary ambient air quality standards * * * and
shall recommend to the Administrator any new * * * standards and
revisions of existing criteria and standards as may be appropriate. * *
*'' This independent review function is performed by the Clean Air
Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.
B. Related Control Requirements
States have primary responsibility for ensuring attainment and
maintenance of ambient air quality standards once EPA has established
them. Under section 110 of the Act (42 U.S.C. 7410) and related
provisions, States are to submit, for EPA approval, State
implementation plans (SIPs) that provide for the attainment and
maintenance of such standards through control programs directed to
emission sources.
The majority of man-made nitrogen oxides (NOX) and
volatile organic compounds (VOC) emissions that contribute to
O3 formation in the United States come from three types of
sources: Mobile sources, industrial processes (which include consumer
and commercial products), and the electric power industry.\3\ Mobile
sources and the electric power industry were responsible for 78 percent
of annual NOX emissions in 2004. That same year, 99 percent
of man-made VOC emissions came from industrial processes (including
solvents) and mobile sources. Emissions from natural sources, such as
trees, may also comprise a significant portion of total VOC emissions
in certain regions of the country, especially during the O3
season, which are considered natural background emissions.
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\3\ See EPA report, Evaluating Ozone Control Programs in the
Eastern United States: Focus on the NOX Budget Trading Program,
2004.
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The EPA has developed new emissions standards for many types of
stationary sources and for nearly every class of mobile sources in the
last decade to reduce O3 by decreasing emissions of
NOX and VOC. These programs complement State and local
efforts to improve O3 air quality and meet the 0.084 ppm 8-
hour national standards. Under title II of the CAA, 42 U.S.C. 7521-
7574), EPA has established new emissions standards for nearly every
type of automobile, truck, bus, motorcycle, earth mover, and aircraft
engine, and for the fuels used to power these engines. EPA also
established new standards for the smaller engines used in small
watercraft, lawn and garden equipment. In March 2008, EPA promulgated
new standards for locomotive and marine diesel engines and in August
2009, proposed to control emissions from ocean-going vessels.
Benefits from engine standards increase modestly each year as
older, more-polluting vehicles and engines are replaced with newer,
cleaner models. In time, these programs will yield substantial emission
reductions. Benefits from fuel programs generally begin as soon as a
new fuel is available.
The reduction of VOC emissions from industrial processes has been
achieved either directly or indirectly through implementation of
control technology standards, including maximum achievable control
technology, reasonably available control technology, and best available
control technology standards; or are anticipated due to proposed or
upcoming proposals based on generally available control technology or
best available controls under provisions related to consumer and
commercial products. These standards have resulted in VOC emission
reductions of almost a million tons per year accumulated starting in
1997 from a variety of sources including combustion sources, coating
categories, and chemical manufacturing. EPA has also finalized emission
standards and fuel requirements for new stationary engines. In the area
of consumer and commercial products, EPA has finalized new national VOC
emission standards for aerosol coatings and is working toward amending
existing rules to establish new nationwide VOC content limits for
household and institutional consumer products and architectural and
industrial maintenance coatings. The aerosol coatings rule took effect
in July 2009; the compliance date for both the amended consumer product
rule and architectural coatings rule is anticipated to be January 2011.
These actions are expected to yield significant new VOC reductions--
about 200,000 tons per year. Additionally, in ozone nonattainment
areas, we anticipate reductions of an additional 25,000 tons per year
as States adopt rules this year implementing control techniques
recommendations issued in 2008 for 4 additional categories of consumer
and commercial products, typically surface coatings and adhesives used
in industrial manufacturing operations. These emission reductions
primarily result from solvent controls and typically occur where and
when the solvent is used, such as during manufacturing processes.
The power industry is one of the largest emitters of NOX
in the United States. Power industry emission sources include large
electric generating units (EGU) and some large industrial boilers and
turbines. The EPA's landmark Clean Air Interstate Rule (CAIR), issued
on March 10, 2005, was designed to permanently cap power industry
emissions of NOX in the eastern United States. The first
phase of the cap was to begin in 2009, and a lower second phase cap was
to begin in 2015. The EPA had projected that by 2015, the CAIR and
other programs would reduce NOX emissions during the
O3 season by about 50 percent and annual NOX
emissions by about 60 percent from 2003 levels in the Eastern U.S.
However, on July 11, 2008 and December 23, 2008, the U.S. Court of
Appeals for the DC Circuit issued decisions on petitions for review of
the CAIR. In its July 11 opinion, the court found CAIR unlawful and
decided to vacate CAIR and its associated Federal implementation plans
(FIPs) in their entirety. On December 23, the court granted EPA's
petition for rehearing to the extent that it remanded without vacatur
for EPA to conduct further proceedings consistent with the Court's
prior opinion. Under this decision, CAIR will remain in place only
until replaced by EPA with a rule that is consistent with the Court's
July
[[Page 2942]]
11 opinion. The EPA recognizes the need in our CAIR replacement effort
to address the reconsidered ozone standard, and we are currently
assessing our options for the best way to accomplish this. It should
also be noted that new electric generating units (EGUs) are also
subject to NOX limits under New Source Performance Standards
(NSPS) under CAA section 111, as well as either nonattainment new
source review or prevention of significant deterioration requirements.
With respect to agricultural sources, the U.S. Department of
Agriculture (USDA) has approved conservation systems and activities
that reduce agricultural emissions of NOX and VOC. Current
practices that may reduce emissions of NOX and VOC include
engine replacement programs, diesel retrofit programs, manipulation of
pesticide applications including timing of applications, and animal
feeding operations waste management techniques. The EPA recognizes that
USDA has been working with the agricultural community to develop
conservation systems and activities to control emissions of
O3 precursors.
These conservation activities are voluntarily adopted through the
use of incentives provided to the agricultural producer. In cases where
the States need these measures to attain the standard, the measures
could be adopted. The EPA will continue to work with USDA on these
activities with efforts to identify and/or improve the control
efficiencies, prioritize the adoption of these conservation systems and
activities, and ensure that appropriate criteria are used for
identifying the most effective application of conservation systems and
activities.
The EPA will work together with USDA and with States to identify
appropriate measures to meet the primary and secondary standards,
including site-specific conservation systems and activities. Based on
prior experience identifying conservation measures and practices to
meet the PM NAAQS requirements, the EPA will use a similar process to
identify measures that could meet the O3 requirements. The
EPA anticipates that certain USDA-approved conservation systems and
activities that reduce agricultural emissions of NOX and VOC
may be able to satisfy the requirements for applicable sources to
implement reasonably available control measures for purposes of
attaining the primary and secondary O3 NAAQS.
C. Review of Air Quality Criteria and Standards for O3
In 1971, EPA first established primary and secondary NAAQS for
photochemical oxidants (36 FR 8186). Both primary and secondary
standards were set at a level of 0.08 parts per million (ppm), 1-hr
average, total photochemical oxidants, not to be exceeded more than one
hr per year. In 1977, EPA announced the first periodic review of the
air quality criteria in accordance with section 109(d)(1) of the Act.
The EPA published a final decision in 1979 (44 FR 8202). Both primary
and secondary standard levels were revised from 0.08 to 0.12 ppm. The
indicator was revised from photochemical oxidants to O3, and
the form of the standards was revised from a deterministic to a
statistical form, which defined attainment of the standards as
occurring when the expected number of days per calendar year with
maximum hourly average concentration greater than 0.12 ppm is equal to
or less than one. In 1983, EPA announced that the second periodic
review of the primary and secondary standards for O3 had
been initiated. Following review and publication of air quality
criteria and a supplement, EPA published a proposed decision (57 FR
35542) in August 1992 that announced EPA's intention to proceed as
rapidly as possible with the next review of the air quality criteria
and standards for O3 in light of emerging evidence of health
effects related to 6- to 8-hr O3 exposures. In March 1993,
EPA concluded the review by deciding that revisions to the standards
were not warranted at that time (58 FR 13008).
In August 1992 (57 FR 35542), EPA announced plans to initiate the
third periodic review of the air quality criteria and O3
NAAQS. On the basis of the scientific evidence contained in the 1996 CD
(U.S. EPA 1996a) and the 1996 Staff Paper (U.S. EPA, 1996b), and
related technical support documents, linking exposures to ambient
O3 to adverse health and welfare effects at levels allowed
by the then existing standards, EPA proposed to revise the primary and
secondary O3 standards in December 1996 (61 FR 65716). The
EPA proposed to replace the then existing 1-hour primary and secondary
standards with 8-hour average O3 standards set at a level of
0.08 ppm (equivalent to 0.084 ppm using standard rounding conventions).
The EPA also proposed, in the alternative, to establish a new distinct
secondary standard using a biologically based cumulative seasonal form.
The EPA completed the review in July 1997 (62 FR 38856) by setting the
primary standard at a level of 0.08 ppm, based on the annual fourth-
highest daily maximum 8-hr average concentration, averaged over three
years, and setting the secondary standard identical to the revised
primary standard.
The EPA initiated the most recent periodic review of the air
quality criteria and standards for O3 in September 2000 with
a call for information (65 FR 57810; September 26, 2000) for the
development of a revised Air Quality Criteria Document for
O3 and Other Photochemical Oxidants (henceforth the ``2006
Criteria Document''). A project work plan (EPA, 2002) for the
preparation of the Criteria Document was released in November 2002 for
CASAC and public review. The EPA held a series of workshops in mid-2003
on several draft chapters of the Criteria Document to obtain broad
input from the relevant scientific communities. These workshops helped
to inform the preparation of the first draft Criteria Document (EPA,
2005a), which was released for CASAC and public review on January 31,
2005; a CASAC meeting was held on May 4-5, 2005 to review the first
draft Criteria Document. A second draft Criteria Document (EPA, 2005b)
was released for CASAC and public review on August 31, 2005, and was
discussed along with a first draft Staff Paper (EPA, 2005c) at a CASAC
meeting held on December 6-8, 2005. In a February 16, 2006 letter to
the Administrator, CASAC provided comments on the second draft Criteria
Document (Henderson, 2006a), and the final 2006 Criteria Document (EPA,
2006a) was released on March 21, 2006. In a June 8, 2006 letter to the
Administrator (Henderson, 2006b), CASAC provided additional advice to
the Agency concerning chapter 8 of the final 2006 Criteria Document
(Integrative Synthesis) to help inform the second draft Staff Paper.
A second draft Staff Paper (EPA, 2006b) was released on July 17,
2006 and reviewed by CASAC on August 24-25, 2006. In an October 24,
2006 letter to the Administrator, CASAC provided advice and
recommendations to the Agency concerning the second draft Staff Paper
(Henderson, 2006c). A final 2007 Staff Paper (EPA, 2007a) was released
on January 31, 2007. In a March 26, 2007 letter (Henderson, 2007),
CASAC offered additional advice to the Administrator with regard to
recommendations and revisions to the primary and secondary
O3 NAAQS.
The schedule for completion of the 2008 rulemaking was governed by
a consent decree resolving a lawsuit filed in March 2003 by a group of
plaintiffs representing national environmental
[[Page 2943]]
and public health organizations, alleging that EPA had failed to
complete the review within the period provided by statute.\4\ The
modified consent decree that governed the 2008 rulemaking, entered by
the court on December 16, 2004, provided that EPA sign for publication
notices of proposed and final rulemaking concerning its review of the
O3 NAAQS no later than March 28, 2007 and December 19, 2007,
respectively. That consent decree was further modified in October 2006
to change these proposed and final rulemaking dates to no later than
May 30, 2007 and February 20, 2008, respectively. These dates for
signing the publication notices of proposed and final rulemaking were
further extended to no later than June 20, 2007 and March 12, 2008,
respectively. The proposed decision was signed on June 20, 2007 and
published in the Federal Register on July 11, 2007 (72 FR 37818).
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\4\ American Lung Association v. Whitman (No. 1:03CV00778, D.DC
2003).
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Public hearings on the proposed decision were held on Thursday,
August 30, 2007 in Philadelphia, PA and Los Angeles, CA. On Wednesday,
September 5, 2007, hearings were held in Atlanta, GA, Chicago, IL, and
Houston, TX. A large number of comments were received from various
commenters on the 2007 proposed revisions to the O3 NAAQS. A
comprehensive summary of all significant comments, along with EPA's
responses (henceforth ``Response to Comments''), can be found in the
docket for the 2008 rulemaking, which is also the docket for this
reconsideration rulemaking.
The EPA's final decision on the O3 NAAAQS was published
in the Federal Register on March 27, 2008 (73 FR 16436). In the 2008
rulemaking, EPA revised the level of the 8-hour primary standard for
O3 to 0.075 parts per million (ppm), expressed to three
decimal places. With regard to the secondary standard for
O3, EPA revised the 8-hour standard by making it identical
to the revised primary standard. The EPA also made conforming changes
to the Air Quality Index (AQI) for O3, setting an AQI value
of 100 equal to 0.075 ppm, 8-hour average, and making proportional
changes to the AQI values of 50, 150 and 200.
D. Reconsideration of the 2008 O3 NAAQS Final Rule
Consistent with a directive of the new Administration regarding the
review of new and pending regulations (Emanuel memorandum, 74 FR 4435;
January 26, 2009), the Administrator reviewed a number of actions that
were taken in the last year by the previous Administration. The 2008
final rule was included in this review in recognition of the central
role that the NAAQS play in enabling EPA to fulfill its mission to
protect the nation's public health and welfare. In her review, the
Administrator was mindful of the need for judgments concerning the
NAAQS to be based on a strong scientific foundation which is developed
through a transparent and credible NAAQS review process, consistent
with the core values highlighted in President Obama's memorandum on
scientific integrity (March 9, 2009).
1. Decision To Initiate a Rulemaking To Reconsider
In her review of the 2008 final rule, several aspects of the final
rule related to the primary and secondary standards stood out to the
Administrator. As an initial matter, the Administrator noted that the
2008 final rule concluded that the 1997 primary and secondary
O3 standards were not adequate to protect public health and
public welfare, and that revisions were necessary to provide increased
protection. With respect to revision of the primary standard, the
Administrator noted that the revised level established in the 2008
final rule was above the range that had been unanimously recommended by
CASAC.\5\ She also noted that EPA received comments from a large number
of commenters from the medical and public health communities, including
EPA's Children's Health Protection Advisory Committee, all of which
endorsed levels within CASAC's recommended range.
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\5\ The level of the 8-hour primary ozone standard was set at
0.075 ppm, while CASAC unanimously recommended a range between 0.060
and 0.070 ppm.
---------------------------------------------------------------------------
With respect to revision of the secondary O3 standard,
the Administrator noted that the 2008 final rule differed substantially
from CASAC's recommendations that EPA adopt a new secondary
O3 standard based on a cumulative, seasonal measure of
exposure. The 2008 final rule revised the secondary standard to be
identical to the revised primary standard, which is based on an 8-hour
daily maximum measure of exposure. She also noted that EPA received
comments from a number of commenters representing environmental
interests, all of which endorsed CASAC;s recommendation for a new
cumulative, seasonal secondary standard.\6\
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\6\ The Administrator also noted the exchange that had occurred
between EPA and the Office of Management and Budget (OMB) with
regard to the final decision on the secondary standard, as discussed
in the 2008 final rule (73 FR 16497).
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Subsequent to issuance of the 2008 final rule, in April 2008, CASAC
took the unusual step of sending EPA a letter expressing strong,
unanimous disagreement with EPA's decisions on both the primary and
secondary standards (Henderson, 2008). The CASAC explained that it did
not endorse the revised primary O3 standard as being
sufficiently protective of public health because it failed to satisfy
the explicit stipulation of the Act to provide an adequate margin of
safety. The CASAC also expressed the view that failing to revise the
secondary standard to a cumulative, seasonal form was not supported by
the available science. In addition to CASAC's letter, the Administrator
noted a recent adverse ruling issued by the U.S. Court of Appeals for
the District of Columbia Circuit on another NAAQS decision. In February
2009, the DC Circuit remanded the Agency's decisions on the primary
annual and secondary standards for fine particles (PM2.5).
In so doing, the Court found that EPA had not adequately explained the
basis for its decisions, including why CASAC's recommendations for a
more health-protective primary annual standard and for secondary
standards different from the primary standards were not accepted.
American Farm Bureau v. EPA, 559 F.3d. 512 (DC Cir. 2009).
Based on her review of the information described above, the
Administrator is initiating a rulemaking to reconsider parts of the
2008 final rule. Specifically, the Administrator is reconsidering the
level of the primary standard to ensure that it is sufficiently
protective of public health, as discussed in section II below, and is
reconsidering all aspects of the secondary standard to ensure that it
appropriately reflects the available science and is sufficiently
protective of public welfare, as discussed in section IV below. Based
on her review, the Administrator has serious cause for concern
regarding whether the revisions to the primary and secondary
O3 standards adopted in the 2008 final rule satisfy the
requirements of the CAA, in light of the body of scientific evidence
before the Agency. In addition, the importance of the O3
NAAQS to public health and welfare weigh heavily in favor of
reconsidering parts of the 2008 final rule as soon as possible, based
on the scientific and technical information upon which the 2008 final
rule was based.
[[Page 2944]]
Also, EPA conducted a provisional assessment of ``new'' scientific
papers (EPA, 2009) of scientific literature evaluating health and
ecological effects of O3 exposure published since the close
of the 2006 Criteria Document upon which the 2008 O3 NAAQS
were based. The Administrator notes that the provisional assessment of
``new'' science found that such studies did not materially change the
conclusions in the 2006 Criteria Document. This provisional assessment
is supportive of the Administrator's decision to reconsider parts of
the 2008 final rule at this time, based on the scientific and technical
information available for the 2008 final rule, as compared to foregoing
such reconsideration and taking appropriate action in the future as
part of the next periodic review of the air quality criteria and NAAQS,
which will include such scientific and technical information.
The reconsideration of parts of the 2008 final rule discussed in
this notice is based on the scientific and technical record from the
2008 rulemaking, including public comments and CASAC advice and
recommendations. The information that was assessed during the 2008
rulemaking includes information in the 2006 Criteria Document (EPA,
2006a), the 2007 Policy Assessment of Scientific and Technical
Information, referred to as the 2007 Staff Paper (EPA, 2007b), and
related technical support documents including the 2007 REAs (U.S. EPA,
2007c; Abt Associates, 2007a,b). Scientific and technical information
developed since the 2006 Criteria Document will be considered in the
next periodic review, instead of this reconsideration rulemaking,
allowing the new information to receive careful and comprehensive
review by CASAC and the public before it is used as a basis in a
rulemaking that determines whether to revise the NAAQS.
2. Ongoing Litigation
In May 2008, following publication of the 2008 final rule, numerous
groups, including state, public health, environmental, and industry
petitioners, challenged EPA's decisions in federal court. The
challenges were consolidated as State of Mississippi, et al. v. EPA
(No. 08-1200, DC Cir. 2008). On March 10, 2009, EPA filed an unopposed
motion requesting that the Court vacate the briefing schedule and hold
the consolidated cases in abeyance. The Agency stated its desire to
allow time for appropriate officials from the new Administration to
review the O3 standards to determine whether they should be
maintained, modified or otherwise reconsidered. The EPA further
requested that it be directed to notify the Court and all the parties
of any actions it has taken or intends to take, if any, within 180 days
of the Court vacating the briefing schedule. On March 19, 2009, the
Court granted EPA's motion. Pursuant to the Court's order, on September
16, 2009 EPA notified the Court and the parties of its decision to
initiate a rulemaking to reconsider the primary and secondary
O3 standards set in March 2008 to ensure they satisfy the
requirements of the CAA.\7\ In its notice to the Court, EPA stated that
this notice of proposed rulemaking would be signed by December 21,
2009, and that the final rule will be signed by August 31, 2010.
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\7\ The EPA also separately announced that it will move quickly
to implement any new standards that might result from this
reconsideration. To reduce the workload for states during the
interim period of reconsideration, the Agency intends to propose to
defer compliance with the CAA requirement to designate areas as
attainment or nonattainment. EPA will work with states, local
governments and tribes to ensure that air quality is protected
during that time.
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II. Rationale for Proposed Decision on the Level of the Primary
Standard
As an initial matter, the Administrator notes that the 2008 final
rule concluded that the 1997 primary O3 standard was ``not
sufficient and thus not requisite to protect public health with an
adequate margin of safety, and that revision is needed to provide
increased public health protection'' (73 FR 16472). The Administrator
is not reconsidering this aspect of the 2008 decision, which is based
on the reasons discussed in section II.B of the 2008 final rule (73 FR
16443-16472). The Administrator also notes that the 2008 final rule
concluded that it was appropriate to retain the O3
indicator, the 8-hour averaging time, and form of the primary
O3 standard (specified as the annual fourth-highest daily
maximum 8-hour concentration, averaged over 3 years), while concluding
that revision of the standard level was appropriate.\8\ The
Administrator is not reconsidering these aspects of the 2008 decision,
which are based on the reasons discussed in sections II.C.1-3 of the
2008 final rule, which address the indicator, averaging time, and form,
respectively, of the primary O3 standard (73 FR 16472-
16475). For these reasons, the Administrator is not reopening the 2008
decision with regard to the need to revise the 1997 primary
O3 standard nor with regard to the indicator, averaging
time, and form of the 2008 primary O3 standard. Thus, the
information that follows in this section specifically focuses on a
reconsideration of level of the primary O3 standard.
---------------------------------------------------------------------------
\8\ The use of O3 as the indicator for photochemical
oxidants was adopted in the 1979 final rule and retained in
subsequent rulemaking. An 8-hour averaging time and a form based on
the annual fourth-highest daily maximum 8-hour concentration,
averaged over 3 years, were adopted in the 1997 final rule and
retained in the 2008 rulemaking.
---------------------------------------------------------------------------
This section presents the rationale for the Administrator's
proposed decision that the O3 primary standard, which was
set at a level of 0.075 ppm in the 2008 final rule, should instead be
set at a lower level within the range from 0.060 to 0.070 ppm. As
discussed more fully below, the rationale for the proposed range of
standard levels is based on a thorough review of the latest scientific
information on human health effects associated with the presence of
O3 in the ambient air presented in the 2006 Criteria
Document. This rationale also takes into account: (1) Staff assessments
of the most policy-relevant information in the 2006 Criteria Document
and staff analyses of air quality, human exposure, and health risks,
presented in the 2007 Staff Paper, upon which staff recommendations for
revisions to the primary O3 standard in the 2008 rulemaking
were based; (2) CASAC advice and recommendations, as reflected in
discussions of drafts of the 2006 Criteria Document and 2007 Staff
Paper at public meetings, in separate written comments, and in CASAC's
letters to the Administrator both before and after the 2008 rulemaking;
and (3) public comments received during the development of these
documents, either in connection with CASAC meetings or separately, and
on the 2007 proposed rule.
In developing this rationale, the Administrator recognizes that the
CAA requires her to reach a public health policy judgment as to what
standard would be requisite to protect public health with an adequate
margin of safety, based on scientific evidence and technical
assessments that have inherent uncertainties and limitations. This
judgment requires making reasoned decisions as to what weight to place
on various types of evidence and assessments, and on the related
uncertainties and limitations. Thus, in selecting standard levels to
propose, and subsequently in selecting a final level, the Administrator
is seeking not only to prevent O3 levels that have been
demonstrated to be harmful but also to prevent lower O3
levels that may pose an unacceptable risk of harm, even if the risk is
not precisely identified as to nature or degree.
In this proposed rule, EPA has drawn upon an integrative synthesis
of the entire body of evidence, published
[[Page 2945]]
through early 2006, on human health effects associated with the
presence of O3 in the ambient air. As discussed below in
section II.A, this body of evidence addresses a broad range of health
endpoints associated with exposure to ambient levels of O3
(EPA, 2006a, chapter 8), and includes over one hundred epidemiologic
studies conducted in the U.S., Canada, and many countries around the
world.\9\ In reconsidering this evidence, EPA focuses on those health
endpoints that have been demonstrated to be caused by exposure to
O3, or for which the 2006 Criteria Document judges
associations with O3 to be causal, likely causal, or for
which the evidence is highly suggestive that O3 contributes
to the reported effects. This rationale also draws upon the results of
quantitative exposure and risk assessments, discussed below in section
II.B. Section II.C focuses on the considerations upon which the
Administrator's proposed conclusions on the level of the primary
standard are based. Policy-relevant evidence-based and exposure/risk-
based considerations are discussed, and the rationale for the 2008
final rulemaking on the primary standard and CASAC advice, given both
prior to the development of the 2007 proposed rule and following the
2008 final rule, are summarized. Finally, the Administrator's proposed
conclusions on the level of the primary standard are presented. Section
II.D summarizes the proposed decision on the level of the primary
O3 standard and the solicitation of public comments.
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\9\ In its assessment of the epidemiological evidence judged to
be most relevant to making decisions on the level of the
O3 primary standard, EPA has placed greater weight on
U.S. and Canadian epidemiologic studies, since studies conducted in
other countries may well reflect different demographic and air
pollution characteristics.
---------------------------------------------------------------------------
Judgments made in the 2006 Criteria Document and 2007 Staff Paper
about the extent to which relationships between various health
endpoints and short-term exposures to ambient O3 are likely
causal have been informed by several factors. As discussed below in
section II.A, these factors include the nature of the evidence (i.e.,
controlled human exposure, epidemiological, and/or toxicological
studies) and the weight of evidence, which takes into account such
considerations as biological plausibility, coherence of evidence,
strength of association, and consistency of evidence.
In assessing the health effects data base for O3, it is
clear that human studies provide the most directly applicable
information for determining causality because they are not limited by
the uncertainties of dosimetry differences and species sensitivity
differences, which would need to be addressed in extrapolating animal
toxicology data to human health effects. Controlled human exposure
studies provide data with the highest level of confidence since they
provide human health effects data under closely monitored conditions
and can provide exposure-response relationships. Epidemiological data
provide evidence of associations between ambient O3 levels
and more serious acute and chronic health effects (e.g., hospital
admissions and mortality) that cannot be assessed in controlled human
exposure studies. For these studies the degree of uncertainty
introduced by potentially confounding variables (e.g., other
pollutants, temperature) and other factors affects the level of
confidence that the health effects being investigated are attributable
to O3 exposures, alone and in combination with other
copollutants.
In using a weight of evidence approach to inform judgments about
the degree of confidence that various health effects are likely to be
caused by exposure to O3, confidence increases as the number
of studies consistently reporting a particular health endpoint grows
and as other factors, such as biological plausibility and strength,
consistency, and coherence of evidence, increase. Conclusions regarding
biological plausibility, consistency, and coherence of evidence of
O3-related health effects are drawn from the integration of
epidemiological studies with mechanistic information from controlled
human exposure studies and animal toxicological studies. As discussed
below, this type of mechanistic linkage has been firmly established for
several respiratory endpoints (e.g., lung function decrements, lung
inflammation) but remains far more equivocal for cardiovascular
endpoints (e.g., cardiovascular-related hospital admissions). For
epidemiological studies, strength of association refers to the
magnitude of the association and its statistical strength, which
includes assessment of both effects estimate size and precision. In
general, when associations yield large relative risk estimates, it is
less likely that the association could be completely accounted for by a
potential confounder or some other bias. Consistency refers to the
persistent finding of an association between exposure and outcome in
multiple studies of adequate power in different persons, places,
circumstances and times. For example, the magnitude of effect estimates
is relatively consistent across recent studies showing association
between short-term, but not long-term, O3 exposure and
mortality.
Based on the information discussed below in sections II.A.1-II.A.3,
judgments concerning the extent to which relationships between various
health endpoints and ambient O3 exposures are likely causal
are summarized below in section II.A.3.c. These judgments reflect the
nature of the evidence and the overall weight of the evidence, and are
taken into consideration in the quantitative exposure and risk
assessments, discussed below in section II.B.
To put judgments about health effects that have been demonstrated
to be caused by exposure to O3, or for which the 2006
Criteria Document judges associations with O3 to be causal,
likely causal, or for which the evidence is highly suggestive that
O3 contributes to the reported effects into a broader public
health context, EPA has drawn upon the results of the quantitative
exposure and risk assessments. These assessments provide estimates of
the likelihood that individuals in particular population groups that
are at risk for various O3-related physiological health
effects would experience ``exposures of concern'' and specific health
endpoints under varying air quality scenarios (i.e., just meeting
various standards \10\), as well as characterizations of the kind and
degree of uncertainties inherent in such estimates.
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\10\ The exposure assessment done as part of the 2008 final
rulemaking considered several air quality scenarios, including just
meeting what was then the current standard set at a level of 0.084
ppm, as well as just meeting alternative standards at levels of
0.080, 0.074, 0.070, and 0.064 ppm.
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In the 2008 final rulemaking and in this reconsideration, the term
``exposures of concern'' is defined as personal exposures while at
moderate or greater exertion to 8-hour average ambient O3
levels at and above specific benchmark levels which represent exposure
levels at which O3-related health effects are known or can
reasonably be inferred to occur in some individuals, as discussed below
in section II.B.1.\11\ The EPA emphasizes
[[Page 2946]]
that although the analysis of ``exposures of concern'' was conducted
using three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060
ppm), the concept is more appropriately viewed as a continuum with
greater confidence and less uncertainty about the existence of health
effects at the upper end and less confidence and greater uncertainty as
one considers increasingly lower O3 exposure levels. The EPA
recognizes that there is no sharp breakpoint within the continuum
ranging from at and above 0.080 ppm down to 0.060 ppm. In considering
the concept of exposures of concern, it is important to balance
concerns about the potential for health effects and their severity with
the increasing uncertainty associated with our understanding of the
likelihood of such effects at lower O3 levels.
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\11\ Exposures of concern were also considered in the 1997
review of the O3 NAAQS, and were judged by EPA to be an
important indicator of the public health impacts of those
O3-related effects for which information was too limited
to develop quantitative estimates of risk but which had been
observed in humans at and above the benchmark level of 0.08 ppm for
6- to 8-hour exposures * * * including increased nonspecific
bronchial responsiveness (for example, aggravation of asthma),
decreased pulmonary defense mechanisms (suggestive of increased
susceptibility to respiratory infection), and indicators of
pulmonary inflammation (related to potential aggravation of chronic
bronchitis or long-term damage to the lungs). (62 FR 38868)
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Within the context of this continuum, estimates of exposures of
concern at discrete benchmark levels provide some perspective on the
public health impacts of O3-related health effects that have
been demonstrated in controlled human exposure and toxicological
studies but cannot be evaluated in quantitative risk assessments, such
as lung inflammation, increased airway responsiveness, and changes in
host defenses. They also help in understanding the extent to which such
impacts have the potential to be reduced by meeting various standards.
These O3-related physiological effects are plausibly linked
to the increased morbidity seen in epidemiological studies (e.g., as
indicated by increased medication use in asthmatics, school absences in
all children, and emergency department visits and hospital admissions
in people with lung disease). Estimates of the number of people likely
to experience exposures of concern cannot be directly translated into
quantitative estimates of the number of people likely to experience
specific health effects, since sufficient information to draw such
comparisons is not available--if such information were available, these
health outcomes would have been included in the quantitative risk
assessment. Due to individual variability in responsiveness, only a
subset of individuals who have exposures at and above a specific
benchmark level can be expected to experience such adverse health
effects, and susceptible subpopulations such as those with asthma are
expected to be affected more by such exposures than healthy
individuals. The amount of weight to place on the estimates of
exposures of concern at any of these benchmark levels depends in part
on the weight of the scientific evidence concerning health effects
associated with O3 exposures at and above that benchmark
level. It also depends on judgments about the importance from a public
health perspective of the health effects that are known or can
reasonably be inferred to occur as a result of exposures at and above
the benchmark level. Such public health policy judgments are embodied
in the NAAQS standard setting criteria (i.e., standards that, in the
judgment of the Administrator, are requisite to protect public health
with an adequate margin of safety).
As discussed below in section II.B.2, the quantitative health risk
assessment conducted as part of the 2008 final rulemaking includes
estimates of risks of lung function decrements in asthmatic and all
school age children, respiratory symptoms in asthmatic children,
respiratory-related hospital admissions, and non-accidental and
cardiorespiratory-related mortality associated with recent ambient
O3 levels, as well as risk reductions and remaining risks
associated with just meeting the then current 0.084 ppm standard and
various alternative O3 standards in a number of example
urban areas. There are two parts to this risk assessment: one part is
based on combining information from controlled human exposure studies
with modeled population exposure, and the other part is based on
combining information from community epidemiological studies with
either monitored or adjusted ambient concentrations levels. This
assessment provides estimates of the potential magnitude of
O3-related health effects, as well as a characterization of
the uncertainties and variability inherent in such estimates. This
assessment also provides insights into the distribution of risks and
patterns of risk reductions associated with meeting alternative
O3 standards.
As discussed below, a substantial amount of new research conducted
since the 1997 review of the O3 NAAQS was available to
inform the 2008 final rulemaking, with important new information coming
from epidemiologic studies as well as from controlled human exposure,
toxicological, and dosimetric studies. The research studies newly
available in the 2008 final rulemaking that were evaluated in the 2006
Criteria Document and the exposure and risk assessments presented in
the 2007 Staff Paper have undergone intensive scrutiny through multiple
layers of peer review and many opportunities for public review and
comment. While important uncertainties remain in the qualitative and
quantitative characterizations of health effects attributable to
exposure to ambient O3, and while different interpretations
of these uncertainties can result in different public health policy
judgments, the review of this information has been extensive and
deliberate. In the judgment of the Administrator, this intensive
evaluation of the scientific evidence provides an adequate basis for
this reconsideration of the 2008 final rulemaking.
A. Health Effects Information
This section outlines key information contained in the 2006
Criteria Document (chapters 4-8) and in the 2007 Staff Paper (chapter
3) on known or potential effects on public health which may be expected
from the presence of O3 in ambient air. The information
highlighted here summarizes: (1) New information available on potential
mechanisms for health effects associated with exposure to
O3; (2) the nature of effects that have been associated
directly with exposure to O3 and indirectly with the
presence of O3 in ambient air; (3) an integrative
interpretation of the evidence, focusing on the biological plausibility
and coherence of the evidence; and (4) considerations in characterizing
the public health impact of O3, including the identification
of ``at risk'' populations.
The decision in the 1997 review focused primarily on evidence from
short-term (e.g., 1 to 3 hours) and prolonged (6 to 8 hours)
controlled-exposure studies reporting lung function decrements,
respiratory symptoms, and respiratory inflammation in humans, as well
as epidemiology studies reporting excess hospital admissions and
emergency department (ED) visits for respiratory causes. The 2006
Criteria Document prepared for the 2008 rulemaking emphasized the large
number of epidemiological studies published since the last review with
these and additional health endpoints, including the effects of acute
(short-term and prolonged) and chronic exposures to O3 on
lung function decrements and enhanced respiratory symptoms in asthmatic
individuals, school absences, and premature mortality. It also
emphasized important new information from toxicology, dosimetry, and
controlled human exposure studies. Highlights of the evidence include:
(1) Two new controlled human-exposure studies are now available
that examine respiratory effects associated with prolonged
O3 exposures at levels below 0.080 ppm, which was the lowest
[[Page 2947]]
exposure level that had been examined in the 1997 review.
(2) Numerous controlled human-exposure studies have examined
indicators of O3-induced inflammatory response in both the
upper respiratory tract (URT) and lower respiratory tract (LRT), and
increased airway responsiveness to allergens in subjects with allergic
asthma and allergic rhinitis exposed to O3, while other
studies have examined changes in host defense capability following
O3 exposure of healthy young adults.
(3) Animal toxicology studies provide new information regarding
mechanisms of action, increased susceptibility to respiratory
infection, and the biological plausibility of acute effects and
chronic, irreversible respiratory damage.
(4) Numerous acute exposure epidemiological studies published
during the past decade offer added evidence of ambient O3-
related lung function decrements and respiratory symptoms in physically
active healthy subjects and greater responses in asthmatic subjects, as
well as evidence on new health endpoints, such as the relationships
between ambient O3 concentrations and asthma medication use
and school absenteeism, and between ambient O3 and cardiac-
related physiological endpoints.
(5) Several additional studies have been published over the last
decade examining the temporal associations between O3
exposures and emergency department visits for asthma and other
respiratory diseases and respiratory-related hospital admissions.
(6) A large number of newly available epidemiological studies have
examined the effects of acute exposure to PM and O3 on
mortality, notably including large multicity studies that provide much
more robust and credible information than was available in the 1997
review, as well as recent meta-analyses that have evaluated potential
sources of heterogeneity in O3-mortality associations.
1. Overview of Mechanisms
Evidence on possible mechanisms by which exposure to O3
may result in acute and chronic health effects is discussed in chapters
5 and 6 of the 2006 Criteria Document.\12\ Evidence from dosimetry,
toxicological, and human exposure studies has contributed to an
understanding of the mechanisms that help to explain the biological
plausibility and coherence of evidence for O3-induced
respiratory health effects reported in epidemiological studies. More
detailed information about the physiological mechanisms related to the
respiratory effects of short- and long-term exposure to O3
can be found in section II.A.3.b.i and II.A.3.b.iii, respectively. In
the past, however, little information was available to help explain
potential biological mechanisms which linked O3 exposure to
premature mortality or cardiovascular effects. As discussed more fully
in section II.A.3.b.ii below, since the 1997 review an emerging body of
animal toxicology and controlled human exposure evidence is beginning
to suggest mechanisms that may mediate acute O3
cardiovascular effects. While much is known about mechanisms that play
a role in O3-related respiratory effects, additional
research is needed to more clearly understand the role that
O3 may have in contributing to cardiovascular effects.
---------------------------------------------------------------------------
\12\ While most of the available evidence addresses mechanisms
for O3, O3 clearly serves as an indicator for
the total photochemical oxidant mixture found in the ambient air.
Some effects may be caused by one or more components in the overall
pollutant mix, either separately or in combination with
O3. However, O3 clearly dominates these other
oxidants with their concentrations only being a few percent of the
O3 concentration.
---------------------------------------------------------------------------
With regard to the mechanisms related to short-term respiratory
effects, scientific evidence discussed in the 2006 Criteria Document
(section 5.2) indicates that reactions of O3 with lipids and
antioxidants in the epithelial lining fluid and the epithelial cell
membranes of the lung can be the initial step in mediating deleterious
health effects of O3. This initial step activates a cascade
of events that lead to oxidative stress, injury, inflammation, airway
epithelial damage and increased alveolar permeability to vascular
fluids. Inflammation can be accompanied by increased airway
responsiveness, which is an increased bronchoconstrictive response to
airway irritants and allergens. Continued respiratory inflammation also
can alter the ability of the body to respond to infectious agents,
allergens and toxins. Acute inflammatory responses to O3 in
some healthy people are well documented, and precursors to lung injury
are observed within 3 hours after exposure in humans. Repeated
respiratory inflammation can lead to a chronic inflammatory state with
altered lung structure and lung function and may lead to chronic
respiratory diseases such as fibrosis and emphysema (EPA, 2006a,
section 8.6.2). The severity of symptoms and magnitude of response to
acute exposures depend on inhaled dose, as well as on individual
susceptibility to O3, as discussed below. At the same
O3 dose, individuals who are more susceptible to
O3 will have a larger response than those who are less
susceptible; among individuals with similar susceptibility, those who
receive a larger dose will have a larger response to O3.
The inhaled dose is the product of O3 concentration (C),
minute ventilation or ventilation rate, and duration of exposure (T),
or (C x ventilation rate x T). A large body of data regarding the
interdependent effect of these components of inhaled dose on pulmonary
responses was assessed in the 1986 and 1996 O3 Criteria
Documents. In an attempt to describe O3 dose-response
characteristics, acute responses were modeled as a function of total
inhaled O3 dose, which was generally found to be a better
predictor of response than O3 concentration, ventilation
rate, or duration of exposure, alone, or as a combination of any two of
these factors (EPA 2006a, section 6.2). Predicted O3-induced
decrements in lung function have been shown to be a function of
exposure concentration, duration and exercise level for healthy, young
adults (McDonnell et al., 1997). A meta-analysis of 21 studies (Mudway
and Kelly, 2004) showed that markers of inflammation and increased
cellular permeability in healthy subjects are associated with total
O3 dose.
The 2006 Criteria Document summarizes information on potentially
susceptible and vulnerable groups in section 8.7. As described there,
the term susceptibility refers to innate (e.g., genetic or
developmental) or acquired (e.g., personal risk factors, age) factors
that make individuals more likely to experience effects with exposure
to pollutants. A number of population groups and lifestages have been
identified as potentially susceptible to health effects as a result of
O3 exposure, including people with existing lung diseases,
including asthma, children and older adults, and people who have larger
than normal lung function responses that may be due to genetic
susceptibility. In addition, some population groups and lifestages have
been identified as having increased vulnerability to O3-
related effects due to increased likelihood of exposure while at
elevated ventilation rates, including healthy children and adults who
are active outdoors, for example, outdoor workers, and joggers. Taken
together, the susceptible and vulnerable groups are more commonly
referred to as ``at-risk'' groups,\13\ as discussed more fully below in
section II.A.4.b.
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\13\ In previous Staff Papers and Federal Register notices
announcing proposed and final decisions on the O3 and
other NAAQS, EPA has used the phrase ``sensitive population groups''
to include both population groups that are at increased risk because
they are more intrinsically susceptible and population groups that
are more vulnerable due to an increased potential for exposure. In
this notice, we use the phrase, ``at risk'' populations to include
both types of population groups.
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[[Page 2948]]
Based on a substantial body of new evidence from animal, controlled
human exposure and epidemiological studies, the 2006 Criteria Document
concludes that people with asthma and other preexisting pulmonary
diseases are likely to be among those at increased risk from
O3 exposure. Altered physiological, morphological and
biochemical states typical of respiratory diseases like asthma, COPD
and chronic bronchitis may render people sensitive to additional
oxidative burden induced by O3 exposure (EPA 2006a, section
8.7). Children and adults with asthma are the group that has been
studied most extensively. Evidence from controlled human exposure
studies indicates that asthmatics may exhibit larger lung function
decrements in response to O3 exposure than healthy controls.
As discussed more fully in section II.A.4.b.ii below, asthmatics
present a differential response profile for cellular, molecular, and
biochemical parameters (EPA, 2006a, section 8.7.1) that are altered in
response to acute O3 exposure. They can have larger
inflammatory responses, as manifested by larger increases in markers of
inflammation such as white bloods cells (e.g., PMNs) or inflammatory
cytokines. Asthmatics, and people with allergic rhinitis, are more
likely to mount an allergic-type response upon exposure to
O3, as manifested by increases in white blood cells
associated with allergy (i.e., eosinophils) and related molecules,
which increase inflammation in the airways. The increased inflammatory
and allergic responses also may be associated with the larger late-
phase responses that asthmatics can experience, which can include
increased bronchoconstrictor responses to irritant substances or
allergens and additional inflammation. In addition to the experimental
evidence of lung function decrements, respiratory symptoms, and other
respiratory effects in asthmatic populations, two large U.S.
epidemiological studies as well as several smaller U.S. and
international studies, have reported fairly robust associations between
ambient O3 concentrations and measures of lung function and
daily symptoms (e.g., chest tightness, wheeze, shortness of breath) in
children with moderate to severe asthma and between O3 and
increased asthma medication use (EPA, 2007a, chapter 6). These
responses in asthmatics and others with lung disease provide biological
plausibility for the more serious respiratory morbidity effects
observed in epidemiological studies, such as emergency department
visits and hospital admissions.
Children with and without asthma were found to be particularly
susceptible to O3 effects on lung function and generally
have greater lung function responses than older people. The American
Academy of Pediatrics (2004) notes that children and infants are among
the population groups most susceptible to many air pollutants,
including O3. This is in part because their lungs are still
developing. For example, eighty percent of alveoli are formed after
birth, and changes in lung development continue through adolescence
(Dietert et al., 2000). Moreover, children have high minute ventilation
rates and relatively high levels of physical activity which also
increases their O3 dose (Plunkett et al., 1992). Thus,
children are at-risk due to both their susceptibility and
vulnerability.
Looking more broadly at age-related differences in susceptibility,
several mortality studies have investigated age-related differences in
O3 effects (EPA, 2006a, section 7.6.7.2), primarily in the
older adult population. Among the studies that observed positive
associations between O3 and mortality, a comparison of all
age or younger age (65 years of age) O3-mortality effect
estimates to that of the elderly population (>65 years) indicates that,
in general, the elderly population is more susceptible to O3
mortality effects. There is supporting evidence of age-related
differences in susceptibility to O3 lung function effects.
The 2006 Criteria Document (section 7.6.7.2) concludes that the elderly
population (>65 years of age) appear to be at greater risk of
O3-related mortality and hospitalizations compared to all
ages or younger populations, and children (<18 years of age) experience
other potentially adverse respiratory health outcomes with increased
O3 exposure.
Controlled human exposure studies have also indicated a high degree
of interindividual variability in some of the pulmonary physiological
parameters, such as lung function decrements. The variable effects in
individuals have been found to be reproducible, in other words, a
person who has a large lung function response after exposure to
O3 will likely have about the same response if exposed again
to the same dose of O3 (EPA 2006a, section 6.1). In
controlled human exposure studies, group mean responses are not
representative of this segment of the population that has much larger
than average responses to O3. Recent studies, discussed in
section II.A.4.b.iv below, reported a role for genetic polymorphism
(i.e., the occurrence together in the same population of more than one
allele or genetic marker at the same locus with the least frequent
allele or marker occurring more frequently than can be accounted for by
mutation alone) in observed differences in antioxidant enzymes and
genes involved in inflammation to modulate pulmonary function and
inflammatory responses to O3 exposure. These observations
suggest a potential role for these markers in the innate susceptibility
to O3, however, the validity of these markers and their
relevance in the context of prediction to population studies needs
additional experimentation.
Controlled human exposure studies that provide information about
mechanisms of the initial response to O3 (e.g., lung
function decrements, inflammation, and injury to the lung) also inform
the selection of appropriate lag times to analyze in epidemiological
studies through elucidation of the time course of these responses (EPA
2006a, section 8.4.3). Based on the results of these studies, it would
be reasonable to expect that lung function decrements could be detected
epidemiologically within lags of 0 (same day) or 1 to 2 days following
O3 exposure, given the rapid onset of lung function changes
and their persistence for 24 to 48 hours among more responsive human
subjects in controlled human exposure studies. Other responses take
longer to develop and can persist for longer periods of time. For
example, although asthmatic individuals may begin to experience
symptoms soon after O3 exposure, it may take anywhere from 1
to 3 days after exposure for these subjects to seek medical attention
as a result of increased airway responsiveness or inflammation that may
persist for 2 to 3 days. This may be reflected by epidemiologic
observations of significantly increased risk for asthma-related
emergency department visits or hospital admissions with 1- to 3-day
lags, or, perhaps, enhanced distributed lag risks (combined across 3
days) for such morbidity indicators. Analogously, one might project
increased mortality within 0- to 3-day lags as a possible consequence
of O3-induced increases in clotting agents arising from the
cascade of events, starting with cell injury described above, occurring
within 12 to 24 hours of O3 exposure. The time course for
many of these initial responses to O3 is highly variable.
[[Page 2949]]
Moreover these observations pertain only to the initial response to
O3. Consequent responses can follow. For example,
J[ouml]rres et al., (1996) found that in subjects with asthma and
allergic rhinitis, a maximum percent fall in FEV1 of 27.9%
and 7.8%, respectively, occurred 3 days after O3 exposure
when they were challenged with of the highest common dose of allergen.
2. Nature of Effects
The 2006 Criteria Document provides new evidence that notably
enhances our understanding of short-term and prolonged exposure
effects, including effects on lung function, symptoms, and inflammatory
effects reported in controlled exposure studies. These studies support
and extend the findings of the previous Criteria Document. There is
also a significant body of new epidemiological evidence of associations
between short-term and prolonged exposure to O3 and effects
such as premature mortality, hospital admissions and emergency
department visits for respiratory (e.g., asthma) causes. Key
epidemiological and controlled human exposure studies are summarized
below and discussed in chapter 3 of the 2007 Staff Paper, which is
based on scientific evidence critically reviewed in chapters 5, 6, and
7 of the 2006 Criteria Document, as well as the Criteria Document's
integration of scientific evidence contained in chapter 8.\14\
Conclusions drawn about O3-related health effects are based
upon the full body of evidence from controlled human exposure,
epidemiological and toxicological data contained in the 2006 Criteria
Document.
---------------------------------------------------------------------------
\14\ Health effects discussions are also drawn from the more
detailed information and tables presented in the Criteria Document's
annexes.
---------------------------------------------------------------------------
a. Morbidity
This section summarizes scientific information on the effects of
inhalation of O3, including public health effects of short-
term, prolonged, and long-term exposures on respiratory morbidity and
cardiovascular system effects, as discussed in chapters 6, 7 and 8 of
the 2006 Criteria Document and chapter 3 of the 2007 Staff Paper. This
section also summarizes the uncertainty about the potential indirect
effects on public health associated with changes due to increases in
UV-B radiation exposure, such as UV-B radiation-related skin cancers,
that may be associated with reductions in ambient levels of ground-
level O3, as discussed in chapter 10 of the 2006 Criteria
Document and chapter 3 of the 2007 Staff Paper.
i. Effects on the Respiratory System From Short-term and Prolonged
O3 Exposures
Controlled human exposure studies have shown that O3
induces a variety of health effects, including: Lung function
decrements, respiratory symptoms, increased airway responsiveness,
respiratory inflammation and permeability, increased susceptibility to
respiratory infection, and acute morphological effects. Epidemiology
studies have reported associations between O3 exposures
(i.e., 1-hour, 8-hour and 24-hour) and a wide range of respiratory-
related health effects including: pulmonary function decrements;
respiratory symptoms; increased asthma medication use; increased school
absences; increased emergency department visits and hospital
admissions.
(a) Pulmonary Function Decrements, Respiratory Symptoms, and Asthma
Medication Use
(i) Results From Controlled Human Exposure Studies
A large number of studies published prior to 1996 that investigated
short-term O3 exposure health effects on the respiratory
system from short-term O3 exposures were reviewed in the
1986 and 1996 Criteria Documents (EPA, 1986, 1996a). In the 1997
review, 0.50 ppm was the lowest O3 concentration at which
statistically significant reductions in forced vital capacity (FVC) and
forced expiratory volume in 1 second (FEV1) were reported in
sedentary subjects. During exercise, spirometric (lung function) and
symptomatic responses were observed at much lower O3
exposures. When minute ventilation was considerably increased by
continuous exercise (CE) during O3 exposures lasting 2 hour
or less at [gteqt] 0.12 ppm, healthy subjects generally experienced
decreases in FEV1, FVC, and other measures of lung function;
increases in specific airway resistance (sRaw), breathing frequency,
and airway responsiveness; and symptoms such as cough, pain on deep
inspiration, shortness of breath, throat irritation, and wheezing. When
exposures were increased to 4- to 8-hours in duration, statistically
significant lung function and symptom responses were reported at
O3 concentrations as low as 0.08 ppm and at lower minute
ventilation (i.e., moderate rather than high level exercise) than the
shorter duration studies.
The most important observations drawn from studies reviewed in the
1996 Criteria Document were that: (1) Young healthy adults exposed to
O3 concentrations = 0.080 ppm develop
significant, reversible, transient decrements in pulmonary function if
minute ventilation or duration of exposure is increased sufficiently;
(2) children experience similar lung function responses but report
lesser symptoms from O3 exposure relative to young adults;
(3) O3-induced lung function responses are decreased in the
elderly relative to young adults; (4) there is a large degree of
intersubject variability in physiological and symptomatic responses to
O3 but responses tend to be reproducible within a given
individual over a period of several months; (5) subjects exposed
repeatedly to O3 for several days show an attenuation of
response upon successive exposures, but this attenuation is lost after
about a week without exposure; and (6) acute O3 exposure
initiates an inflammatory response which may persist for at least 18 to
24 hours post exposure.
The development of these respiratory effects is time-dependent
during both exposure and recovery periods, with great overlap for
development and disappearance of the effects. In healthy human subjects
exposed to typical ambient O3 levels near 0.120 ppm, lung
function responses largely resolve within 4 to 6 hours postexposure,
but cellular effects persist for about 24 hours. In these healthy
subjects, small residual lung function effects are almost completely
gone within 24 hours, while in hyperresponsive subjects, recovery can
take as much as 48 hour to return to baseline. The majority of these
responses are attenuated after repeated consecutive exposures, but such
attenuation to O3 is lost one week postexposure.
Since 1996, there have been a number of studies published
investigating lung function and symptomatic responses that generally
support the observations previously drawn. Recent studies for acute
exposures of 1 to 2 hours and 6 to 8 hours in duration are compiled in
the 2007 Staff Paper (Appendix 3C). As summarized in more detail in the
2007 Staff Paper (section 3.3.1.1), among the more important of the
recent studies that examined changes in FEV1 in large
numbers of subjects over a range of 1-2 hours at exposure levels of
0.080 to 0.40 ppm were studies by McDonnell et al. (1997) and Ultman et
al. (2004). These studies observed considerable intersubject
variability in FEV1 decrements, which was consistent with
findings in the 1996 Criteria Document.
For prolonged exposures (4 to 8 hours) in the range of 0.080 to
0.160 ppm O3 using moderate intermittent
[[Page 2950]]
exercise and typically using square-wave exposure patterns (i.e., a
constant exposure level during time of exposure), several pre- and
post-1996 studies (Folinsbee et al., 1988,1994; Horstman et al., 1990;
Adams, 2002, 2003a, 2006) have reported statistically significant lung
function responses and increased symptoms in healthy adults with
increasing duration of exposure, O3 concentration, and
minute ventilation. Studies that employed triangular exposure patterns
(i.e., integrated exposures that begin at a low level, rise to a peak,
and return to a low level during the exposure) (Hazucha et al., 1992;
Adams 2003a, 2006) suggest that the triangular exposure pattern can
potentially lead to greater FEV1 decrements and respiratory
symptoms than square-wave exposures (when the overall O3
doses are equal). These results suggest that peak exposures, reflective
of the pattern of ambient O3 concentrations in some
locations, are important in terms of O3 health effects.
McDonnell (1996) used data from a series of studies to investigate
the frequency distributions of FEV1 decrements following 6.6
hour exposures and found statistically significant, but relatively
small, group mean decreases in average FEV1 responses
(between 5 and 10 percent) at 0.080 ppm O3.\15\ Notably,
about 26 percent of the 60 exposed subjects had lung function
decrements > 10 percent, including about 8 percent of the subjects that
experienced large decrements (> 20 percent) (EPA, 2007b, Figure 3-1A).
These results (which were not corrected for exercise in filtered air
responses) demonstrate that while average responses may be relatively
small at the 0.080 ppm exposure level, some individuals experience more
severe effects that may be clinically significant. Similar results at
the 0.080 ppm exposure level (for 6.6 hours during intermittent
exercise) were seen in more recent studies of 30 healthy young adults
by Adams (2002, 2006).\16\ In Adams (2006), relatively small but
statistically significant lung function decrements and respiratory
symptom responses were found (for both square-wave and triangular
exposure patterns), with 17 percent of the subjects (5 of 30)
experiencing [gteqt] 10 percent FEV1 decrements (comparing
pre- and post-exposures) when the results were not corrected for the
effects of exercise alone in filtered air (EPA, 2007b, Figure 3-1B) and
with 23 percent of subjects (7 of 30) experiencing such effects when
the results were corrected (EPA, 2007b, p. 3-6).\17\
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\15\ This study and other studies (Folinsbee et al., 1988;
Horstman et al., 1990; and McDonnell et al., 1991), conducted in
EPA's human studies research facility in Chapel Hill, NC, measured
ozone concentrations to within +/- 5 percent or +/- 0.004 ppm at the
0.080 ppm exposure level.
\16\ These studies, conducted at a facility at the University of
California, in Davis, CA, reported O3 concentrations to
be accurate within +/- 0.003 ppm over the range of concentrations
included in these studies.
\17\ These distributional results presented in the Criteria
Document and Staff Paper for the Adams (2006) study are based on
data for squate-wave exposures to 0.080 ppm that were not included
in the publication but were obtained from the author.
---------------------------------------------------------------------------
These studies by Adams (2002, 2006) were notable in that they were
the only controlled exposure human studies available at the time of the
2008 rulemaking that examined respiratory effects associated with
prolonged O3 exposures at levels below 0.080 ppm, which was
the lowest exposure level that had been examined in the 1997 review.
The Adams (2006) study investigated a range of exposure levels (0.000,
0.040, 0.060, and 0.080 ppm O3) using square-wave and
triangular exposure patterns. The study was designed to examine hour-
by-hour changes in pulmonary function (FEV1) and respiratory
symptom responses (total subjective symptoms (TSS) and pain on deep
inspiration (PDI)) between these various exposure protocols at six
different time points within the exposure periods to investigate the
effects of different patterns of exposure. At the 0.060 ppm exposure
level, the author reported no statistically significant differences for
FEV1 decrements nor for most respiratory symptoms responses.
Statistically significant responses were reported only for TSS for the
triangular exposure pattern toward the end of the exposure period, with
the PDI responses being noted as following a closely similar pattern
(Adams, 2006, p. 131-132). EPA's reanalysis of the data from the Adams
(2006) study addressed the more fundamental question of whether there
were statistically significant differences in responses before and
after the 6.6 hour exposure period (Brown, 2007), and used a standard
statistical method appropriate for a simple before-and-after
comparison. The statistical method used by EPA had been used previously
by other researchers to address this same question. EPA's reanalysis of
the data from the Adams (2006) study, comparing FEV1
responses pre- and post-exposure at the 0.060 ppm exposure level, found
small group mean differences from responses to filtered air that were
statistically significant (Brown, 2007).\18\
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\18\ Dr. Adams submitted comments on EPA's reanalysis in which
he concluded that the FEV1 response in healthy young
adults at the 0.060 ppm exposure level in his study (Adams, 2006a)
does not demonstrate a significant mean effect by ordinarily
acceptable statistical analysis, but is rather in somewhat of a gray
area, both in terms of a biologically meaningful response and a
statistically significant response (Adams, 2007). The EPA responded
to these comments in the 2008 final rule (73 FR 16455) and in the
Response to Comments (EPA, 2008, pp. 26-28).
---------------------------------------------------------------------------
Further examination of the post-exposure FEV1 data and
mean data at other time points and concentrations also suggest a
pattern of response at 0.06 ppm that is consistent with a dose-response
relationship rather than random variability. For example, the response
at 5.6 hours was similar to that of the post-exposure 6.6 hour response
and appeared to also differ from the FA response. At the 0.08 ppm
level, the subjects in this study did not appear to be more responsive
to O3 than subjects in previous studies, as the observed
response was similar to that of previous studies (Adams, 2003a,b;
Horstman et al., 1990; McDonnell et al., 1991). Although of much
smaller magnitude, the temporal pattern of the 0.06 ppm response was
generally consistent with the temporal patterns of response to higher
concentrations of O3 in this and other studies. These
findings are not unexpected because the previously observed group mean
FEV1 responses to 0.08 ppm were in the range of 6-9%
suggesting that exposure to lower concentrations of O3 would
result in smaller, but real group mean FEV1 decrements,
i.e., the responses to 0.060 ppm O3 are consistent with the
presence of a smooth exposure-response curve with responses that do not
end abruptly below 0.080 ppm.
Moreover, the Adams studies (2002, 2006) also report a small
percentage of subjects experiencing moderate lung function decrements
([gteqt] 10 percent) at the 0.060 ppm exposure level. Based on study
data (Adams, 2006) provided by the author, 7 percent of the subjects (2
of 30 subjects) experienced notable FEV1 decrements (>= 10
percent) with the square wave exposure pattern at the 0.060 ppm
exposure level (comparing pre- and post-exposures) when the results
were corrected for the effects of exercise alone in filtered air (EPA,
2007b, p. 3-6). Furthermore, in a prior publication (Adams, 2002), the
author stated that, ``some sensitive subjects experience notable
effects at 0.06 ppm,'' based on the observation that 20% of subjects
exposed to 0.06 ppm O3 (in a face mask exposure study) had
greater than a 10% decrement in FEV1 even though the group
mean response was not statistically different from the filtered air
response. The effects described by Adams (2002), along with
[[Page 2951]]
the reanalysis of the Adams (2006) data as described above, demonstrate
considerable inter-individual variability in responses of healthy
adults at the 0.060 ppm level with some individuals experiencing
greater than 10% decrements in FEV1. The observation of
statistically significant small group mean lung function decrements in
healthy adults at 0.060 ppm O3 lowers the lowest-observed-
effects level found in controlled human exposure studies for lung
function decrements and respiratory symptoms.
Of potentially greater concern is the magnitude of the lung
function decrements in the small group of healthy subjects who had the
largest responses (i.e., FEV1 decrements [gteqt] 10%). This
is a concern because for active healthy people, moderate levels of
functional responses (e.g., FEV1 decrements of [gteqt] 10%
but < 20%) and/or moderate symptomatic responses would likely interfere
with normal activity for relatively few responsive individuals.
However, for people with lung disease, even moderate functional or
symptomatic responses would likely interfere with normal activity for
many individuals, and would likely result in more frequent use of
medication (see section II.A.4 below).
(ii) Results of Epidemiological and Field Studies
A relatively large number of field studies investigating the
effects of ambient O3 concentrations, in combination with
other air pollutants, on lung function decrements and respiratory
symptoms has been published over the last decade that support the major
findings of the 1996 Criteria Document that lung function changes, as
measured by decrements in FEV1 or peak expiratory flow
(PEF), and respiratory symptoms in healthy adults and asthmatic
children are closely correlated to ambient O3
concentrations. Pre-1996 field studies focused primarily on children
attending summer camps and found O3-related impacts on
measures of lung function, but not respiratory symptoms, in healthy
children. The newer studies have expanded to evaluate O3-
related effects on outdoor workers, athletes, the elderly, hikers,
school children, and asthmatics. Collectively, these studies confirm
and extend clinical observations that prolonged (i.e., 6-8 hour)
exposure periods, combined with elevated levels of exertion or
exercise, increase the dose of O3 to the lungs at a given
ambient exposure level and result in larger lung function effects. The
results of one large study of hikers (Korrick et al., 1998), which
reported outcome measures stratified by several factors (e.g., gender,
age, smoking status, presence of asthma) within a population capable of
more than normal exertion, provide useful insight. In this study, lung
function was measured before and after hiking, and individual
O3 exposures were estimated by averaging hourly
O3 concentrations from ambient monitors located at the base
and summit. The mean 8-hour average O3 concentration was
0.040 ppm (8-hour average concentration range of 0.021 ppm to 0.074 ppm
O3). Decreased lung function was associated with
O3 exposure, with the greatest effect estimates reported for
the subgroup that reported having asthma or wheezing, and for those who
hiked for longer periods of time.
Asthma panel studies conducted both in the U.S. and in other
countries have reported that decrements in PEF are associated with
routine O3 exposures among asthmatic and healthy people. One
large U.S. multicity study, the National Cooperative Inner City Asthma
Study or NCICAS, (Mortimer et al., 2002) examined O3-related
changes in PEF in 846 asthmatic children from 8 urban areas and
reported that the incidence of [gteqt] 10 percent decrements in morning
PEF are associated with increases in 8-hour average O3 for a
5-day cumulative lag, suggesting that O3 exposure may be
associated with clinically significant changes in PEF in asthmatic
children; however, no associations were reported with evening PEF. The
mean 8-hour average O3 was 0.048 ppm across the 8 cities.
Excluding days when 8-hour average O3 was greater than 0.080
ppm (less than 5 percent of days), the associations with morning PEF
remained statistically significant. Mortimer et al. (2002) discussed
potential biological mechanisms for delayed effects on pulmonary
function in asthma, which included increased nonspecific airway
responsiveness secondary to airway inflammation due to O3
exposure. Two other panel studies (Romieu et al., 1996, 1997) carried
out simultaneously in northern and southwestern Mexico City with mildly
asthmatic school children reported statistically significant
O3-related reductions in PEF, with variations in effect
depending on lag time and time of day. Mean 1-hour maximum
O3 concentrations in these locations ranged from 0.190 ppm
in northern Mexico City to 0.196 ppm in southwestern Mexico City. While
several studies report statistically significant associations between
O3 exposure and reduced PEF in asthmatics, other studies did
not, possibly due to low levels of O3 exposure. EPA
concludes that these studies collectively indicate that O3
may be associated with short-term declines in lung function in
asthmatic individuals and that the Mortimer et al. (2002) study showed
statistically significant effects at concentrations in the range below
0.080 ppm O3.
Most of the panel studies which have investigated associations
between O3 exposure and respiratory symptoms or increased
use of asthma medication are focused on asthmatic children. Two large
U.S. studies (Mortimer et al., 2002; Gent et al., 2003) have reported
associations between ambient O3 concentrations and daily
symptoms/asthma medication use, even after adjustment for copollutants.
Results were more mixed, meaning that a greater proportion of studies
were not both positive and statistically significant, across smaller
U.S. and international studies that focused on these health endpoints.
The NCICAS reported morning symptoms in 846 asthmatic children from
8 U.S. urban areas to be most strongly associated with a cumulative 1-
to 4-day lag of O3 concentrations (Mortimer et al., 2002).
The NCICAS used standard protocols that included instructing caretakers
of the subjects to record symptoms (including cough, chest tightness,
and wheeze) in the daily diary by observing or asking the child. While
these associations were not statistically significant in several
cities, when the individual data are pooled from all eight cities,
statistically significant effects were observed for the incidence of
symptoms. The authors also reported that the odds ratios remained
essentially the same and statistically significant for the incidence of
morning symptoms when days with 8-hour O3 concentrations
above 0.080 ppm were excluded. These days represented less than 5
percent of days in the study.
Gent and colleagues (2003) followed 271 asthmatic children under
age 12 and living in southern New England for 6 months (April through
September) using a daily symptom diary. They found that mean 1-hour max
O3 and 8-hour max O3 concentrations were 0.0586
ppm and 0.0513 ppm, respectively. The data were analyzed for two
separate groups of subjects, those who used maintenance asthma
medications during the follow-up period and those who did not. The need
for regular medication was considered to be a proxy for more severe
asthma. Not taking any medication on a regular basis and not needing to
use a bronchodilator would suggest the
[[Page 2952]]
presence of very mild asthma. Statistically significant effects of 1-
day lag O3 were observed on a variety of respiratory
symptoms only in the medication user group. Both daily 1-hour max and
8-hour max O3 concentrations were similarly related to
symptoms such as chest tightness and shortness of breath. Effects of
O3, but not PM2.5, remained significant and even
increased in magnitude in two-pollutant models. Some of the
associations were noted at 1-hour max O3 levels below 0.060
ppm. In contrast, no effects were observed among asthmatics not using
maintenance medication. In terms of person-days of follow-up, this is
one of the larger studies currently available that address symptom
outcomes in relation to O3 and provides supportive evidence
for effects of O3 independent of PM2.5. Study
limitations include the post-hoc nature of the population
stratification by medication use. Also, the study did not account for
all of the important meteorological factors that might influence these
results, such as relative humidity or dew point.
The multicity study by Mortimer et al. (2002), which examined an
asthmatic population representative of the United States, and several
single-city studies indicate a robust association of O3
concentrations with respiratory symptoms and increased medication use
in asthmatics. While there are a number of well-conducted, albeit
relatively smaller, U.S. studies which showed only limited or a lack of
evidence for symptom increases associated with O3 exposure,
these studies had less statistical power and/or were conducted in areas
with relatively low 1-hour maximum average O3 levels, in the
range of 0.03 to 0.09 ppm. The 2006 Criteria Document concludes that
the asthma panel studies, as a group, and the NCICAS in particular,
indicate a positive association between ambient concentrations and
respiratory symptoms and increased medication use in asthmatics. The
evidence has continued to expand since 1996 and now is considered to be
much stronger than in the 1997 review of the O3 primary
standard.
School absenteeism is another potential surrogate for the health
implications of O3 exposure in children. The association
between school absenteeism and ambient O3 concentrations was
assessed in two relatively large field studies. The first study, Chen
et al. (2000), examined total daily school absenteeism in about 28,000
elementary school students in Nevada over a 2-year period (after
adjusting for PM10 and CO concentrations) and found that
ambient O3 concentrations with a distributed lag of 14 days
were statistically significantly associated with an increased rate of
school absences. The second study, Gilliland et al. (2001), studied
O3-related absences among about 2,000 4th grade students in
12 southern California communities and found statistically significant
associations between 8-hour average O3 concentrations (with
a distributed lag out to 30 days) and all absence categories, and
particularly for respiratory causes. Neither PM10 nor
NO2 were associated with any respiratory or nonrespiratory
illness-related absences in single pollutant models. The 2006 Criteria
Document concludes that these studies of school absences suggest that
ambient O3 concentrations, accumulated over two to four
weeks, may be associated with school absenteeism, and particularly
illness-related absences, but further replication is needed before firm
conclusions can be reached regarding the effect of O3 on
school absences. In addition, more research is needed to help shed
light on the implications of variation in the duration of the lag
structures (i.e., 1 day, 5 days, 14 days, and 30 days) found both
across studies and within data sets by health endpoint and exposure
metric.
(b) Increased Airway Responsiveness
As discussed in more detail in the 2006 Criteria Document (section
6.8) and the 2007 Staff Paper (section 3.3.1.1.2), increased airway
responsiveness, also known as airway hyperresponsiveness (AHR) or
bronchial hyperreactivity, refers to a condition in which the
propensity for the airways to bronchoconstrict due to a variety of
stimuli (e.g., exposure to cold air, allergens, or exercise) becomes
augmented. This condition is typically quantified by measuring the
decrement in pulmonary function after inhalation exposure to specific
(e.g., antigen, allergen) or nonspecific (e.g., methacholine,
histamine) bronchoconstrictor stimuli. Exposure to O3 causes
an increase in airway responsiveness as indicated by a reduction in the
concentration of stimuli required to produce a given reduction in
FEV1 or increase in airway obstruction. Increased airway
responsiveness is an important consequence of exposure to O3
because its presence means that the airways are predisposed to
narrowing on exposure to various stimuli, such as specific allergens,
cold air or SO2. Statistically significant and clinically
relevant decreases in pulmonary function have been observed in early
phase allergen response in subjects with allergic rhinitis after
consecutive (4-day) 3-hour exposures to 0.125 ppm O3 (Holz
et al., 2002). Similar increased airway responsiveness in asthmatics to
house dust mite antigen 16 to 18 hours after exposure to a single dose
of O3 (0.160 ppm for 7.6 hours) was observed. These
observations, based on O3 exposures to levels much higher
than the 0.084 ppm standard level suggest that O3 exposure
may be a clinically important factor that can exacerbate the response
to ambient bronchoconstrictor substances in individuals with
preexisting allergic asthma or rhinitis. Further, O3 may
have an immediate impact on the lung function of asthmatics as well as
contribute to effects that persist for longer periods.
Kreit et al. (1989) found that O3 can induce increased
airway responsiveness in asthmatic subjects to O3, who
typically have increased airway responsiveness at baseline. A
subsequent study (J[ouml]rres et al., 1996) suggested an increase in
specific (i.e., allergen-induced) airway reactivity in subjects with
allergic asthma, and to a lesser extent in subjects with allergic
rhinitis after short-term exposure to higher O3 levels;
other studies reported similar results. According to one study
(Folinsbee and Hazucha, 2000), changes in airway responsiveness after
O3 exposure resolve more slowly than changes in
FEV1 or respiratory symptoms. Other studies of repeated
exposure to O3 suggest that changes in airway responsiveness
tend to be somewhat less affected by attenuation with consecutive
exposures than changes in FEV1 (EPA, 2006a, section 6.8).
The 2006 Criteria Document (section 6.8) concludes that
O3 exposure is linked with increased airway responsiveness.
Both human and animal studies indicate that increased airway
responsiveness is not mechanistically associated with inflammation, and
does not appear to be strongly associated with initial decrements in
lung function or increases in symptoms. As a result of increased airway
responsiveness induced by O3 exposure, human airways may be
more susceptible to a variety of stimuli, including antigens,
chemicals, and particles. Because asthmatic subjects typically have
increased airway responsiveness at baseline, enhanced bronchial
response to antigens in asthmatics raises potential public health
concerns as they could lead to increased morbidity (e.g., medication
usage, school absences, emergency room visits, hospital admissions) or
to more persistent alterations in airway
[[Page 2953]]
responsiveness (EPA 2006a, p. 8-21). As such, increased airway
responsiveness after O3 exposure represents a plausible link
between O3 exposure and increased hospital admissions.
(c) Respiratory Inflammation and Increased Permeability
Based on evidence from the 1997 review, acute inflammatory
responses in the lung have been observed subsequent to 6.6 hour
O3 exposures to the lowest tested level--0.080 ppm--in
healthy adults engaged in moderately high exercise (section 6.9 of the
2006 Criteria Document and section 3.3.1.3 of the 2007 Staff Paper).
Some of these prior studies suggest that inflammatory responses may be
detected in some individuals following O3 exposures in the
absence of O3-induced pulmonary decrements in those
subjects. These studies also demonstrate that short-term exposures to
O3 also can cause increased permeability in the lungs of
humans and experimental animals. Inflammatory responses and epithelial
permeability have been seen to be independent of spirometric responses.
Not only are the newer lung inflammation and increased cellular
permeability findings discussed in the 2006 Criteria Document (section
8.4.2) consistent with the 1997 review, but they provide better
characterization of the physiological mechanisms by which O3
causes these effects.
Lung inflammation and increased permeability, which are distinct
events controlled by different mechanisms, are two commonly observed
effects of O3 exposure observed in all of the species
studied. Increased cellular permeability is a disruption of the lung
barrier that leads to leakage of serum proteins, influx of
polymorphonuclear leukocytes (neutrophils or PMNs), release of
bioactive mediators, and movement of compounds from the airspaces into
the blood.
A number of controlled human exposure studies have analyzed
bronchoalveolar lavage (BAL) and nasal lavage (NL) \19\ fluids and
cells for markers of inflammation and lung damage (EPA, 2006a, Annex
AX6). Increased lung inflammation is demonstrated by the presence of
neutrophils found in BAL fluid in the lungs, which has long been
accepted as a hallmark of inflammation. It is apparent, however, that
inflammation within airway tissues may persist beyond the point that
inflammatory cells are found in the BAL fluid. Soluble mediators of
inflammation, such as cytokines and arachidonic acid metabolites have
been measured in the BAL fluid of humans exposed to O3. In
addition to their role in inflammation, many of these compounds have
bronchoconstrictive properties and may be involved in increased airway
responsiveness following O3 exposure. An in vitro study of
epithelial cells from nonatopic and atopic asthmatics exposed to 0.010
to 0.100 ppm O3 showed significantly increased permeability
compared to cells from normal persons. This indicates a potentially
inherent susceptibility of cells from asthmatic individuals for
O3-induced permeability.
---------------------------------------------------------------------------
\19\ Graham and Koren (1990) compared inflammatory mediators
present in NL and BAL fluids of humans exposed to 0.4 ppm
O3 for 2 hours and found similar increases in PMNs in
both fluids, suggesting a qualitative correlation between
inflammatory changes in the lower airways (BAL) and upper
respiratory tract (NL).
---------------------------------------------------------------------------
In the 1996 Criteria Document, assessment of controlled human
exposure studies indicated that a single, acute (1 to 4 hours)
O3 exposure (>= 0.080 to 0.100 ppm) of subjects engaged in
moderate to heavy exercise could induce a number of cellular and
biochemical changes suggestive of pulmonary inflammation and lung
permeability (EPA, 2006a, p. 8-22). These changes persisted for at
least 18 hours. Markers from BAL fluid following both 2-hour and 4-hour
O3 exposures repeated up to 5 days indicate that there is
ongoing cellular damage irrespective of attenuation of some cellular
inflammatory responses of the airways, pulmonary function, and symptom
scores (EPA, 2006a, p. 8-22). Acute airway inflammation was shown in
Devlin et al. (1990) to occur among adults exposed to 0.080 ppm
O3 for 6.6 hours with exercise. McBride et al. (1994)
reported that asthmatic subjects were more sensitive than non-
asthmatics to upper airway inflammation for O3 exposures
that did not affect pulmonary function (EPA, 2006a, p. 6-33). However,
the public health significance of these changes is not entirely clear.
The studies reporting inflammatory responses and markers of lung
injury have clearly demonstrated that there is significant variation in
response of subjects exposed, especially to 6.6 hours O3
exposures at 0.080 and 0.100 ppm. To provide some perspective on the
public health impact for these effects, the 2007 Staff Paper (section
3.3.1.1.3) notes that one study (Devlin et al., 1991) showed that
roughly 10 to 50 percent of the 18 young healthy adult subjects
experienced notable increases (i.e., >= 2 fold increase) in most of the
inflammatory and cellular injury indicators analyzed, associated with
6.6-hour exposures at 0.080 ppm. Similar, although in some cases
higher, fractions of the population of 10 healthy adults tested saw > 2
fold increases associated with 6.6-hour exposures to 0.100 ppm. The
authors of this study expressed the view that ``susceptible
subpopulations such as the very young, elderly, and people with
pulmonary impairment or disease may be even more affected'' (Devlin et
al., 1991).
Since 1996, a substantial number of human exposure studies have
been published which have provided important new information on lung
inflammation and epithelial permeability. Mudway and Kelly (2004)
examined O3-induced inflammatory responses and epithelial
permeability with a meta-analysis of 21 controlled human exposure
studies and showed that an influx in neutrophils and protein in healthy
subjects is associated with total O3 dose (product of
O3 concentration, exposure duration, and minute ventilation)
(EPA, 2006a, p. 6-34). Results of the analysis suggest that the time
course for inflammatory responses (including recruitment of neutrophils
and other soluble mediators) is not clearly established, but there is
evidence that attenuation profiles for many of these parameters are
different (EPA, 2006a, p. 8-22).
The 2006 Criteria Document (chapter 8) concludes that interaction
of O3 with lipid constituents of epithelial lining fluid
(ELF) and cell membranes and the induction of oxidative stress is
implicated in injury and inflammation. Alterations in the expression of
cytokines, chemokines, and adhesion molecules, indicative of an ongoing
oxidative stress response, as well as injury repair and regeneration
processes, have been reported in animal toxicology and human in vitro
studies evaluating biochemical mediators implicated in injury and
inflammation. While antioxidants in ELF confer some protection,
O3 reactivity is not eliminated at environmentally relevant
exposures (2006 Criteria Document, p. 8-24). Further, antioxidant
reactivity with O3 is both species-specific and dose-
dependent.
(d) Increased Susceptibility to Respiratory Infection
As discussed in more detail in the 2006 Criteria Document (sections
5.2.2, 6.9.6, and 8.4.2), short-term exposures to O3 have
been shown to impair physiological defense capabilities in experimental
animals by depressing alveolar macrophage (AM) functions and by
altering the mucociliary clearance of inhaled particles and microbes
resulting in increased susceptibility to respiratory infection.
[[Page 2954]]
Short-term O3 exposures also interfere with the clearance
process by accelerating clearance for low doses and slowing clearance
for high doses. Animal toxicological studies have reported that acute
O3 exposures suppress alveolar phagocytosis and immune
system functions. Impairment of host defenses and subsequent increased
susceptibility to bacterial lung infection in laboratory animals has
been induced by short-term exposures to O3 levels as low as
0.080 ppm.
A single controlled human exposure study reviewed in the 1996
Criteria Document (p. 8-26) reported that exposure to 0.080 to 0.100
ppm O3 for 6.6 hours (with moderate exercise) induced
decrements in the ability of AMs to phagocytose microorganisms.
Integrating the recent animal study results with human exposure
evidence available in the 1996 Criteria Document, the 2006 Criteria
Document concludes that available evidence indicates that short-term
O3 exposures have the potential to impair host defenses in
humans, primarily by interfering with AM function. Any impairment in AM
function may lead to decreased clearance of microorganisms or nonviable
particles. Compromised AM functions in asthmatics may increase their
susceptibility to other O3 effects, the effects of
particles, and respiratory infections (EPA, 2006a, p. 8-26).
(e) Morphological Effects
The 1996 Criteria Document found that short-term O3
exposures cause similar alterations in lung morphology in all
laboratory animal species studied, including primates. As discussed in
the 2007 Staff Paper (section 3.3.1.1.5), cells in the centriacinar
region (CAR) of the lung (the segment between the last conducting
airway and the gas exchange region) have been recognized as a primary
target of O3-induced damage (epithelial cell necrosis and
remodeling of respiratory bronchioles), possibly because epithelium in
this region receives the greatest dose of O3 delivered to
the lower respiratory tract. Following chronic O3 exposure,
structural changes have been observed in the CAR, the region typically
affected in most chronic airway diseases of the human lung (EPA, 2006a,
p. 8-24).
Ciliated cells in the nasal cavity and airways, as well as Type I
cells in the gas-exchange region, are also identified as targets. While
short-term O3 exposures can cause epithelial cell
profileration and fibrolitic changes in the CAR, these changes appear
to be transient with recovery occurring after exposure, depending on
species and O3 dose. The potential impacts of repeated
short-term and chronic morphological effects of O3 exposure
are discussed below in the section on effects from long-term exposures.
Long-term or prolonged exposure has been found to cause chronic lesions
similar to early lesions found in individuals with respiratory
bronchiolitis, which have the potential to progress to fibrotic lung
disease (2006 Criteria Document, p. 8-25).
Recent studies continue to show that short-term and sub-chronic
exposures to O3 cause similar alterations in lung structure
in a variety of experimental animal species. For example, a series of
new studies that used infant rhesus monkeys and simulated seasonal
ambient exposure (0.5 ppm 8 hours/day for 5 days, every 14 days for 11
episodes) reported remodeling in the distal airways; abnormalities in
tracheal basement membrane; eosinophil accumulation in conducting
airways; and decrements in airway innervation (2006 Criteria Document,
p. 8-25). Based on evidence from animal toxicological studies, short-
term and sub-chronic exposures to O3 can cause morphological
changes in the respiratory systems, particularly in the CAR, of a
number of laboratory animal species (EPA, 2006a, section 5.2.4).
(f) Emergency Department Visits/Hospital Admissions for Respiratory
Causes
Increased summertime emergency department visits and hospital
admissions for respiratory causes have been associated with ambient
exposures to O3. As discussed in section 3.3.1.1.6 of the
2007 Staff Paper, numerous studies conducted in various locations in
the U.S. and Canada consistently have shown a relationship between
ambient O3 levels and increased incidence of emergency
department visits and hospital admissions for respiratory causes, even
after controlling for modifying factors, such as weather and
copollutants. Such associations between elevated ambient O3
during summer months and increased hospital admissions have a plausible
biological basis in the human and animal evidence of functional,
symptomatic, and physiologic effects discussed above and in the
increased susceptibility to respiratory infections observed in
laboratory animals.
In the 1997 review of the O3 NAAQS, the Criteria
Document evaluated emergency department visits and hospital admissions
as possible outcomes following exposure to O3 (EPA, 2006a,
section 7.3). The evidence was limited for emergency department visits,
but results of several studies generally indicated that short-term
exposures to O3 were associated with respiratory emergency
department visits. The strongest and most consistent evidence, at both
lower levels (i.e., below 0.120 ppm 1-hour max O3) and at
higher levels (above 0.120 ppm 1-hour max O3), was found in
the group of studies which investigated summertime \20\ daily hospital
admissions for respiratory causes in different eastern North American
cities. These studies consistently demonstrated that ambient
O3 levels were associated with increased hospital admissions
and accounted for about one to three excess respiratory hospital
admissions per million persons with each 0.100 ppm increase in 1-hour
max O3, after adjustment for possible confounding effects of
temperature and copollutants. Overall, the 1996 Criteria Document
concluded that there was strong evidence that ambient O3
exposures can cause significant exacerbations of preexisting
respiratory disease in the general public. Excess respiratory-related
hospital admissions associated with O3 exposures for the New
York City area (based on Thurston et al., 1992) were included in the
quantitative risk assessment in the 1997 review and are included in the
current assessment along with estimates for respiratory-related
hospital admissions in Cleveland, Detroit, and Los Angeles based on
more recent studies (2007 Staff Paper, chapter 5). Significant
uncertainties and the difficulty of obtaining reliable baseline
incidence numbers resulted in emergency department visits not being
used in the quantitative risk assessment in either the 1997 or the 2008
O3 NAAQS review.
---------------------------------------------------------------------------
\20\ Discussion of the reasons for focusing on warm season
studies is found in the section 2.A.3.a below.
---------------------------------------------------------------------------
In the past decade, a number of studies have examined the temporal
pattern associations between O3 exposures and emergency
department visits for respiratory causes (EPA, 2006a, section 7.3.2).
These studies are summarized in the 2006 Criteria Document (chapter 7
Annex) and some are shown in Figure 1 (in section II.A.3). Respiratory
causes for emergency department visits include asthma, bronchitis,
emphysema, pneumonia, and other upper and lower respiratory infections,
such as influenza, but asthma visits typically dominate the daily
incidence counts. Most studies report positive associations with
O3. Among studies with adequate controls for seasonal
patterns, many reported at least one significant positive association
involving O3.
[[Page 2955]]
In reviewing evidence for associations between emergency department
visits for asthma and short-term O3 exposures, the 2006
Criteria Document (Figure 7-8, p. 7-68) notes that in general,
O3 effect estimates from summer only analyses tended to be
positive and larger compared to results from cool season or all year
analyses. Several of the studies reported significant associations
between O3 concentrations and emergency department visits
for respiratory causes, in particular asthma. However, inconsistencies
were observed which were at least partially attributable to differences
in model specifications and analysis approach among various studies.
For example, ambient O3 concentrations, length of the study
period, and statistical methods used to control confounding by seasonal
patterns and copollutants appear to affect the observed O3
effect on emergency department visits.
Hospital admissions studies focus specifically on unscheduled
admissions because unscheduled hospital admissions occur in response to
unanticipated disease exacerbations and are more likely than scheduled
admissions to be affected by variations in environmental factors, such
as daily O3 levels. Results of a fairly large number of
these studies published during the past decade are summarized in 2006
Criteria Document (chapter 7 Annex), and results of U.S. and Canadian
studies are shown in Figure 1 below (in section II.A.3). As a group,
these hospital admissions studies tend to be larger geographically and
temporally than the emergency department visit studies and provide
results that are generally more consistent. The strongest associations
of respiratory hospital admissions with O3 concentrations
were observed using short lag periods, in particular for a 0-day lag
(same day exposure) and a 1-day lag (previous day exposure). Most
studies in the United States and Canada indicated positive,
statistically significant associations between ambient O3
concentrations and respiratory hospital admissions in the warm season.
However, not all studies found a statistically significant relationship
with O3, possibly because of very low ambient O3
levels. Analyses for confounding using multipollutant regression models
suggest that copollutants generally do not confound the association
between O3 and respiratory hospitalizations. Ozone effect
estimates were robust to PM adjustment in all-year and warm-season only
data.
Overall, the 2006 Criteria Document concludes that positive and
robust associations were found between ambient O3
concentrations and various respiratory disease hospitalization
outcomes, when focusing particularly on results of warm-season
analyses. Recent studies also generally indicate a positive association
between O3 concentrations and emergency department visits
for asthma during the warm season (EPA, 2006a, p. 7-175). These
positive and robust associations are supported by the controlled human
exposure, animal toxicological, and epidemiological evidence for lung
function decrements, increased respiratory symptoms, airway
inflammation, and increased airway responsiveness. Taken together, the
overall evidence supports a causal relationship between acute ambient
O3 exposures and increased respiratory morbidity outcomes
resulting in increased emergency department visits and hospitalizations
during the warm season (EPA, 2006a, p. 8-77).
ii. Effects on the Respiratory System of Long-Term O3
Exposures
The 1996 Criteria Document concluded that there was insufficient
evidence from the limited number of studies to determine whether long-
term O3 exposures resulted in chronic health effects at
ambient levels observed in the U.S. However, the aggregate evidence
suggested that O3 exposure, along with other environmental
factors, could be responsible for health effects in exposed
populations. Animal toxicological studies carried out in the 1980's and
1990's demonstrated that long-term exposures can result in a variety of
morphological effects, including permanent changes in the small airways
of the lungs, including remodeling of the distal airways and CAR and
deposition of collagen, possibly representing fibrotic changes. These
changes result from the damage and repair processes that occur with
repeated exposure. Fibrotic changes were also found to persist after
months of exposure providing a potential pathophysiologic basis for
changes in airway function observed in children in some recent
epidemiological studies. It appears that variable seasonal ambient
patterns of exposure may be of greater concern than continuous daily
exposures.
Several studies published since 1996 have investigated lung
function changes over seasonal time periods (EPA, 2006a, section
7.5.3). The 2006 Criteria Document (p. 7-114) summarizes these studies
which collectively indicate that seasonal O3 exposure is
associated with smaller growth-related increases in lung function in
children than they would have experienced living in areas with lower
O3 levels. There is some limited evidence that seasonal
O3 also may affect lung function growth in young adults,
although the uncertainty about the role of copollutants makes it
difficult to attribute the effects to O3 alone.
Lung capacity grows during childhood and adolescence as body size
increases, reaches a maximum during the twenties, and then begins to
decline steadily and progressively with age. Long-term exposure to air
pollution has long been thought to contribute to slower growth in lung
capacity, diminished maximally attained capacity, and/or more rapid
decline in lung capacity with age (EPA, 2006a, section 7.5.4).
Toxicological findings evaluated in the 1996 Criteria Document
demonstrated that repeated daily exposure of rats to an episodic
profile of O3 caused small, but significant, decrements in
growth-related lung function that were consistent with early indicators
of focal fibrogenesis in the proximal alveolar region, without overt
fibrosis. Because O3 at sufficient concentrations is a
strong respiratory irritant and has been shown to cause inflammation
and restructuring of the respiratory airways, it is plausible that
long-term O3 exposures might have a negative impact on
baseline lung function, particularly during childhood when these
exposures might be associated with long-term risks.
Several epidemiological studies published since 1996 have examined
the relationship between lung function development and long-term
O3 exposure. The most extensive and robust study of
respiratory effects in relation to long-term air pollution exposures
among children in the U.S. is the Children's Health Study carried out
in 12 communities of southern California starting in 1993. One analysis
(Peters et al., 1999a) examined the relationship between long-term
O3 exposures and self-reports of respiratory symptoms and
asthma in a cross sectional analysis and found a limited relationship
between outcomes of current asthma, bronchitis, cough and wheeze and a
0.040 ppm increase in 1-hour max O3 (EPA, 2006a, p. 7-115).
Another analysis (Peters et al., 1999b) examined the relationship
between lung function at baseline and levels of air pollution in the
community. They reported evidence that annual mean O3 levels
were associated with decreases in FVC, FEV1, PEF and forced
expiratory flow (FEF25-75) (the latter two being
statistically significant) among females but not males. In a separate
analysis (Gauderman et al., 2000) of 4th, 7th, and
[[Page 2956]]
10th grade students, a longitudinal analysis of lung function
development over four years found no association with O3
exposure. The Children's Health Study enrolled a second cohort of more
than 1500 fourth graders in 1996 (Gauderman et al., 2002). While the
strongest associations with negative lung function growth were observed
with acid vapors in this cohort, children from communities with higher
4-year average O3 levels also experienced smaller increases
in various lung function parameters. The strongest relationship with
O3 was with PEF. Specifically, children from the least-
polluted community had a small but statistically significant increase
in PEF as compared to those from the most-polluted communities. In two-
pollutant models, only 8-hour average O3 and NO2
were significant joint predictors of FEV1 and maximal
midexpiratory flow (MMEF). Although results from the second cohort of
children are supportive of a weak association, the definitive 8-year
follow-up analysis of the first cohort (Gauderman et al., 2004a)
provides little evidence that long-term exposure to ambient
O3 at current levels is associated with significant deficits
in the growth rate of lung function in children. Avol et al. (2001)
examined children who had moved away from participating communities in
southern California to other states with improved air quality. They
found that a negative, but not statistically significant, association
was observed between O3 and lung function parameters.
Collectively, the results of these reports from the children's health
cohorts provide little evidence to support an impact of long-term
O3 exposures on lung function development.
Evidence for a significant relationship between long-term
O3 exposures and decrements in maximally attained lung
function was reported in a nationwide study of first year Yale students
(Kinney et al., 1998; Galizia and Kinney, 1999) (EPA, 2006a, p. 7-120).
Males had much larger effect estimates than females, which might
reflect higher outdoor activity levels and correspondingly higher
O3 exposures during childhood. A similar study of college
freshmen at University of California at Berkeley also reported
significant effects of long-term O3 exposures on lung
function (K[uuml]nzli et al., 1997; Tager et al., 1998). In a
comparison of students whose city of origin was either Los Angeles or
San Francisco, long-term O3 exposures were associated with
significant changes in mid- and end-expiratory flow measures, which
could be considered early indicators for pathologic changes that might
progress to COPD.
There have been a few studies that investigated associations
between long-term O3 exposures and the onset of new cases of
asthma (EPA, 2006a, section 7.5.6). The Adventist Health and Smog
(AHSMOG) study cohort of about 4,000 was drawn from nonsmoking, non-
Hispanic white adult Seventh Day Adventists living in California (Greer
et al., 1993; McDonnell et al., 1999). During the ten-year follow-up in
1987, a statistically significant increased relative risk of asthma
development was observed in males, compared to a nonsignificant
relative risk in females (Greer et al., 1993). In the 15-year follow-up
in 1992, it was reported that for males, there was a statistically
significant increased relative risk of developing asthma associated
with 8-hour average O3 exposures, but there was no evidence
of an association in females. Consistency of results in the two studies
with different follow-up times provides supportive evidence of the
potential for an association between long-term O3 exposure
and asthma incidence in adult males; however, representativeness of
this cohort to the general U.S. population may be limited (EPA, 2006a,
p. 7-125).
In a similar study (McConnell et al., 2002) of incident asthma
among children (ages 9 to 16 at enrollment), annual surveys of 3,535
children initially without asthma were used to identify new-onset
asthma cases as part of the Children's Health Study. Six high-
O3 and six low-O3 communities were identified
where the children resided. There were 265 children who reported new-
onset asthma during the follow-up period. Although asthma risk was no
higher for all residents of the six high-O3 communities
versus the six low-O3 communities, asthma risk was 3.3 times
greater for children who played three or more sports as compared with
children who played no sports within the high-O3
communities. This association was absent in the communities with lower
O3 concentrations. No other pollutants were found to be
associated with new-onset asthma (EPA, 2006a, p. 7-125). Playing sports
may result in extended outdoor activity and exposure occurring during
periods when O3 levels are higher. It should be noted,
however, that the results of the Children's Health Study were based on
a small number of new-onset asthma cases among children who played
three or more sports. Future replication of these findings in other
cohorts would help determine whether a causal interpretation is
appropriate.
In animal toxicology studies, the progression of morphological
effects reported during and after a chronic exposure in the range of
0.50 to 1.00 ppm O3 (well above current ambient levels) is
complex, with inflammation peaking over the first few days of exposure,
then dropping, then plateauing, and finally, largely disappearing (EPA,
2006a, section 5.2.4.4). By contrast, fibrotic changes in the tissue
increase very slowly over months of exposure, and, after exposure
ceases, the changes sometimes persist or increase. Epithelial
hyperplasia peaks soon after the inflammatory response but is usually
maintained in both the nose and lungs with continuous exposure; it also
does not return to pre-exposure levels after the end of exposure.
Patterns of exposure in this same concentration range determine
effects, with 18 months of daily exposure, causing less morphologic
damage than exposures on alternating months. This is important as
environmental O3 exposure is typically seasonal. Long-term
studies by Plopper and colleagues (Evans et al., 2003; Schelegle et
al., 2003; Chen et al., 2003; Plopper and Fanucchi, 2000) investigated
infant rhesus monkeys exposed to simulated, seasonal O3 and
demonstrated: (1) Remodeling in the distal airways, (2) abnormalities
in tracheal basement membrane; (3) eosinophil accumulation in
conducting airways; and (4) decrements in airway innervation (EPA,
2006a, p. 5-45). These findings provide additional information
regarding possible injury-repair processes occurring with long-term
O3 exposures suggesting that these processes are only
partially reversible and may progress following cessation of
O3 exposure. Further, these processes may lead to
nonreversible structural damage to lung tissue; however, there is still
too much uncertainty to characterize the significance of these findings
to human exposure profiles and effect levels (EPA, 2006a, p. 8-25).
In summary, in the past decade, important new longitudinal studies
have examined the effect of chronic O3 exposure on
respiratory health outcomes. Limited evidence from recent long-term
morbidity studies have suggested in some cases that chronic exposure to
O3 may be associated with seasonal declines in lung function
or reduced lung function development, increases in inflammation, and
development of asthma in children and adults. Seasonal decrements or
smaller increases in lung function measures have been reported in
several studies; however, the extent to which these
[[Page 2957]]
changes are transient remains uncertain. While there is supportive
evidence from animal studies involving effects from chronic exposures,
large uncertainties still remain as to whether current ambient levels
and exposure patterns might cause these same effects in human
populations. The 2006 Criteria Document concludes that epidemiological
studies of new asthma development and longer-term lung function
declines remain inconclusive at present (EPA, 2006a, p. 7-134).
iii. Effects on the Cardiovascular System of O3 Exposure
At the time of the 1997 review, the possibility of O3-
induced cardiovascular effects was largely unrecognized. Since then, a
very limited body of evidence from animal, controlled human exposure,
and epidemiologic studies has emerged that provides evidence for some
potential plausible mechanisms for how O3 exposures might
exert cardiovascular system effects, however further research is needed
to substantiate these potential mechanisms. Possible mechanisms may
involve O3-induced secretions of vasoconstrictive substances
and/or effects on neuronal reflexes that may result in increased
arterial blood pressure and/or altered electrophysiologic control of
heart rate or rhythm. Some animal toxicology studies have shown
O3-induced decreases in heart rate, mean arterial pressure,
and core temperature. One controlled human exposure study that
evaluated effects of O3 exposure on cardiovascular health
outcomes found no significant O3-induced differences in ECG
or blood pressure in healthy or hypertensive subjects but did observe a
significant O3-induced increase the alveolar-to-arterial
PO2 gradient and heart rate in both groups resulting in an
overall increase in myocardial work and impairment in pulmonary gas
exchange (Gong et al., 1998). In another controlled human exposure
study, inhalation of a mixture of PM2.5 and O3 by
healthy subjects increased brachial artery vasoconstriction and
reactivity (Brook et al., 2002).
The evidence from a few animal studies also includes potential
direct effects such as O3-induced release from lung
epithelial cells of platelet activating factor (PAF) that may
contribute to blood clot formation that would have the potential to
increase the risk of serious cardiovascular outcomes (e.g., heart
attack, stroke, mortality). Also, interactions of O3 with
surfactant components in epithelial lining fluid of the lung may result
in production of oxysterols and reactive oxygen species that may
exhibit PAF-like activity contributing to clotting and also may exert
cytotoxic effects on lung and heart muscle cells.
Epidemiological panel and field studies that examined associations
between O3 and various cardiac physiologic endpoints have
yielded limited evidence suggestive of a potential association between
acute O3 exposure and altered heart rate variability (HRV),
ventricular arrhythmias, and incidence of heart attacks (myocardial
infarction or MI). A number of epidemiological studies have also
reported associations between short-term exposures and hospitalization
for cardiovascular diseases. As shown in Figure 7-13 of the 2006
Criteria Document, many of the studies reported negative or
inconsistent associations. Some other studies, especially those that
examined the relationship when O3 exposures were higher,
have found robust positive associations between O3 and
cardiovascular hospital admissions (EPA, 2006a, p. 7-82). For example,
one study reported a positive association between O3 and
cardiovascular hospital admissions in Toronto, Canada in a summer-only
analysis (Burnett et al., 1997b). The results were robust to adjustment
for various PM indices, whereas the PM effects diminished when adjusted
for gaseous pollutants. Other studies stratified their analysis by
temperature (i.e., by warms days versus cool days). Several analyses
using warm season days consistently produced positive associations.
The epidemiologic evidence for cardiovascular morbidity is much
weaker than for respiratory morbidity, with only one of several U.S.
and Canadian studies showing statistically significant positive
associations of cardiovascular hospitalizations with warm-season
O3 concentrations. Most of the available European and
Australian studies, all of which conducted all-year O3
analyses, did not find an association between short-term O3
concentrations and cardiovascular hospitalizations. Overall, the
currently available evidence is inconclusive regarding an association
between cardiovascular hospital admissions and ambient O3
exposure (EPA, 2006a, p. 7-83).
In summary, based on the evidence from animal toxicology,
controlled human exposure, and epidemiological studies, from the 2006
Criteria Document (p. 8-77) concludes that this generally limited body
of evidence is suggestive that O3 can directly and/or
indirectly contribute to cardiovascular-related morbidity, but that
much needs to be done to more fully integrate links between ambient
O3 exposures and adverse cardiovascular outcomes.
b. Mortality
i. Mortality and Short-term O3 Exposure
The 1996 Criteria Document concluded that an association between
daily mortality and O3 concentration for areas with high
O3 levels (e.g., Los Angeles) was suggested. However, due to
a very limited number of studies available at that time, there was
insufficient evidence to conclude that the observed association was
likely causal.
The 2006 Criteria Document included results from numerous
epidemiological analyses of the relationship between O3 and
mortality. Additional single city analyses have also been conducted
since 1996, however, the most pivotal studies in EPA's (and CASAC's)
finding of increased support for the relationship between premature
mortality and O3 is in part related to differences in study
design--limiting analyses to warm seasons, better control for
copollutants, particularly PM, and use of multicity designs (both time
series and meta-analytic designs). Key findings are available from
multicity time-series studies that report associations between
O3 and mortality. These studies include analyses using data
from 90 U.S. cities in the National Mortality, Morbidity and Air
Pollution (NMMAPS) study (Dominici et al., 2003) and from 95 U.S.
communities in an extension to the NMMAPS analyses (Bell et al., 2004).
The original 90-city NMMAPS analysis, with data from 1987 to 1994,
was primarily focused on investigating effects of PM10 on
mortality. A significant association was reported between mortality and
24-hour average O3 concentrations in analyses using all
available data as well as in the warm season only analyses (Dominici et
al., 2003). The estimate using all available data was about half that
for the summer-only data at a lag of 1-day. The extended NMMAPS
analysis included data from 95 U.S. cities and included an additional 6
years of data, from 1987-2000 (Bell et al., 2004). Significant
associations were reported between O3 and mortality in
analyses using all available data. The effect estimate for increased
mortality was approximately 0.5 percent per 0.020 ppm change in 24-hour
average O3 measured on the same day, and approximately 1.04
percent per 0.020 ppm change in 24-hour average O3 in a 7-
day distributed lag model (EPA, 2006a, p. 7-88). In analyses using only
data from the warm season, the results were not significantly different
from the full-year results. The authors also report
[[Page 2958]]
that O3-mortality associations were robust to adjustment for
PM (EPA, 2006a, p. 7-100). Using a subset of the NMMAPS data set, Huang
et al. (2005) focused on associations between cardiopulmonary mortality
and O3 exposure (24-hour average) during the summer season
only. The authors report an approximate 1.47 percent increase per 0.020
ppm change in O3 concentration measured on the same day and
an approximate 2.52 percent increase per 0.020 ppm change in
O3 concentration using a 7-day distributed lag model. These
findings suggest that the effect of O3 on mortality is
immediate but also persists for several days.
As discussed below in section II.A.3.a, confounding by weather,
especially temperature, is complicated by the fact that higher
temperatures are associated with the increased photochemical activities
that are important for O3 formation. Using a case-crossover
study design, Schwartz (2005) assessed associations between daily
maximum concentrations and mortality, matching case and control periods
by temperature, and using data only from the warm season. The reported
effect estimate of approximately 0.92 percent change in mortality per
0.040 ppm O3 (1-hour maximum) was similar to time-series
analysis results with adjustment for temperature (approximately 0.76
percent per 0.040 ppm O3), suggesting that associations
between O3 and mortality were robust to the different
adjustment methods for temperature.
An initial publication from APHEA, a European multicity study,
reported statistically significant associations between daily maximum
O3 concentrations and mortality in four cities in a full
year analysis (Toulomi et al., 1997). An extended analysis was done
using data from 23 cities throughout Europe (Gryparis et al., 2004). In
this report, a positive but not statistically significant association
was found between mortality and 1-hour daily maximum O3 in a
full year analysis. Gryparis et al. (2004) noted that there was a
considerable seasonal difference in the O3 effect on
mortality; thus, the small effect for the all-year data might be
attributable to inadequate adjustment for confounding by seasonality.
Focusing on analyses using summer measurements, the authors report
statistically significant associations with total mortality,
cardiovascular mortality and respiratory mortality (EPA, 2006a, p. 7-
93, 7-99).
Numerous single-city analyses have also reported associations
between mortality and short-term O3 exposure, especially for
those analyses using warm season data. As shown in Figure 7-21 of the
2006 Criteria Document, the results of recent publications show a
pattern of positive, often statistically significant associations
between short-term O3 exposure and mortality during the warm
season. In considering results from year-round analyses, there remains
a pattern of positive results but the findings are less consistent. In
most single-city analyses, effect estimates were not substantially
changed with adjustment for PM (EPA, 2006a, Figure 7-22).
In addition, several meta-analyses have been conducted on the
relationship between O3 and mortality. As described in
section 7.4.4 of the 2006 Criteria Document, these analyses reported
fairly consistent and positive combined effect estimates ranging from
approximately 1.5 to 2.5 percent increase in mortality for a
standardized change in O3 (EPA, 2006a, Figure 7-20). Three
recent meta-analyses evaluated potential sources of heterogeneity in
O3-mortality associations (Bell et al., 2005; Ito et al.,
2005; Levy et al., 2005). The 2006 Criteria Document (p. 7-96) observes
common findings across all three analyses, in that all reported that
effect estimates were larger in warm season analyses, reanalysis of
results using default convergence criteria in generalized additive
models (GAM) did not change the effect estimates, and there was no
strong evidence of confounding by PM. Bell et al. (2005) and Ito et al.
(2005) both provided suggestive evidence of publication bias, but
O3-mortality associations remained after accounting for that
potential bias. The 2006 Criteria Document concludes that the
``positive O3 effects estimates, along with the sensitivity
analyses in these three meta-analyses, provide evidence of a robust
association between ambient O3 and mortality'' (EPA, 2006a,
p. 7-97).
Most of the single-pollutant model estimates from single-city
studies range from 0.5 to 5 percent excess deaths per standardized
increments. Corresponding summary estimates in large U.S. multicity
studies ranged between 0.5 to 1 percent with some studies noting
heterogeneity across cities and studies (EPA, 2006a, p. 7-110).
Finally, from those studies that included assessment of
associations with specific causes of death, it appears that effect
estimates for associations with cardiovascular mortality are larger
than those for total mortality. The meta-analysis by Bell et al. (2005)
observed a slightly larger effect estimate for cardiovascular mortality
compared to mortality from all causes. The effect estimate for
respiratory mortality was approximately one-half that of cardiovascular
mortality in the meta-analysis. However, other studies have observed
larger effect estimates for respiratory mortality compared to
cardiovascular mortality. The apparent inconsistency regarding the
effect size of O3-related respiratory mortality may be due
to reduced statistical power in this subcategory of mortality (EPA,
2006a, p. 7-108).
In summary, many single- and multi-city studies observed positive
associations of ambient O3 concentrations with total
nonaccidental and cardiopulmonary mortality. The 2006 Criteria Document
finds that the results from U.S. multicity time-series studies provide
the strongest evidence to date for O3 effects on acute
mortality. Recent meta-analyses also indicate positive risk estimates
that are unlikely to be confounded by PM; however, future work is
needed to better understand the influence of model specifications on
the risk coefficient (EPA, 2006a, p. 7-175). A meta-analysis that
examined specific causes of mortality found that the cardiovascular
mortality risk estimates were higher than those for total mortality.
For cardiovascular mortality, the 2006 Criteria Document (Figure 7-25,
p. 7-106) suggests that effect estimates are consistently positive and
more likely to be larger and statistically significant in warm season
analyses. The findings regarding the effect size for respiratory
mortality have been less consistent, possibly because of lower
statistical power in this subcategory of mortality. The 2006 Criteria
Document (p. 8-78) concludes that these findings are highly suggestive
that short-term O3 exposure directly or indirectly
contribute to non-accidental and cardiopulmonary-related mortality, but
additional research is needed to more fully establish underlying
mechanisms by which such effects occur.\21\
---------------------------------------------------------------------------
\21\ In commenting on the Criteria Document, the CASAC Ozone
Panel raised questions about the implications of these time-series
results in a policy context, emphasizing that ``* * * while the
time-series study design is a powerful tool to detect very small
effects that could not be detected using other designs, it is also a
blunt tool'' (Henderson, 2006b). They note that ``* * * not only is
the interpretation of these associations complicated by the fact
that the day-to-day variation in concentrations of these pollutants
is, to a varying degree, determined by meteorology, the pollutants
are often part of a large and highly correlated mix of pollutants,
only a very few of which are measured'' (Henderson, 2006b). Even
with these uncertainties, the CASAC Ozone Panel, in its review of
the Staff Paper, found ``* * * premature total non-accidental and
cardiorespiratory mortality for inclusion in the quantitative risk
assessment to be appropriate.'' (Henderson, 2006b)
---------------------------------------------------------------------------
[[Page 2959]]
ii. Mortality and Long-Term O3 Exposure
Little evidence was available in the 1997 review on the potential
for associations between mortality and long-term exposure to
O3. In the Harvard Six City prospective cohort analysis, the
authors report that mortality was not associated with long-term
exposure to O3 (Dockery et al., 1993). The authors note that
the range of O3 concentrations across the six cities was
small, which may have limited the power of the study to detect
associations between mortality and O3 levels (EPA, 2006a, p.
7-127).
As discussed in section 7.5.8 of the 2006 Criteria Document, in
this review there are results available from three prospective cohort
studies: the American Cancer Society (ACS) study (Pope et al., 2002),
the Adventist Health and Smog (AHSMOG) study (Beeson et al., 1998;
Abbey et al., 1999), and the U.S. Veterans Cohort study (Lipfert et
al., 2000, 2003). In addition, a major reanalysis report includes
evaluation of data from the Harvard Six City cohort study (Krewski et
al., 2000).\22\ This reanalysis also includes additional evaluation of
data from the initial ACS cohort study report that had only reported
results of associations between mortality and long-term exposure to
fine particles and sulfates (Pope et al., 1995). This reanalysis was
discussed in the 2007 Staff Paper (section 3.3.2.2) but not in the 2006
Criteria Document.
---------------------------------------------------------------------------
\22\ This reanalysis report and the original prospective cohort
study findings are discussed in more detail in section 8.2.3 of the
Air Quality Criteria for Particulate Matter (EPA, 2004).
---------------------------------------------------------------------------
In this reanalysis of data from the previous Harvard Six City
prospective cohort study, the investigators replicated and validated
the findings of the original studies, and the report included
additional quantitative results beyond those available in the original
report (Krewski et al., 2000). In the reanalysis of data from the
Harvard Six Cities study, the effect estimate for the association
between long-term O3 concentrations and mortality was
negative and nearly statistically significant (relative risk = 0.87, 95
percent CI: 0.76, 1.00).
The ACS study is based on health data from a large prospective
cohort of approximately 500,000 adults and air quality data from about
150 U.S. cities. The initial report (Pope et al., 1995) focused on
associations with fine particles and sulfates, for which significant
associations had been reported in the earlier Harvard Six Cities study
(Dockery et al., 1993). As part of the major reanalysis of these data,
results for associations with other air pollutants were also reported,
and the authors report that no significant associations were found
between O3 and all-cause mortality. However, a significant
association was reported for cardiopulmonary mortality in the warm
season (Krewski et al., 2000). The ACS II study (Pope et al., 2002)
reported results of associations with an extended data base; the
mortality records for the cohort had been updated to include 16 years
of follow-up (compared with 8 years in the first report) and more
recent air quality data were included in the analyses. Similar to the
earlier reanalysis, a marginally significant association was observed
between long-term exposure to O3 and cardiopulmonary
mortality in the warm season. No other associations with mortality were
observed in both the full-year and warm season analyses.
The Adventist Health and Smog (AHSMOG) cohort includes about 6,000
adults living in California. In two studies from this cohort, a
significant association has been reported between long-term
O3 exposure and increased risk of lung cancer mortality
among males only (Beeson et al., 1998; Abbey et al., 1999). No
significant associations were reported between long-term O3
exposure and mortality from all causes or cardiopulmonary causes. Due
to the small numbers of lung cancer deaths (12 for males, 18 for
females) and the precision of the effect estimate (i.e., the wide
confidence intervals), the 2006 Criteria Document (p. 7-130) discussed
concerns about the plausibility of the reported association with lung
cancer.
The U.S. Veterans Cohort study (Lipfert et al., 2000, 2003) of
approximately 50,000 middle-aged males diagnosed with hypertension,
reported some positive associations between mortality and peak
O3 exposures (95th percentile level for several years of
data). The study included numerous analyses using subsets of exposure
and mortality follow-up periods which spanned the years 1960 to 1996.
In the results of analyses using deaths and O3 exposure
estimates concurrently across the study period, there were positive,
statistically significant associations between peak O3 and
mortality (EPA, 2006a, p. 7-129).
Overall, the 2006 Criteria Document (p. 7-130) concludes that
consistent associations have not been reported between long-term
O3 exposure and all-cause, cardiopulmonary or lung cancer
mortality.
c. Role of Ground-Level O3 in Solar Radiation-Related Human
Health Effects
Beyond the direct health effects attributable to inhalation
exposure to O3 in the ambient air discussed above, the 2006
Criteria Document also assesses potential indirect effects related to
the presence of O3 in the ambient air by considering the
role of ground-level O3 in mediating human health effects
that may be directly attributable to exposure to solar ultraviolet
radiation (UV-B). The 2006 Criteria Document (chapter 10) focuses this
assessment on three key factors, including those factors that govern
(1) UV-B radiation flux at the earth's surface, (2) human exposure to
UV-B radiation, and (3) human health effects due to UV-B radiation. In
so doing, the 2006 Criteria Document provides a thorough analysis of
the current understanding of the relationship between reducing ground-
level O3 concentrations and the potential impact these
reductions might have on increasing UV-B surface fluxes and indirectly
contributing to UV-B related health effects.
There are many factors that influence UV-B radiation penetration to
the earth's surface, including latitude, altitude, cloud cover, surface
albedo, PM concentration and composition, and gas phase pollution. Of
these, only latitude and altitude can be defined with small uncertainty
in any effort to assess the changes in UV-B flux that may be
attributable to any changes in tropospheric O3 as a result
of any revision to the O3 NAAQS. Such an assessment of UV-B
related health effects would also need to take into account human
habits, such as outdoor activities (including age- and occupation-
related exposure patterns), dress and skin care to adequately estimate
UV-B exposure levels. However, little is known about the impact of
these factors on individual exposure to UV-B.
Moreover, detailed information does not exist regarding other
factors that are relevant to assessing changes in disease incidence,
including: Type (e.g., peak or cumulative) and time period (e.g.,
childhood, lifetime, current) of exposures related to various adverse
health outcomes (e.g., damage to the skin, including skin cancer;
damage to the eye, such as cataracts; and immune system suppression);
wavelength dependency of biological responses; and interindividual
variability in UV-B resistance to such health outcomes. Beyond these
well recognized adverse health effects associated with various
wavelengths of UV radiation, the 2006 Criteria Document (section
10.2.3.6) also
[[Page 2960]]
discusses protective effects of UV-B radiation. Recent reports indicate
the necessity of UV-B in producing vitamin D. Vitamin D deficiency can
cause metabolic bone disease among children and adults, and may also
increase the risk of many common chronic diseases (e.g., type I
diabetes and rheumatoid arthritis) as well as the risk of various types
of cancers. Thus, the 2006 Criteria Document concludes that any
assessment that attempts to quantify the consequences of increased UV-B
exposure on humans due to reduced ground-level O3 must
include consideration of both negative and positive effects. However,
as with other impacts of UV-B on human health, this beneficial effect
of UV-B radiation has not been studied in sufficient detail to allow
for a credible health benefits or risk assessment. In conclusion, the
effect of changes in surface-level O3 concentrations on UV-
B-induced health outcomes cannot yet be critically assessed within
reasonable uncertainty (2006 Criteria Document, p. 10-36).
The Agency last considered indirect effects of O3 in the
ambient air in its 2003 final response to a remand of the Agency's 1997
decision to revise the O3 NAAQS. In so doing, based on the
available information in the 1997 review, EPA determined that the
information linking (a) changes in patterns of ground-level
O3 concentrations likely to occur as a result of programs
implemented to attain the 1997 O3 NAAQS to (b) changes in
relevant exposures to UV-B radiation of concern to public health was
too uncertain at that time to warrant any relaxation in the level of
public health protection previously determined to be requisite to
protect against the demonstrated direct adverse respiratory effects of
exposure to O3 in the ambient air (68 FR 614). At that time,
the more recent information on protective effects of UV-B radiation was
not available, such that only adverse UV-B-related effects could be
considered. Taking into consideration the more recent information
available for the 2008 review, the 2006 Criteria Document and 2007
Staff Paper conclude that the effect of changes in ground-level
O3 concentrations, likely to occur as a result of revising
the O3 NAAQS, on UV-B-induced health outcomes, including
whether these changes would ultimately result in increased or decreased
incidence of UV-B-related diseases, cannot yet be critically assessed.
3. Interpretation and Integration of Health Evidence
As discussed below, in assessing the health evidence, the 2006
Criteria Document integrates findings from experimental (e.g.,
toxicological, dosimetric and controlled human exposure) and
epidemiological studies, to make judgments about the extent to which
causal inferences can be made about observed associations between
health endpoints and exposure to O3. In evaluating the
evidence from epidemiological studies, the EPA focuses on well-
recognized criteria, including: The strength of reported associations,
including the magnitude and precision of reported effect estimates and
their statistical significance; the robustness of reported
associations, or stability in the effect estimates after considering
factors such as alternative models and model specification, potential
confounding by co-pollutants, and issues related to the consequences of
exposure measurement error; potential aggregation bias in pooling data;
and the consistency of the effects associations as observed by looking
across results of multiple- and single-city studies conducted by
different investigators in different places and times. Consideration is
also given to evaluating concentration-response relationships observed
in epidemiological studies to inform judgments about the potential for
threshold levels for O3-related effects. Integrating more
broadly across epidemiological and experimental evidence, the 2006
Criteria Document also focuses on the coherence and plausibility of
observed O3-related health effects to reach judgments about
the extent to which causal inferences can be made about observed
associations between health endpoints and exposure to O3 in
the ambient air.
a. Assessment of Evidence From Epidemiological Studies
Key elements of the evaluation of epidemiological studies are
briefly summarized below.
(1) The strength of associations most directly refers to the
magnitude of the reported relative risk estimates. Taking a broader
view, the 2006 Criteria Document draws upon the criteria summarized in
a recent report from the U.S. Surgeon General, which define strength of
an association as ``the magnitude of the association and its
statistical strength'' which includes assessment of both effect
estimate size and precision, which is related to the statistical power
of the study (CDC, 2004). In general, when associations are strong in
terms of yielding large relative risk estimates, it is less likely that
the association could be completely accounted for by a potential
confounder or some other source of bias, whereas with associations that
yield small relative risk estimates it is especially important to
consider potential confounding and other factors in assessing
causality. Effect estimates between O3 and some of the
health outcomes are generally small in size and could thus be
characterized as weak. For example, effect estimates for associations
with mortality generally range from 0.5 to 5 percent increases per
0.040 ppm increase in 1-hour maximum O3 or equivalent,
whereas associations for hospitalization range up to 50 percent
increases per standardized O3 increment. However, the 2006
Criteria Document notes that there are large multicity studies that
find small associations between short-term O3 exposure and
mortality or morbidity and have done so with great precision due to the
statistical power of the studies (p. 8-40). That is, the power of the
studies allows the authors to reliably distinguish even weak
relationships from the null hypothesis with statistical confidence.
(2) In evaluating the robustness of associations, the 2006 Criteria
Document (sections 7.1.3 and 8.4.4.3) and 2007 Staff Paper (section
3.4.2) have primarily considered the impact of exposure error,
potential confounding by copollutants, and alternative models and model
specifications.
In time-series and panel studies, the temporal (e.g., daily or
hourly) changes in ambient O3 concentrations measured at
centrally-located ambient monitoring stations are generally used to
represent a community's exposure to ambient O3. In
prospective cohort or cross-sectional studies, air quality data
averaged over a period of months to years are used as indicators of a
community's long-term exposure to ambient O3 and other
pollutants. In both types of analyses, exposure error is an important
consideration, as actual exposures to individuals in the population
will vary across the community.
Ozone concentrations measured at central ambient monitoring sites
may explain, at least partially, the variance in individual exposures
to ambient O3; however, this relationship is influenced by
various factors related to building ventilation practices and personal
behaviors. Further, the pattern of exposure misclassification error and
the influence of confounders may differ across the outcomes of interest
as well as in susceptible populations. As discussed in the 2006
Criteria Document
[[Page 2961]]
(section 3.9), only a limited number of studies have examined the
relationship between ambient O3 concentrations and personal
exposures to ambient O3. One of the strongest predictors of
the relationship between ambient concentrations and personal exposures
appears to be time spent outdoors. The strongest relationships were
observed in outdoor workers (Brauer and Brook, 1995, 1997; O'Neill et
al., 2004). Statistically significant correlations between ambient
concentrations and personal exposures were also observed for children,
who likely spend more time outdoors in the warm season (Linn et al.,
1996; Xu et al., 2005). There is some concern about the extent to which
ambient concentrations are representative of personal O3
exposures of another particularly susceptible group of individuals, the
debilitated elderly, since those who suffer from chronic cardiovascular
or respiratory conditions may tend to protect themselves more than
healthy individuals from environmental threats by reducing their
exposure to both O3 and its confounders, such as high
temperature and PM. Studies by Sarnat et al. (2001, 2005) that included
this susceptible group reported mixed results for associations between
ambient O3 concentrations and personal exposures to
O3. Collectively, these studies observed that the daily
averaged personal O3 exposures tend to be well correlated
with ambient O3 concentrations despite the substantial
variability that existed among the personal measurements. These studies
provide supportive evidence that ambient O3 concentrations
from central monitors may serve as valid surrogate measures for mean
personal exposures experienced by the population, which is of most
relevance for time-series studies. A better understanding of the
relationship between ambient concentrations and personal exposures, as
well as of the other factors that affect relationship will improve the
interpretation of concentration-population health response associations
observed.
The 2006 Criteria Document (section 7.1.3.1) also discusses the
potential influence of exposure error on epidemiologic study results.
Zeger et al. (2000) outlined the components to exposure measurement
error, finding that ambient exposure can be assumed to be the product
of the ambient concentration and an attenuation factor (i.e., building
filter) and that panel studies and time-series studies that use ambient
concentrations instead of personal exposure measurements will estimate
a health risk that is attenuated by that factor. Navidi et al. (1999)
used data from a children's cohort study to compare effect estimates
from a simulated ``true'' exposure level to results of analyses from
O3 exposures determined by several methods, finding that
O3 exposures based on the use of ambient monitoring data
overestimate the individual's O3 exposure and thus generally
result in O3 effect estimates that are biased downward (EPA,
2006a, p. 7-8). Similarly, in a reanalysis of a study by Burnett et al.
(1994) on the acute respiratory effects of ambient air pollution, Zidek
et al. (1998) reported that accounting for measurement error, as well
as making a few additional changes to the analysis, resulted in
qualitatively similar conclusions, but the effects estimates were
considerably larger in magnitude (EPA, 2006a, p. 7-8). A simulation
study by Sheppard et al. (2005) also considered attenuation of the risk
based on personal behavior, their microenvironment, and the qualities
of the pollutant in time-series studies. Of particular interest is
their finding that risk estimates were not further attenuated in time-
series studies even when the correlations between personal exposures
and ambient concentrations were weak. In addition to overestimation of
exposure and the resulting underestimation of effects, the use of
ambient O3 concentrations may obscure the presence of
thresholds in epidemiologic studies (EPA, 2006a, p. 7-9).
As discussed in the 2006 Criteria Document (section 3.9), using
ambient concentrations to determine exposure generally overestimates
true personal O3 exposures by approximately 2- to 4-fold in
available studies, resulting in attenuated risk estimates. The
implication is that the effects being estimated occur at fairly low
exposures and the potency of O3 is greater than these
effects estimates indicate. As very few studies evaluating
O3 health effects with personal O3 exposure
measurements exist in the literature, effect estimates determined from
ambient O3 concentrations must be evaluated and used with
caution to assess the health risks of O3. In the absence of
available data on personal O3 exposure, the use of routinely
monitored ambient O3 concentrations as a surrogate for
personal exposures is not generally expected to change the principal
conclusions from O3 epidemiologic studies. Therefore,
population health risk estimates derived using ambient O3
levels from currently available observational studies, with appropriate
caveats about personal exposure considerations, remain useful. The 2006
Criteria Document recommends caution in the quantitative use of effect
estimates calculated using ambient O3 concentrations as they
may lead to underestimation of the potency of O3. However,
the 2007 Staff Paper observes that the use of these risk estimates for
comparing relative risk reductions between alternative ambient
O3 standards considered in the risk assessment (discussed
below in section II.B.2) is less likely to suffer from this concern.
Confounding occurs when a health effect that is caused by one risk
factor is attributed to another variable that is correlated with the
causal risk factor; epidemiological analyses attempt to adjust or
control for potential confounders. Copollutants (e.g., PM, CO,
SO2 and NO2) can meet the criteria for potential
confounding in O3-health associations if they are potential
risk factors for the health effect under study and are correlated with
O3. Effect modifiers include variables that may influence
the health response to the pollutant exposure (e.g., co-pollutants,
individual susceptibility, smoking or age). Both are important
considerations for evaluating effects in a mixture of pollutants, but
for confounding, the emphasis is on controlling or adjusting for
potential confounders in estimating the effects of one pollutant, while
the emphasis for effect modification is on identifying and assessing
the effects for different modifiers.
The 2006 Criteria Document (p. 7-148) observes that O3
is generally not highly correlated with other criteria pollutants
(e.g., PM10, CO, SO2 and NO2), but may
be more highly correlated with secondary fine particles, especially
during the summer months, and that the degree of correlation between
O3 and other pollutants may vary across seasons. For
example, positive associations are observed between O3 and
pollutants such as fine particles during the warmer months, but
negative correlations may be observed during the cooler months (EPA,
2006a, p. 7-17). Thus, the 2006 Criteria Document (section 7.6.4) pays
particular attention to the results of season-specific analyses and
studies that assess effects of PM in potential confounding of
O3-health relationships. The 2006 Criteria Document also
discussed the limitations of commonly used multipollutant models that
include the difficulty in interpreting results where the copollutants
are highly colinear, or where correlations between pollutants change by
season (EPA, 2006a, p. 7-150). This is particularly the situation where
O3 and a copollutant, such as
[[Page 2962]]
sulfates, are formed under the same atmospheric condition; in such
cases multipollutant models would produce unstable and possibly
misleading results (EPA, 2006a, p. 7-152).
For mortality, the results from numerous multicity and single-city
studies indicate that O3-mortality associations do not
appear to be substantially changed in multipollutant models including
PM10 or PM2.5 (EPA, 2006a, p. 7-101; Figure 7-
22). Focusing on results of warm season analyses, effect estimates for
O3-mortality associations are fairly robust to adjustment
for PM in multipollutant models (EPA, 2006a, p. 7-102; Figure 7-23).
The 2006 Criteria Document concludes that in the few multipollutant
analyses conducted for these endpoints, copollutants generally do not
confound the relationship between O3 and respiratory
hospitalization (EPA, 2006a, p. 7-79 to 7-80; Figure 7-12).
Multipollutant models were not used as commonly in studies of
relationships between respiratory symptoms or lung function with
O3, but the 2006 Criteria Document reports that results of
available analyses indicate that such associations generally were
robust to adjustment for PM2.5 (p. 7-154). For example, in a
large multicity study of asthmatic children (Mortimer et al., 2002),
the O3 effect was attenuated, but there was still a positive
association; in Gent et al. (2003), effects of O3, but not
PM2.5, remained statistically significant and even increased
in magnitude in two-pollutant models (EPA, 2006a, p. 7-53). Considering
this body of studies, the 2006 Criteria Document (p. 7-154) concludes:
``Multipollultant regression analyses indicated that O3 risk
estimates, in general, were not sensitive to the inclusion of
copollutants, including PM2.5 and sulfate. These results
suggest that the effects of O3 on respiratory health
outcomes appear to be robust and independent of the effects of other
copollutants.''
The 2006 Criteria Document (p. 7-14) observes that another
challenge of time-series epidemiological analysis is assessing the
relationship between O3 and health outcomes while avoiding
bias due to confounding by other time-varying factors, particularly
seasonal trends and weather variables. These variables are of
particular interest because O3 concentrations have a well-
characterized seasonal pattern and are also highly correlated with
changes in temperature, such that it can be difficult to distinguish
whether effects are associated with O3 or with seasonal or
weather variables in statistical analyses.
The 2006 Criteria Document (section 7.1.3.4) discusses statistical
modeling approaches that have been used to adjust for time-varying
factors, highlighting a series of analyses that were done in a Health
Effects Institute-funded reanalysis of numerous time-series studies.
While the focus of these reanalyses was on associations with PM, a
number of investigators also examined the sensitivity of O3
coefficients to the extent of adjustment for temporal trends and
weather factors. In addition, several recent studies, including U.S.
multicity studies (Bell et al., 2005; Huang et al., 2005; Schwartz et
al., 2005) and a meta-analysis study (Ito et al., 2005), evaluated the
effect of model specification on O3-mortality associations.
As discussed in the 2006 Criteria Document (section 7.6.3.1), these
studies generally report that associations reported with O3
are not substantially changed with alternative modeling strategies for
adjusting for temporal trends and meteorologic effects. In the meta-
analysis by Ito et al. (2005), a separate multicity analysis was
presented that found that alternative adjustments for weather resulted
in up to 2-fold difference in the O3 effect estimate.
Significant confounding can occur when strong seasonal cycles are
present, suggesting that season-specific results are more generally
robust than year-round results in such cases. A number of
epidemiological studies have conducted season-specific analyses, and
have generally reported stronger and more precise effect estimates for
O3 associations in the warm season than in analyses
conducted in the cool seasons or over the full year.
(3) Consistency refers to the persistent finding of an association
between exposure and outcome in multiple studies of adequate power in
different persons, places, circumstances and times (CDC, 2004). In
considering results from multicity studies and single-city studies in
different areas, the 2006 Criteria Document (p. 8-41) observes general
consistency in effects of short-term O3 exposure on
mortality, respiratory hospitalization and other respiratory health
outcomes. The variations in effects that are observed may be
attributable to differences in relative personal exposure to
O3, as well as varying concentrations and composition of
copollutants present in different regions. Thus, the 2006 Criteria
Document (p. 8-41) concludes that ``consideration of consistency or
heterogeneity of effects is appropriately understood as an evaluation
of the similarity or general concordance of results, rather than an
expectation of finding quantitative results with a very narrow range.''
(4) The 2007 Staff Paper recognizes that it is likely that there
are biological thresholds for different health effects in individuals
or groups of individuals with similar innate characteristics and health
status. For O3 exposure, individual thresholds would
presumably vary substantially from person to person due to individual
differences in genetic susceptibility, pre-existing disease conditions
and possibly individual risk factors such as diet or exercise levels
(and could even vary from one time to another for a given person).
Thus, it would be difficult to detect a distinct threshold at the
population level below which no individual would experience a given
effect, especially if some members of a population are unusually
sensitive even down to very low concentrations (EPA, 2004, p. 9-43, 9-
44).
Some studies have tested associations between O3 and
health outcomes after removal of days with higher O3 levels
from the data set; such analyses do not necessarily indicate the
presence or absence of a threshold, but provide some information on
whether the relationship is found using only lower-concentration data.
For example, using data from 95 U.S. cities, Bell et al. (2004) found
that the effect estimate for an association between short-term
O3 exposure and mortality was little changed when days
exceeding 0.060 ppm (24-hour average) were excluded in the analysis.
Using data from 8 U.S. cities, Mortimer and colleagues (2002) also
reported that associations between O3 and both lung function
and respiratory symptoms remained statistically significant and of the
same or greater magnitude in effect size when concentrations greater
than 0.080 ppm (8-hour average) were excluded (EPA, 2006a, p. 7-46).
Several single-city studies also report similar findings of
associations that remain or are increased in magnitude and statistical
significance when data at the upper end of the concentration range are
removed (EPA, 2006a, section 7.6.5).
Other time-series epidemiological studies have used statistical
modeling approaches to evaluate whether thresholds exist in
associations between short-term O3 exposure and mortality.
As discussed in section 7.6.5 of the 2006 Criteria Document, one
European multicity study included evaluation of the shape of the
concentration-response curve, and observed no deviation from a linear
function across the range of O3 measurements from the study
(Gryparis et al., 2004; EPA, 2006a p. 7-154). Several single-city
studies also observed a monotonic increase in associations between
O3 and morbidity that suggest
[[Page 2963]]
that no population threshold exists (EPA, 2006a, p. 7-159).
On the other hand, a study in Korea used several different modeling
approaches and reported that a threshold model provided the best fit
for the data. The results suggested a potential threshold level of
about 0.045 ppm (1-hour maximum concentration; < 0.035 ppm, 8-hour
average) for an association between mortality and short-term
O3 exposure during the summer months (Kim et al., 2004; EPA,
2006a, p. 8-43). The authors reported larger effect estimates for the
association for data above the potential threshold level, suggesting
that an O3-mortality association might be underestimated in
the non-threshold model. A threshold analysis recently reported by Bell
et al. (2006) for 98 U.S. communities, including the same 95
communities in Bell et al. (2004), indicated that if a population
threshold existed for mortality, it would likely fall below a 24-hour
average O3 concentration of 0.015 ppm (< 0.025 ppm, 8-hour
average). In addition, Burnett and colleagues (1997a,b) plotted the
relationships between air pollutant concentrations and both respiratory
and cardiovascular hospitalization, and it appears in these results
that the associations with O3 are found in the concentration
range above about 0.030 ppm (1-hour maximum; < 0.025 ppm, 8-hour
average). Vedal and colleagues (2003) reported a significant
association between O3 and mortality in British Columbia
where O3 concentrations were quite low (mean 1-hour maximum
concentration of 0.0273 ppm). The authors did not specifically test for
threshold levels, but the fact that the association was found in an
area with such low O3 concentrations suggests that any
potential threshold level would be quite low in this data set.
In summary, the 2006 Criteria Document finds that, taken together,
the available evidence from controlled human exposure and
epidemiological studies suggests that no clear conclusion can now be
reached with regard to possible threshold levels for O3-
related effects (EPA, 2006a, p. 8-44). Thus, the available
epidemiological evidence neither supports nor refutes the existence of
thresholds at the population level for effects such as increased
hospital admissions and premature mortality. There are limitations in
epidemiological studies that make discerning thresholds in populations
difficult, including low data density in the lower concentration
ranges, the possible influence of exposure measurement error, and
interindividual differences in susceptibility to O3-related
effects in populations. There is the possibility that thresholds for
individuals may exist in reported associations at fairly low levels
within the range of air quality observed in the studies but not be
detectable as population thresholds in epidemiological analyses.
b. Biological Plausibility and Coherence of Evidence
The body of epidemiological studies discussed in the 2007 Staff
Paper emphasizes the role of O3 in association with a
variety of adverse respiratory and cardiovascular effects. While
recognizing a variety of plausible mechanisms, there exists a general
consensus suggesting that O3, could either directly or
through initiation, interfere with basic cellular oxidation processes
responsible for inflammation, reduced antioxidant capacity,
atherosclerosis and other effects. Reasoning that O3
influences cellular chemistry through basic oxidative properties (as
opposed to a unique chemical interaction), other reactive oxidizing
species (ROS) in the atmosphere acting either independently or in
combination with O3 may also contribute to a number of
adverse respiratory and cardiovascular health effects. Consequently,
the role of O3 should be considered more broadly as
O3 behaves as a generator of numerous oxidative species in
the atmosphere.
In considering the biological plausibility of reported
O3-related effects, the 2007 Staff Paper (section 3.4.6)
considers this broader question of health effects of pollutant mixtures
containing O3. The potential for O3-related
enhancements of PM formation, particle uptake, and exacerbation of PM-
induced cardiovascular effects underscores the importance of
considering contributions of O3 interactions with other
often co-occurring air pollutants to health effects due to
O3-containing pollutant mixes. The 2007 Staff Paper
summarizes some examples of important pollutant mixture effects from
studies that evaluate interactions of O3 with other co-
occurring pollutants, as discussed in chapters 4, 5, and 6 of the 2006
Criteria Document.
All of the types of interactive effects of O3 with other
co-occurring gaseous and nongaseous viable and nonviable PM components
of ambient air mixes noted above argue that O3 acts not only
alone but that O3 also is a surrogate indicator for air
pollution mixes which may enhance the risk of adverse effects due to
O3 acting in combination with other pollutants. Viewed from
this perspective, those epidemiologic findings of morbidity and
mortality associations, with ambient O3 concentrations
extending to quite low levels in many cases, become more understandable
and plausible.
The 2006 Criteria Document integrates epidemiological studies with
mechanistic information from controlled human exposure studies and
animal toxicological studies to draw conclusions regarding the
coherence of evidence and biological plausibility of O3-
related health effects to reach judgments about the causal nature of
observed associations. As summarized below, coherence and biological
plausibility is discussed for each of the following types of
O3-related effects: Short-term effects on the respiratory
system, effects on the cardiovascular system, effects related to long-
term O3 exposure, and short-term mortality-related health
endpoints.
i. Coherence and Plausibility of Short-Term Effects on the Respiratory
System
Acute respiratory morbidity effects that have been associated with
short-term exposure to O3 include such health endpoints as
decrements in lung function, increased respiratory symptoms, increased
airway responsiveness, airway inflammation, increased permeability
related to epithelial injury, immune system effects, emergency
department visits for respiratory diseases, and hospitalization due to
respiratory illness.
Recent epidemiological studies have supported evidence available in
the previous O3 NAAQS review on associations between ambient
O3 exposure and decline in lung function for children. The
2006 Criteria Document (p. 8-34) concludes that exposure to ambient
O3 has a significant effect on lung function and is
associated with increased respiratory symptoms and medication use,
particularly in asthmatics. Short-term exposure to O3 has
also been associated with more severe morbidity endpoints, such as
emergency department visits and hospital admissions for respiratory
cases, including specific respiratory illness (e.g., asthma) (EPA,
2006a, sections 7.3.2 and 7.3.3). In addition, a few epidemiological
studies have reported positive associations between short-term
O3 exposure and respiratory mortality, though the
associations are not generally statistically significant (EPA, 2006a,
p. 7-108).
Considering the evidence from epidemiological studies, the results
described above provide evidence for coherence in O3-related
effects on the respiratory system. Effect estimates from U.S. and
Canadian studies are shown in
[[Page 2964]]
Figure 1, where it can be seen that mostly positive associations have
been reported with respiratory effects ranging from respiratory
symptoms, such as cough or wheeze, to hospitalization for various
respiratory diseases, and there is suggestive evidence for associations
with respiratory mortality. Many of the reported associations are
statistically significant, particularly in the warm season. In Figure
1, the central effect estimate is indicated by a square for each
result, with the vertical bar representing the 95 percent confidence
interval around the estimate. In the discussions that follow, an
individual study result is considered to be statistically significant
if the 95 percent confidence interval does not include zero.\23\
Positive effect estimates indicate increases in the health outcome with
O3 exposure. In considering these results as a whole, it is
important to consider not only whether statistical significance at the
95 percent confidence level is reported in individual studies but also
the general pattern of results, focusing in particular on studies with
greater statistical power that report relatively more precise results.
---------------------------------------------------------------------------
\23\ Results for studies of respiratory symptoms are presented
as odds ratios; an odds ratio of 1.0 is equivalent to no effect, and
thus is presented as equivalent to the zero effect estimate line.
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Considering also evidence from toxicological, controlled human
exposure, and field studies, the 2006 Criteria Document (section 8.6)
discusses biological plausibility and coherence of evidence for acute
O3-induced respiratory health effects. Inhalation of
O3 for several hours while subjects are physically active
can elicit both acute adverse pathophysiological changes and subjective
respiratory tract symptoms (EPA, 2006a, section 8.4.2). Acute pulmonary
responses observed in healthy humans exposed to O3 at
ambient concentrations include: decreased inspiratory capacity; mild
bronchoconstriction; rapid, shallow breathing during exercise;
subjective symptoms of tracheobronchial airway irritation, including
cough and pain on deep inspiration; decreases in measures of lung
function; and increased airway resistance. The severity of symptoms and
magnitude of response depends on inhaled dose, individual O3
sensitivity, and the degree of attenuation or enhancement of response
resulting from previous O3 exposures. Lung function studies
of several animal species acutely exposed to relatively low
O3 levels from a toxicological perspective (i.e., 0.25 to
0.4 ppm) show responses similar to those observed in humans, including
increased breathing frequency, decreased tidal volume, increased
resistance, and decreased FVC. Alterations in breathing pattern return
to normal within hours of exposure, and
[[Page 2966]]
attenuation in functional responses following repeated O3
exposures is similar to those observed in humans.
Physiological and biochemical alterations investigated in
controlled human exposure and animal toxicology studies tend to support
certain hypotheses of underlying pathological mechanisms which lead to
the development of respiratory-related effects reported in epidemiology
studies (e.g., increased hospitalization and medication use). Some of
these are: (a) Decrements in lung function, (b) bronchoconstriction,
(c) increased airway responsiveness, (d) airway inflammation, (e)
epithelial injury, (f) immune system activation, (g) host defense
impairment, and (h) sensitivity of individuals, which depends on at
least a person's age, disease status, genetic susceptibility, and the
degree of attenuation present due to prior exposures. The time
sequence, magnitude, and overlap of these complex events, both in terms
of development and recovery, illustrate the inherent difficulty of
interpreting the biological plausibility of O3-induced
cardiopulmonary health effects (EPA, 2006a, p. 8-48).
The interaction of O3 with airway epithelial cell
membranes and ELF to form lipid ozonation products and ROS is supported
by numerous human, animal and in vitro studies. Ozonation products and
ROS initiate a cascade of events that lead to oxidative stress, injury,
inflammation, airway epithelial damage and increased epithelial damage
and increased alveolar permeability to vascular fluids. Repeated
respiratory inflammation can lead to a chronic inflammatory state with
altered lung structure and lung function and may lead to chronic
respiratory diseases such as fibrosis and emphysema (EPA, 2006a,
section 8.6.2). Continued respiratory inflammation also can alter the
ability to respond to infectious agents, allergens and toxins. Acute
inflammatory responses to O3 are well documented, and lung
injury appears within 3 hours after exposure in humans.
Taken together, the 2006 Criteria Document concludes that the
evidence from experimental human and animal toxicology studies
indicates that acute O3 exposure is causally associated with
respiratory system effects. These effects include O3-induced
pulmonary function decrements; respiratory symptoms; lung inflammation
and increased lung permeability; airway hyperresponsiveness; increased
uptake of nonviable and viable particles; and consequent increased
susceptibility to PM-related toxic effects and respiratory infections
(EPA, 2006a, p. 8-48).
ii. Coherence and Plausibility of Effects on the Cardiovascular System
There is very limited experimental evidence of animals and humans
that has evaluated possible mechanisms or physiological pathways by
which acute O3 exposures may induce cardiovascular system
effects. Ozone induces lung injury, inflammation, and impaired
mucociliary clearance, with a host of associated biochemical changes
all leading to increased lung epithelial permeability. As noted above
in section II.A.2.a, the generation of lipid ozonation products and ROS
in lung tissues can influence pulmonary hemodynamics, and ultimately
the cardiovascular system. Other potential mechanisms by which
O3 exposure may be associated with cardiovascular disease
outcomes have been described. Laboratory animals exposed to relatively
high O3 concentrations (>= 0.5 ppm) demonstrate tissue edema
in the heart and lungs. Ozone-induced changes in heart rate, edema of
heart tissue, and increased tissue and serum levels of ANF found with
8-hour 0.5 ppm O3 exposure in animal toxicology studies
(Vesely et al., 1994a,b,c) also raise the possibility of potential
cardiovascular effects of acute ambient O3 exposures.
Animal toxicology studies have found both transient and persistent
ventilatory responses with and without progressive decreases in heart
rate (Arito et al., 1997). Observations of O3-induced
vasoconstriction in a controlled human exposure study by Brook et al.
(2002) suggests another possible mechanism for O3-related
exacerbations of preexisting cardiovascular disease. One controlled
human study (Gong et al., 1998) evaluated potential cardiovascular
health effects of O3 exposure. The overall results did not
indicate acute cardiovascular effects of O3 in either the
hypertensive or control subjects. The authors observed an increase in
rate-pressure product and heart rate, a decrement for FEV1,
and a > 10 mm Hg increase in the alveolar/arterial pressure difference
for O2 following O3 exposure. Foster et al.
(1993) demonstrated that even in relatively young healthy adults,
O3 exposure can cause ventilation to shift away from the
well-perfused basal lung. This effect of O3 on ventilation
distribution may persist beyond 24-hours post-exposure (Foster et al.,
1997). These findings suggest that O3 may exert
cardiovascular effects indirectly by impairing alveolar-arterial
O2 transfer and potentially reducing O2 supply to
the myocardium. Ozone exposure may increase myocardial work and impair
pulmonary gas exchange to a degree that could perhaps be clinically
important in persons with significant preexisting cardiovascular
impairment.
As noted above in section II.A.2.a, a limited number of new
epidemiological studies have reported associations between short-term
O3 exposure and effects on the cardiovascular system. Among
these studies, three were population-based and involved relatively
large cohorts; two of these studies evaluated associations between
O3 and HRV and the other study evaluated the association
between O3 levels and the relative risk of MI or heart
attack. Such studies may offer more informative results based on their
large subject-pool and design. Results from these three studies were
suggestive of an association between O3 exposure and the
cardiovascular endpoints studied. In other recent studies on the
incidence of heart attacks and some more subtle cardiovascular health
endpoints, such as changes in HRV or cardiac arrhythmia, some but not
all studies reported associations with short-term exposure to
O3 (EPA, 2006a, section 7.2.7.1). From these studies, the
2006 Criteria Document concludes that the ``current evidence is rather
limited but suggestive of a potential effect on HRV, ventricular
arrhythmias, and MI incidence'' (EPA, 2006a, p. 7-65).
An increasing number of studies have evaluated the association
between O3 exposure and cardiovascular hospital admissions.
As discussed in section 7.3.4 of the 2006 Criteria Document, many
reported negative or inconsistent associations, whereas other studies,
especially those that examined the relationship when O3
exposures were higher, have found positive and robust associations
between O3 and cardiovascular hospital admissions. The 2006
Criteria Document (p. 7-83) finds that the overall evidence from these
studies remains inconclusive regarding the effect of O3 on
cardiovascular hospitalizations. The 2006 Criteria Document notes that
the suggestive positive epidemiologic findings of O3
exposure on cardiac autonomic control, including effects on HRV,
ventricular arrhythmias and heart attacks, and reported associations
between O3 exposure and cardiovascular hospitalizations
generally in the warm season gain credibility and scientific support
from the results of experimental animal toxicology and controlled human
exposure studies, which are indicative of plausible pathways by which
O3 may exert cardiovascular effects (EPA, 2006a, section
8.6.1).
[[Page 2967]]
iii. Coherence and Plausibility of Effects Related to Long-Term
O3 Exposure
Controlled human exposure studies cannot evaluate effects of long-
term exposures to O3; there is some evidence available from
toxicological studies. While early animal toxicology studies of long-
term O3 exposures were conducted using continuous exposures,
more recent studies have focused on exposures which mimic diurnal and
seasonal patterns and more realistic O3 exposure levels
(EPA, 2006a, p. 8-50). Studies of monkeys that compared these two
exposure scenarios found increased airway pathology only with the
latter design. Persistent and irreversible effects reported in chronic
animal toxicology studies suggest that additional complementary human
data are needed from epidemiologic studies (EPA, 2006a, p. 8-50).
There is limited evidence from human studies for long-term
O3-induced effects on lung function. As discussed in section
8.6.2 of the 2006 Criteria Document, previous epidemiological studies
have provided only inconclusive evidence for either mortality or
morbidity effects of long-term O3 exposure. The 2006
Criteria Document (p. 8-50) observes that the inconsistency in findings
may be due to a lack of precise exposure information, the possibility
of selection bias, and the difficulty of controlling for confounders.
Several new longitudinal epidemiology studies have evaluated
associations between long-term O3 exposures and morbidity
and mortality and suggest that these long-term exposures may be related
to changes in lung function in children; however, little evidence is
available to support a relationship between chronic O3
exposure and mortality or lung cancer incidence (EPA, 2006a, p. 8-50).
The 2006 Criteria Document (p. 8-51) concludes that evidence from
animal toxicology studies strongly suggests that chronic O3
exposure is capable of damaging the distal airways and proximal
alveoli, resulting in lung tissue remodeling leading to apparent
irreversible changes. Such structural changes and compromised lung
function caused by persistent inflammation may exacerbate the
progression and development of chronic lung disease. Together with the
limited evidence available from epidemiological studies, these findings
offer some insight into potential biological mechanisms for suggested
associations between long-term or seasonal exposures to O3
and reduced lung function development in children which have been
observed in epidemiologic studies (EPA, 2006a, p. 8-51).
iv. Coherence and Plausibility of Short-Term Mortality-Related Health
Endpoints
An extensive epidemiological literature on air pollution related
mortality risk estimates from the U.S., Canada, and Europe is discussed
in the 2006 Criteria Document (sections 7.4 and 8.6.3). These single-
and multicity mortality studies coupled with results from meta-analyses
generally indicate associations between acute O3 exposure
and elevated risk for all-cause mortality, even after adjustment for
the influence of season and PM exposure. Several single-city studies
that specifically evaluated the relationship between O3
exposure and cardiopulmonary mortality also reported results suggestive
of a positive association (EPA, 2006a, p. 8-51). These mortality
studies suggest a pattern of effects for causality that have
biologically plausible explanations, but our knowledge regarding
potential underlying mechanisms is very limited at this time and
requires further research. Most of the physiological and biochemical
parameters investigated in human and animal studies suggest that
O3-induced biochemical effects are relatively transient and
attenuate over time. The 2006 Criteria Document (p. 8-52) hypothesizes
a generic pathway of O3-induced lung damage, potentially
involving oxidative lung damage with subsequent inflammation and/or
decline in lung function leading to respiratory distress in some
sensitive population groups (e.g., asthmatics), or other plausible
pathways noted below that may lead to O3-related
contributions to cardiovascular effects that ultimately increase risk
of mortality.
The third National Health and Nutrition Examination Survey follow-
up data analysis indicates that about 20 percent of the adult
population has reduced FEV1 values, suggesting impaired lung
function in a significant portion of the population. Most of these
individuals have COPD, asthma or fibrotic lung disease (Manino et al.,
2003), which are associated with persistent low-grade inflammation.
Furthermore, patients with COPD are at increased risk for
cardiovascular disease. Also, lung disease with underlying inflammation
may be linked to low-grade systemic inflammation associated with
atherosclerosis, independent of cigarette smoking (EPA, 2006a, p. 8-
52). Lung function decrements in persons with cardiopulmonary disease
have been associated with inflammatory markers, such as C-reactive
protein (CRP) in the blood. At a population level it has been found
that individuals with the lowest FEV1 values have the
highest levels of CRP, and those with the highest FEV1
values have the lowest CRP levels (Manino et al., 2003; Sin and Man,
2003). This complex series of physiological and biochemical reactions
following O3 exposure may tilt the biological homeostasis
mechanisms which could lead to adverse health effects in people with
compromised cardiopulmonary systems.
Several other types of newly available data also support reasonable
hypotheses that may help to explain the findings of O3-
related increases in cardiovascular mortality observed in some
epidemiological studies. These include the direct effect of
O3 on increasing PAF in lung tissue that can then enter the
general circulation and possibly contribute to increased risk of blood
clot formation and the consequent increased risk of heart attacks,
cerebrovascular events (stroke), or associated cardiovascular-related
mortality. Ozone reactions with cholesterol in lung surfactant to form
epoxides and oxysterols that are cytotoxic to lung and heart muscles
and that contribute to atherosclerotic plaque formation in arterial
walls represent another potential pathway. Stimulation of airway
irritant receptors may lead to increases in tissue and serum levels of
ANF, changes in heart rate, and edema of heart tissue. A few new field
and panel studies of human adults have reported associations between
ambient O3 concentrations and changes in cardiac autonomic
control (e.g., HRV, ventricular arrhythmias, and MI). These represent
plausible pathways that may lead to O3-related contributions
to cardiovascular effects that ultimately increase the risk of
mortality.
In addition, O3-induced increases in lung permeability
allow more ready entry for inhaled PM into the blood stream, and thus
O3 exposure may increase the risk of PM-related
cardiovascular effects. Furthermore, increased ambient O3
levels contribute to ultrafine PM formation in the ambient air and
indoor environments. Thus, the contributions of elevated ambient
O3 concentrations to ultrafine PM formation and human
exposure, along with the enhanced uptake of inhaled fine particles,
consequently may contribute to exacerbation of PM-induced
cardiovascular effects in addition to those more directly induced by
O3 (EPA, 2006a, p. 8-53).
[[Page 2968]]
c. Summary
Judgments concerning the extent to which relationships between
various health endpoints and ambient O3 exposures are likely
to be causal are informed by the conclusions and discussion in the 2006
Criteria Document as discussed above and summarized in section 3.7.5 of
the 2007 Staff Paper. These judgments reflect the nature of the
evidence and the overall weight of the evidence, and are taken into
consideration in the quantitative risk assessment discussed below in
section II.B.2.
For example, there is a very high level of confidence that
O3 induces lung function decrements in healthy adults and
children due in part to the dozens of controlled human exposure and
epidemiological studies consistently showing such effects. The 2006
Criteria Document (p. 8-74) states that these studies provide clear
evidence of causality for associations between short-term O3
exposures and statistically significant declines in lung function in
children, asthmatics and adults who exercise outdoors. An increase in
respiratory symptoms (e.g., cough, shortness of breath) has been
observed in controlled human exposure studies of short-term
O3 exposures, and significant associations between ambient
O3 exposures and a wide variety of respiratory symptoms have
been reported in epidemiology studies (EPA, 2006a, p. 8-75). Population
time-series studies showing robust associations between O3
exposures and respiratory hospital admissions and emergency department
visits are strongly supported by controlled human exposure, animal
toxicological, and epidemiological evidence for O3-related
lung function decrements, respiratory symptoms, airway inflammation,
and airway hyperreactivity. The 2006 Criteria Document (p. 8-77)
concludes that, taken together, the overall evidence supports the
inference of a causal relationship between acute ambient O3
exposures and increased respiratory morbidity outcomes resulting in
increased emergency department visits and hospitalizations during the
warm season. Further, recent epidemiologic evidence has been
characterized in the 2006 Criteria Document (p. 8-78) as highly
suggestive that O3 directly or indirectly contributes to
non-accidental and cardiopulmonary-related mortality.
4. O3-Related Impacts on Public Health
The following discussion draws from chapters 6 and 7 and section
8.7 of the 2006 Criteria Document and section 3.6 of the 2007 Staff
Paper to characterize factors which modify responsiveness to
O3, populations potentially at risk for O3-
related health effects, the adversity of O3-related effects,
and the size of the at-risk populations in the U.S. These
considerations are all important elements in characterizing the
potential public health impacts associated with exposure to ambient
O3.
a. Factors That Modify Responsiveness to Ozone
There are numerous factors that can modify individual
responsiveness to O3. These include: influence of physical
activity; age; gender and hormonal influences; racial, ethnic and
socioeconomic status (SES) factors; environmental factors; and oxidant-
antioxidant balance. These factors are discussed in more detail in
section 6.5 of the 2006 Criteria Document.
It is well established that physical activity increases an
individual's minute ventilation and will thus increase the dose of
O3 inhaled (EPA, 2006a, section 6.5.4). Increased physical
activity results in deeper penetration of O3 into more
distal regions of the lungs, which are more sensitive to acute
O3 response and injury. This will result in greater lung
function decrements for acute exposures of individuals during increased
physical activity. Research has shown that respiratory effects are
observed at lower O3 concentrations if the level of exertion
is increased and/or duration of exposure and exertion are extended.
Predicted O3-induced decrements in lung function have been
shown to be a function of exposure concentration, duration and exercise
level for healthy, young adults (McDonnell et al., 1997).
Most of the studies investigating the influence of age have used
lung function decrements and symptoms as measures of response. For
healthy adults, lung function and symptom responses to O3
decline as age increases. The rate of decline in O3
responsiveness appears greater in those 18 to 35 years old compared to
those 35 to 55 years old, while there is very little change after age
55. In one study (Seal et al., 1996) analyzing a large data set, a 5.4%
decrement in FEV1 on average was estimated for 20-year-old
individuals exposed to 0.12 ppm O3 for 2.3 hours, whereas
similar exposure of 35-year-old individuals resulted in a 2.6%
decrement on average. While healthy children tend not to report
respiratory symptoms when exposed to low levels of O3, for
subjects 18 to 36 years old symptom responses induced by O3
are observed but tend to decrease with increasing age within this range
(McDonnell et al., 1999).
Limited evidence of gender differences in response to O3
exposure has suggested that females may be predisposed to a greater
susceptibility to O3. Lower plasma and NL fluid levels of
the most prevalent antioxidant, uric acid, in females relative to males
may be a contributing factor. Consequently, reduced removal of
O3 in the upper airways may promote deeper penetration.
However, most of the evidence on gender differences appears to be
equivocal, with one study (Hazucha et al., 2003) suggesting that
physiological responses of young healthy males and females may be
comparable (EPA, 2006a, section 6.5.2).
A few studies have suggested that ethnic minorities might be more
responsive to O3 than Caucasian population groups (EPA,
2006a, section 6.5.3). This may be more the result of a lack of
adequate health care and socioeconomic status (SES) than any
differences in sensitivity to O3. The limited data
available, which have investigated the influence of race, ethnic or
other related factors on responsiveness to O3, prevent
drawing any clear conclusions at this time.
Few human studies have examined the potential influence of
environmental factors such as the sensitivity of individuals who
voluntarily smoke tobacco (i.e., smokers) and the effect of high
temperatures on O3 responsiveness. New controlled human
exposure studies have confirmed that smokers are less responsive to
O3 than nonsmokers; however, time course of development and
recovery of these effects, as well as reproducibility, was not
different from nonsmokers (EPA, 2006a, section 6.5.5). Influence of
ambient temperature on pulmonary effects induced by O3 has
been studied very little, but additive effects of heat and
O3 exposure have been reported.
Antioxidants, which scavenge free radicals and limit lipid
peroxidation in the ELF, are the first line of defense against
oxidative stress. Ozone exposure leads to absorption of O3
in the ELF with subsequent depletion of antioxidant in the nasal ELF,
but concentration and antioxidant enzyme activity in ELF or plasma do
not appear related to O3 responsiveness (EPA 2006a, section
6.5.6). Controlled studies of dietary antioxidant supplements have
shown some protective effects on lung function decrements but not on
symptoms and airway inflammatory responses. Dietary antioxidant
supplements have provided some protection to asthmatics by attenuating
post-exposure airway hyperresponsiveness. Animal studies
[[Page 2969]]
have also supported the protective effects of ELF antioxidants.
b. At-Risk Subgroups for O3-Related Effects
Several characteristics may increase the extent to which a
population group shows increased susceptibility or vulnerability.
Information on potentially susceptible and vulnerable groups is
summarized in section 8.7 of the 2006 Criteria Document. As described
there, the term susceptibility refers to innate (e.g., genetic or
developmental) or acquired (e.g., personal risk factors, age) factors
that make individuals more likely to experience effects with exposure
to pollutants. A number of population groups have been identified as
potentially susceptible to health effects as a result of O3
exposure, including people with existing lung diseases, including
asthma, children and older adults, and people who have larger than
normal lung function responses that may be due to genetic
susceptibility. In addition, some population groups have been
identified as having increased vulnerability to O3-related
effects due to increased likelihood of exposure while at elevated
ventilation rates, including healthy children and adults who are active
outdoors, for example, outdoor workers and joggers. Taken together, the
susceptible and vulnerable groups make up ``at-risk'' groups.\24\
---------------------------------------------------------------------------
\24\ In the Staff Paper and documents from previous
O3 NAAQS reviews, ``at-risk'' groups have also been
called ``sensitive'' groups, to mean both groups with greater
inherent susceptibility and those more likely to be exposed.
---------------------------------------------------------------------------
i. Active People
A large group of individuals at risk from O3 exposure
consists of outdoor workers and children, adolescents, and adults who
engage in outdoor activities involving exertion or exercise during
summer daylight hours when ambient O3 concentrations tend to
be higher. This conclusion is based on a large number of controlled-
human exposure studies and several epidemiologic field/panel studies
which have been conducted with healthy children and adults and those
with preexisting respiratory diseases (EPA 2006a, sections 6.2, 6.3,
7.2, and 8.4.4). The controlled human exposure studies show a clear
O3 exposure-response relationship with increasing
spirometric and symptomatic response as exercise level increases.
Furthermore, O3-induced response increases as time of
exposure increases. Studies of outdoor workers and others who
participate in outdoor activities indicate that extended exposures to
O3 at elevated exertion levels can produce marked effects on
lung function, as discussed above in section IIA.2 (Brauer et al.,
1996; H[ouml]ppe et al., 1995; Korrick et al., 1998; McConnell et al.,
2002).
These field studies with subjects at elevated exertion levels
support the extensive evidence derived from controlled human exposure
studies. The majority of controlled human exposure studies has examined
the effects of O3 exposure in subjects performing continuous
or intermittent exercise for variable periods of time and has reported
significant O3-induced respiratory responses. The
epidemiologic studies discussed above also indicate that prolonged
exposure periods, combined with elevated levels of exertion or
exercise, may magnify O3 effects on lung function. Thus,
outdoor workers and others who participate in higher exertion
activities outdoors during the time of day when high peak O3
concentrations occur appear to be particularly vulnerable to
O3 effects on respiratory health. Although these studies
show a wide variability of response and sensitivity among subjects and
the factors contributing to this variability continue to be
incompletely understood, the effect of increased exertion is
consistent. It should be noted that this wide variability of response
and sensitivity among subjects may be in part due to the wide range of
other highly reactive photochemical oxidants coexisting with
O3 in the ambient air.
ii. People With Lung Disease
People with preexisting pulmonary disease are among those at
increased risk from O3 exposure. Altered physiological,
morphological, and biochemical states typical of respiratory diseases
like asthma, COPD, and chronic bronchitis may render people sensitive
to additional oxidative burden induced by O3 exposure. At
the time of the 1997 review, it was concluded that these groups were at
greater risk because the impact of O3-induced responses on
already-compromised respiratory systems would noticeably impair an
individual's ability to engage in normal activity or would be more
likely to result in increased self-medication or medical treatment. At
that time there was little evidence that people with pre-existing
disease were more responsive than healthy individuals in terms of the
magnitude of lung function decrements or symptomatic responses. The new
results from controlled exposure and epidemiologic studies continue to
indicate that individuals with preexisting pulmonary disease are a
sensitive population for O3-related health effects.
Several controlled human exposure studies reviewed in the 1996
Criteria Document on atopic and asthmatic subjects have suggested but
not clearly demonstrated enhanced responsiveness to acute O3
exposure compared to healthy subjects. The majority of the newer
studies reviewed in Chapter 6 of the 2006 Criteria Document indicate
that asthmatics are more sensitive than normal subjects in manifesting
O3-induced lung function decrements. In one key study
(Horstman et al., 1995), the FEV1 decrement observed in the
asthmatics was significantly larger than in the healthy subjects (19%
versus 10%, respectively). There was also a notable tendency for a
greater group mean O3-induced decrease in
FEF25-75 in asthmatics relative to the healthy subjects (24%
versus 15%, respectively). A significant positive correlation in
asthmatics was also reported between the magnitude of O3-
induced spirometric responses and baseline lung function, i.e.,
responses increased with severity of disease.
Asthmatics present a differential response profile for cellular,
molecular, and biochemical parameters (2006 Criteria Document, Figure
8-1) that are altered in response to acute O3 exposure.
Ozone-induced increases in neutrophils, IL-8 and protein were found to
be significantly higher in the BAL fluid from asthmatics compared to
healthy subjects, suggesting mechanisms for the increased sensitivity
of asthmatics (Basha et al., 1994; McBride et al., 1994; Scannell et
al., 1996; Hiltermann et al., 1999; Holz et al., 1999; Bosson et al.,
2003). Neutrophils, or PMNs, are the white blood cells most associated
with inflammation. IL-8 is an inflammatory cytokine with a number of
biological effects, primarily on neutrophils. The major role of this
cytokine is to attract and activate neutrophils. Protein in the airways
is leaked from the circulatory system, and is a marker for increased
cellular permeability.
Bronchial constriction following provocation with O3
and/or allergens presents a two-phase response. The early response is
mediated by release of histamine and leukotrienes that leads to
contraction of smooth muscle cells in the bronchi, narrowing the lumen
and decreasing the airflow. In people with allergic airway disease,
including people with rhinitis and asthma, these mediators also cause
accumulation of eosinophils in the airways (Bascom et al., 1990; Jorres
et al., 1996; Peden et al., 1995 and 1997; Frampton et al., 1997;
Michelson et al., 1999; Hiltermann et al., 1999; Holz et al., 2002;
Vagaggini et al., 2002). In asthma, the eosinophil,
[[Page 2970]]
which increases inflammation and allergic responses, is the cell most
frequently associated with exacerbations of the disease. A study by
Bosson et al. (2003) evaluated the difference in O3-induced
bronchial epithelial cytokine expression between healthy and asthmatic
subjects. After O3 exposure the epithelial expression of IL-
5 and GM-CSF increased significantly in asthmatics, compared to healthy
subjects. Asthma is associated with Th2-related airway response
(allergic response), and IL-5 is an important Th2-related cytokine. The
O3-induced increase in IL-5, and also in GM-CSF, which
affects the growth, activation and survival of eosinophils, may
indicate an effect on the Th2-related airway response and on airway
eosinophils. The authors reported that the O3-induced Th2-
related cytokine responses that were found within the asthmatic group
may indicate a worsening of their asthmatic airway inflammation and
thus suggest a plausible link to epidemiological data indicating
O3-associated increases in bronchial reactivity and hospital
admissions.
The accumulation of eosinophils in the airways of asthmatics is
followed by production of mucus and a late-phase bronchial constriction
and reduced airflow. In a study of 16 intermittent asthmatics,
Hiltermann et al. (1999) found that there was a significant inverse
correlation between the O3-induced change in the percentage
of eosinophils in induced sputum and the change in PC20, the
concentration of methacholine causing a 20% decrease in
FEV1. Characteristic O3-induced inflammatory
airway neutrophilia at one time was considered a leading mechanism of
airway hyperresponsiveness. However, Hiltermann et al. (1999)
determined that the O3-induced change in percentage
neutrophils in sputum was not significantly related to the change in
PC20. These results are consistent with the results of Zhang
et al. (1995), which found neutrophilia in a murine model to be only
coincidentally associated with airway hyperresponsiveness, i.e., there
was no cause and effect relationship. (2006 Criteria Document, AX 6-
26). Hiltermann et al. (1999) concluded that the results point to the
role of eosinophils in O3-induced airway
hyperresponsiveness. Increases in O3-induced nonspecific
airway responsiveness incidence and duration could have important
clinical implications for asthmatics.
Two studies (J[ouml]rres et al., 1996; Holz et al., 2002) observed
increased airway responsiveness to O3 exposure with
bronchial allergen challenge in subjects with preexisting allergic
airway disease. J[ouml]rres et al. (1996) found that O3
causes an increased response to bronchial allergen challenge in
subjects with allergic rhinitis and mild allergic asthma. The subjects
were exposed to 0.25 ppm O3 for 3 hours with IE. Airway
responsiveness to methacholine was determined 1 hour before and after
exposure; responsiveness to allergen was determined 3 hours after
exposure. Statistically significant decreases in FEV1
occurred in subjects with allergic rhinitis (13.8%) and allergic asthma
(10.6%), and in healthy controls (7.3%). Methacholine responsiveness
was statistically increased in asthmatics, but not in subjects with
allergic rhinitis or healthy controls. Airway responsiveness to an
individual's historical allergen (either grass and birch pollen, house
dust mite, or animal dander) was significantly increased after
O3 exposure when compared to FA exposure. In subjects with
asthma and allergic rhinitis, a maximum percent fall in FEV1
of 27.9% and 7.8%, respectively, occurred 3 days after O3
exposure when they were challenged with of the highest common dose of
allergen. The authors concluded that subjects with asthma or allergic
rhinitis, without asthma, could be at risk if a high O3
exposure is followed by a high dose of allergen. Holz et al. (2002)
reported an early phase lung function response in subjects with
rhinitis after a consecutive 4-day exposure to 0.125 ppm O3
that resulted in a clinically relevant (>20%) decrease in
FEV1. Ozone-induced exacerbation of airway responsiveness
persists longer and attenuates more slowly than O3-induced
lung function decrements and respiratory symptom responses and can have
important clinical implications for asthmatics.
A small number of in vitro studies corroborate the differences in
the responses of asthmatic and healthy subject generally found in
controlled human exposure studies. In vitro studies (Schierhorn et al.,
1999) of nasal mucosal biopsies from atopic and nonatopic subjects
exposed to 0.1 ppm O3 found significant differences in
release of IL-4, IL-6, IL-8, and TNF-[alpha]. Another study by
Schierhorn et al. (2002) found significant differences in the
O3-induced release of the neuropeptides neurokinin A and
substance P for allergic patients in comparison to nonallergic
controls, suggesting increased activation of sensory nerves by
O3 in the allergic tissues. Another study by Bayram et al.
(2002) using in vitro culture of bronchial epithelial cells recovered
from atopic and nonatopic asthmatics also found significant increases
in epithelial permeability in response to O3 exposure.
The new data on airway responsiveness, inflammation, and various
molecular markers of inflammation and bronchoconstriction indicate that
people with asthma and allergic rhinitis (with or without asthma)
comprise susceptible groups for O3-induced adverse effects.
This body of evidence indicates that controlled human exposure and
epidemiological panel studies of lung function decrements and
respiratory symptoms that evaluate only healthy, non-asthmatic subjects
likely underestimate the effects of O3 exposure on
asthmatics and other susceptible populations. The effects of
O3 on lung function, inflammation, and increased airway
responsiveness demonstrated in subjects with asthma and other allergic
airway diseases, provide plausible mechanisms underlying the more
serious respiratory morbidity effects, such as emergency department
visits and hospital admissions, and respiratory mortality effects.
A number of epidemiological studies have been conducted using
asthmatic study populations. The majority of epidemiological panel
studies that evaluated respiratory symptoms and medication use related
to O3 exposures focused on children. These studies suggest
that O3 exposure is associated with increased respiratory
symptoms and medication use in children with asthma. Other reported
effects include respiratory symptoms, lung function decrements, and
emergency department visits, as discussed in the 2006 Criteria Document
(section 7.6.7.1). Strong evidence from a large multicity study
(Mortimer et al., 2002), along with support from several single-city
studies indicate that O3 exposure is associated with
increased respiratory symptoms and medication use in children with
asthma. With regard to ambient O3 levels and increased
hospital admissions and emergency department visits for asthma and
other respiratory causes, strong and consistent evidence establishes a
correlation between O3 exposure and increased exacerbations
of preexisting respiratory disease for 1-hour maximum O3
concentrations <0.12 ppm. As discussed above and in the 2006 Criteria
Document, section 7.3, several hospital admission and emergency
department visit studies in the U.S., Canada, and Europe have reported
positive associations between increase in O3 and increased
risk of emergency department visits and hospital admissions for asthma
other
[[Page 2971]]
respiratory diseases, especially during the warm season.
In summary, based on a substantial new body of evidence from
animal, controlled human exposure and epidemiological studies the 2006
Criteria Document (section x.x) concludes that people with asthma and
other preexisting pulmonary diseases are among those at increased risk
from O3 exposure. Evidence from controlled human exposure
studies indicates that asthmatics may exhibit larger lung function
decrements and can have larger inflammatory responses in response to
O3 exposure than healthy controls. Asthmatics present a
different response profile for cellular, molecular, and biochemical
parameters that are altered in response to acute O3
exposure. Asthmatics, and people with allergic rhinitis, are more
likely to mount an allergic-type response upon exposure to
O3, as manifested by increases in white blood cells
associated with allergy and related molecules, which increase
inflammation in the airways. The increased inflammatory and allergic
responses also may be associated with the larger late-phase responses
that asthmatics can experience, which can include increased
bronchoconstrictor responses to irritant substances or allergens and
additional inflammation. Epidemiological studies have reported fairly
robust associations between ambient O3 concentrations and
measures of lung function and daily respiratory symptoms (e.g., chest
tightness, wheeze, shortness of breath) in children with moderate to
severe asthma and between O3 and increased asthma medication
use. These more serious responses in asthmatics and others with lung
disease provide biological plausibility for the respiratory morbidity
effects observed in epidemiological studies, such as emergency
department visits and hospital admissions. The body of evidence from
controlled human exposure and epidemiological studies, which includes
asthmatic as well as non-asthmatic subjects, indicates that controlled
human exposure studies of lung function decrements and respiratory
symptoms that evaluate only healthy, non-asthmatic subjects likely
underestimate the effects of O3 exposure on asthmatics and
other susceptible populations.
Newly available reports from controlled human exposure studies (see
chapter 6 in the 2006 Criteria Document) utilized subjects with
preexisting cardiopulmonary diseases such as COPD, asthma, allergic
rhinitis, and hypertension. The data generated from these studies that
evaluated changes in spirometry did not find clear differences between
filtered air and O3 exposure in COPD subjects. However, the
new data on airway responsiveness, inflammation, and various molecular
markers of inflammation and bronchoconstriction indicate that people
with atopic asthma and allergic rhinitis comprise susceptible groups
for O3-induced adverse health effects.
Although controlled human exposure studies have not found evidence
of larger spirometric responses to O3 in people with COPD
relative to healthy subjects, this may be due to the fact that most
people with COPD are older adults who would not be expected to be as
responsive based on their age. However, in section 8.7.1, the 2006
Criteria Document notes that new epidemiological evidence indicates
that people with COPD may be more likely to experience other effects,
including emergency room visits, hospital admissions, or premature
mortality. For example, results from an analysis of five European
cities indicated strong and consistent O3 effects on
unscheduled respiratory hospital admissions, including COPD (Anderson
et al., 1997). Also, an analysis of a 9-year data set for the whole
population of the Netherlands provided risk estimates for more specific
causes of mortality, including COPD (Hoek et al., 2000, 2001;
reanalysis Hoek, 2003); a positive, but nonsignificant, excess risk of
COPD-related mortality was found to be associated with short-term
O3 concentrations. Moreover, as indicated by Gong et al.
(1998), the effects of O3 exposure on alveolar-arterial
oxygen gradients may be more pronounced in patients with preexisting
obstructive lung diseases. Relative to healthy elderly subjects, COPD
patients have reduced gas exchange and low SaO2. Any
inflammatory or edematous responses due to O3 delivered to
the well-ventilated regions of the lung in COPD subjects could further
inhibit gas exchange and reduce oxygen saturation. In addition,
O3-induced vasoconstriction could also acutely induce
pulmonary hypertension. Inducing pulmonary vasoconstriction and
hypertension in these patients would perhaps worsen their condition,
especially if their right ventricular function was already compromised
(EPA, 2006a, section 6.10). These controlled human exposure and
epidemiological studies indicate that people with pre-existing lung
diseases other than asthma are also at greater risk from O3
exposure than people without lung disease.
iii. Children and Older Adults
Supporting evidence exists for heterogeneity in the effects of
O3 by age. As discussed in section 6.5.1 of the 2006
Criteria Document, children, adolescents, and young adults (<18 yrs of
age) appear, on average, to have nearly equivalent spirometric
responses to O3, but have greater responses than middle-aged
and older adults when exposed to comparable O3 doses.
Symptomatic responses to O3 exposure, however, do not appear
to occur in healthy children, but are observed in asthmatic children,
particularly those who use maintenance medications. For adults (>17 yrs
of age) symptoms gradually decrease with increasing age. In contrast to
young adults, the diminished symptomatic responses in children and the
diminished symptomatic and spirometric responses in older adults
increases the likelihood that these groups continue outdoor activities
leading to greater O3 exposure and dose.
As described in the section 7.6.7.2 of the 2006 Criteria Document,
many epidemiological field studies focused on the effect of
O3 on the respiratory health of school children. In general,
children experienced decrements in lung function parameters, including
PEF, FEV1, and FVC. Increases in respiratory symptoms and
asthma medication use were also observed in asthmatic children. In one
German study, children with and without asthma were found to be
particularly susceptible to O3 effects on lung function.
Approximately 20 percent of the children, both with and without asthma,
experienced a greater than 10 percent change in FEV1,
compared to only 5 percent of the elderly population and athletes
(H[ouml]ppe et al., 2003).
The American Academy of Pediatrics (2004) notes that children and
infants are among the population groups most susceptible to many air
pollutants, including O3. This is in part because their
lungs are still developing. For example, eighty percent of alveoli are
formed after birth, and changes in lung development continue through
adolescence (Dietert et al., 2000). Children are also likely to spend
more time outdoors than adults, which results in increased exposure to
air pollutants (Wiley et al., 1991a,b). Moreover, children have high
minute ventilation rates and high levels of physical activity which
also increases their dose (Plunkett et al., 1992).
Several mortality studies have investigated age-related differences
in O3 effects (EPA, 2006a, section 7.6.7.2). Older adults
are also often classified as
[[Page 2972]]
being particularly susceptible to air pollution. The 2006 Criteria
Document (p. 8-60) concludes that the basis for increased O3
sensitivity among the elderly is not known, but one hypothesis is that
it may be related to changes in the respiratory tract lining fluid
antioxidant defense network (Kelly et al., 2003). Older adults have
lower baseline lung function than younger people, and are also more
likely to have preexisting lung and heart disease. Increased
susceptibility of older adults to O3 health effects is most
clearly indicated in the newer mortality studies. Among the studies
that observed positive associations between O3 and
mortality, a comparison of all age or younger age (<= 65 years of age)
O3-mortality effect estimates to that of the elderly
population (> 65 years) indicates that, in general, the elderly
population is more susceptible to O3 mortality effects. The
meta-analysis by Bell et al. (2005) found a larger mortality effect
estimate for the elderly than for all ages. In the large U.S. 95
communities study (Bell et al., 2004), mortality effect estimates were
slightly higher for those aged 65 to 74 years, compared to individuals
less than 65 years and 75 years or greater. The absolute effect of
O3 on premature mortality may be substantially greater in
the elderly population because of higher rates of preexisting
respiratory and cardiac diseases. The 2006 Criteria Document (p. 7-177)
concludes that the elderly population (>65 years of age) appear to be
at greater risk of O3-related mortality and hospitalizations
compared to all ages or younger populations.
The 2006 Criteria Document notes that, collectively, there is
supporting evidence of age-related differences in susceptibility to
O3 lung function effects. The elderly population (> 65 years
of age) appear to be at increased risk of O3-related
mortality and hospitalizations, and children (< 18 years of age)
experience other potentially adverse respiratory health outcomes with
increased O3 exposure (EPA, 2006a, section 7.6.7.2).
iv. People With Increased Responsiveness to Ozone
New animal toxicology studies using various strains of mice and
rats have identified O3-sensitive and resistant strains and
illustrated the importance of genetic background in determining
O3 susceptibility (EPA, 2006a, section 8.7.4). Controlled
human exposure studies have also indicated a high degree of variability
in some of the pulmonary physiological parameters. The variable effects
in individuals have been found to be reproducible, in other words, a
person who has a large lung function response after exposure to
O3 will likely have about the same response if exposed again
to the same dose of O3. In controlled human exposure
studies, group mean responses are not representative of this segment of
the population that has much larger than average responses to
O3. Recent studies of asthmatics by David et al. (2003) and
Romieu et al. (2004) reported a role for genetic polymorphism in
observed differences in antioxidant enzymes and genes involved in
inflammation to modulate lung function and inflammatory responses to
O3 exposure.\25\
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\25\ Similar to animal toxicology studies referred above, a
polymorphism in a specific proinflammatory cytokine gene has been
implicated in O3-induced lung function changes in
healthy, mild asthmatics and individuals with rhinitis. These
observations suggest a potential role for these markers in the
innate susceptibility to O3, however, the validity of
these markers and their relevance in the context of prediction to
population studies requires additional research.
---------------------------------------------------------------------------
Biochemical and molecular parameters extensively evaluated in these
experiments were used to identify specific loci on chromosomes and, in
some cases, to relate the differential expression of specific genes to
biochemical and physiological differences observed among these species.
Utilizing O3-sensitive and O3-resistant species,
it has been possible to identify the involvement of increased airway
reactivity and inflammation processes in O3 susceptibility.
However, most of these studies were carried out using relatively high
doses of O3, making the relevance of these studies
questionable in human health effects assessment. The genes and genetic
loci identified in these studies may serve as useful biomarkers in the
future.
v. Other Population Groups
There is limited, new evidence supporting associations between
short-term O3 exposures and a range of effects on the
cardiovascular system. Some but not all, epidemiological studies have
reported associations between short-term O3 exposures and
the incidence of heart attacks and more subtle cardiovascular health
endpoints, such as changes in HRV and cardiac arrhythmia. Others have
reported associations with hospitalization or emergency department
visits for cardiovascular diseases, although the results across the
studies are not consistent. Studies also report associations between
short-term O3 exposure and mortality from cardiovascular or
cardiopulmonary causes. The 2006 Criteria Document (p. 7-65) concludes
that current cardiovascular effects evidence from some field studies is
rather limited but supportive of a potential effect of short-term
O3 exposure and HRV, cardiac arrhythmia, and heart attack
incidence. In the 2006 Criteria Document's evaluation of studies of
hospital admissions for cardiovascular disease (EPA 2006a, section
7.3.4), it is concluded that evidence from this growing group of
studies is generally inconclusive regarding an association with
O3 in studies conducted during the warm season (EPA 2006a,
p. 7-83). This body of evidence suggests that people with heart disease
may be at increased risk from short-term exposures to O3;
however, more evidence is needed to conclude that people with heart
disease are a susceptible population.
Other groups that might have enhanced sensitivity to O3,
but for which there is currently very little evidence, include groups
based on race, gender and SES, and those with nutritional deficiencies,
which presents factors which modify responsiveness to O3.
c. Adversity of Effects
In the 2008 rulemaking, in making judgments as to when various
O3-related effects become regarded as adverse to the health
of individuals, EPA looked to guidelines published by the American
Thoracic Society (ATS) and the advice of CASAC. While recognizing that
perceptions of ``medical significance'' and ``normal activity'' may
differ among physicians, lung physiologists and experimental subjects,
the ATS (1985) \26\ defined adverse respiratory health effects as
``medically significant physiologic changes generally evidenced by one
or more of the following: (1) Interference with the normal activity of
the affected person or persons, (2) episodic respiratory illness, (3)
incapacitating illness, (4) permanent respiratory injury, and/or (5)
progressive respiratory dysfunction.'' During the 1997 review, it was
concluded that there was evidence of causal associations from
controlled human exposure studies for effects in the first of these
five ATS-defined categories, evidence of statistically significant
associations from epidemiological studies for effects in the second and
third categories, and evidence from animal toxicology
[[Page 2973]]
studies, which could be extrapolated to humans only with a significant
degree of uncertainty, for the last two categories.
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\26\ In 2000, the American Thoracic Society (ATS) published an
official statement on ``What Constitutes an Adverse Health Effect of
Air Pollution?'' (ATS, 2000), which updated its earlier guidance
(ATS, 1985). Overall, the new guidance does not fundamentally change
the approach previously taken to define adversity, nor does it
suggest a need at this time to change the structure or content of
the tables describing gradation of severity and adversity of effects
described below.
---------------------------------------------------------------------------
For ethical reasons, clear causal evidence from controlled human
exposure studies still covers only effects in the first category.
However, for this review there are results from epidemiological
studies, upon which to base judgments about adversity, for effects in
all of the categories. Statistically significant and robust
associations have been reported in epidemiology studies falling into
the second and third categories. These more serious effects include
respiratory events (e.g., triggering asthma attacks) that may require
medication (e.g., asthma), but not necessarily hospitalization, as well
as respiratory hospital admissions and emergency department visits for
respiratory causes. Less conclusive, but still positive associations
have been reported for school absences and cardiovascular hospital
admissions. Human health effects for which associations have been
suggested through evidence from epidemiological and animal toxicology
studies, but have not been conclusively demonstrated still fall
primarily into the last two categories. In the 1997 review of the
O3 standard, evidence for these more serious effects came
from studies of effects in laboratory animals. Evidence from animal
studies evaluated in the 2006 Criteria Document strongly suggests that
O3 is capable of damaging the distal airways and proximal
alveoli, resulting in lung tissue remodeling leading to apparently
irreversible changes. Recent advancements of dosimetry modeling also
provide a better basis for extrapolation from animals to humans.
Information from epidemiological studies provides supporting, but
limited evidence of irreversible respiratory effects in humans than was
available in the prior review. Moreover, the findings from single-city
and multicity time-series epidemiology studies and meta-analyses of
these epidemiological studies are highly suggestive of an association
between short-term O3 exposure and mortality particularly in
the warm season.
While O3 has been associated with effects that are
clearly adverse, application of these guidelines, in particular to the
least serious category of effects related to ambient O3
exposures, involves judgments about which medical experts on the CASAC
panel and public commenters have expressed diverse views in the past.
To help frame such judgments, EPA staff have defined specific ranges of
functional responses (e.g., decrements in FEV1 and airway
responsiveness) and symptomatic responses (e.g., cough, chest pain,
wheeze), together with judgments as to the potential impact on
individuals experiencing varying degrees of severity of these
responses, that have been used in previous NAAQS reviews. These ranges
of pulmonary responses and their associated potential impacts are
summarized in Tables 3-2 and 3-3 of the 2007 Staff Paper.
For active healthy people, moderate levels of functional responses
(e.g., FEV1 decrements of >= 10 percent but < 20 percent,
lasting up to 24 hours) and/or moderate symptomatic responses (e.g.,
frequent spontaneous cough, marked discomfort on exercise or deep
breath, lasting up to 24 hours) would likely interfere with normal
activity for relatively few responsive individuals. On the other hand,
EPA staff determined that large functional responses (e.g.,
FEV1 decrements >= 20 percent, lasting longer than 24 hours)
and/or severe symptomatic responses (e.g., persistent uncontrollable
cough, severe discomfort on exercise or deep breath, lasting longer
than 24 hours) would likely interfere with normal activities for many
responsive individuals. EPA staff determined that these would be
considered adverse under ATS guidelines. In the context of standard
setting, CASAC indicated that a focus on the mid to upper end of the
range of moderate levels of functional responses (e.g., FEV1
decrements >= 15 percent but < 20 percent) is appropriate for
estimating potentially adverse lung function decrements in active
healthy people. However, for people with lung disease, even moderate
functional (e.g., FEV1 decrements >= 10 percent but < 20
percent, lasting up to 24 hours) or symptomatic responses (e.g.,
frequent spontaneous cough, marked discomfort on exercise or with deep
breath, wheeze accompanied by shortness of breath, lasting up to 24
hours) would likely interfere with normal activity for many
individuals, and would likely result in more frequent use of
medication. For people with lung disease, large functional responses
(e.g., FEV1 decrements >= 20 percent, lasting longer than 24
hours) and/or severe symptomatic responses (e.g., persistent
uncontrollable cough, severe discomfort on exercise or deep breath,
persistent wheeze accompanied by shortness of breath, lasting longer
than 24 hours) would likely interfere with normal activity for most
individuals and would increase the likelihood that these individuals
would seek medical treatment. In the context of standard setting, the
CASAC indicated (Henderson, 2006c) that a focus on the lower end of the
range of moderate levels of functional responses (e.g., FEV1
decrements >= 10 percent) is most appropriate for estimating
potentially adverse lung function decrements in people with lung
disease.
In judging the extent to which these impacts represent effects that
should be regarded as adverse to the health status of individuals, an
additional factor that has been considered in previous NAAQS reviews is
whether such effects are experienced repeatedly during the course of a
year or only on a single occasion. While some experts would judge
single occurrences of moderate responses to be a ``nuisance,''
especially for healthy individuals, a more general consensus view of
the adversity of such moderate responses emerges as the frequency of
occurrence increases.
The new guidance builds upon and expands the 1985 definition of
adversity in several ways. There is an increased focus on quality of
life measures as indicators of adversity. There is also a more specific
consideration of population risk. Exposure to air pollution that
increases the risk of an adverse effect to the entire population is
adverse, even though it may not increase the risk of any individual to
an unacceptable level. For example, a population of asthmatics could
have a distribution of lung function such that no individual has a
level associated with significant impairment. Exposure to air pollution
could shift the distribution to lower levels that still do not bring
any individual to a level that is associated with clinically relevant
effects. However, this would be considered to be adverse because
individuals within the population would have diminished reserve
function, and therefore would be at increased risk if affected by
another agent.
Of the various effects of O3 exposure that have been
studied, many would meet the ATS definition of adversity. Such effects
include, for example, any detectible level of permanent lung function
loss attributable to air pollution, including both reductions in lung
growth or acceleration of the age-related decline of lung function;
exacerbations of disease in individuals with chronic cardiopulmonary
diseases; reversible loss of lung function in combination with the
presence of symptoms; as well as more serious effects such as those
requiring medical care including hospitalization and, obviously,
mortality.
[[Page 2974]]
d. Size of At-Risk Populations
Although O3-related health risk estimates may appear to
be small, their significance from an overall public health perspective
is determined by the large numbers of individuals in the population
groups potentially at risk for O3-related health effects
discussed above. For example, a population of concern includes people
with respiratory disease, which includes approximately 11 percent of
U.S. adults and 13 percent of children who have been diagnosed with
asthma and 6 percent of adults with chronic obstructive pulmonary
disease (chronic bronchitis and/or emphysema) in 2002 and 2003 (Table
8-4 in the 2006 Criteria Document, section 8.7.5.2). More broadly,
individuals with preexisting cardiopulmonary disease may constitute an
additional population of concern, with potentially tens of millions of
people included in each disease category. In addition, populations
based on age group also comprise substantial segments of the population
that may be potentially at risk for O3-related health
impacts. Based on U.S. census data from 2003, about 26 percent of the
U.S. population are under 18 years of age and 12 percent are 65 years
of age or older. Hence, large proportions of the U.S. population are
included in life stages that are most likely to have increased
susceptibility to the health effects of O3 and/or those with
the highest ambient O3 exposures.
The 2006 Criteria Document (section 8.7.5.2) notes that the health
statistics data illustrate what is known as the ``pyramid'' of effects.
At the top of the pyramid, there are approximately 2.5 millions deaths
from all causes per year in the U.S. population, with about 100,000
deaths from chronic lower respiratory diseases. For respiratory health
diseases, there are nearly 4 million hospital discharges per year, 14
million emergency department visits, 112 million ambulatory care
visits, and an estimated 700 million restricted activity days per year
due to respiratory conditions from all causes per year. Applying small
risk estimates for the O3-related contribution to such
health effects with relatively large baseline levels of health outcomes
can result in quite large public health impacts related to ambient
O3 exposure. Thus, even a small percentage reduction in
O3 health impacts on cardiopulmonary diseases would reflect
a large number of avoided cases. In considering this information
together with the concentration-response relationships that have been
observed between exposure to O3 and various health
endpoints, the 2006 Criteria Document (section 8.7.5.2) concludes that
exposure to ambient O3 likely has a significant impact on
public health in the U.S.
B. Human Exposure and Health Risk Assessments
To put judgments about health effects that are adverse for
individuals into a broader public health context, EPA has developed and
applied models to estimate human exposures and health risks. This
broader context includes consideration of the size of particular
population groups at risk for various effects, the likelihood that
exposures of concern will occur for individuals in such groups under
varying air quality scenarios, estimates of the number of people likely
to experience O3-related effects, the variability in
estimated exposures and risks, and the kind and degree of uncertainties
inherent in assessing the exposures and risks involved.
As discussed below there are a number of important uncertainties
that affect the exposure and health risk estimates. It is also
important to note that there have been significant improvements in both
the exposure and health risk model. CASAC expressed the view that the
exposure analysis represents a state-of-the-art modeling approach and
that the health risk assessment was ``well done, balanced and
reasonably communicated (Henderson, 2006c). While recognizing and
considering the kind and degree of uncertainties in both the exposure
and health risk estimates, the 2007 Staff Paper (pp. 6-20 to 6-21)
judged that the quality of the estimates is such that they are suitable
to be used as an input to the Administrator's decisions on the
O3 primary standard.
In modeling exposures and health risks associated with just meeting
the current and alternative O3 standards, EPA has simulated
air quality to represent conditions just meeting these standards based
on O3 air quality patterns in several recent years and on
how the shape of the O3 air quality distribution have
changed over time based on historical trends in monitored O3
air quality data. As described in the 2007 Staff Paper (EPA, 2007b,
section 4.5.8) and discussed below, recent O3 air quality
distributions have been statistically adjusted to simulate just meeting
the current and selected alternative standards. These simulations do
not reflect any consideration of specific control programs or
strategies designed to achieve the reductions in emissions required to
meet the specified standards. Further, these simulations do not
represent predictions of when, whether, or how areas might meet the
specified standards.\27\
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\27\ Modeling that projects whether and how areas might attain
alternative standards in a future year is presented in the
Regulatory Impact Analysis being prepared in connection with this
rulemaking.
---------------------------------------------------------------------------
As noted in section I.C above, around the time of the release of
the final 2007 Staff Paper in January 2007, EPA discovered a small
error in the exposure model that when corrected resulted in slight
increases in the simulated exposures. Since the exposure estimates are
an input to the lung function portion of the health risk assessment,
this correction also resulted in slight increases in the lung function
risk estimates as well. The exposure and risk estimates discussed in
this notice reflect the corrected estimates, and thus are slightly
different than the exposure and risk estimates cited in the January 31,
2007 Staff Paper.\28\
---------------------------------------------------------------------------
\28\ EPA made available corrected versions of the final 2007
Staff Paper, and human exposure and health risk assessment technical
support documents in July 2007 on the EPA Web site listed in the
Availability of Related Information section of this notice.
---------------------------------------------------------------------------
1. Exposure Analyses
a. Overview
As part of the 2008 rulemaking, the EPA conducted exposure analyses
using a simulation model to estimate O3 exposures for the
general population, school age children (ages 5-18), and school age
children with asthma living in 12 U.S. metropolitan areas representing
different regions of the country where the then current 8-hour
O3 standard is not met. The emphasis on children reflects
the finding of the 1997 O3 NAAQS review that children are an
important at-risk group. The 12 modeled areas combined represent a
significant fraction of the U.S. urban population, 89 million people,
including 18 million school age children of whom approximately 2.6
million have asthma. The selection of urban areas to include in the
exposure analysis took into consideration the location of O3
epidemiological studies, the availability of ambient O3
data, and the desire to represent a range of geographic areas,
population demographics, and O3 climatology. These selection
criteria are discussed further in chapter 5 of the 2007 Staff Paper
(EPA, 2007b). The geographic extent of each modeled area consists of
the census tracts in the combined statistical area (CSA) as defined by
OMB (OMB, 2005).\29\
---------------------------------------------------------------------------
\29\ The 12 CSAs modeled are: Atlanta-Sandy Springs-Gainesville,
GA-AL; Boston-Worcester-Manchester, MA-NH; Chicago-Naperville-
Michigan City, IL-IN-WI; Cleveland-Akron-Elyria, OH; Detroit-Warren-
Flint, MI; Houston-Baytown-Huntsville, TX; Los Angeles-Long Beach-
Riverside, CA; New York-Newark-Bridgeport, NY-NJ-CT-PA;
Philadelphia-Camden-Vineland, PA-NJ-DE-MD; Sacramento--Arden-
Arcade--Truckee, CA-NV; St. Louis-St. Charles-Farmington, MO-IL;
Washington-Baltimore-N. Virginia, DC-MD-VA-WV.
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[[Page 2975]]
Exposure estimates were developed using a probabilistic exposure
model that is designed to explicitly model the numerous sources of
variability that affect people's exposures. As discussed below, the
model estimates population exposures by simulating human activity
patterns, air conditioning prevalence, air exchange rates, and other
factors. The modeled exposure estimates were developed for three recent
years of ambient O3 concentrations (2002, 2003, and 2004),
as well as for O3 concentrations adjusted to simulate
conditions associated with just meeting the then current NAAQS and
various alternative 8-hour standards based on the three year period
2002-2004.\30\ This exposure assessment is more fully described and
presented in the 2007 Staff Paper and in a technical support document,
Ozone Population Exposure Analysis for Selected Urban Areas (EPA,
2007c; hereafter Exposure Analysis TSD). The scope and methodology for
this exposure assessment were developed over the last few years with
considerable input from the CASAC Ozone Panel and the public.\31\
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\30\ All 12 of the CSAs modeled did not meet the 0.084 ppm
O3 NAAQS for the three year period examined.
\31\ The general approach used in the human exposure assessment
was described in the draft Health Assessment Plan (EPA, 2005d) that
was released to the CASAC and general public in April 2005 and was
the subject of a consultation with the CASAC O3 Panel on
May 5, 2005. In October 2005, OAQPS released the first draft of the
Staff Paper containing a chapter discussing the exposure analyses
and first draft of the Exposure Analyses TSD for CASAC consultation
and public review on December 8, 2005. In July 2006, OAQPS released
the second draft of the Staff Paper and second draft of the Exposure
Analyses TSD for CASAC review and public comment which was held by
the CASAC O3 Panel on August 24-25, 2006.
---------------------------------------------------------------------------
The goals of the O3 exposure assessment were: (1) To
provide estimates of the size of at-risk populations exposed to various
levels associated with recent O3 concentrations, and with
just meeting the current O3 NAAQS and alternative
O3 standards, in specific urban areas; (2) to provide
distributions of exposure estimates over the entire range of ambient
O3 concentrations as an important input to the lung function
risk assessment summarized below in section II.B.2; (3) to develop a
better understanding of the influence of various inputs and assumptions
on the exposure estimates; and (4) to gain insight into the
distribution of exposures and patterns of exposure reductions
associated with meeting alternative O3 standards.
The EPA recognizes that there are many sources of variability and
uncertainty inherent in the inputs to this assessment and that there is
uncertainty in the resulting O3 exposure estimates. With
respect to variability, the exposure modeling approach accounts for
variability in ambient O3 levels, demographic
characteristics, physiological attributes, activity patterns, and
factors affecting microenvironmental (e.g., indoor) concentrations. In
EPA's judgment, the most important uncertainties affecting the exposure
estimates are related to the modeling of human activity patterns over
an O3 season, the modeling of variations in ambient
concentrations near roadways, and the modeling of air exchange rates
that affect the amount of O3 that penetrates indoors.
Another important uncertainty that affects the estimation of how many
exposures are associated with moderate or greater exertion is the
characterization of energy expenditure for children engaged in various
activities. As discussed in more detail in the 2007 Staff Paper (EPA,
2007b, section 4.3.4.7), the uncertainty in energy expenditure values
carries over to the uncertainty of the modeled breathing rates, which
are important since they are used to classify exposures occurring at
moderate or greater exertion which are the relevant exposures since
O3-related effects observed in controlled human exposure
studies only are observed when individuals are engaged in some form of
exercise. The uncertainties in the exposure model inputs and the
estimated exposures have been assessed using quantitative uncertainty
and sensitivity analyses. Details are discussed in the 2007 Staff Paper
(section 4.6) and in a technical memorandum describing the exposure
modeling uncertainty analysis (Langstaff, 2007).
b. Scope and Key Components
Population exposures to O3 are primarily driven by
ambient outdoor concentrations, which vary by time of day, location,
and peoples' activities. Outdoor O3 concentration estimates
used in the exposure assessment are provided by measurements and
statistical adjustments to the measured concentrations. The current
exposure analysis allows comparisons of population exposures to
O3 within each urban area, associated with current
O3 levels and with O3 levels just meeting several
potential alternative air quality standards or scenarios. Human
exposure, regardless of the pollutant, depends on where individuals are
located and what they are doing. Inhalation exposure models are useful
in realistically estimating personal exposures to O3 based
on activity-specific breathing rates, particularly when recognizing
that large scale population exposure measurement studies have not been
conducted that are representative of the overall population or at risk
subpopulations.
The model EPA used to simulate O3 population exposure is
the Air Pollutants Exposure Model (APEX), the human inhalation exposure
model within the Total Risk Integrated Methodology (TRIM) framework
(EPA, 2006c,d). APEX is conceptually based on the probabilistic NAAQS
exposure model for O3 (pNEM/O3) used in the last
O3 NAAQS review. Since that time the model has been
restructured, improved, and expanded to reflect conceptual advances in
the science of exposure modeling and newer input data available for the
model. Key improvements to algorithms include replacement of the cohort
approach with a probabilistic sampling approach focused on individuals,
accounting for fatigue and oxygen debt after exercise in the
calculation of breathing rates, and a new approach for construction of
longitudinal activity patterns for simulated persons. Major
improvements to data input to the model include updated air exchange
rates, more recent census and commuting data, and a greatly expanded
daily time-activities database.
APEX is a probabilistic model designed to explicitly model the
numerous sources of variability that affect people's exposures. APEX
simulates the movement of individuals through time and space and
estimates their exposures to O3 in indoor, outdoor, and in-
vehicle microenvironments. The exposure model takes into account the
most significant factors contributing to total human O3
exposure, including the temporal and spatial distribution of people and
O3 concentrations throughout an urban area, the variation of
O3 levels within each microenvironment, and the effects of
exertion on breathing rate in exposed individuals. A more detailed
description of APEX and its application is presented in chapter 4 of
the 2007 Staff Paper and associated technical documents (EPA,
2006b,c,d).
Several methods have been used to evaluate the APEX model and to
characterize the uncertainty of the model estimates. These include
conducting model evaluation, sensitivity analyses, and a detailed
uncertainty analysis for one urban area.
[[Page 2976]]
These are discussed fully in the 2007 Staff Paper (section 4.6) and in
Langstaff (2007). The uncertainty of model structure was judged to be
of lesser importance than the uncertainties of the model inputs and
parameters. Model structure refers to the algorithms in APEX designed
to simulate the processes that result in people's exposures, for
example, the way that APEX models exposures to individuals when they
are near roads. The uncertainties in the model input data (e.g.,
measurement error, ambient concentrations, air exchange rates, and
activity pattern data) have been assessed individually, and their
impact on the uncertainty in the modeled exposure estimates was
assessed in a unified quantitative analysis with results expressed in
the form of estimated confidence ranges around the estimated measures
of exposure. This uncertainty analysis was conducted for one urban area
(Boston) using the observed 2002 O3 concentrations and 2002
concentrations adjusted to simulate just meeting the current standard,
with the expectation that the results would be similar for other cities
and years. One significant source of uncertainty, due to limitations in
the database used to model peoples' daily activities, was not included
in the unified analysis, and was assessed through separate sensitivity
analyses. This analysis indicates that the uncertainty of the exposure
results is relatively small. For example, 95 percent uncertainty
intervals were calculated for the APEX estimates of the percent of
children or asthmatic children with exposures above 0.060, 0.070, or
0.080 ppm under moderate exertion, for two air quality scenarios
(current 2002 and 2002 adjusted to simulate just meeting the current
standard) in Boston (Langstaff, 2007, Tables 26 and 27). The 95 percent
uncertainty intervals for this set of 12 exposure estimates indicate
the possibility of underpredictions of the exposure estimates ranging
from 3 to 25 percent of the modeled estimates, and overpredictions
ranging from 4 to 11 percent of the estimates. For example, APEX
estimates the percent of asthmatic children with exposures above 0.070
ppm under moderate exertion to be 24 percent, for Boston 2002
O3 concentrations adjusted to simulate just meeting the
current standard. The 95 percent uncertainty interval for this estimate
is 23-30 percent, or -4 to +25 percent of the estimate. These
uncertainty intervals do not include the uncertainty engendered by
limitations of the activity database, which is in the range of one to
ten percent.
The exposure periods modeled here are the O3 seasons in
2002, 2003, and 2004. The O3 season in each area includes
the period of the year where elevated O3 levels tend to be
observed and for which routine hourly O3 monitoring data are
available. Typically this period spans from March or April through
September or October, or in some areas, spanning the entire year. Three
years were modeled to reflect the substantial year-to-year variability
that occurs in O3 levels and related meteorological
conditions, and because the standard is specified in terms of a three-
year period. The year-to-year variability observed in O3
levels is due to a combination of different weather patterns and the
variation in emissions of O3 precursors. Nationally, 2002
was a relatively high year with respect to the 4th highest daily
maximum 8-hour O3 levels observed in urban areas across the
U.S. (EPA, 2007b, Figure 2-16), with the mean of the distribution of
O3 levels for the urban monitors being in the upper third
among the years 1990 through 2006. In contrast, on a national basis,
2004 is the lowest year on record through 2006 for this same air
quality statistic, and 8-hour daily maximum O3 levels
observed in most, but not all of the 12 urban areas included in the
exposure and risk analyses were relatively low compared to other recent
years. The 4th highest daily maximum 8-hour O3 levels
observed in 2003 in the 12 urban areas and nationally generally were
between those observed in 2002 and 2004.
Regulatory scenarios examined in the 2008 rulemaking include the
then current 0.08 ppm, average of the 4th daily maximum 8-hour averages
over a three year period standard; standards with the same form but
with alternative levels of 0.080, 0.074, 0.070, and 0.064 ppm;
standards specified as the average of the 3rd highest daily maximum 8-
hour averages over a three year period with alternative levels of 0.084
and 0.074 ppm; and a standard specified as the average of the 5th
highest daily maximum 8-hour averages over a three year period with a
level of 0.074 ppm.\32\ The then current standard used a rounding
convention that allows areas to have an average of the 4th daily
maximum 8-hour averages as high as 0.084 ppm and still meet the
standard. All alternative standards analyzed were intended to reflect
improved precision in the measurement of ambient concentrations (in
ppm), where the precision would extend to three instead of two decimal
places.
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\32\ The 8-hour O3 standard established in 1997 was
0.08 ppm, but the rounding convention specified that the average of
the 4th daily maximum 8-hour average concentrations over a three-
year period must be at 0.084 ppm or lower to be in attainment of
this standard. When EPA staff selected alternative standards to
analyze, it was presumed that the same type of rounding convention
would be used, and thus alternative standards of 0.084, 0.074, 0.064
ppm were chosen.
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The then current standard and all alternative standards were
modeled using a quadratic rollback approach to adjust the hourly
concentrations observed in 2002-2004 to yield a design value \33\
corresponding to the standard being analyzed. The quadratic rollback
technique reduces higher concentrations more than lower concentrations
near ambient background levels.\34\ This procedure was considered in a
sensitivity analysis in the 1997 review of the O3 standard
and has been shown to be more realistic than a linear, proportional
rollback method, where all of the ambient concentrations are reduced by
the same factor.
---------------------------------------------------------------------------
\33\ A design value is a statistic that describes the air
quality status of a given area relative to the level of the NAAQS.
Design values are often based on multiple years of data, consistent
with specification of the NAAQS in Part 50 of the CFR. For the 8-
hour O3 NAAQS, the 3-year average of the annual 4th-
highest daily maximum 8-hour average concentrations, based on the
monitor within (or downwind of) an urban area yielding the highest
3-year average, is the design value.
\34\ The quadratic rollback approach and evaluation of this
approach are described by Johnson (1997), Duff et al. (1998) and
Rizzo (2005, 2006).
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c. Exposure Estimates and Key Observations
The exposure assessment, which provides estimates of the number of
people exposed to different levels of ambient O3 while at
specified exertion levels,\35\ serve two purposes. First, the entire
range of modeled personal exposures to ambient O3 is an
essential input to the portion of the health risk assessment based on
exposure-response functions from controlled human exposure studies,
discussed in the next section. Second, estimates of personal exposures
to ambient O3 concentrations at and above specific benchmark
levels provide some perspective on the public
[[Page 2977]]
health impacts of health effects that cannot currently be evaluated in
quantitative risk assessments that may occur at current air quality
levels, and the extent to which such impacts might be reduced by
meeting the current and alternative standards. This is especially true
when there are exposure levels at which it is known or can reasonably
be inferred that specific O3-related health effects are
occurring. In this notice, exposures at and above these benchmark
concentrations are referred to as ``exposures of concern.''
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\35\ As discussed above in Section II.A, O3 health
responses observed in controlled human exposure studies are
associated with exposures while engaged in moderate or greater
exertion and, therefore, these are the exposure measures of
interest. The level of exertion of individuals engaged in particular
activities is measured by an equivalent ventilation rate (EVR),
ventilation normalized by body surface area (BSA, in m\2\), which is
calculated as VE/BSA, where VE is the ventilation rate (liters/
minute). Moderate and greater exertion levels were defined as EVR >
13 liters/min-m\2\ (Whitfield et al., 1996) to correspond to the
exertion levels measured in most subjects studied in the controlled
human exposure studies that reported health effects associated with
6.6 hour O3 exposures.
---------------------------------------------------------------------------
It is important to note that although the analysis of ``exposures
of concern'' was conducted using three discrete benchmark levels (i.e.,
0.080, 0.070, and 0.060 ppm), the concept is more appropriately viewed
as a continuum with greater confidence and less uncertainty about the
existence of health effects at the upper end and less confidence and
greater uncertainty as one considers increasingly lower O3
exposure levels. The EPA recognizes that there is no sharp breakpoint
within the continuum ranging from at and above 0.080 ppm down to 0.060
ppm. In considering the concept of exposures of concern, it is
important to balance concerns about the potential for health effects
and their severity with the increasing uncertainty associated with our
understanding of the likelihood of such effects at lower O3
levels.
Within the context of this continuum, estimates of exposures of
concern at discrete benchmark levels provide some perspective on the
public health impacts of O3-related health effects that have
been demonstrated in controlled human exposure and toxicological
studies but cannot be evaluated in quantitative risk assessments, such
as lung inflammation, increased airway responsiveness, and changes in
host defenses. They also help in understanding the extent to which such
impacts have the potential to be reduced by meeting the current and
alternative standards. In the selection of specific benchmark
concentrations for this analysis, staff first considered the exposure
level of 0.080 ppm, at which there is a substantial amount of
controlled human exposure evidence demonstrating a range of
O3-related health effects including lung inflammation and
airway responsiveness in healthy individuals. Thus, as in the 1997
review, this level was selected as a benchmark level for this
assessment of exposures of concern. Evidence newly available in this
review is the basis for identifying additional, lower benchmark levels
of 0.070 and 0.060 ppm for this assessment.
More specifically, as discussed above in section II.A.2, evidence
available from controlled human exposure and epidemiological studies
indicates that people with asthma have larger and more serious effects
than healthy individuals, including lung function, respiratory
symptoms, increased airway responsiveness, and pulmonary inflammation,
which has been shown to be a more sensitive marker than lung function
responses. Further, a substantial new body of evidence from
epidemiological studies shows associations with serious respiratory
morbidity and cardiopulmonary mortality effects at O3 levels
that extend below 0.080 ppm. Additional, but very limited new evidence
from controlled human exposure studies shows lung function decrements
and respiratory symptoms in healthy subjects at an O3
exposure level of 0.060 ppm. The selected benchmark level of 0.070 ppm
reflects the new information that asthmatics have larger and more
serious effects than healthy people and therefore controlled human
exposure studies done with healthy subjects may underestimate effects
in this group, as well as the substantial body of epidemiological
evidence of associations with O3 levels below 0.080 ppm. The
selected benchmark level of 0.060 ppm additionally reflects the very
limited new evidence from controlled human exposure studies that show
lung function decrements and respiratory symptoms in some healthy
subjects at the 0.060 ppm exposure level, recognizing that asthmatics
are likely to have more serious responses and that lung function is not
likely to be as sensitive a marker for O3 effects as is lung
inflammation.
The estimates of exposures of concern were reported in terms of
both ``people exposed'' (the number and percent of people who
experience a given level of O3 concentrations, or higher, at
least one time during the O3 season in a given year) and
``occurrences of exposure'' (the number of times a given level of
pollution is experienced by the population of interest, expressed in
terms of person-days of occurrences). Estimating exposures of concern
is important because it provides some indication of the potential
public health impacts of a range of O3-related health
outcomes, such as lung inflammation, increased airway responsiveness,
and changes in host defenses. These particular health effects have been
demonstrated in controlled human exposure studies of healthy
individuals to occur at levels as low as 0.080 ppm O3, but
have not been evaluated at lower levels in controlled human exposure
studies. The EPA did not include these effects in the quantitative risk
assessment due to a lack of adequate information on the exposure-
response relationships.
The 1997 O3 NAAQS review estimated exposures associated
with 1-hour heavy exertion, 1-hour moderate exertion, and 8-hour
moderate exertion for children, outdoor workers, and the general
population. The EPA's analysis in the 1997 Staff Paper showed that
exposure estimates based on the 8-hour moderate exertion scenario for
children yielded the largest number of children experiencing exposures
at or above exposures of concern. Consequently, EPA chose to focus on
the 8-hour moderate and greater exertion exposures in all and asthmatic
school age children in the current exposure assessment. While outdoor
workers and other adults who engage in moderate or greater exertion for
prolonged durations while outdoors during the day in areas experiencing
elevated O3 concentrations also are at risk for experiencing
exposures associated with O3-related health effects, EPA did
not focus on quantitative estimates for these populations due to the
lack of information about the number of individuals who regularly work
or exercise outdoors. Thus, the exposure estimates presented here and
in the 2007 Staff Paper are most useful for making relative comparisons
across alternative air quality scenarios and do not represent the total
exposures in all children or other groups within the general population
associated with the air quality scenarios.
Population exposures to O3 were estimated in 12 urban
areas for 2002, 2003, and 2004 air quality, and also using
O3 concentrations adjusted to just meet the then current and
several alternative standards. The estimates of 8-hour exposures of
concern at and above benchmark levels of 0.080, 0.070, and 0.060 ppm
aggregated across all 12 areas are shown in Table 1 for air quality
scenarios just meeting the current and four alternative 8-hour average
standards.\36\ Table 1 provides estimates of the number and percent of
school age children and asthmatic school age children exposed, with
daily 8-hour maximum exposures at or above each O3 benchmark
level of exposures of concern, while at intermittent moderate or
greater exertion and based on O3 concentrations observed in
2002 and
[[Page 2978]]
2004. Table 1 summarizes estimates for 2002 and 2004 because these
years reflect years that bracket relatively higher and lower
O3 levels, with year 2003 generally containing O3
levels in between when considering the 12 urban areas modeled. This
table also reports the percent change in the number of persons exposed
when a given alternative standard is compared with the then current
standard.
---------------------------------------------------------------------------
\36\ The full range of quantitative exposure estimates
associated with just meeting the 0.084 ppm and alternative
O3 standards are presented in chapter 4 and Appendix 4A
of the 2007 Staff Paper.
---------------------------------------------------------------------------
Key observations important in comparing exposure estimates
associated with just meeting the current NAAQS and alternative
standards under consideration include:
(1) As shown in Table 6-1 of the 2007 Staff Paper, the patterns of
exposure in terms of percentages of the population exceeding a given
exposure level are very similar for the general population and for
asthmatic and all school age (5-18) children, although children are
about twice as likely to be exposed, based on the percent of the
population exposed, at any given level.
(2) As shown in Table 1 below, the number and percentage of
asthmatic and all school-age children aggregated across the 12 urban
areas estimated to experience one or more exposures of concern decline
from simulations of just meeting the then current 0.084 ppm standard to
simulations of alternative 8-hour standards by varying amounts
depending on the benchmark level, the population subgroup considered,
and the year chosen. For example, the estimated percentage of school
age children experiencing one or more exposures >= 0.070 ppm, while
engaged in moderate or greater exertion, during an O3 season
is about 18 percent of this population when the 0.084 ppm standard is
met using the 2002 simulation; this is reduced to about 12, 4, 1, and
0.2 percent of children upon meeting alternative standards of 0.080,
0.074, 0.070, and 0.064 ppm, respectively (all specified in terms of
the 4th highest daily maximum 8-hour average), using the 2002
simulation.
Table 1--Number and Percent of All and Asthmatic School Age Children in 12 Urban Areas Estimated To Experience 8-Hour Ozone Exposures Above 0.080,
0.070, and 0.060 ppm While at Moderate or Greater Exertion, One or More Times per Season, and the Number of Occurrences Associated With Just Meeting
Alternative 8-Hour Standards Based on Adjusting 2002 and 2004 Air Quality Data1 2
--------------------------------------------------------------------------------------------------------------------------------------------------------
All children, ages 5-18 Aggregate for 12 urban Asthmatic children, ages 5-18 Aggregate for 12
8-Hour air areas Number of children exposed (% of all) [% urban areas Number of children exposed (% of
Benchmark levels of exposures of quality reduction from 0.084 ppm standard] group) [% reduction from 0.084 ppm standard]
concern (ppm) standards \3\ ----------------------------------------------------------------------------------------------------
(ppm) 2002 2004 2002 2004
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.080.............................. 0.084 700,000 (4%) 30,000 (0%) 110,000 (4%) 0 (0%)
0.080 290,000 (2%) [70%] 10,000 (0%) [67%] 50,000 (2%) [54%] 0 (0%)
0.074 60,000 (0%) [91%] 0 (0%) [100%] 10,000 (0%) [91%] 0 (0%)
0.070 10,000 (0%) [98%] 0 (0%) [100%] 0 (0%) [100%] 0 (0%)
0.064 0 (0%) [100%] 0 (0%) [100%] 0 (0%) [100%] 0 (0%)
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.070.............................. 0.084 3,340,000 (18%) 260,000 (1%) 520,000 (20%) 40,000 (1%)
0.080 2,160,000 (12%) [35%] 100,000 (1%) [62%] 330,000 (13%) [36%] 10,000 (0%) [75%]
0.074 770,000 (4%) [77%] 20,000 (0%) [92%] 120,000 (5%) [77% ] 0 (0%) [100%]
0.070 270,000 (1%) [92%] 0 (0%) [100%] 50,000 (2%) [90%] 0 (0%) [100%]
0.064 30,000 (0.2%) [99%] 0 (0%) [100%] 10,000 (0.2%) [98% ] 0 (0%) [100%]
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.060.............................. 0.084 7,970,000 (44%) 1,800,000 (10%) 1,210,000 (47%) 270,000 (11%)
0.080 6,730,000 (37%) [16%] 1,050,000 (6%) [42%] 1,020,000 (40%) [16%] 150,000 (6%) [44%]
0.074 4,550,000 (25%) [43%] 350,000 (2%) [80%] 700,000 (27%) [42%] 50,000 (2%) [81%]
0.070 3,000,000 (16%) [62%] 110,000 (1%) [94%] 460,000 (18%) [62%] 10,000 (1%) [96%]
0.064 950,000 (5%) [88%] 10,000 (0%) [99%] 150,000 (6%) [88%] 0 (0%) [100%]
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate = 13 l-min/m\2\.
\2\ Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New
York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston, Los Angeles and
Sacramento and March or April to September or October for the remaining urban areas.
\3\ All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of the annual
4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the 2007 Staff Paper
(EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard and
selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might meet the specified standards.
(3) Substantial year-to-year variability in exposure estimates is
observed over the three-year modeling period. For example, the
estimated number of school age children experiencing one or more
exposures >= 0.070 ppm during an O3 season when a 0.084 ppm
standard is met in the 12 urban areas included in the analysis is 3.3,
1.0, or 0.3 million for the 2002, 2003, and 2004 simulations,
respectively.
(4) There is substantial variability observed across the 12 urban
areas in the percent of the population subgroups estimated to
experience exposures of concern. For example, when 2002 O3
concentrations are simulated to just meet a 0.084 ppm standard, the
aggregate 12 urban area estimate is 18 percent of all school age
children are estimated to experience O3 exposures >= 0.070
ppm (Table 1 below), while the range of exposure estimates in the 12
urban areas considered separately for all children range from 1 to 38
percent (EPA, 2007b, p. 4-48, Exhibit 2). There was also variability in
exposure estimates among the modeled areas when using the 2004 air
quality simulation for the same scenario; however it was reduced and
ranged from 0 to 7 percent in the 12 urban areas (EPA, 2007b, p. 4-60,
Exhibit 8).
(5) Of particular note, as discussed above in section II.A of this
notice, high inter-individual variability in responsiveness means that
only a subset of individuals in these groups who are exposed at and
above a given benchmark level would actually be expected to experience
such adverse health effects.
[[Page 2979]]
(6) In considering these observations, it is important to take into
account the variability, uncertainties, and limitations associated with
this assessment, including the degree of uncertainty associated with a
number of model inputs and uncertainty in the model itself, as
discussed above.
2. Quantitative Health Risk Assessment
This section discusses the approach used to develop quantitative
health risk estimates associated with exposures to O3
building upon a more limited risk assessment that was conducted during
the last review.\37\ As part of the 1997 review, EPA conducted a health
risk assessment that produced risk estimates for the number and percent
of children and outdoor workers experiencing lung function and
respiratory symptoms associated with O3 exposures for 9
urban areas.\38\ The risk assessment for the 1997 review also included
risk estimates for excess respiratory-related hospital admissions
related to O3 concentrations for New York City. In the last
review, the risk estimates played a significant role in both the staff
recommendations and in the proposed and final decisions to revise the
O3 standards. The health risk assessment conducted for the
current review builds upon the methodology and lessons learned from the
prior review.
---------------------------------------------------------------------------
\37\ The methodology, scope, and results from the risk
assessment conducted in the last review are described in Chapter 6
of the 1996 Staff Paper (EPA, 1996) and in several technical reports
(Whitfield et al., 1996; Whitfield, 1997) and publication (Whitfield
et al., 1998).
\38\ The 9 urban study areas included in the exposure and risk
analyses conducted during the last review were: Chicago, Denver,
Houston, Los Angeles, Miami, New York City, Philadelphia, St. Louis,
and Washington, DC.
---------------------------------------------------------------------------
a. Overview
The updated health risk assessment conducted as part of the 2008
rulemaking includes estimates of (1) risks of lung function decrements
in all and asthmatic school age children, respiratory symptoms in
asthmatic children, respiratory-related hospital admissions, and non-
accidental and cardiorespiratory-related mortality associated with
recent ambient O3 levels; (2) risk reductions and remaining
risks associated with just meeting the then current 0.084 ppm 8-hour
O3 NAAQS; and (3) risk reductions and remaining risks
associated with just meeting various alternative 8-hour O3
NAAQS in a number of example urban areas. This risk assessment is more
fully described and presented in chapter 5 of the 2007 Staff Paper and
in a technical support document (TSD), Ozone Health Risk Assessment for
Selected Urban Areas (Abt Associates, 2007a, hereafter referred to as
``Risk Assessment TSD''). The scope and methodology for this risk
assessment were developed over the last few years with considerable
input from the CASAC O3 Panel and the public.\39\ The
information contained in these documents included specific criteria for
the selection of health endpoints, studies, and locations to include in
the assessment. In a peer review letter sent by CASAC to the
Administrator documenting its advice in October 2006 (Henderson,
2006c), the CASAC O3 Panel concluded that the risk
assessment was ``well done, balanced, and reasonably communicated'' and
that the selection of health endpoints for inclusion in the
quantitative risk assessment was appropriate.
---------------------------------------------------------------------------
\39\ The general approach used in the health risk assessment was
described in the draft Health Assessment Plan (EPA, 2005d) that was
released to the CASAC and general public in April 2005 and was the
subject of a consultation with the CASAC O3 Panel on May
5, 2005. In October 2005, OAQPS released the first draft of the
Staff Paper containing a chapter discussing the risk assessment and
first draft of the Risk Assessment TSD for CASAC consultation and
public review on December 8, 2005. In July 2006, OAQPS released the
second draft of the Staff Paper and second draft of the Risk
Assessment TSD for CASAC review and public comment which was held by
the CASAC O3 Panel on August 24-25, 2006.
---------------------------------------------------------------------------
The goals of the risk assessment are: (1) To provide estimates of
the potential magnitude of several morbidity effects and mortality
associated with current O3 levels, and with meeting the then
current 0.084 ppm standard and alternative 8-hour O3
standards in specific urban areas; (2) to develop a better
understanding of the influence of various inputs and assumptions on the
risk estimates; and (3) to gain insights into the distribution of risks
and patterns of risk reductions associated with meeting alternative
O3 standards. The health risk assessment is intended to be
dependent on and reflect the overall weight and nature of the health
effects evidence discussed above in section II.A and in more detail in
the 2006 Criteria Document and 2007 Staff Paper. While not independent
of the overall evaluation of the health effects evidence, the
quantitative health risk assessment provides additional insights
regarding the relative public health implications associated with just
meeting a 0.084 ppm standard and several alternative 8-hour standards.
The risk assessment covers a variety of health effects for which
there is adequate information to develop quantitative risk estimates.
However, as noted by CASAC (Henderson, 2007) and in the 2007 Staff
Paper, there are a number of health endpoints (e.g., increased lung
inflammation, increased airway responsiveness, impaired host defenses,
increased medication usage for asthmatics, increased emergency
department visits for respiratory causes, and increased school
absences) for which there currently is insufficient information to
develop quantitative risk estimates, but which are important to
consider in assessing the overall public health impacts associated with
exposures to O3. These additional health endpoints are
discussed above in section II.A.2 and are also taken into account in
considering the level of exposures of concern in populations
particularly at risk, discussed above in this notice.
There are two parts to the health risk assessment: One based on
combining information from controlled human exposure studies with
modeled population exposure and the other based on combining
information from community epidemiological studies with either
monitored or adjusted ambient concentrations levels. Both parts of the
risk assessment were implemented within a new probabilistic version of
TRIM.Risk, the component of EPA's Total Risk Integrated Methodology
(TRIM) model framework that estimates human health risks.
The EPA recognizes that there are many sources of uncertainty and
variability in the inputs to this assessment and that there is
significant variability and uncertainty in the resulting O3
risk estimates. As discussed in chapters 2, 5, and 6 of the 2007 Staff
Paper, there is significant year-to-year and city-to-city variability
related to the air quality data that affects both the controlled human
exposure studies-based and epidemiological studies-based parts of the
risk assessment. There are also uncertainties associated with the air
quality adjustment procedure used to simulate just meeting various
alternative standards. In the prior review, different statistical
approaches using alternative functional forms (i.e., quadratic,
proportional, Weibull) were used to reflect how O3 air
quality concentrations have historically changed. Based on sensitivity
analyses conducted in the prior review, the choice of alternative air
quality adjustment procedures had only a modest impact on the risk
estimates (EPA, 2007b, p. 6-20). With respect to uncertainties about
estimated background concentrations, as discussed below and in the 2007
Staff Paper (section 5.4.3), alternative assumptions about background
levels have a variable impact depending on the location, standard, and
health endpoint analyzed.
[[Page 2980]]
With respect to the lung function part of the health risk
assessment, key uncertainties include uncertainties in the exposure
estimates, discussed above, and uncertainties associated with the shape
of the exposure-response relationship, especially at levels below 0.08
ppm, 8-hour average, where only very limited data are available down to
0.04 ppm and there is an absence of data below 0.04 ppm (EPA, 2007b,
pp. 6-20 to 6-21). Concerning the part of the risk assessment based on
effects reported in epidemiological studies, important uncertainties
include uncertainties (1) surrounding estimates of the O3
coefficients for concentration-response relationships used in the
assessment, (2) involving the shape of the concentration-response
relationship and whether or not a population threshold or non-linear
relationship exists within the range of concentrations examined in the
studies, (3) related to the extent to which concentration-response
relationships derived from studies in a given location and time when
O3 levels were higher or behavior and/or housing conditions
were different provide accurate representations of the relationships
for the same locations with lower air quality distributions and/or
different behavior and/or housing conditions, and (4) concerning the
possible role of co-pollutants which also may have varied between the
time of the studies and the current assessment period. An important
additional uncertainty for the mortality risk estimates is the extent
to which the associations reported between O3 and non-
accidental and cardiorespiratory mortality actually reflect causal
relationships.
As discussed below, some of these uncertainties have been addressed
quantitatively in the form of estimated confidence ranges around
central risk estimates; others are addressed through separate
sensitivity analyses (e.g., the influence of alternative estimates for
policy-relevant background levels) or are characterized qualitatively.
For both parts of the health risk assessment, statistical uncertainty
due to sampling error has been characterized and is expressed in terms
of 95 percent credible intervals. The EPA recognizes that these
credible intervals do not reflect all of the uncertainties noted above.
b. Scope and Key Components
The health risk assessment is based on the information evaluated in
the 2006 Criteria Document. The risk assessment includes several
categories of health effects and estimates risks associated with just
meeting a 0.084 ppm standard and alternative 8-hour O3 NAAQS
and with several individual recent years of air quality (i.e., 2002,
2003, and 2004). The risk assessment considers the same alternative air
quality scenarios that were examined in the human exposure analyses
described above. Risk estimates were developed for up to 12 urban areas
selected to illustrate the public health impacts associated with these
air quality scenarios.\40\ As discussed above in section II.B.1, the
selection of urban areas was largely determined by identifying areas in
the U.S. which represented a range of geographic areas, population
demographics, and climatology; with an emphasis on areas that did not
meet the then current 0.084 ppm 8-hour O3 NAAQS and which
included the largest areas with O3 nonattainment problems.
The selection criteria also included whether or not there were
acceptable epidemiological studies available that reported
concentration-response relationships for the health endpoints selected
for inclusion in the assessment.
---------------------------------------------------------------------------
\40\ The 12 urban areas are the same urban areas evaluated in
the exposure analysis discussed in the prior section. However, for
most of the health endpoints based on findings from epidemiological
studies, the geographic areas and populations examined in the health
risk assessment were limited to those counties included in the
original epidemiological studies that served as the basis for the
concentration-response relationships.
---------------------------------------------------------------------------
The short-term exposure related health endpoints selected for
inclusion in the quantitative risk assessment include those for which
the 2006 Criteria Document or the 2007 Staff Paper concluded that the
evidence as a whole supports the general conclusion that O3,
acting alone and/or in combination with other components in the ambient
air pollution mix, is either clearly causal or is judged to be likely
causal. Some health effects met this criterion of likely causality, but
were not included in the risk assessment for other reasons, such as
insufficient exposure-response data or lack of baseline incidence data.
As discussed in the section above describing the exposure analysis,
in order to estimate the health risks associated with just meeting
various alternative 8-hour O3 NAAQS, it is necessary to
estimate the distribution of hourly O3 concentrations that
would occur under any given standard. Since compliance is based on a 3-
year average, the amount of control has been applied to each year of
data (i.e., 2002 to 2004) to estimate risks for a single O3
season or single warm O3 season, depending on the health
effect, based on a simulation that adjusted each of these individual
years so that the three year period would just meet the specified
standard.
Consistent with the risk assessment approach used in the last
review, the risk estimates developed for both recent air quality levels
and just meeting the then current 0.084 ppm standard and selected
alternative 8-hour standards represent risks associated with
O3 levels attributable to anthropogenic sources and
activities (i.e., risk associated with concentrations above ``policy-
relevant background''). Policy-relevant background O3
concentrations used in the O3 risk assessment were defined
in chapter 2 of the 2007 Staff Paper (pp. 2-48--2-55) as the
O3 concentrations that would be observed in the U.S. in the
absence of anthropogenic emissions of precursors (e.g., VOC,
NOX, and CO) in the U.S., Canada, and Mexico. The results of
a global tropospheric O3 model (GEOS-CHEM) have been used to
estimate monthly background daily diurnal profiles for each of the 12
urban areas for each month of the O3 season using
meteorology for the year 2001. Based on the results of the GEOS-CHEM
model, the Criteria Document indicates that background O3
concentrations are generally predicted to be in the range of 0.015 to
0.035 ppm in the afternoon, and they are generally lower under
conditions conducive to man-made O3 episodes.\41\
---------------------------------------------------------------------------
\41\ EPA notes that the estimated level of policy-relevant
background O3 used in the prior risk assessment was a
single concentration of 0.04 ppm, which was the midpoint of the
range of levels for policy-relevant background that was provided in
the 1996 Criteria Document.
---------------------------------------------------------------------------
This approach of estimating risks in excess of background is judged
to be more relevant to policy decisions regarding ambient air quality
standards than risk estimates that include effects potentially
attributable to uncontrollable background O3 concentrations.
Sensitivity analyses examining the impact of alternative estimates for
background on lung function and mortality risk estimates have been
developed and are included in the 2007 Staff Paper and Risk Assessment
TSD and key observations are discussed below. Further, CASAC noted the
difficulties and complexities associated with available approaches to
estimating policy-relevant background concentrations (Henderson, 2007).
In the first part of the risk assessment, lung function decrement,
as measured by FEV1, is the only health response that is
based on data from controlled human exposure studies. As discussed
above, there is clear evidence of a causal relationship between lung
function decrements and O3 exposures for school age children
engaged in moderate
[[Page 2981]]
exertion based on numerous controlled human exposure and summer camp
field studies conducted by various investigators. Risk estimates have
been developed for O3-related lung function decrements
(measured as changes in FEV1) for all school age children
(ages 5 to 18) and a subset of this group, asthmatic school age
children (ages 5 to 18), whose average exertion over an 8-hour period
was moderate or greater. The exposure period and exertion level were
chosen to generally match the exposure period and exertion level used
in the controlled human exposure studies that were the basis for the
exposure-response relationships. A combined data set including
individual level data from the Folinsbee et al. (1988), Horstman et al.
(1990), and McDonnell et al. (1991) studies, used in the previous risk
assessment, and more recent data from Adams (2002, 2003a, 2006) have
been used to estimate probabilistic exposure-response relationships for
8-hour exposures under different definitions of lung function response
(i.e., >= 10, 15, and 20 percent decrements in FEV1). As
discussed in the 2007 Staff Paper (p. 5-27), while these specific
controlled human exposure studies only included healthy adults aged 18-
35, findings from other controlled human exposure studies and summer
camp field studies involving school age children in at least six
different locations in the northeastern United States, Canada, and
Southern California indicated changes in lung function in healthy
children similar to those observed in healthy adults exposed to
O3 under controlled chamber conditions.
Consistent with advice from CASAC (Henderson, 2006c), EPA has
considered both linear and logistic functional forms in estimating the
probabilistic exposure-response relationships for lung function
responses. A Bayesian Markov Chain Monte Carlo approach, described in
more detail in the Risk Assessment TSD, has been used that incorporates
both model uncertainty and uncertainty due to sample size in the
combined data set that served as the basis for the assessment. The EPA
has chosen a model reflecting a 90 percent weighting on a logistic form
and a 10 percent weighting on a linear form as the base case for the
risk assessment. The basis for this choice is that the logistic form
provides a very good fit to the combined data set, but a linear model
cannot be entirely ruled out since there are only very limited data
(i.e., 30 subjects) at the two lowest exposure levels (i.e., 0.040 and
0.060 ppm). The EPA has conducted a sensitivity analysis which examines
the impact on the lung function risk estimates of two alternative
choices, an 80 percent logistic/20 percent linear split and a 50
percent logistic/50 percent linear split.
As noted above, risk estimates have been developed for three
measures of lung function response (i.e., >= 10, 15, and 20 percent
decrements in FEV1). However, the 2007 Staff Paper and risk
estimates summarized below focus on FEV1 decrements >= 15
percent for all school age children and >= 10 percent for asthmatic
school age children, consistent with the advice from CASAC (Henderson,
2006c) that these levels of response represent indicators of adverse
health effects in these populations. The Risk Assessment TSD and 2007
Staff Paper present the broader range of risk estimates including all
three measures of lung function response.
Developing risk estimates for lung function decrements involved
combining probabilistic exposure-response relationships based on the
combined data set from several controlled human exposure studies with
population exposure distributions for all and asthmatic school age
children associated with recent air quality and air quality simulated
to just meet the then current 0.084 ppm standard and alternative 8-hour
O3 NAAQS based on the results from the exposure analysis
described in the previous section. The risk estimates have been
developed for 12 large urban areas for the O3 season.\42\
These 12 urban areas include approximately 18.3 million school age
children, of which 2.6 million are asthmatic school age children.\43\
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\42\ As discussed above in section II.B.1, the urban areas were
defined using the consolidated statistical areas definition and the
total population residing in the 12 urban areas was approximately
88.5 million people.
\43\ For 9 of the 12 urban areas, the O3 season is
defined as a period running from March or April to September or
October. In 3 of the urban areas (Houston, Los Angeles, and
Sacramento), the O3 season is defined as the entire year.
---------------------------------------------------------------------------
In addition to uncertainties arising from sample size
considerations, which are quantitatively characterized and presented as
95 percentile credible intervals, there are additional uncertainties
and caveats associated with the lung function risk estimates. These
include uncertainties about the shape of the exposure-response
relationship, particularly at levels below 0.080 ppm, and about policy-
relevant background levels, for which sensitivity analyses have been
conducted. Additional important caveats and uncertainties concerning
the lung function portion of the health risk assessment include: (1)
The uncertainties and limitations associated with the exposure
estimates discussed above and (2) the inability to account for some
factors which are known to affect the exposure-response relationships
(e.g., assigning healthy and asthmatic children the same responses as
observed in healthy adult subjects and not adjusting response rates to
reflect the increase and attenuation of responses that have been
observed in studies of lung function responses upon repeated
exposures). A more complete discussion of assumptions and uncertainties
is contained in chapter 5 of the 2007 Staff Paper and in the Risk
Assessment TSD.
The second part of the risk assessment is based on health effects
observed in epidemiological studies. Based on a review of the evidence
evaluated in the 2006 Criteria Document and 2007 Staff Paper, as well
as the criteria discussed in chapter 5 of the 2007 Staff Paper, the
following categories of health endpoints associated with short-term
exposures to ambient O3 concentrations were included in the
risk assessment: respiratory symptoms in moderate to severe asthmatic
children, hospital admissions for respiratory causes, and non-
accidental and cardiorespiratory mortality. As discussed above, there
is strong evidence of a causal relationship for the respiratory
morbidity endpoints included in the risk assessment. With respect to
nonaccidental and cardiorespiratory mortality, the 2006 Criteria
Document concludes that there is strong evidence which is highly
suggestive of a causal relationship between nonaccidental and
cardiorespiratory-related mortality and O3 exposures during
the warm O3 season. As discussed in the 2007 Staff Paper
(chapter 5), EPA also recognizes that for some of the effects observed
in epidemiological studies, such as increased respiratory-related
hospital admissions and nonaccidental and cardiorespiratory mortality,
O3 may be serving as an indicator for reactive oxidant
species in the overall photochemical oxidant mix and that these other
constituents may be responsible in whole or part for the observed
effects.
Risk estimates for each health endpoint category were only
developed for areas that were the same or close to the location where
at least one concentration-response function for the health endpoint
had been estimated.\44\
[[Page 2982]]
Thus, for respiratory symptoms in moderate to severe asthmatic children
only the Boston urban area was included and four urban areas were
included for respiratory-related hospital admissions. Nonaccidental
mortality risk estimates were developed for 12 urban areas and 8 urban
areas were included for cardiorespiratory mortality.
---------------------------------------------------------------------------
\44\ The geographic boundaries for the urban areas included in
this portion of the risk assessment were generally matched to the
geographic boundaries used in the epidemiological studies that
served as the basis for the concentration-response functions. In
most cases, the urban areas were defined as either a single county
or a few counties for this portion of the risk assessment.
---------------------------------------------------------------------------
The concentration-response relationships used in the assessment are
based on findings from human epidemiological studies that have relied
on fixed-site ambient monitors as a surrogate for actual ambient
O3 exposures. In order to estimate the incidence of a
particular health effect associated with recent air quality in a
specific county or set of counties attributable to ambient
O3 exposures in excess of background, as well as the change
in incidence corresponding to a given change in O3 levels
resulting from just meeting various 8-hour O3 standards,
three elements are required for this part of the risk assessment. These
elements are: (1) Air quality information (including recent air quality
data for O3 from ambient monitors for the selected location,
estimates of background O3 concentrations appropriate for
that location, and a method for adjusting the recent data to reflect
patterns of air quality estimated to occur when the area just meets a
given O3 standard); (2) relative risk-based concentration-
response functions that provide an estimate of the relationship between
the health endpoints of interest and ambient O3
concentration; and (3) annual or seasonal baseline health effects
incidence rates and population data, which are needed to provide an
estimate of the seasonal baseline incidence of health effects in an
area before any changes in O3 air quality.
A key component in the portion of the risk assessment based on
epidemiological studies is the set of concentration-response functions
which provide estimates of the relationships between each health
endpoint of interest and changes in ambient O3
concentrations. Studies often report more than one estimated
concentration-response function for the same location and health
endpoint. Sometimes models include different sets of co-pollutants and/
or different lag periods between the ambient concentrations and
reported health responses. For some health endpoints, there are studies
that estimated multicity and single-city O3 concentration-
response functions. While the Risk Assessment TSD and chapter 5 of the
2007 Staff Paper present a more comprehensive set of risk estimates,
EPA has focused on estimates based on multicity studies where
available. As discussed in chapter 5 of the 2007 Staff Paper, the
advantages of relying more heavily on concentration-response functions
based on multicity studies include: (1) More precise effect estimates
due to larger data sets, reducing the uncertainty around the estimated
coefficient; (2) greater consistency in data handling and model
specification that can eliminate city-to-city variation due to study
design; and (3) less likelihood of publication bias or exclusion of
reporting of negative or nonsignificant findings. Where studies
reported different effect estimates for varying lag periods, consistent
with the 2006 Criteria Document, single day lag periods of 0 to 1 days
were used for associations with respiratory hospital admissions and
mortality. For mortality associated with exposure to O3
which may result over a several day period after exposure, distributed
lag models, which take into account the contribution to mortality
effects over several days, were used where available
One of the most important elements affecting uncertainties in the
epidemiological-based portion of the risk assessment is the
concentration-response relationships used in the assessment. The
uncertainty resulting from the statistical uncertainty associated with
the estimate of the O3 coefficient in the concentration-
response function was characterized either by confidence intervals or
by Bayesian credible intervals around the corresponding point estimates
of risk. Confidence and credible intervals express the range within
which the true risk is likely to fall if the only uncertainty
surrounding the O3 coefficient involved sampling error.
Other uncertainties, such as differences in study location, time period
(i.e., the years in which the study was conducted), and model
uncertainties are not represented by the confidence or credible
intervals presented, but were addressed by presenting estimates for
different urban areas, by including risk estimates based on studies
using different time periods and models, where available, and/or are
discussed throughout section 5.3 of the 2007 Staff Paper. Because
O3 effects observed in the epidemiological studies have been
more clearly and consistently shown for warm season analyses, all
analyses for this portion of the risk assessment were carried out for
the same time period, April through September.
The 2006 Criteria Document (p. 8-44) finds that no definitive
conclusion can be reached with regard to the existence of population
thresholds in epidemiological studies. The EPA recognizes, however, the
possibility that thresholds for individuals may exist for reported
associations at fairly low levels within the range of air quality
observed in the studies, but not be detectable as population thresholds
in epidemiological analyses. Based on the 2006 Criteria Document's
conclusions, EPA judged and CASAC concurred, that there is insufficient
evidence to support use of potential population threshold levels in the
quantitative risk assessment. However, EPA recognizes that there is
increasing uncertainty about the concentration-response relationship at
lower concentrations which is not captured by the characterization of
the statistical uncertainty due to sampling error. Therefore, the risk
estimates for respiratory symptoms in moderate to severe asthmatic
children, respiratory-related hospital admissions, and premature
mortality associated with exposure to O3 must be considered
in light of uncertainties about whether or not these O3-
related effects occur in these populations at very low O3
concentrations.
With respect to variability within this portion of the risk
assessment, there is variability among concentration-response functions
describing the relation between O3 and both respiratory-
related hospital admissions and nonaccidental and cardiorespiratory
mortality across urban areas. This variability is likely due to
differences in population (e.g., age distribution), population
activities that affect exposure to O3 (e.g., use of air
conditioning), levels and composition of co-pollutants, baseline
incidence rates, and/or other factors that vary across urban areas. The
risk assessment incorporates some of the variability in key inputs to
the analysis by using location-specific inputs (e.g., location-specific
concentration-response functions, baseline incidence rates, and air
quality data). Although spatial variability in these key inputs across
all U.S. locations has not been fully characterized, variability across
the selected locations is imbedded in the analysis by using, to the
extent possible, inputs specific to each urban area.
c. Risk Estimates and Key Observations
The 2007 Staff Paper (chapter 5) and Risk Assessment TSD present
risk estimates associated with just meeting the then current 0.084 ppm
standard and several alternative 8-hour standards, as well as three
recent years of air quality as represented by 2002,
[[Page 2983]]
2003, and 2004 monitoring data. As discussed in the exposure analysis
section above, there is considerable city-to-city and year-to-year
variability in the O3 levels during this period, which
results in significant variability in both portions of the health risk
assessment.
In the 1997 risk assessment, risks for lung function decrements
associated with 1-hour heavy exertion, 1-hour moderate exertion, and 8-
hour moderate exertion exposures were estimated. Since the 8-hour
moderate exertion exposure scenario for children clearly resulted in
the greatest health risks in terms of lung function decrements, EPA
chose to include only the 8-hour moderate exertion exposures in the
risk assessment for this health endpoint. Thus, the risk estimates
presented here and in the 2007 Staff Paper are most useful for making
relative comparisons across alternative air quality scenarios and do
not represent the total risks for lung function decrements in children
or other groups within the general population associated with any of
the air quality scenarios. Thus, some outdoor workers and adults
engaged in moderate exertion over multi-hour periods (e.g., 6-8 hour
exposures) also would be expected to experience similar lung function
decrements. However, the percentage of each of these other
subpopulations expected to experience these effects is expected to be
smaller than all school age children who tend to spend more hours
outdoors while active based on the exposure analyses conducted during
the prior review.
Table 2 presents a summary of the risk estimates for lung function
decrements for the 0.084 ppm standard set in 1997 and several
alternative 8-hour standard levels with the same form.
Table 2--Number and Percent of All and Asthmatic School Age Children in Several Urban Areas Estimated To
Experience Moderate or Greater Lung Function Responses One or More Times per Season Associated With 8-Hour Ozone
Exposures Associated With Just Meeting Alternative 8-Hour Standards Based on Adjusting 2002 and 2004 Air Quality
Data 1 2
----------------------------------------------------------------------------------------------------------------
All children, ages 5-18 FEV1 >= 15 Asthmatic Children, ages 5-18 FEV1 >=
percent Aggregate for 12 urban areas 10 percent Aggregate for 5 urban
Number of children affected (% of all) areas Number of children affected (%
8-Hour air quality standards [% reduction from 0.084 ppm standard] of group) [% reduction from 0.084 ppm
\3\ ----------------------------------------- standard]
---------------------------------------
2002 2004 2002 2004
----------------------------------------------------------------------------------------------------------------
0.084 ppm (Standard set in 610,000 (3.3%) 230,000 (1.2%) 130,000 (7.8%) 70,000 (4.2%)
1997).
0.080 ppm...................... 490,000 (2.7%) [20% 180,000 (1.0%) NA \4\ NA
reduction] [22% reduction]
0.074 ppm...................... 340,000 (1.9%) [44% 130,000 (0.7%) 90,000 (5.0%) [31% 40,000 (2.7%) [43%
reduction] [43% reduction] reduction] reduction]
0.070 ppm...................... 260,000 (1.5%) [57% 100,000 (0.5%) NA NA
reduction] [57% reduction]
0.064 ppm...................... 180,000 (1.0%) [70% 70,000 (0.4%) [70% 50,000 (3.0%) [62% 20,000 (1.5%) [71%
reduction] reduction] reduction] reduction]
----------------------------------------------------------------------------------------------------------------
\1\ Associated with exposures while engaged in moderate or greater exertion, which is defined as having an 8-
hour average equivalent ventilation rate >= 13 l-min/m \2\.
\2\ Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston,
Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and
Washington, DC) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, New York). Estimates are for the O3
season which is all year in Houston, Los Angeles and Sacramento and March or April to September or October for
the remaining urban areas.
\3\ All standards summarized here have the same form as the 8-hour standard set in 1997, which is specified as
the 3-year average of the annual 4th highest daily maximum 8-hour average concentrations. As described in the
2007 Staff Paper (section 4.5.8), recent O3 air quality distributions have been statistically adjusted to
simulate just meeting the 0.084 ppm standard set in 1997 and selected alternative standards. These simulations
do not represent predictions of when, whether, or how areas might meet the specified standards
\4\ NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic
school age children population.
The estimates are for the aggregate number and percent of all
school age children across 12 urban areas and the aggregate number and
percent of asthmatic school age children across 5 urban areas \45\ who
are estimated to have at least 1 moderate or greater lung function
response (defined as FEV1 >= 15 percent in all children and
>= 10 percent in asthmatic children) associated with 8-hour exposures
to O3 while engaged in moderate or greater exertion on
average over the 8-hour period. The lung function risk estimates
summarized in Table 2 illustrate the year-to-year variability in both
remaining risk associated with a relatively high year (i.e., based on
adjusting 2002 O3 air quality data) and relatively low year
(based on adjusting 2004 O3 air quality data) as well as the
year-to-year variability in the risk reduction estimated to occur
associated with various alternative standards relative to just meeting
the then current 0.084 ppm standard. For example, it is estimated that
about 610,000 school age children (3.2 percent of school age children)
would experience 1 or more moderate lung function decrements for the 12
urban areas associated with O3 levels just meeting a 0.084
ppm standard based on 2002 air quality data compared to 230,000 (1.2
percent of children) associated with just meeting a 0.084 ppm standard
based on 2004 air quality data.
---------------------------------------------------------------------------
\45\ Due to time constraints, lung function risk estimates for
asthmatic school age children were developed for only 5 of the 12
urban areas, and the areas were selected to represent different
geographic regions. The 5 areas were: Atlanta, Chicago, Houston, Los
Angeles, and New York City.
---------------------------------------------------------------------------
As discussed in the 2007 Staff Paper, a child may experience
multiple occurrences of a lung function response during the
O3 season. For example, upon meeting a 0.084 ppm 8-hour
standard, the median estimates are that about 610,000 children would
experience a moderate or greater lung function response 1 or more times
for the aggregate of the 12 urban areas over a single O3
season (based on the 2002 simulation), and that there would be almost
3.2 million total occurrences. Thus, on average it is estimated that
there would be about 5 occurrences per O3 season per
responding child for air quality just meeting a 0.084 ppm 8-hour
[[Page 2984]]
standard across the 12 urban areas. While the estimated number of
occurrences per O3 season is lower when based on the 2004
simulation than for the 2002 simulation, the estimated number of
occurrences per responding child is similar. The EPA recognizes that
some children in the population might have only 1 or 2 occurrences
while others may have 6 or more occurrences per O3 season.
Risk estimates based on adjusting 2003 air quality to simulate just
meeting the a 0.084 ppm standard and alternative 8-hour standards are
intermediate to the estimates presented in Table 2 above in this notice
and are presented in the 2007 Staff Paper (chapter 5) and Risk
Assessment TSD.
For just meeting a 0.084 ppm 8-hour standard, Table 5-8 in the 2007
Staff Paper shows that median estimates across the 12 urban areas for
all school age children experiencing 1 or more moderate lung function
decrements ranges from 0.9 to 5.4 percent based on the 2002 simulation
and from 0.8 to 2.2 percent based on the 2004 simulation. Risk
estimates for each urban area included in the assessment, for each of
the three years analyzed, and for additional alternative standards are
presented in chapter 5 of the 2007 Staff Paper and in the Risk
Assessment TSD.
For just meeting a 0.084 ppm 8-hour standard, the median estimates
across the 5 urban areas for asthmatic school age children range from
3.4 to 10.9 percent based on the 2002 simulation and from 3.2 to 6.9
percent based on the 2004 simulation.
Key observations important in comparing estimated lung function
risks associated with just meeting the 0.084 ppm NAAQS and alternative
standards under consideration include:
(1) As discussed above, there is significant year to year
variability in the range of median estimates of the number of school
age children (ages 5-18) estimated to experience at least one
FEV1 decrement >= 15 percent due to 8-hour O3
exposures across the 12 urban areas analyzed, and similarly across the
5 urban areas analyzed for asthmatic school age children (ages 5-18)
estimated to experience at least one FEV1 decrement >= 10
percent, when various 8-hour standards are just met.
(2) For asthmatic school age children, the median estimates of
occurrences of FEV1 decrements >= 10% range from 52,000 to
nearly 510,000 responses associated with just meeting a 0.084 ppm
standard (based on the 2002 simulation) and range from 61,000 to about
240,000 occurrences (based on the 2004 simulation). These risk
estimates would be reduced to a range of 14,000 to about 275,000
occurrences (2002 simulation) and to about 18,000 to nearly 125,000
occurrences (2004 simulation) upon just meeting the most stringent
alternative 8-hour standard (0.064 ppm, 4th highest). The average
number of occurrences per asthmatic child in an O3 season
ranged from about 6 to 11 associated with just meeting a 0.084 ppm
standard (2002 simulation). The average number of occurrences per
asthmatic child ranged from 4 to 12 upon meeting the most stringent
alternative examined (0.064 ppm, 4th-highest) based on the 2002
simulation. The number of occurrences per asthmatic child is similar
for the scenarios based on the 2004 simulation.
As discussed above, several epidemiological studies have reported
increased respiratory morbidity outcomes (e.g., respiratory symptoms in
moderate to severe asthmatic children, respiratory-related hospital
admissions) and increased nonaccidental and cardiorespiratory mortality
associated with exposure to ambient O3 concentrations. The
results and key observations from this portion of the risk assessment
are presented below:
(1) Estimates for increased respiratory symptoms (i.e., chest
tightness, shortness of breath, and wheeze) in moderate/severe
asthmatic children (ages 0-12) were developed for the Boston urban area
only. The median estimated number of days involving chest tightness
(using the concentration-response relationship with only O3
in the model) is about 6,100 (based on the 2002 simulation) and about
4,500 (based on the 2004 simulation) upon meeting a 0.084 ppm 8-hour
standard and this is reduced to about 4,600 days (2002 simulation) and
3,100 days (2004 simulation) upon meeting the most stringent
alternative examined (0.064 ppm, 4th-highest daily maximum 8-hour
average). This corresponds to 11 percent (2002 simulation) and 8
percent (2004 simulation) of total incidence of chest tightness upon
meeting a 0.084 ppm 8-hour standard and to about 8 percent (2002
simulation) and 5.5 percent (2004 simulation) of total incidence of
chest tightness upon meeting a 0.064 ppm, 4th-highest daily maximum 8-
hour average standard. Similar patterns of effects and reductions in
effects are observed for each of the respiratory symptoms examined.
(2) The 2007 Staff Paper and Risk Assessment TSD present
unscheduled hospital admission risk estimates for respiratory illness
and asthma in New York City associated with short-term exposures to
O3 concentrations in excess of background levels from April
through September for several recent years (2002, 2003, and 2004) and
upon just meeting a 0.084 ppm standard and alternative 8-hour standards
based on simulating O3 levels using 2002-2004 O3
air quality data. For total respiratory illness, EPA estimates about
6.4 cases per 100,000 relevant population (2002 simulation) and about
4.6 cases per 100,000 relevant population (2004 simulation), which
represents 1.5 percent (2002 simulation) and 1.0 percent (2004
simulation) of total incidence or about 510 cases (2002 simulation) and
about 370 cases (2004 simulation) upon just meeting a 0.084 ppm 8-hour
standard. For asthma-related hospital admissions, which are a subset of
total respiratory illness admissions, the estimates are about 5.5 cases
per 100,000 relevant population (2002 simulation) and about 3.9 cases
per 100,000 relevant population (2004 simulation), which represents
about 3.3 percent (2002 simulation) and 2.4 percent (2004 simulation)
of total incidence or about 440 cases (2002) and about 310 cases (2004)
for this same air quality scenario.
For increasingly more stringent alternative 8-hour standards, there
is a gradual reduction in respiratory illness cases per 100,000
relevant population from 6.4 cases per 100,000 upon just meeting a
0.084 ppm 8-hour standard to 4.6 cases per 100,000 under the most
stringent 8-hour standard (i.e., 0.064 ppm, average 4th-highest daily
maximum) analyzed based on the 2002 simulation. Similarly, based on the
2004 simulation there is a gradual reduction from 4.6 cases per 100,000
relevant population upon just meeting a 0.084 ppm 8-hour standard to
3.0 cases per 100,000 under a 0.064 ppm, average 4th-highest daily
maximum standard.
Additional respiratory-related hospital admission estimates for
three other locations are provided in the Risk Assessment TSD. The EPA
notes that the concentration-response functions for each of these
locations examined different outcomes in different age groups (e.g., >
age 30 in Los Angeles, > age 64 in Cleveland and Detroit, vs. all ages
in New York City), making comparison of the risk estimates across the
areas very difficult.
(3) Based on the median estimates for incidence for nonaccidental
mortality (based on the Bell et al. (2004) 95 cities concentration-
response function), meeting the most stringent standard (0.064 ppm) is
estimated to reduce mortality by 40 percent of what it would be
associated with just meeting a 0.084 ppm standard (based on the 2002
simulation). The patterns for cardiorespiratory mortality are similar.
[[Page 2985]]
The aggregate O3-related cardiorespiratory mortality upon
just meeting the most stringent standard shown is estimated to be about
42 percent of what it would be upon just meeting a 0.084 ppm standard,
using simulated O3 concentrations that just meet a 0.084 ppm
standard and alternative 8-hour standards based on the 2002 simulation.
Using the 2004 simulation, the corresponding reductions show a similar
pattern but are somewhat greater.
(4) Much of the contribution to the risk estimates for non-
accidental and cardiorespiratory mortality upon just meeting a 0.084
ppm 8-hour standard is associated with 24-hour O3
concentrations between background and 0.040 ppm. Based on examining
relationships between 24-hour concentrations averaged across the
monitors within an urban area and 8-hour daily maximum concentrations,
8-hour daily maximum levels at the highest monitor in an urban area
associated with these averaged 24-hour levels are generally about twice
as high as the 24-hour levels. Thus, most O3-related
nonaccidental mortality is estimated to occur when O3
concentrations are between background and when the highest monitor in
the urban area is at or below 0.080 ppm, 8-hour average concentration.
The discussion below highlights additional observations and
insights from the O3 risk assessment, together with
important uncertainties and limitations.
(1) As discussed in the 2007 Staff Paper (section 5.4.5), EPA has
greater confidence in relative comparisons in risk estimates between
alternative standards than in the absolute magnitude of risk estimates
associated with any particular standard.
(2) Significant year-to-year variability in O3
concentrations combined with the use of a 3-year design value to
determine the amount of air quality adjustment to be applied to each
year analyzed, results in significant year-to-year variability in the
annual health risk estimates upon just meeting various 8-hour
standards.
(3) There is noticeable city-to-city variability in estimated
O3-related incidence of morbidity and mortality across the
12 urban areas analyzed for both recent years of air quality and for
air quality adjusted to simulate just meeting a 0.084 ppm standard and
selected potential alternative standards. This variability is likely
due to differences in air quality distributions, differences in
exposure related to many factors including varying activity patterns
and air exchange rates, differences in baseline incidence rates, and
differences in susceptible populations and age distributions across the
12 urban areas.
(4) With respect to the uncertainties about estimated policy-
relevant background concentrations, as discussed in the 2007 Staff
Paper (section 5.4.3), alternative assumptions about background levels
had a variable impact depending on the health effect considered and the
location and standard analyzed in terms of the absolute magnitude and
relative changes in the risk estimates. There was relatively little
impact on either absolute magnitude or relative changes in lung
function risk estimates due to alternative assumptions about background
levels. With respect to O3-related non-accidental mortality,
while notable differences (i.e., greater than 50 percent) \46\ were
observed for nonaccidental mortality in some areas, particularly for
more stringent standards, the overall pattern of estimated reductions,
expressed in terms of percentage reduction relative to the 0.084 ppm
standard, was significantly less impacted.
---------------------------------------------------------------------------
\46\ For example, assuming lower background levels resulted in
increased estimates of non-accidental mortality incidence per
100,000 that were often 50 to 100 percent greater than the base case
estimates; assuming higher background levels resulted in decreased
estimates of non-accidental mortality incidence per 100,000 that
were less than the base case estimates by 50 percent or more in many
of the areas.
---------------------------------------------------------------------------
C. Reconsideration of the Level of the Primary Standard
1. Evidence and Exposure/Risk-Based Considerations
The approach used in the 2007 Staff Paper as a basis for staff
recommendations on standard levels builds upon and broadens the general
approach used by EPA in the 1997 review. This approach reflects the
more extensive and stronger body of evidence available for the 2008
rulemaking on a broader range of health effects associated with
exposure to O3, including: (1) Additional respiratory-
related endpoints; (2) new information about the mechanisms underlying
respiratory morbidity effects supporting a judgment that the link
between O3 exposure and these effects is causal; (3) newly
identified cardiovascular-related health endpoints from animal
toxicology and controlled human exposures studies that are highly
suggestive that O3 can directly or indirectly contribute to
cardiovascular morbidity, and (4) new U.S. multicity time series
studies, single city studies, and several meta-analyses of these
studies that provide relatively strong evidence for associations
between short-term O3 exposures and all-cause
(nonaccidental) mortality, at levels below the current primary
standard: As well as (5) a substantial body of new evidence of
increased susceptibility in people with asthma and other lung diseases.
In evaluating evidence-based and exposure/risk-based considerations,
the 2007 Staff Paper considered: (1) The ranges of levels of
alternative standards that are supported by the evidence, and the
uncertainties and limitations in that evidence and (2) the extent to
which specific levels of alternative standards reduce the estimated
exposures of concern and risks attributable to O3 and other
photochemical oxidants, and the uncertainties associated with the
estimated exposure and risk reductions.
a. Evidence-Based Considerations
In taking into account evidence-based considerations, the 2007
Staff Paper evaluated available evidence from controlled human exposure
studies and epidemiological studies, as well as the uncertainties and
limitations in that evidence. In particular, it focused on the extent
to which controlled human exposure studies provide evidence of lowest-
observed-effects levels and the extent to which epidemiological studies
provide evidence of associations that extend down to the lower levels
of O3 concentrations observed in the studies or some
indication of potential effect thresholds in terms of 8-hour average
O3 concentrations.
The most certain evidence of adverse health effects from exposure
to O3 comes from the controlled human exposure studies, as
discussed above in section II.A.2, and the large bulk of this evidence
derives from studies of exposures at levels of 0.080 ppm and above. At
those levels, there is consistent evidence of lung function decrements
and respiratory symptoms in healthy young adults, as well as evidence
of inflammation and other medically significant airway responses.
Two studies by Adams (2002, 2006), newly available for
consideration in the 2008 rulemaking, are the only available controlled
human exposure studies that examine respiratory effects associated with
prolonged O3 exposures at levels below 0.080 ppm, which was
the lowest exposure level that had been examined in the 1997 review. As
discussed above in section II.A.2.a.i.(a)(i), the Adams (2006) study
investigated a range of exposure levels, including 0.060 and 0.080 ppm
O3, and analyzed hour-by-hour changes in responses,
including lung function (measured in term of decrements in
FEV1) and respiratory
[[Page 2986]]
symptoms, to investigate the effects of different patterns of exposure.
At the 0.060 ppm exposure level, the author reported no statistically
significant differences for lung function decrements; statistically
significant responses were reported for total subjective respiratory
symptoms toward the end of the exposure period for one exposure
pattern. The EPA's reanalysis (Brown, 2007) of the data from the Adams
(2006) study addressed the more fundamental question of whether there
were statistically significant changes in lung function from a 6.6-hour
exposure to 0.060 ppm O3 versus filtered air and used a
standard statistical method appropriate for a simple paired comparison.
This reanalysis found small group mean lung function decrements in
healthy adults at the 0.060 ppm exposure level to be statistically
significantly different from responses associated with filtered air
exposure.
Moreover, the Adams' studies also report a small percentage of
subjects (7 to 20 percent) experienced lung function decrements (> 10
percent) at the 0.060 ppm exposure level. This is a concern because,
for active healthy people, moderate levels of functional responses
(e.g., FEV1 decrements of > 10% but < 20%) and/or moderate
respiratory symptom responses would likely interfere with normal
activity for relatively few responsive individuals. However, for people
with lung disease, even moderate functional or symptomatic responses
would likely interfere with normal activity for many individuals, and
would likely result in more frequent use of medication. In the context
of standard setting, the CASAC indicated (Henderson, 2006c) that a
focus on the lower end of the range of moderate levels of functional
responses (e.g., FEV1 decrements >= 10%) is most appropriate
for estimating potentially adverse lung function decrements in people
with lung disease. Therefore, the results of the Adams studies which
indicate that a small percentage of healthy, non-asthmatic subjects are
likely to experience FEV1 decrements >= 10% when exposed to
0.060 ppm O3 have implications for setting a standard that
protects public health, including the health of sensitive populations
such as asthmatics, with an adequate margin of safety.
In considering these most recent controlled human exposure studies,
the 2007 Staff Paper concluded that these studies provide evidence of a
lowest-observed-effects level of 0.060 ppm for potentially adverse lung
function decrements and respiratory symptoms in some healthy adults
while at prolonged moderate exertion. It further concluded that since
people with asthma, particularly children, have been found to be more
sensitive and to experience larger decrements in lung function in
response to O3 exposures than would healthy adults, the
0.060 ppm exposure level also can be interpreted as representing a
level likely to cause adverse lung function decrements and respiratory
symptoms in children with asthma and more generally in people with
respiratory disease.
In considering controlled human exposure studies of pulmonary
inflammation, airway responsiveness, and impaired host defense
capabilities, discussed above in section II.A.2.a.i, the 2007 Staff
Paper noted that these studies provide evidence of a lowest-observed-
effects level for such effects in healthy adults at prolonged moderate
exertion of 0.080 ppm, the lowest level tested. Moreover there is no
evidence that the 0.080 ppm level is a threshold for these effects.
Studies reporting inflammatory responses and markers of lung injury
have clearly demonstrated that there is significant variation in
response of subjects exposed, even to O3 exposures at 0.080
ppm. One study showed notable interindividual variability in young
healthy adult subjects in most of the inflammatory and cellular injury
indicators analyzed at 0.080 ppm. This inter-individual variability
suggests that some portion of the population would likely experience
such effects at exposure levels extending well below 0.080 ppm.
As discussed above, these physiological effects have been linked to
aggravation of asthma and increased susceptibility to respiratory
infection, potentially leading to increased medication use, increased
school and work absences, increased visits to doctors' offices and
emergency departments, and increased hospital admissions. Further,
pulmonary inflammation is related to increased cellular permeability in
the lung, which may be a mechanism by which O3 exposure can
lead to cardiovascular system effects, and to potential chronic effects
such as chronic bronchitis or long-term damage to the lungs that can
lead to reduced quality of life. These are all indicators of adverse
O3-related morbidity effects, which are consistent with and
lend plausibility to the adverse morbidity effects and mortality
effects observed in epidemiological studies.
Significant associations between ambient O3 exposures
and a wide variety of respiratory symptoms and other morbidity outcomes
(e.g., asthma medication use, school absences, emergency department
visits, and hospital admissions) have been reported in epidemiological
studies, as discussed above in section II.A.2.a.i. Overall, the 2006
Criteria Document concludes that positive and robust associations were
found between ambient O3 concentrations and various
respiratory disease hospitalization outcomes, when focusing
particularly on results of warm-season analyses. Recent studies also
generally indicate a positive association between O3
concentrations and emergency department visits for asthma during the
warm season. These positive and robust associations are supported by
the controlled human exposure, animal toxicological, and
epidemiological evidence for lung function decrements, increased
respiratory symptoms, airway inflammation, and increased airway
responsiveness. Taken together, the overall evidence supports a causal
relationship between acute ambient O3 exposures and
increased respiratory morbidity outcomes resulting in increased
emergency department visits and hospitalizations during the warm season
(EPA, 2006a, p. 8-77).
Moreover, many single- and multicity epidemiological studies
observed positive associations of ambient O3 concentrations
with total nonaccidental and cardiopulmonary mortality. As discussed
above in section II.A.2.b.i, the 2006 Criteria Document finds that the
results from U.S. multicity time-series studies provide the strongest
evidence to date for O3 effects on acute mortality. Recent
meta-analyses also indicate positive risk estimates that are unlikely
to be confounded by PM; however, future work is needed to better
understand the influence of model specifications on the magnitude of
risk. The 2006 Criteria Document concludes that the ``positive
O3 effects estimates, along with the sensitivity analyses in
these three meta-analyses, provide evidence of a robust association
between ambient O3 and mortality'' (EPA, 2006a, p. 7-97). In
summary, the 2006 Criteria Document (p. 8-78) concludes that these
findings are highly suggestive that short-term O3 exposure
directly or indirectly contribute to non-accidental and
cardiopulmonary-related mortality, but additional research is needed to
more fully establish underlying mechanisms by which such effects occur.
The 2007 Staff Paper considered the epidemiological studies to
evaluate evidence related to potential effects thresholds at the
population level for morbidity and mortality effects. As discussed
above in section II.A.3.a (and more fully in the 2007 Staff Paper in
chapter 3 and the 2006 Criteria
[[Page 2987]]
Document in chapter 7), a number of time-series studies have used
statistical modeling approaches to evaluate potential thresholds at the
population level. A few such studies reported some suggestive evidence
of possible thresholds for morbidity and mortality outcomes in terms of
24-hour, 8-hour, and 1-hour averaging times. These results, taken
together, provide some indication of possible 8-hour average threshold
levels from below about 0.025 to 0.035 ppm (within the range of
background concentrations) up to approximately 0.050 ppm. Other
studies, however, observe linear concentration-response functions
suggesting no effect threshold. The 2007 Staff Paper (p.6-60) concluded
that the statistically significant associations between ambient
O3 concentrations and lung function decrements, respiratory
symptoms, indicators of respiratory morbidity including increase
emergency department visits and hospital admissions, and possibly
mortality reported in a large number of studies likely extend down to
ambient O3 concentrations that are well below the level of
the then current standard (0.084 ppm). These associations also extend
well below the level of the standard set in 2008 (0.075 ppm) in that
the highest level at which there is any indication of a threshold is
approximately 0.050 ppm. Toward the lower end of the range of
O3 concentrations observed in such studies, ranging down to
background levels (i.e., 0.035 to 0.015 ppm), however, the 2007 Staff
Paper stated that there is increasing uncertainty as to whether the
observed associations remain plausibly related to exposures to ambient
O3, rather than to the broader mix of air pollutants present
in the ambient atmosphere.
The 2007 Staff Paper also considered studies that did subset
analyses, which included only days with ambient O3
concentrations below the level of the then current standard, or below
even lower O3 concentrations, and continue to report
statistically significant associations. Notably, as discussed above,
Bell et al. (2006) conducted a subset analysis that continued to show
statistically significant mortality associations even when only days
with a maximum 8-hour average O3 concentration below a value
of approximately 0.061 ppm were included.\47\ Also of note is the large
multicity NCICAS (Mortimer et al., 2002) that reported statistically
significant associations between ambient O3 concentrations
and lung function decrements even when days with 8-hour average
O3 levels greater than 0.080 ppm were excluded (which
consisted of less than 5 percent of the days in the eight urban areas
in the study).
---------------------------------------------------------------------------
\47\ Bell et al. (2006) referred to this level as being
approximately equivalent to 120 [micro]g/m\3\, daily 8-hour maximum,
the World Health Organization guideline and European Commission
target value for O3.
---------------------------------------------------------------------------
Further, as discussed above in section II.A.3.a, there are
limitations in epidemiological studies that make discerning thresholds
in populations difficult, including low data density in the lower
concentration ranges, the possible influence of exposure measurement
error, and interindividual differences in susceptibility to
O3-related effects in populations. There is the possibility
that thresholds for individuals may exist in reported associations at
fairly low levels within the range of air quality observed in the
studies but not be detectable as population thresholds in
epidemiological analyses.
Based on the above considerations, the 2007 Staff Paper recognized
that the available evidence neither supports nor refutes the existence
of effect thresholds at the population level for morbidity and
mortality effects, and that if a population threshold level does exist,
it would likely be well below the level of the then current standard
and possibly within the range of background levels. Taken together,
these considerations also support the conclusion that if a population
threshold level does exist, it would likely be well below the level of
the 0.075 ppm, 8-hour average, standard set in 2008.
In looking more broadly at evidence from animal toxicological,
controlled human exposure, and epidemiological studies, the 2006
Criteria Document found substantial evidence, newly available in the
2008 rulemaking, that people with asthma and other preexisting
pulmonary diseases are among those at increased risk from O3
exposure. Altered physiological, morphological, and biochemical states
typical of respiratory diseases like asthma, COPD, and chronic
bronchitis may render people sensitive to additional oxidative burden
induced by O3 exposure (EPA, 2006a, section 8.7). Children
and adults with asthma are the groups that have been studied most
extensively. Evidence from controlled human exposure studies indicates
that asthmatics may exhibit larger lung function decrements in response
to O3 exposure than healthy controls. As discussed more
fully in section II.A.4 above, asthmatics present a different response
profile for cellular, molecular, and biochemical parameters (EPA,
2006a, Figure 8-1) that are altered in response to acute O3
exposure. They can have larger inflammatory responses, as manifested by
larger increases in markers of inflammation such as white bloods cells
(e.g., PMNs) or inflammatory cytokines. Asthmatics, and people with
allergic rhinitis, are more likely to have an allergic-type response
upon exposure to O3, as manifested by increases in white
blood cells associated with allergy (i.e., eosinophils) and related
molecules, which increase inflammation in the airways. The increased
inflammatory and allergic responses also may be associated with the
larger late-phase responses that asthmatics can experience, which can
include increased bronchoconstrictor responses to irritant substances
or allergens and additional inflammation.
In addition to the experimental evidence of lung function
decrements, respiratory symptoms, and other respiratory effects in
asthmatic populations, two large U.S. epidemiological studies as well
as several smaller U.S. and international studies, have reported fairly
robust associations between ambient O3 concentrations and
measures of lung function and daily respiratory symptoms (e.g., chest
tightness, wheeze, shortness of breath) in children with moderate to
severe asthma and between O3 and increased asthma medication
use (EPA, 2007a, chapter 6). These more serious responses in asthmatics
and others with lung disease provide biological plausibility for the
respiratory morbidity effects observed in epidemiological studies, such
as emergency department visits and hospital admissions.
The body of evidence from controlled human exposure and
epidemiological studies, which includes asthmatic as well as non-
asthmatic subjects, indicates that controlled human exposure studies of
lung function decrements and respiratory symptoms that evaluate only
healthy, non-asthmatic subjects likely underestimate the effects of
O3 exposure on asthmatics and other susceptible populations.
Therefore, relative to the healthy, non-asthmatic subjects used in most
controlled human exposure studies, including the Adams (2002, 2006)
studies, a greater proportion of people with asthma may be affected,
and those who are affected may have as large or larger lung function
and symptomatic responses at ambient exposures to 0.060 ppm
O3. This indicates that the lowest-observed-effects levels
demonstrated in controlled human exposure studies that use only healthy
subjects may not
[[Page 2988]]
reflect the lowest levels at which people with asthma or other lung
diseases may respond.
Being mindful of the uncertainties and limitations inherent in
interpreting the available evidence, the 2007 Staff Paper stated the
view that the range of alternative O3 standards for
consideration should take into account information on lowest-observed-
effects levels in controlled human exposure studies as well as
indications of possible effects thresholds reported in some
epidemiological studies and questions of biological plausibility in
attributing associations observed down to background levels to
O3 exposures alone. Based on the evidence and these
considerations, it concluded that the upper end of the range of
consideration should be somewhat below 0.080 ppm, the lowest-observed-
effects level for effects such as pulmonary inflammation, increased
airway responsiveness and impaired host-defense capabilities in healthy
adults while at prolonged moderate exertion. The 2007 Staff Paper also
concluded that the lower end of the range of alternative O3
standards appropriate for consideration should be the lowest-observed-
effects level for potentially adverse lung function decrements and
respiratory symptoms in some healthy adults, 0.060 ppm.
b. Exposure and Risk-Based Considerations
In addition to the evidence-based considerations informing staff
recommendations on alternative levels, as discussed above in section
II.B, the 2007 Staff Paper also evaluated quantitative exposures and
health risks estimated to occur upon meeting the then current 0.084 ppm
standard and alternative standards.\48\ In so doing, it presented the
important uncertainties and limitations associated with these exposure
and risk assessments (discussed above in section II.B and more fully in
chapters 4 and 5 of the 2007 Staff Paper).
---------------------------------------------------------------------------
\48\ As described in the 2007 Staff Paper (section 4.5.8) and
discussed above in section II.B, recent O3 air quality
distributions have been statistically adjusted to simulate just
meeting the then current 0.084 ppm standard and selected alternative
standards. These simulations do not represent predictions of when,
whether, or how areas might meet the specified standards. Modeling
that projects whether and how areas might attain alternative
standards in a future year is presented in the Regulatory Impact
Analysis being prepared in connection with this rulemaking.
---------------------------------------------------------------------------
The 2007 Staff Paper (and the CASAC) also recognized that the
exposure and risk analyses could not provide a full picture of the
O3 exposures and O3-related health risks posed
nationally. The EPA did not have sufficient information to evaluate all
relevant at-risk groups (e.g., outdoor workers) or all O3-
related health outcomes (e.g., increased medication use, school
absences, and emergency department visits that are part of the broader
pyramid of effects discussed above in section II.A.4.d), and the scope
of the 2007 Staff Paper analyses was generally limited to estimating
exposures and risks in 12 urban areas across the U.S., and to only five
or just one area for some health effects included in the risk
assessment. Thus, national-scale public health impacts of ambient
O3 exposures are clearly much larger than the quantitative
estimates of O3-related incidences of adverse health effects
and the numbers of children likely to experience exposures of concern
associated with meeting the 0.084 ppm standard or alternative
standards. On the other hand, inter-individual variability in
responsiveness means that only a subset of individuals in each group
estimated to experience exposures exceeding a given benchmark exposure
of concern level would actually be expected to experience such adverse
health effects.
The 2007 Staff Paper focused on alternative standards with the same
form as the then current 0.084 ppm O3 standard (i.e. the
0.074/4, 0.070/4 and 0.064/4 scenarios).\49\ Having concluded in the
2007 Staff Paper that it was appropriate to consider a range of
standard levels from somewhat below 0.080 ppm down to as low as 0.060
ppm, the 2007 Staff Paper looked to results of the analyses of exposure
and risk for the 0.074/4 scenario to represent the public health
impacts of selecting a standard in the upper part of the range, the
results of analyses of the 0.070/4 scenario to represent the impacts in
the middle part of the range, and the results of the analyses of the
0.064/4 scenario to represent the lower part of the range.
---------------------------------------------------------------------------
\49\ The abbreviated notation used to identify the then current
0.084 ppm standard and alternative standards in this section and in
the risk assessment section of the Staff Paper is in terms of ppm
and the nth highest daily maximum 8-hour average. For example, the
8-hour standard established in 1997 is identified as ``0.084/4.''
---------------------------------------------------------------------------
As discussed in section II.B.1 of this notice, the exposure
estimates presented in the 2007 Staff Paper are for the number and
percent of all children and asthmatic children exposed, and the number
of person-days (occurrences) of exposures, with daily 8-hour maximum
exposures at or above several benchmark levels while at intermittent
moderate or greater exertion. Exposures above selected benchmark levels
provide some perspective on the public health impacts of health effects
that cannot currently be evaluated in quantitative risk assessments but
that may occur at existing air quality levels, and the extent to which
such impacts might be reduced by meeting alternative standard levels.
As described in section II.B.1.c above, the 2007 Staff Paper refers to
exposures at and above these benchmark levels as ``exposures of
concern.'' The 2007 Staff Paper notes that exposures of concern, and
the health outcomes they represent, likely occur across a range of
O3 exposure levels, such that there is no one exposure level
that addresses all public health concerns. As noted above in section
II.B., EPA also has acknowledged that the concept is more appropriately
viewed as a continuum with greater confidence and less uncertainty
about the existence of health effects at the upper end and less
confidence and greater uncertainty as one considers increasingly lower
O3 exposure levels.
Consistent with advice from CASAC, the 2007 Staff Paper estimates
exposures of concern not only at 0.080 ppm O3, a level at
which there are clearly demonstrated effects, but also at 0.070 and
0.060 ppm O3 levels where there is some evidence that health
effects are likely to occur in some individuals. The 2007 Staff Paper
recognizes that there will be varying degrees of concern about
exposures at each of these levels, based in part on the population
groups experiencing them. Given that there is clear evidence of
inflammation, increased airway responsiveness, and changes in host
defenses in healthy people exposed to 0.080 ppm and reason to infer
that such effects will continue at lower exposure levels, but with
increasing uncertainty about the extent to which such effects occur at
lower O3 concentrations, the 2007 Staff Paper and discussion
below, focus on exposures of concern at or above benchmark levels of
0.070 and 0.060 ppm O3 for purposes of evaluating
alternative standards. The focus on these two benchmark levels reflects
the following evidence-based considerations, discussed above in section
II.C.1, that raise concerns about adverse health effects likely
occurring at levels below 0.080 ppm: (1) That there is limited, but
important, new evidence from controlled human exposure studies showing
lung function decrements and respiratory symptoms in some healthy
subjects at 0.060 ppm; (2) that asthmatics are likely to have more
serious responses than healthy individuals; (3) that lung function is
not likely to be as sensitive a marker for O3
[[Page 2989]]
effects as lung inflammation; and (4) that there is epidemiological
evidence which reports associations with O3 levels that
extend well below 0.080 ppm.
Table 3 below summarizes the exposure estimates for all children
and asthmatic children for the 0.060 and 0.070 ppm health effect
benchmark levels associated with O3 levels adjusted to just
meet 0.074/4, 0.070/4, and 0.064/4 alternative 8-hour standards based
on a generally poorer year of air quality (2002) and based on a
generally better year of air quality (2004). This table includes
exposure estimates reflecting the aggregate estimate for the 12 urban
areas as well as the range across these same 12 areas. As shown in
Table 3 below, the percent of population exposed over the selected
benchmark levels is very similar for all and asthmatic school age
children. Thus, the following discussion focuses primarily on the
exposure estimates for asthmatic children, recognizing that the pattern
of exposure estimates is similar for all children when expressed in
terms of percentage of the population.
As noted in section II.B.2 and shown in Tables 1 and 3 of this
notice, substantial year-to-year variability is observed, ranging to
over an order of magnitude at the higher alternative standard levels,
in estimates of the number of children and the number of occurrences of
exposures of concern at both the 0.060 and 0.070 ppm benchmark levels.
As shown in Table 3, and discussed more fully below, aggregate
estimates of exposures of concern for the 12 urban areas included in
the assessment are considerably larger for the benchmark level of >=
0.060 ppm O3, compared to the 0.070 ppm benchmark, while the
pattern of year-to-year variability is fairly similar.
As shown in Table 3, aggregate estimates of exposures of concern
for a 0.060 ppm benchmark level vary considerably among the three
alternative standards included in this table, particularly for the 2002
simulations (a year with generally poorer air quality in most, but not
all areas). For air quality just meeting a 0.074/4 standard
approximately 27% of asthmatic children, based on the 2002 simulation,
and approximately 2% of asthmatic children based on the 2004 simulation
(a year with better air quality in most but not all areas), are
estimated to experience one or more exposures of concern at the
benchmark level of >= 0.060 ppm O3. Considering a 0.070/4
standard using the same benchmark level (0.060 ppm), about 18% of
asthmatic children are estimated to experience one or more exposures of
concern, in a year with poorer air quality (2002), and only about 1% in
a year with better air quality (2004). For the most stringent standard
examined (a 0.064/4 standard), about 6% of asthmatic children are
estimated to experience one or more exposures of concern in the
simulation based on the year with poorer air quality (2002), and
exposures of concern at the 0.060 ppm benchmark level are essentially
eliminated based on a year with better air quality (2004).
Table 3 also provides aggregate exposure estimates for the 12 urban
areas where a benchmark level of >= 0.070 ppm is used. Based on the
year with poorer air quality (2002), the estimate of the percent of
asthmatic children exposed one or more times is about 5% when a 0.074/4
standard is just met; based on a year with better air quality (2004),
exposures of concern are essentially eliminated. For this same
benchmark (0.070 ppm), when a 0.070/4 standard is just met, estimates
range from about 2% of asthmatic children exposed one or more times
over this benchmark based on a year with poorer air quality (2002), and
exposures of concern are essentially eliminated based on a year with
better air quality (2004). At the 0.070 ppm benchmark, just meeting a
0.064/4 standard essentially eliminates exposures of concern regardless
of the year that is used as the basis for the analysis.
The 2007 Staff Paper also notes that there is substantial city-to-
city variability in these estimates, and notes that it is appropriate
to consider not just the aggregate estimates across all cities, but
also to consider the public health impacts in cities that receive
relatively less protection from the alternative standards. As shown in
Table 3, in considering the benchmark level of >= 0.060 ppm, while the
aggregate percentage of asthmatic children estimated to experience one
or more exposures of concern across all 12 cities for a 0.074/4
standard is about 27% based on the year with poorer air quality (2002),
it ranges up to approximately 51% for asthmatic children in the city
with the least degree of protection from that alternative standard.
Similarly, for air quality just meeting a 0.070/4 standard, the
aggregate percentage of asthmatic children estimated to experience one
or more exposures of concern across all 12 cities is 18% based on the
year with poorer air quality, but it ranges up to about 41% in the city
with the least degree of protection associated with just meeting that
alternative standard. For just meeting a 0.064/4 standard, the
aggregate estimate of asthmatic children experiencing exposures of
concern for the 0.060 ppm benchmark is about 6% based on the year with
poorer air quality and ranges up to 16% in the city with the least
degree of protection.
This pattern of city-to-city variability also occurs at the
benchmark level of >= 0.070 ppm associated with air quality just
meeting these same three alternative standards (i.e., 0.074/4, 0.070/4,
and 0.064/4). While the aggregate percentage of asthmatic children
estimated to experience such exposures of concern across all 12 cities
is about 5% based on the year with poorer air quality for just meeting
the 0.074/4 standard, it ranges up to 14% in the city with the least
degree of protection associated with that alternative standard. For
just meeting a 0.070/4 standard the aggregate estimate is 2% of
asthmatic children experiencing exposures of concern for the 0.070 ppm
benchmark based on the year with poorer air quality and ranges up to 6%
in the city with the least degree of protection. The aggregate estimate
for exposures of concern is further reduced to 0.2% of asthmatic
children for this same benchmark level for air quality just meeting a
0.064/4 standard based on the year with poorer air quality and ranges
up to 1% in the city with the least degree of protection.
In addition to observing the fraction of the population estimated
to experience exposures of concern associated with just meeting
alternative standards, EPA also took into consideration in the 2007
Staff Paper the percent reduction in exposures of concern and health
risks associated with alternative standards relative to just meeting
the then current 0.084/4 standards. For the current decision it is also
informative to consider the incremental reductions in exposures of
concern associated with more stringent alternative standards relative
to the 0.075 ppm standard. As shown in Table 1 above, at the >= 0.060
ppm benchmark level based on a year with poorer air quality, the
reduction in exposures of concern for asthmatic children in going from
the 0.074/4 standard (which approximates the 0.075 ppm standard adopted
in 2008) down to a 0.064/4 standard is observed to be very similar to
the reduction estimated to occur in going from then current 0.084/4
standard down to a 0.074/4 standard. More specifically, the estimates
for asthmatic children are reduced from 47% (about 1.2 million
children) associated with meeting a 0.084/4 standard down to 27% (about
700,000 children) for just meeting a 0.074/4 standard and the estimates
are reduced further to about 6% (about 150,000 children) associated
with just meeting a
[[Page 2990]]
0.064/4 standard in the 12 urban areas included in the assessment. In a
year with better air quality (2004), exposures estimated to exceed the
0.060 ppm benchmark in asthmatic children one or more times in a year
are reduced from 11% associated with just meeting a 0.084/4 standard
down to about 2% for a 0.074/4 standard and are essentially eliminated
when a 0.064/4 standard is just met.
Turning to consideration of the risk assessment estimates, Table 2
above summarizes the risk estimates for moderate lung function
decrements in both all school age children and asthmatic school age
children associated with just meeting several alternative standards
based on simulations involving a year with relatively poorer air
quality (2002) and a year with relatively better air quality (2004). As
shown in Table 2, for the 2002 simulation the reduction in the number
of asthmatic children estimated to experience one or more moderate lung
function decrements going from a 0.074/4 standard down to a 0.064/4
standard is roughly equivalent to the additional health protection
afforded associated with just meeting a 0.074/4 standard relative to
then current 0.084/4 standard. More specifically, for just 5 urban
areas, it is estimated that nearly 8% of asthmatic children (130,000
children) would experience one or more occurrences of moderate lung
function decrements per year at a 0.084/4 standard and this would be
reduced to about 5% (90,000 children) at a 0.074/4 standard and further
reduced down to about 3% (50,000 children) at a 0.064/4 standard. Based
on the 2002 simulations, the percent reduction associated with just
meeting a 0.064/4 standard relative to then current 0.084/4 standard is
about 62% which is about twice the reduction in risk compared to the
estimated 31% reduction associated with just meeting a 0.074/4
standard. As shown in Table 2 above, similar patterns were observed in
reductions in lung function risk for all school age children in 12
urban areas associated with these alternative standards.
Figures 6-5 and 6-6 in the 2007 Staff Paper (EPA, 2007b) show the
percent reduction in non-accidental mortality risk estimates associated
with just meeting the same alternative standards discussed above
relative to just meeting the then current 0.084/4 standard for 12 urban
areas, based on adjusting 2002 and 2004 air quality data. These figures
also provide perspective on the extent to which the risks in these
years (i.e., 2002 and 2004) are greater than those estimated to occur
upon meeting the then current 0.084/4 standard (in terms of a negative
percent reduction relative to a 0.084/4 standard). Based on the 2002
simulations (EPA, 2007b, Figure 6-5), the estimated reduction in non-
accidental mortality is about 30 to 70% across the 12 urban areas for
just meeting a 0.064/4 standard relative to the then current 0.084/4
standard. This reduction is roughly twice the 15 to 30% estimated
reduction across the 12 urban areas associated with just meeting a
0.074/4 standard relative to a 0.084/4 standard. While the estimated
incidence is lower based on the 2004 simulations (EPA, 2007b, Figure 6-
6), the pattern of risk reductions among alternative standards is
roughly similar to that observed for the 2002 simulations.
In addition to the risk estimates for lung function decrements in
all school age children and non-accidental mortality that were
estimated for 12 urban areas and lung function decrements in asthmatic
children for 5 urban areas, a similar pattern of incremental reductions
in health risks was shown for two health outcomes where risks were
estimated in one city only for each of these outcomes. These included
reductions in respiratory symptoms in asthmatic children (EPA, 2007b;
Boston, Table 6-9) and respiratory-related hospital admissions (EPA,
2007a; New York City, Table 6-10) associated with just meeting
alternative 8-hour standards set at 0.074 ppm, 0.070 ppm, and 0.064 ppm
relative to just meeting the then current 0.084 ppm standard. Using the
2002 simulation, a standard set at 0.074/4 is estimated to reduce the
incidence of symptom days in children with moderate to severe asthma in
the Boston area by about 15 percent relative to a 0.084/4 standard.
With this reduction, it is estimated that about 1 respiratory symptom
day in 8 during the O3 season would be attributable to
O3 exposure. A standard set at 0.064/4 is estimated, based
on the 2002 simulation, to reduce the incidence of symptom days in
children with moderate to severe asthma in the Boston area by about a
25 to 30 percent reduction relative to a 0.084 ppm standard, which is
roughly twice the reduction compared to that provided by a 0.074/4
standard. But even with this reduction, it is estimated that 1
respiratory symptom day in 10 during the O3 season is
attributable to O3 exposure.
As shown in Table 6-10 (EPA, 2007b) estimated incidence of
respiratory-related hospital admissions in one urban area (New York
City) was reduced by 14 to 17 percent by a standard set at 0.074/4
relative to then current 0.084/4 standard, in the year with relatively
high and relatively low O3 air quality levels, respectively.
Similar to the pattern observed for the other health outcomes discussed
above, the reduction in incidence of respiratory-related hospital
admissions for a 0.064/4 standard relative to a 0.084/4 standard is
about twice that associated with a 0.074/4 standard relative to a
0.084/4 standard.
Table 3--Number and Percent of All and Asthmatic School Age Children in 12 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above 0.060 and
0.070 ppm While at Moderate or Greater Exertion, One or More Times per Season Associated With Just Meeting Alternative 8-Hour Standards Based on
Adjusting 2002 and 2004 Air Quality Data1 2
--------------------------------------------------------------------------------------------------------------------------------------------------------
All children, ages 5-18 Aggregate for Asthmatic children, ages 5-18
12 urban areas Number of children Aggregate for 12 urban areas Number
8-Hour air quality exposed (% of all children) [Range of children exposed (% of group)
Benchmark levels of exposures of concern (ppm) standards \3\ across 12 cities, % of all children] [Range across 12 cities, % of group]
(ppm) -------------------------------------------------------------------------------
2002 2004 2002 2004
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.070............................................... 0.074 770,000 (4%) 20,000 (0%) 120,000 (5%) 0 (0%)
[0-13%] [0-1%] [0-14%] [0-1%]
0.070 270,000 (1%) 0 (0%) 50,000 (2%) 0 (0%)
[0-5%] [0%] [0-6%] [0%]
0.064 30,000 (0.2%) 0 (0%) 10,000 (0.2%) 0 (0%)
[0-1%] [0%] [0-1% ] [0%]
[[Page 2991]]
0.060............................................... 0.074 4,550,000 (25%) 350,000 (2%) 700,000 (27%) 50,000 (2%)
[1-48%] [0-9%] [1-51%] [0-9%]
0.070 3,000,000 (16%) 110,000 (1%) 460,000 (18%) 10,000 (1%)
[1-36%] [0-4%] [0-41%] [0-3%]
0.064 950,000 (5%) 10,000 (0%) 150,000 (6%) 0 (0%)
[0-17%] [0-1%] [0-16%] [0-1%]
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate >= 13 1-min/m\2\.
\2\ Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New
York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston, Los Angeles and
Sacramento and March or April to September or October for the remaining urban areas.
\3\ All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of the annual
4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the 2007 Staff Paper
(EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard and
selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might meet the specified standards.
2. CASAC Views Prior to 2008 Decision
In comments on the second draft Staff Paper, CASAC stated in its
letter to the Administrator, ``the CASAC unanimously recommends that
the current primary ozone NAAQS be revised and that the level that
should be considered for the revised standard be from 0.060 to 0.070
ppm'' (Henderson, 2006c, p. 5). This recommendation followed from its
more general recommendation that the 0.084 ppm standard needed to be
substantially reduced to be protective of human health, particularly in
at-risk subpopulations.
The CASAC Panel noted that beneficial reductions in some adverse
health effects were estimated to occur upon meeting the lowest standard
level (0.064 ppm) considered in the risk assessment (Henderson, 2006c,
p. 4). The lower end of this range reflects CASAC's views that
``[w]hile data exist that adverse health effects may occur at levels
lower than 0.060 ppm, these data are less certain and achievable gains
in protecting human health can be accomplished through lowering the
ozone NAAQS to a level between 0.060 and 0.070 ppm.'' (id.).
In a subsequent letter sent specifically to offer advice to aid the
Administrator and Agency staff in developing the O3
proposal, the CASAC reiterated that the Panel members ``were unanimous
in recommending that the level of the current primary ozone standard
should be lowered from 0.08 ppm to no greater than 0.070 ppm''
(Henderson, 2007, p. 2). Further, the CASAC Panel expressed the view
that the 2006 Criteria Document and 2007 Staff Paper, together with the
information in its earlier letter, provide ``overwhelming scientific
evidence for this recommendation,'' and emphasized the Clean Air Act
requirement that the primary standard must be set to protect the public
health with an adequate margin of safety (id.).
3. Basis for 2008 Decision on the Primary Standard
This section presents the rationale for the 2008 final decision on
the primary O3 standard as presented in the 2008 final rule
(73 FR 16475). The EPA's conclusions on the level of the standard began
by noting that, having carefully considered the public comments on the
appropriate level of the O3 standard, EPA concluded that the
fundamental scientific conclusions on the effects of O3
reached in the 2006 Criteria Document and 2007 Staff Paper remained
valid. In considering the level at which the primary O3
standard should be set, EPA placed primary consideration on the body of
scientific evidence available in the 2008 final rulemaking on the
health effects associated with O3 exposure, while viewing
the results of exposure and risk assessments as providing information
in support of the decision. In considering the available scientific
evidence, EPA concluded that a focus on the proposed range of 0.070 to
0.075 ppm was appropriate in light of the large body of controlled
human exposure and epidemiological and other scientific evidence. The
notice stated that this body of evidence did not support retaining the
then current 0.084 ppm 8-hour O3 standard, as suggested by
some commenters, nor did it support setting a level just below 0.080
ppm, because, based on the entire body of evidence, such a level would
not provide a significant increase in protection compared to the 0.084
ppm standard. Further, such a level would not be appreciably below the
level in controlled human exposure studies at which adverse effects
have been demonstrated (i.e., 0.080 ppm). The notice also stated that
the body of evidence did not support setting a level of 0.060 ppm or
below, as suggested by other commenters. In evaluating the information
from the exposure assessment and the risk assessment, EPA judged that
this information did not provide a clear enough basis for choosing a
specific level within the range of 0.075 to 0.070 ppm.
In making a final judgment about the level of the primary
O3 standard, EPA noted that the level of 0.075 ppm is above
the range recommended by the CASAC (i.e., 0.070 to 0.060 ppm). The
notice stated that in placing great weight on the views of CASAC,
careful consideration had been given to CASAC's stated views and the
scientific basis and policy views for the range it recommended. In so
doing, EPA fully agreed that the scientific evidence supports the
conclusion that the current standard was not adequate and must be
revised.
[[Page 2992]]
With respect to CASAC's recommended range of standard levels, EPA
observed that the basis for CASAC's recommendation appeared to be a
mixture of scientific and policy considerations. While in general
agreement with CASAC's views concerning the interpretation of the
scientific evidence, EPA noted that there was no bright line clearly
directing the choice of level, and the choice of what was appropriate
was clearly a public health policy judgment entrusted to the EPA
Administrator. This judgment must include consideration of the
strengths and limitations of the evidence and the appropriate
inferences to be drawn from the evidence and the exposure and risk
assessments. In reviewing the basis for the CASAC Panel's
recommendation for the range of the O3 standard, EPA
observed that it reached a different policy judgment than the CASAC
Panel based on apparently placing different weight in two areas: The
role of the evidence from the Adams studies and the relative weight
placed on the results from the exposure and risk assessments. While EPA
found the evidence reporting effects at the 0.060 ppm level from the
Adams studies to be too limited to support a primary focus at this
level, EPA observed that the CASAC Panel appeared to place greater
weight on this evidence, as indicated by its recommendation of a range
down to 0.060 ppm. It was noted that while the CASAC Panel supported a
level of 0.060 ppm, they also supported a level above 0.060, which
indicated that they did not believe that the results of Adams studies
meant that the level of the standard had to be set at 0.060 ppm. The
EPA also observed that the CASAC Panel appeared to place greater weight
on the results of the risk assessment as a basis for its recommended
range. In referring to the risk assessment results for lung function,
respiratory symptoms, hospital admissions and mortality, the CASAC
Panel concluded that: ``beneficial effects in terms of reduction of
adverse health effects were calculated to occur at the lowest
concentration considered (i.e., 0.064 ppm)'' (Henderson, 2006c, p. 4).
However, EPA more heavily weighed the implications of the uncertainties
associated with the Agency's quantitative human exposure and health
risk assessments. Given these uncertainties, EPA did not agree that
these assessment results appropriately served as a primary basis for
concluding that levels at or below 0.070 ppm were required for the 8-
hour O3 standard.
The notice stated that after carefully taking the above comments
and considerations into account, and fully considering the scientific
and policy views of the CASAC, EPA decided to revise the level of the
primary 8-hour O3 standard to 0.075 ppm. The EPA judged,
based on the available evidence, that a standard set at this level
would be requisite to protect public health with an adequate margin of
safety, including the health of sensitive subpopulations, from serious
health effects including respiratory morbidity, that were judged to be
causally associated with short-term and prolonged exposures to
O3, and premature mortality. The EPA also judged that a
standard set at this level provides a significant increase in
protection compared to the 0.084 ppm standard, and is appreciably below
0.080 ppm, the level in controlled human exposure studies at which
adverse effects have been demonstrated. At a level of 0.075 ppm,
exposures at and above the benchmark of 0.080 ppm are essentially
eliminated, and exposures at and above the benchmark of 0.070 are
substantially reduced or eliminated for the vast majority of people in
at-risk groups. A standard set at a level lower than 0.075 would only
result in significant further public health protection if, in fact,
there is a continuum of health risks in areas with 8-hour average
O3 concentrations that are well below the concentrations
observed in the key controlled human exposure studies and if the
reported associations observed in epidemiological studies are, in fact,
causally related to O3 at those lower levels. Based on the
available evidence, EPA was not prepared to make these assumptions.
Taking into account the uncertainties that remained in interpreting the
evidence from available controlled human exposure and epidemiological
studies at very low levels, EPA noted that the likelihood of obtaining
benefits to public health decreased with a standard set below 0.075 ppm
O3, while the likelihood of requiring reductions in ambient
concentrations that go beyond those that are needed to protect public
health increased. The EPA judged that the appropriate balance to be
drawn, based on the entire body of evidence and information available
in the 2008 final rulemaking, was to set the 8-hour primary standard at
0.075 ppm. The EPA expressed the belief that a standard set at 0.075
ppm would be sufficient to protect public health with an adequate
margin of safety, and did not believe that a lower standard was needed
to provide this degree of protection. The EPA further asserted that
this judgment appropriately considered the requirement for a standard
that was neither more nor less stringent than necessary for this
purpose and recognized that the CAA does not require that primary
standards be set at a zero-risk level, but rather at a level that
reduces risk sufficiently so as to protect public health with an
adequate margin of safety.
4. CASAC Advice Following 2008 Decision
Following the 2008 decision on the O3 standard, serious
questions were raised as to whether the standard met the requirements
of the CAA. In April 2008, the members of the CASAC Ozone Review Panel
sent a letter to EPA stating ``In our most-recent letters to you on
this subject--dated October 2006 and March 2007--the CASAC unanimously
recommended selection of an 8-hour average Ozone NAAQS within the range
of 0.060 to 0.070 parts per million for the primary (human health-
based) Ozone NAAQS'' (Henderson, 2008). The letter continued: ``The
CASAC now wishes to convey, by means of this letter, its additional,
unsolicited advice with regard to the primary and secondary Ozone
NAAQS. In doing so, the participating members of the CASAC Ozone Review
Panel are unanimous in strongly urging you or your successor as EPA
Administrator to ensure that these recommendations be considered during
the next review cycle for the Ozone NAAQS that will begin next year''
(id.). Moreover, the CASAC Panel noted that ``numerous medical
organizations and public health groups have also expressed their
support of these CASAC recommendations.'' (id.) The letter further
stated the following strong, unanimous view:
[the CASAC did] ``not endorse the new primary ozone standard as
being sufficient protective of public health. The CASAC--as the
Agency's statutorily-established science advisory committee for
advising you on the national ambient air quality standards--unanimously
recommended decreasing the primary standard to within the range of
0.060-0.070 ppm. It is the Committee's consensus scientific opinion
that your decision to set the primary ozone standard above this range
fails to satisfy the explicit stipulations of the Clean Air Act that
you ensure an adequate margin of safety for all individuals, including
sensitive populations'' (Henderson, 2008).
5. Administrator's Proposed Conclusions
For the reasons discussed below, the Administrator proposes to set
a new level for the 8-hour primary O3 within
[[Page 2993]]
the range from 0.060 to 0.070 ppm.\50\ In reaching this proposed
decision, the Administrator has considered: the evidence-based
considerations from the 2006 Criteria Document and the 2007 Staff
Paper; the results of the exposure and risk assessments discussed above
and in the 2007 Staff Paper; CASAC advice and recommendations provided
in CASAC's letters to the Administrator both during and following the
2008 rulemaking; EPA staff recommendations; and public comments
received in conjunction with review of drafts of these documents and on
the 2007 proposed rule. In considering what level of an 8-hour
O3 standard is requisite to protect public health with an
adequate margin of safety, the Administrator is mindful that this
choice requires judgments based on an interpretation of the evidence
and other information that neither overstates nor understates the
strength and limitations of the evidence and information.
---------------------------------------------------------------------------
\50\ As discussed above at the beginning of section II, the
Administrator has focused her reconsideration of the primary
O3 standard set in the 2008 final rule on the level of
the standard, having decided not to reopen the 2008 final rule with
regard to the need to revise the 1997 primary O3 standard
to provide increased public health protection nor with regard to the
indicator, averaging period, and form of the 2008 standard.
---------------------------------------------------------------------------
The Administrator notes that the most certain evidence of adverse
health effects from exposure to O3 comes from the controlled
human exposure studies, and that the large bulk of this evidence
derives from studies of exposures at levels of 0.080 ppm and above. At
those levels, there is consistent evidence of lung function decrements
and respiratory symptoms in healthy young adults, as well as evidence
of O3-induced pulmonary inflammation, airway responsiveness,
impaired host defense capabilities, and other medically significant
airway responses. Moreover, there is no evidence that the 0.080 ppm
exposure level is a threshold for any of these types of respiratory
effects. Rather, there is now controlled human exposure evidence,
including studies of lung function decrements and respiratory symptoms
at the 0.060 ppm exposure level, that strengthens our previous
understanding that this array of respiratory responses are likely to
occur in some healthy adults at such lower levels.
In particular, the Administrator notes two studies by Adams (2002,
2006), newly available in the 2008 rulemaking, that examined lung
function and respiratory symptom effects associated with prolonged
O3 exposures at levels below 0.080 ppm, as well as EPA's
reanalysis of the data from the Adams (2006) study at a 0.060 ppm
exposure level. As discussed above, while the author's analysis focused
on hour-by-hour comparisons of effects, for the purpose of exploring
responses associated with different patterns of exposure, EPA's
reanalysis focused on addressing the more fundamental question of
whether the pre- to post-exposure change in lung function differed
between a 6.6-hour exposure to 0.060 ppm O3 versus a 6.6
hour exposure to clean filtered air. The Administrator notes that this
reanalysis found small, but statistically significant group mean
differences in lung function decrements in healthy adults at the 0.060
ppm exposure level, which is now the lowest-observed-effects level for
these effects. Moreover, these studies also report a small percentage
of subjects (7 to 20 percent) experienced moderate lung function
decrements (>= 10 percent) at the 0.060 ppm exposure level. While for
active healthy people, moderate levels of functional responses (e.g.,
FEV1 decrements of >= 10% but < 20%) and/or moderate
respiratory symptom responses would likely interfere with normal
activity for relatively few responsive individuals, the Administrator
notes that for people with lung disease, even moderate functional or
symptomatic responses would likely interfere with normal activity for
many individuals, and would likely result in more frequent use of
medication. Further, she notes that CASAC indicated that a focus on the
lower end of the range of moderate levels of functional responses
(e.g., FEV1 decrements >= 10%) is most appropriate for
estimating potentially adverse lung function decrements in people with
lung disease (Henderson, 2006c).
The Administrator also notes that many public commenters on the
2007 proposed rule raised a number of questions about the weight that
should be placed on the Adams studies and EPA's reanalysis of data from
the Adams (2006) study. Some commenters expressed the view that the
results of these studies and EPA's reanalysis provided support for
setting a standard level below the proposed range, while others raised
questions about EPA's reanalysis and generally expressed the view that
the study results were not robust enough to reach conclusions about
respiratory effects at the 0.060 ppm exposure level.\51\
---------------------------------------------------------------------------
\51\ The EPA responded to these comments in the 2008 final rule
(73 FR 16454-5).
---------------------------------------------------------------------------
Based on all the above considerations, the Administrator concludes
that the Adams studies provide limited but important evidence which
adds to the overall body of evidence that informs her proposed decision
on the range of levels within which a standard could be set that would
be requisite to protect public health with an adequate margin of
safety, including the health of at-risk populations such as people with
lung disease.
In considering controlled human exposure studies reporting
O3-induced pulmonary inflammation, airway responsiveness,
and impaired host defense capabilities at exposure levels down to 0.080
ppm, the lowest level at which these effects have been tested, the
Administrator notes that these physiological effects have been linked
to aggravation of asthma and increased susceptibility to respiratory
infection, potentially leading to increased medication use, increased
school and work absences, increased visits to doctors' offices and
emergency departments, and increased hospital admissions, especially in
people with lung disease. These physiological effects are all
indicators of potential adverse O3-related morbidity
effects, which are consistent with and lend plausibility to the
associations observed between O3 and adverse morbidity
effects and mortality effects in epidemiological studies.
With regard to epidemiological studies, the Administrator observes
that statistically significant associations between ambient
O3 levels and a wide array of respiratory symptoms and other
morbidity outcomes including school absences, emergency department
visits, and hospital admissions have been reported in a large number of
studies. More specifically, positive and robust associations were found
between ambient O3 concentrations and respiratory hospital
admissions and emergency department visits, when focusing particularly
on the results of warm season analyses. Taken together, the overall
body of evidence from controlled human exposure, toxicological, and
epidemiological studies supports the inference of a causal relationship
between acute ambient O3 exposures and increased respiratory
morbidity outcomes resulting in increased emergency department visits
and hospitalizations during the warm season. Further, the Administrator
notes that recent epidemiological evidence is highly suggestive that
O3 directly or indirectly contributes to non-accidental and
cardiopulmonary-related mortality.
The Administrator also considered the epidemiological evidence with
regard to considering potential effects thresholds at the population
level for
[[Page 2994]]
morbidity and mortality effects. As discussed above, while some studies
provide some indication of possible 8-hour average threshold levels
from below about 0.025 to 0.035 ppm (within the range of background
concentrations) up to approximately 0.050 ppm, other studies observe
linear concentration-response functions suggesting that there may be no
effects thresholds at the population level above background
concentrations. In addition, other studies conducted subset analyses
that included only days with ambient O3 concentrations below
the level of the then current standard, or below even lower
O3 concentrations, including a level as low as 0.061 ppm,
and continue to report statistically significant associations. The
Administrator notes that the relationships between ambient
O3 concentrations and lung function decrements, respiratory
symptoms, indicators of respiratory morbidity including increased
respiratory-related emergency department visits and hospital
admissions, and possibly mortality reported in a large number of
studies likely extend down to ambient O3 concentrations well
below the level of the standard set in 2008 (0.075 ppm), in that the
highest level at which there is any indication of a threshold is
approximately 0.050 ppm. The Administrator notes as well that toward
the lower end of the range of O3 concentrations observed in
such studies, ranging down to background levels (i.e., 0.035 to 0.015
ppm), there is increasing uncertainty as to whether the observed
associations remain plausibly related to exposures to ambient
O3, rather than to the broader mix of air pollutants present
in the ambient atmosphere. She also notes that there are limitations in
epidemiological studies that make discerning population thresholds
difficult, as discussed above, such that there is the possibility that
thresholds for individuals may exist in reported associations at fairly
low levels within the range of air quality observed in the studies but
not be detectable as population thresholds in epidemiological analyses.
In looking more broadly at evidence from animal toxicological,
controlled human exposure, and epidemiological studies, the
Administrator finds substantial evidence, newly available for
consideration in the 2008 rulemaking, that people with asthma and other
preexisting pulmonary diseases are among those at increased risk from
O3 exposure. As discussed above, altered physiological,
morphological, and biochemical states typical of respiratory diseases
like asthma, COPD, and chronic bronchitis may render people sensitive
to additional oxidative burden induced by O3 exposure.
Children and adults with asthma are the group that has been studied
most extensively. Evidence from controlled human exposure studies
indicates that asthmatics and people with allergic rhinitis may exhibit
larger lung function decrements in response to O3 exposure
than healthy subjects and that they can have larger inflammatory
responses. The Administrator also notes that two large U.S.
epidemiological studies, as well as several smaller U.S. and
international studies, have reported fairly robust associations between
ambient O3 concentrations and measures of lung function and
daily symptoms (e.g., chest tightness, wheeze, shortness of breath) in
children with moderate to severe asthma and between O3 and
increased asthma medication use. These more serious responses in
asthmatics and others with lung disease provide biological plausibility
for the respiratory morbidity effects observed in epidemiological
studies, such as respiratory-related emergency department visits and
hospital admissions.
The Administrator also observes that a substantial body of evidence
from controlled human exposure and epidemiological studies indicates
that relative to the healthy, non-asthmatic subjects used in most
controlled human exposure studies, a greater proportion of people with
asthma may be affected, and those who are affected may have as large or
larger lung function and symptomatic responses to O3
exposures. Thus, the Administrator concludes that controlled human
exposure studies of lung function decrements and respiratory symptoms
that evaluate only healthy, non-asthmatic subjects likely underestimate
the effects of O3 exposure on asthmatics and other
susceptible populations.
In addition to the evidence-based considerations discussed above,
the Administrator also considered quantitative exposures and health
risks estimated to occur associated with air quality simulated to just
meet various standard levels to help inform judgments about a range of
standard levels for consideration that could provide an appropriate
degree of public health protection. In so doing, she is mindful of the
important uncertainties and limitations that are associated with the
exposure and risk assessments, as discussed in more detail in the 2007
Staff Paper, and above in sections II.B and II.C.1.b. Beyond these
uncertainties, the Administrator also recognized important limitations
related to the exposure and risk analyses. For example, EPA did not
have sufficient information to evaluate all relevant at-risk groups
(e.g., outdoor workers) or all O3-related health outcomes
(e.g., increased medication use, school absences, emergency department
visits), and the scope of the analyses was generally limited to
estimating exposures and risks in 12 urban areas across the U.S., and
to only five or just one area for some health effects. Thus, it is
clear that national-scale public health impacts of ambient
O3 exposures are much larger than the quantitative estimates
of O3-related incidences of adverse health effects and the
numbers of children likely to experience exposures of concern
associated with meeting the then current standard or alternative
standards. Taking these limitations into account, the CASAC advised EPA
not to rely solely on the results of the exposure and risk assessments
in considering alternative standards, but also to place significant
weight on the body of evidence of O3-related health effects
in drawing conclusions about an appropriate range of levels for
consideration. The Administrator agrees with this advice.
Turning first to the results of the exposure assessment, the
Administrator focused on the extent to which alternative standard
levels, approximately at and below the 0.075 ppm O3 standard
set in the 2008 final rule, are estimated to reduce exposures over the
0.060 and 0.070 ppm health effects benchmark levels, for all and
asthmatic school age children in the 12 urban areas included in the
assessment.\52\ The Administrator also took note that the lowest
standard level included in the exposure and health risk assessments was
0.064 ppm and that additional reductions in exposures over the selected
health benchmark levels would be anticipated for just meeting a 0.060
ppm standard.
---------------------------------------------------------------------------
\52\ As noted in section II.C.1.b.above, the Administrator
focused on alternative standards with different levels but the same
form and averaging time as the primary standard set in 2008.
---------------------------------------------------------------------------
As an initial matter, the Administrator recognized that the concept
of ``exposures of concern'' is more appropriately viewed as a
continuum, with greater confidence and less uncertainty about the
existence of health effects at the upper end and less confidence and
greater uncertainty as one considers increasingly lower O3
exposure levels. In considering the concept of exposures of concern,
the Administrator also noted that it is important to balance concerns
about the potential for health effects and their
[[Page 2995]]
severity with the increasing uncertainty associated with our
understanding of the likelihood of such effects at lower O3
levels. Within the context of this continuum, estimates of exposures of
concern at discrete benchmark levels provide some perspective on the
public health impacts of O3-related physiological effects
that have been demonstrated in controlled human exposure and
toxicological studies but cannot be evaluated in quantitative risk
assessments, such as lung inflammation, increased airway
responsiveness, and changes in host defenses. They also help in
understanding the extent to which such impacts have the potential to be
reduced by meeting alternative standards. As discussed in II.C.1.a
above, these O3-related physiological effects are plausibly
linked to the increased morbidity seen in epidemiological studies
(e.g., as indicated by increased medication use in asthmatics, school
absences in all children, and emergency department visits and hospital
admissions in people with lung disease).
Estimates of the number of people likely to experience exposures of
concern cannot be directly translated into quantitative estimates of
the number of people likely to experience specific health effects,
since sufficient information to draw such comparisons is not
available--if such information were available, these health outcomes
would have been included in the quantitative risk assessment. Due to
individual variability in responsiveness, only a subset of individuals
who have exposures at and above a specific benchmark level are expected
to experience such adverse health effects, and susceptible population
groups such as those with asthma are expected to be affected more by
such exposures than healthy individuals.
For the reasons discussed in section II.C.1.b above, the
Administrator has concluded that it is appropriate to focus on both the
0.060 and 0.070 ppm health effect benchmarks for her decision on the
primary standard. In summary, the focus on these two benchmark levels
reflects the following evidence-based considerations, discussed above
in section II.C.1.a, that raise concerns about adverse health effects
likely occurring at levels below 0.080 ppm: (1) That there is limited,
but important, new evidence from controlled human exposure studies
showing lung function decrements and respiratory symptoms in some
healthy subjects at 0.060 ppm; (2) that asthmatics are likely to have
more serious responses than healthy individuals; (3) that lung function
is not likely to be as sensitive a marker for O3 effects as
lung inflammation; and (4) that there is epidemiological evidence which
reports associations between ambient O3 concentrations and
respiratory symptoms, ED visits, hospital admissions, and premature
mortality in areas with O3 levels that extend well below
0.080 ppm.
Based on the exposure and risk considerations discussed in detail
in the 2007 Staff Paper and presented in sections II.B and II.C.1.b
above, the Administrator notes the following important observations
from these assessments: (1) There is a similar pattern for all children
and asthmatic school age children in terms of exposures of concern over
selected benchmark levels when estimates are expressed in terms of
percentage of the population; (2) the aggregate estimates of exposures
of concern reflecting estimates for the 12 urban areas included in the
assessment are considerably larger for the benchmark level of 0.060 ppm
compared to the 0.070 ppm benchmark; (3) there is notable year-to-year
variability in exposure and risk estimates with higher exposure and
risk estimates occurring in simulations involving a year with generally
poorer air quality in most areas (2002) compared to a year with
generally better air quality (2004); and (4) there is significant city-
to-city variability in exposure and risk estimates, with some cities
receiving considerably less protection associated with air quality just
meeting the same standard. As discussed above, the Administrator
believes that it is appropriate to consider not just the aggregate
estimates across all cities, but also to consider the public health
impacts in cities that receive relatively less protection from
alternative standards under consideration. Similarly, the Administrator
believes that year-to-year variability should also be considered in
making judgments about which standards will protect public health with
an adequate margin of safety.
In addition, significant reductions in exposures of concern and
risk have been estimated to occur across standard levels analyzed. The
magnitudes of exposure and risk reductions estimated to occur in going
from a 0.074 ppm standard to a 0.064 ppm standard are as large as those
estimated to occur in going from the then current 0.084 ppm standard to
a 0.074 ppm standard. Consequently, the reduction in risk that can be
achieved by going from a standard of 0.074 ppm to a standard of 0.064
ppm is comparable to the risk reduction that can be achieved by moving
from the 1997 O3 standard, effectively a 0.084 ppm standard,
to a standard very close to the 2008 standard of 0.075 ppm.
The Administrator also observes that estimates of exposures of
concern associated with air quality just meeting the alternative
standards below 0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm, the
levels included in the assessment) are notably lower than estimates for
alternative standards set at and above 0.080 ppm. As shown in Table 6-8
in the 2007 Staff Paper, just meeting a 0.080 ppm standard is
associated with an aggregate estimate of exposures of concern of about
13% of asthmatic children at the 0.070 ppm benchmark level, ranging up
to 31% in the city with the least degree of protection in a year with
generally poorer air quality, and an aggregate estimate of exposures of
concern of about 40% of asthmatic children, ranging up to 63% in the
city with the least degree of protection at the 0.060 ppm benchmark
level. Based on the exposure estimates presented in Table 3 in this
notice, she observes that standards included in the assessment below
0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm), are estimated to have
substantially lower estimates of exposures of concern at the 0.070 ppm
benchmark level. Similarly, she notes that exposures of concern at the
0.060 ppm benchmark associated with alternative standards below 0.080
ppm are appreciably lower than exposures associated with standards at
or above 0.080 ppm, especially for standards set at 0.064 and 0.070
ppm.
As noted previously, the Administrator also recognizes that the
risk estimates for health outcomes included in the risk assessment are
limited and that the overall health effects evidence is indicative of a
much broader array of O3-related health effects that are
part of a ``pyramid of effects'' that include various indicators of
morbidity that could not be included in the risk assessment (e.g.,
school absences, increased medication use, doctor's visits, and
emergency department visits), some of which have a greater impact on
at-risk groups. Consideration of such unquantified risks for this array
of health effects, taken together with the estimates of exposures of
concern and the quantified health risks discussed above, supports the
Administrator's evidence-based conclusion that revising the standard
level to a level well below 0.080 ppm will provide important increased
public health protection, especially for at-risk groups such as people
with asthma or other lung disease, as well as children and older
adults, particularly those active outdoors, and outdoor workers.
[[Page 2996]]
Based on the evidence- and exposure/risk-based considerations
discussed above, the Administrator concludes that it is appropriate to
set the level of the primary O3 standard to a level well
below 0.080 ppm, a level at which the evidence provides a high degree
of certainty about the adverse effects of O3 exposure in
healthy people, to provide an adequate margin of safety for at-risk
groups. In selecting a proposed range of levels, the Administrator
believes it is appropriate to consider the following information: (1)
The strong body of evidence from controlled human exposure studies
evaluating healthy people at exposure levels of 0.080 ppm and above
that demonstrated lung function decrements, respiratory symptoms,
pulmonary inflammation, and other medically significant airway
responses, as well as limited but important evidence of lung function
decrements and respiratory symptoms in healthy people down to
O3 exposure levels of 0.060 ppm; (2) the substantial body of
evidence from controlled human exposure and epidemiological studies
indicating that people with asthma are likely to experience larger and
more serious effects than healthy people; (3) the body of
epidemiological evidence indicating associations are observed for a
wide range of serious health effects, including respiratory-related
emergency department visits and hospital admissions and premature
mortality, across distributions of ambient O3 concentrations
that extend below the current standard level of 0.075 ppm, as well as
questions of biological plausibility in attributing the observed
effects to O3 alone at the lower end of the concentration
ranges extending down to background levels; and (4) the estimates of
exposures of concern and risks for a range of health effects that
indicate that important improvements in public health are very likely
associated with O3 levels just meeting alternative
standards, especially for standards set at 0.070 and 0.064 ppm (the
lowest levels included in the assessment), relative to standards set at
and above 0.080 ppm.
The Administrator next considered what standard level well below
0.080 ppm would be requisite to protect public health, including the
health of at-risk groups, with an adequate margin of safety that is
sufficient but not more than necessary to achieve that result. The
assessment of a standard level calls for consideration of both the
degree of risk to public health at alternative levels of the standard
as well as the certainty that such risk will occur at any specific
level. Based on the information available in the 2008 rulemaking, there
is no evidence-based bright line that indicates a single appropriate
level. Instead there is a combination of scientific evidence and other
information that needs to be considered as a whole in making this
public health policy judgment, and selecting a standard level from a
range of potentially reasonable values.
As an initial matter, the Administrator considered whether the
standard level of 0.075 ppm set in the 2008 final rule is sufficiently
below 0.080 ppm to be requisite to protect public health with an
adequate margin of safety. In considering this standard level, the
Administrator looked to the rationale for selecting this level
presented in the 2008 final rule, as summarized above in section
II.C.3. In that rationale, EPA observed that a level of 0.075 ppm is
above the range of 0.060 to 0.070 ppm recommended by CASAC, and that
the CASAC Panel appeared to place greater weight on the evidence from
the Adams studies and on the results of the exposure and risk
assessments, whereas EPA placed greater weight on the limitations and
uncertainties associated with that evidence and the quantitative
exposure and risk assessments. Additionally, EPA's rationale did not
discuss and thus placed no weight on exposures of concern relative to
the 0.060 ppm benchmark. Further, EPA concluded that ``[a] standard set
at a lower level than 0.075 ppm would only result in significant
further public health protection if, in fact, there is a continuum of
health risks in areas with 8-hour average O3 concentrations
that are well below the concentrations observed in the key controlled
human exposure studies and if the reported associations observed in
epidemiological studies are, in fact, causally related to O3
at those lower levels. Based on the available evidence, [EPA] is not
prepared to make these assumptions'' (73 FR 16483).
In reconsidering the entire body of evidence available in the 2008
rulemaking, including the Agency's own assessment of the
epidemiological evidence in the 2006 Criteria Document, and placing
significant weight on the views of CASAC, the Administrator now
concludes that important and significant risks to public health are
likely to occur at a standard level of 0.075 ppm. She judges that a
standard level of 0.075 ppm is not sufficient to provide protection
with an adequate margin of safety. In support of this conclusion, the
Administrator finds that setting a standard that would protect public
health, including the health of at-risk populations, with an adequate
margin of safety should reasonably depend upon giving some weight to
the results of the Adams studies and EPA's reanalysis of the Adams's
data, and to how effectively alternative standard levels would serve to
limit exposures of concern relative to the 0.060 ppm benchmark level as
well as to the 0.070 ppm benchmark level. The Administrator notes that
EPA's risk assessment estimates comparable risk reductions in going
from a 0.074 ppm standard to a 0.064 ppm standard as were estimated in
going from the then current 0.084 ppm standard down to a 0.074 ppm
standard for an array of health effects analyzed. These estimates
include reductions in risk for lung function decrements in all and
asthmatic school age children, respiratory symptoms in asthmatic
children, respiratory-related hospital admissions, and non-accidental
mortality.
Further, based on the exposure assessment estimates discussed
above, the Administrator notes that for air quality just meeting a
0.074 ppm standard, approximately 27% of asthmatic school age children
and 25% of all school age children are estimated to experience one or
more exposures of concern over the 0.060 ppm benchmark level based on
simulations for a year with generally poorer air quality; this estimate
increases to about 50% of asthmatic and all children in the city with
the least degree of protection. The Administrator judges that these
estimates are large and strongly suggest significant public health
impacts would likely remain in many areas with air quality just meeting
a 0.075 ppm O3 standard.
In light of these estimates and the available evidence, the
Administrator agrees with CASAC's conclusion that important public
health protections can be achieved by a standard set below 0.075 ppm,
within the range of 0.060 to 0.070 ppm. In addition, based on both the
evidence- and exposure/risk-based considerations summarized above, the
Administrator concludes that a standard set as high as 0.075 would not
be considered requisite to protect public health with an adequate
margin of safety, and that consideration of lower levels is warranted.
In considering such lower levels, the Administrator recognizes that the
CAA requires her to reach a public health policy judgment as to what
standard would be requisite to protect public health with an adequate
margin of safety, based on scientific evidence and technical
assessments that have inherent uncertainties and limitations. This
judgment requires making reasoned decisions as to what weight to place
on various types of
[[Page 2997]]
evidence and assessments and on the related uncertainties and
limitations.
In selecting a level below 0.075 ppm that would serve as an
appropriate upper end for a range of levels to propose, the
Administrator has considered a more cautious approach to interpreting
the available evidence and exposure/risk-based information--that is, an
approach that places significant weight on uncertainties and
limitations in the information so as to avoid potentially
overestimating public health risks and protection likely to be
associated with just meeting a particular standard level. In so doing,
she notes that the most certain evidence of adverse health effects from
exposure to O3 comes from the controlled human exposure
studies, and that the large bulk of this evidence derives from studies
of exposures at levels of 0.080 ppm and above. At those levels, there
is consistent evidence of lung function decrements and respiratory
symptoms in healthy young adults, as well as evidence of inflammation
and other medically significant airway responses. Further, she takes
note of the limited but important evidence from controlled human
exposure studies indicating that lung function decrements and symptoms
can occur in healthy people at levels as low as 0.060 ppm, while also
recognizing the limitations in that evidence, as discussed above in
sections II.A.1 and II.C.1.a. She also notes that some people with
asthma are likely to experience larger and more serious effects than
the healthy subjects evaluated in the controlled exposure studies,
while recognizing that there is uncertainty about the magnitude of such
differences. In considering the available epidemiological studies, she
recognizes that they provide evidence of serious respiratory morbidity
effects, including respiratory-related emergency department visits and
hospital admissions, and non-accidental mortality at levels well below
0.080 ppm, while also recognizing that there is increasing uncertainty
associated with the likelihood that such effects occur at decreasing
O3 levels down to background levels. Considering the
exposure/risk information, as shown in Table 3, the Administrator
observes that a standard set at 0.070 ppm would likely substantially
limit exposures of concern relative to the 0.070 ppm benchmark level,
while affording far less protection against exposures of concern
relative to the 0.060 ppm benchmark level. To the extent that more
weight is placed on protection relative to the higher benchmark level,
and more weight is placed on the uncertainties associated with the
epidemiological evidence, a standard set at 0.070 ppm might be
considered to be adequately protective. Taken together, this type of
cautious approach to interpreting the evidence and the exposure/risk
information serves as the basis for the Administrator's conclusion that
the upper end of the proposed range should be set at 0.070 ppm
O3.
In selecting a level that would serve as an appropriate lower end
for a range of levels to propose, the Administrator has considered a
more precautionary approach to interpreting the available evidence and
exposure/risk-based information--that is, an approach that places less
weight on uncertainties and limitations in the information so as to
avoid potentially underestimating public health improvements likely to
be associated with just meeting a particular standard level. In so
doing, the Administrator notes the limited, but important evidence of a
lowest-observed-effects level at 0.060 ppm O3 from
controlled human exposure studies reporting lung function decrements
and respiratory symptoms in healthy subjects. Notably, these studies
also report that a small percentage of subjects (7 to 20 percent)
experienced moderate lung function decrements (>= 10 percent) at the
0.060 ppm exposure level, recognizing that for people with lung
disease, such moderate functional or symptomatic responses would likely
interfere with normal activity for many individuals, and would likely
result in more frequent use of medication. In addition, a substantial
body of evidence indicates that people with asthma are likely to
experience larger and more serious effects than healthy people and
therefore controlled human exposure studies done with healthy subjects
likely underestimate effects in this at-risk population.
Moreover, epidemiological studies provide evidence of serious
respiratory morbidity effects, including respiratory-related emergency
department visits and hospital admissions, and non-accidental mortality
at O3 levels that may plausibly extend down to at least
0.060 ppm even when considering the uncertainties inherent in such
studies. The Administrator notes that the controlled human exposure
studies conducted at 0.060 ppm provide some biological plausibility for
associations between respiratory morbidity and mortality effects found
in epidemiological studies and O3 exposures down to 0.060
ppm. Considering the exposure information, as shown in Table 3, the
Administrator observes that a standard set at 0.064 ppm would likely
essentially eliminate exposures of concern relative to the 0.070 ppm
benchmark level, while appreciably limiting exposures of concern
relative to the 0.060 ppm benchmark level to approximately 6 percent of
asthmatic children in the aggregate across 12 cities and up to 16
percent in the city that would receive the least protection. While not
addressed in the exposure assessment done as part of the 2008
rulemaking, a standard set at 0.060 ppm would be expected to provide
somewhat greater protection from such exposures, which is important to
the extent that more weight is placed on providing protection relative
to the lower benchmark level. Taken together, the Administrator
concludes that this precautionary approach to interpreting the evidence
and the exposure/risk information supports a level of 0.060 ppm as the
lower end of the proposed range.
The Administrator has also concluded that the lower end of the
proposed range should not extend below 0.060 ppm O3. In
reaching this conclusion, she gives significant weight to the
recommendation of the CASAC panel that 0.060 ppm should be the lower
end of the range for consideration (Henderson, 2006c). In the
Administrator's view, the evidence from controlled human exposure
studies at the 0.060 ppm exposure level, the lowest level tested, is
not robust enough to support consideration of a lower level. While some
epidemiological studies provide evidence of serious respiratory
morbidity effects and non-accidental mortality with no evidence of a
threshold, the Administrator notes that other studies provide evidence
of a potential threshold somewhat below 0.060 ppm. Moreover, there are
limitations in epidemiological studies that make discerning population
thresholds difficult, including fewer observations in the range of
lower concentrations, concerns related to exposure measurement error,
the possible role of copollutants and effects modifiers, and
interindividual differences in susceptibility to O3-related
effects. In the Administrator's judgment, these limitations in
epidemiological studies, including the limitations in judging the
causality of observed associations at lower O3 levels, and
the lack of robust controlled human exposure data at 0.060 ppm make it
difficult to interpret this evidence as a basis for a standard level
set below 0.060 ppm. Thus, in selecting 0.060 ppm as the lower end of
the range for the proposed level of the O3 standard, the
Administrator has taken into
[[Page 2998]]
account information on the lowest-observed-effects levels in controlled
human exposure studies, indications of possible thresholds reported in
some epidemiological studies, the increasing uncertainty in the
epidemiological evidence at even lower levels, as well as evidence
about increased susceptibility of people with asthma and also other
lung diseases. In so doing, she concludes that a primary O3
standard set below 0.060 ppm would be more than is necessary to protect
public health with an adequate margin of safety for at-risk groups.
In reaching her proposed decision, the Administrator has also
considered the public comments that were received on the 2007 proposed
rule (72 FR 37818). The Administrator notes that there were sharply
divergent views expressed by two general sets of commenters with regard
to considering the health effects evidence, results of exposure and
risk assessments, and the advice of the CASAC panel. On one hand,
medical groups, health effects researchers, public health
organizations, environmental groups, and some state, tribal and local
air pollution control agencies strongly supported a standard set within
the range recommended by the CASAC. These commenters generally placed
significant weight on the more recent evidence from controlled human
exposure studies, down to the 0.060 ppm exposure level, as well as on
the epidemiological studies and the results of the exposure and risk
assessment conducted for the 2008 rulemaking. Many of these commenters
took a more precautionary view and supported a standard set at 0.060
ppm O3, the lower end of the CASAC recommended range. The
Administrator notes that these views are generally consistent with her
proposed conclusions. On the other hand, another group of commenters
primarily representing industry associations and businesses and some
state environmental agencies, primarily expressed the view that the
more recent evidence from controlled human exposure, the
epidemiological studies, and the results of exposure and human health
risk assessments were so uncertain that they did not provide a basis
for making any changes to the then current 0.084 ppm O3
standard set in 1997. This group of commenters generally argued that
the health effects evidence newly available in the 2008 rulemaking, the
results of the exposure and health risk assessments, and the advice of
the CASAC were flawed. For the reasons discussed above, the
Administrator does not agree with the later group of commenters that
essentially no weight should be placed on any of the new evidence or
assessments that were available for consideration in the 2008
rulemaking.
Based on consideration of the entire body of evidence and
information available in the 2008 rulemaking, including exposure and
risk estimates, as well as the recommendations of CASAC, the
Administrator proposes to set the level of the primary 8-hour
O3 standard to a level within the range of 0.060 to 0.070
ppm. A standard level within this range would reduce the risk of a
variety of health effects associated with exposure to O3,
including the respiratory symptoms and lung function effects
demonstrated in the controlled human exposure studies, and the
respiratory-related emergency department visits, hospital admissions
and mortality effects observed in the epidemiological studies. All of
these effects are indicative of a much broader array of O3-
related health endpoints, such as school absences and increased
medication use, that are plausibly linked to these observed effects.
Depending on the weight placed on the evidence and information
available in the 2008 rulemaking, as well as the uncertainties and
limitations in the evidence and information, a standard could be set
within this range at a level that would be requisite to protect public
health with an adequate margin of safety.
In reaching this proposed decision, as discussed above, the
Administrator has focused on the nature of the increased public health
protection that would be afforded by a standard set within the proposed
range of levels relative to the protection afforded by the standard set
in 2008. Having considered the public comments received on the 2007
proposed rule in reaching this proposed decision that reconsiders the
2008 final rule, the Administrator is interested in again receiving
public comment on the benefits to public health associated with a
standard set at specific levels within the proposed range relative to
the benefits associated with the standard set in 2008.
D. Proposed Decision on the Level of the Primary Standard
For the reasons discussed above, and taking into account
information and assessments presented in the 2006 Criteria Document and
2007 Staff Paper, the advice and recommendations of CASAC, and public
comments received during the 2008 rulemaking, the Administrator
proposes to set a new level for the 8-hour primary O3
standard. Specifically, the Administrator proposes to set the level of
the 8-hour primary O3 standard to within a range of 0.060 to
0.070 ppm. The proposed 8-hour primary standard would be met at an
ambient air monitoring site when the 3-year average of the annual
fourth-highest daily maximum 8-hour average O3 concentration
is less than or equal to the level of the standard that is promulgated.
Thus, the Administrator proposes to set a standard with a level within
this range. She solicits comment on this range and on the appropriate
weight to place on the various types of available evidence, the
exposure and risk assessment results, and the uncertainties and
limitations related to this information, as well as on the benefits to
public health associated with a standard set within this range relative
to the benefits associated with the standard set in 2008.
III. Communication of Public Health Information
Information on the public health implications of ambient
concentrations of criteria pollutants is currently made available
primarily through EPA's Air Quality Index (AQI) program. The current
Air Quality Index has been in use since its inception in 1999 (64 FR
42530). It provides accurate, timely, and easily understandable
information about daily levels of pollution (40 CFR 58.50). The AQI
establishes a nationally uniform system of indexing pollution levels
for O3, carbon monoxide, nitrogen dioxide, particulate
matter and sulfur dioxide. The AQI converts pollutant concentrations in
a community's air to a number on a scale from 0 to 500. Reported AQI
values enable the public to know whether air pollution levels in a
particular location are characterized as good (0-50), moderate (51-
100), unhealthy for sensitive groups (101-150), unhealthy (151-200),
very unhealthy (201-300), or hazardous (300-500). The AQI index value
of 100 typically corresponds to the level of the short-term NAAQS for
each pollutant. An AQI value greater than 100 means that a pollutant is
in one of the unhealthy categories (i.e., unhealthy for sensitive
groups, unhealthy, very unhealthy, or hazardous) on a given day;
whereas an AQI value at or below 100 means that a pollutant
concentration is in one of the satisfactory categories (i.e., moderate
or good). Decisions about the pollutant concentrations at which to set
the various AQI breakpoints, that delineate the various AQI categories,
draw directly from the underlying health information that supports the
NAAQS review.
[[Page 2999]]
In the 2008 rulemaking, the AQI for O3 was revised by
setting an AQI value of 100 equal to 0.075 ppm, 8-hour average, the
level of the revised primary O3 standard. The other AQI
breakpoints were also revised as follows: An AQI value of 50 is set at
0.059 ppm; an AQI value of 150 was set at 0.095 ppm; and an AQI value
of 200 was set at 0.115 ppm. All these levels are averaged over 8
hours. These levels were developed by making proportional adjustments
to the other AQI breakpoints (i.e., AQI values of 50, 150 and 200).
The Agency recognizes the importance of revising the AQI in a
timely manner to be consistent with any revisions to the NAAQS.
Therefore, having proposed to set a new level for the 2008 primary 8-
hour O3 standard in this action, EPA also proposes to
finalize conforming changes to the AQI in connection with the Agency's
final decision on the level of the primary O3 standard.
These conforming changes would include setting the 100 level of the AQI
at the same level as that set for the primary O3 standard
resulting from this rulemaking, and also making proportional
adjustments to AQI breakpoints at the lower end of the range (i.e., AQI
values of 50, 150 and 200). EPA does not propose to change breakpoints
at the higher end of the range (from 300 to 500), which would apply to
state contingency plans or the Significant Harm Level (40 CFR 51.16),
because the information from this reconsideration of the 2008 final
rule does not inform decisions about breakpoints at those higher
levels.
With respect to reporting requirements (40 CFR Part 58, Sec.
58.50), EPA proposes to require that the AQI be reported in all
metropolitan and micropolitan statistical areas where O3
monitoring is required, as discussed below in section VI. The Agency
solicits comments on our proposed approach to AQI reporting
requirements. We are also revising 40 CFR Part 58, Sec. 58.50(c) to
require the reporting requirements to be based on the latest available
census figures, rather than the most recent decennial U.S. census. This
change is consistent with our current practice of using the latest
population figures to make monitoring requirements more responsive to
changes in population.
IV. Rationale for Proposed Decision on the Secondary Standard
As an initial matter, the Administrator notes that the 2008 final
rule concluded that (1) the protection afforded by the 1997 secondary
O3 standard was ``not sufficient and that the standard needs
to be revised to provide additional protection from known and
anticipated adverse effects on sensitive natural vegetation and
sensitive ecosystems, and that such a revised standard could also be
expected to provide additional protection to sensitive ornamental
vegetation'' and (2) ``that there is not adequate information to
establish a separate secondary standard based on other effects of
O3 on public welfare'' (73 FR 16497). The Administrator is
not reconsidering these aspects of the 2008 decision, which are based
on the reasons discussed in section IV.B of the 2008 final rule (73 FR
16489-16497). The Administrator also notes that the 2008 final rule
concluded that it was appropriate to retain the O3 indicator
for the secondary O3 standard. The Administrator is not
reconsidering this aspect of the 2008 decision, which was based on the
reasons discussed in sections IV.B and IV.C of the 2008 final rule (73
FR 16489-16497). For these reasons, the Administrator is not reopening
the 2008 decision with regard to the need to revise the 1997 secondary
O3 standard to provide additional protection from known and
anticipated adverse effects on sensitive natural vegetation and
sensitive ecosystems, nor with regard to the appropriate indicator for
the secondary standard. Thus, the information that follows in this
section specifically focuses on a reconsideration of the 8-hour
secondary O3 standard set in the 2008 final rule for the
purpose of determining whether and, if so, how to revise the form,
averaging time, and level of the standard to provide appropriate
protection from known and anticipated adverse effects on sensitive
natural vegetation and sensitive ecosystems.
This section presents the rationale for the Administrator's
proposed decision that the secondary O3 standard, which was
set identical to the revised primary standard in the 2008 final rule,
should instead be a new cumulative, seasonal standard. This standard is
expressed in terms of a concentration-weighted form commonly called
W126, which uses a sigmoidal weighting function to assign a weight to
each hourly O3 concentration within the 12-hour daylight
period (8 am to 8 pm). This daily ozone index is defined as follows:
[GRAPHIC] [TIFF OMITTED] TP19JA10.000
The daily index values are then summed over each month within the
O3 season, and the annual highest consecutive three month
sum is determined. The proposed standard consists of the three-year
average of this highest three-month statistic, set at a level within
the range of 7 to 15 ppm-hours.
As discussed more fully below, the rationale for this proposed new
standard is based on a thorough review, in the 2006 Criteria Document,
of the latest scientific information on vegetation, ecological and
other public welfare effects associated with the presence of
O3 in the ambient air. This rationale also takes into
account and is consistent with: (1) Staff assessments of the most
policy-relevant information in the 2006 Criteria Document and staff
analyses of air quality, vegetation effects evidence, exposure, and
risks, presented in the 2007 Staff Paper, upon which staff
recommendations for revisions to the secondary O3 standard
are based; (2) CASAC advice and recommendations as reflected in
discussions of drafts of the 2006 Criteria Document and 2007 Staff
Paper at public meetings, in separate written comments, and in CASAC's
letters to the Administrator, both before and after the 2008
rulemaking, and (3) public comments received during development of
these documents, either in conjunction with CASAC meetings or
separately; and on the 2007 proposed rule, and (4) consideration of the
degree of protection to vegetation potentially afforded by the 2008 8-
hour standard.
In developing this rationale, the Administrator has again focused
on direct O3 effects on vegetation, specifically drawing
upon an integrative synthesis of the entire body of evidence (EPA,
2006a, chapter 9), published through early 2006, on the broad array of
vegetation effects associated with the presence of O3 in the
ambient air. In addition, because O3 can also indirectly
affect other ecosystem components such as soils, water, and wildlife,
and their associated ecosystem goods and services, through its effects
on vegetation, a qualitative discussion of these other indirect impacts
is also
[[Page 3000]]
included, though these effects were not quantifiable at the time of the
2008 rulemaking. As discussed below in section IV.A, the peer-reviewed
literature includes studies conducted in the U.S., Canada, Europe, and
many other countries around the world.\53\ In reconsidering this
evidence, as was concluded in the 2008 rulemaking, and based on the
body of scientific literature assessed in the 2006 Criteria Document,
the Administrator continues to believe that it is reasonable to
conclude that a secondary standard protecting the public welfare from
known or anticipated adverse effects to trees and native vegetation
would also afford increased protection from adverse effects to other
environmental components relevant to the public welfare, including
ecosystem services and function. Section IV.B focuses on considerations
related to biologically relevant exposure indices. This rationale also
draws upon the results of quantitative exposure and risk assessments,
discussed below in section IV.C. Section IV.D focuses on the
considerations upon which the Administrator's proposed conclusions are
based. Considerations regarding a cumulative seasonal standard as well
as an 8-hour standard are discussed, and the rationale for the 2008
decision on the secondary standard and CASAC advice, given both prior
to the development of the 2007 proposed rule and following the 2008
final rule, are summarized. Finally, the Administrator's proposed
conclusions on the secondary standard are presented. Section IV.E
summarizes the proposed decision on the secondary O3
standard and the solicitation of public comments.
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\53\ In its assessment of the evidence judged to be most
relevant to making decisions on the level of the O3
secondary standard, however, EPA has placed greater weight on U.S.
studies, due to the often species-, site- and climate-specific
nature of O3-related vegetation response.
---------------------------------------------------------------------------
As with virtually any policy-relevant vegetation effects research,
there is uncertainty in the characterization of vegetation effects
attributable to exposure to ambient O3. As discussed below,
however, research conducted since the 1997 review provides important
information coming from field-based exposure studies, including free
air, gradient, and biomonitoring surveys, in addition to the more
traditional open top chamber (OTC) studies. Moreover, the newly
available studies evaluated in the 2006 Criteria Document have
undergone intensive scrutiny through multiple layers of peer review and
many opportunities for public review and comment. While important
uncertainties remain, the review of the vegetation effects information
has been extensive and deliberate. In the judgment of the
Administrator, the intensive evaluation of the scientific evidence that
has occurred provides an adequate basis for this reconsideration of the
2008 rulemaking.
A. Vegetation Effects Information
This section outlines key information contained in the 2006
Criteria Document (chapter 9) and in the 2007 Staff Paper (chapter 7)
on known or anticipated effects on public welfare associated with the
presence of O3 in ambient air. The information highlighted
here summarizes: (1) New information available in the 2008 rulemaking
on potential mechanisms for vegetation effects associated with exposure
to O3; (2) the nature of effects on vegetation that have
been associated with exposure to O3 and consequent potential
impacts on ecosystems; and (3) considerations in characterizing what
constitutes an adverse welfare impact of O3.
Exposures to O3 have been associated quantitatively and
qualitatively with a wide range of vegetation effects. The decision in
the 1997 review to set a more protective secondary standard primarily
reflected consideration of the quantitative information on vegetation
effects available at that time, particularly growth impairment (e.g.,
biomass loss) in sensitive forest tree species during the seedling
growth stage and yield loss in important commercial crops. This
information, derived mainly using the open top chamber (OTC) exposure
method, found cumulative, seasonal O3 exposures were most
strongly associated with observed vegetation response. The 2006
Criteria Document discusses a number of additional studies that support
and strengthen key conclusions regarding O3 effects on
vegetation and ecosystems found in the previous Criteria Document (EPA,
1996a, 2006a), including further clarification of the underlying
mechanistic and physiological processes at the sub-cellular, cellular,
and whole system levels within the plant. More importantly, however, in
the context of this review, new quantitative information is now
available across a broader array of vegetation effects (e.g., growth
impairment during seedlings, saplings and mature tree growth stages,
visible foliar injury, and yield loss in annual crops) and across a
more diverse set of exposure methods, including chamber, free air,
gradient, model, and field-based observation. The non-chambered, field-
based study results begin to address one of the key data gaps cited by
EPA in the 1997 review.
The following discussion of the policy-relevant science regarding
vegetation effects associated with cumulative, seasonal exposures to
ambient levels of O3 integrates information from the 2006
Criteria Document (chapter 9) and the 2007 Staff Paper (chapter 7).
1. Mechanisms
Scientific understanding regarding O3 impacts at the
genetic, physiological, and mechanistic levels helps to explain the
biological plausibility and coherence of the evidence for
O3-induced vegetation effects and informs the interpretation
of predictions of risk associated with vegetation response at ambient
O3 exposure levels. In most cases, the mechanisms of
response are similar regardless of the degree of sensitivity of the
species. The evidence assessed in the 2006 Criteria Document (EPA,
2006a) regarding the O3-induced changes in physiology
continues to support the information discussed in the 1997 review (EPA,
1996a, 2006a). In addition, during the last decade understanding of the
cellular processes within plants has been further clarified and
enhanced. This section reviews the key scientific conclusions
identified in 1996 Criteria Document (EPA, 1996a), and incorporates
recent information from the Criteria Document (EPA, 2006a). This
section describes: (1) Plant uptake of O3, (2)
O3-induced cellular to systemic response, (3) plant
compensation and detoxification mechanisms, (4) O3-induced
changes to plant metabolism, and (5) plant response to chronic
O3 exposures.
a. Plant Uptake of Ozone
To cause injury, O3 must first enter the plant through
openings in the leaves called stomata. Leaves exist in a three
dimensional environment called the plant canopy, where each leaf has a
unique orientation and receives a different exposure to ambient air,
microclimatological conditions, and sunlight. In addition, a plant may
be located within a stand of other plants which further modifies
ambient air exchange with individual leaves. Not all O3
entering a plant canopy is absorbed into the leaf stomata, but may be
adsorbed to other surfaces e.g., leaf cuticles, stems, and soil (termed
non-stomatal deposition) or scavenged by reactions with intra-canopy
biogenic VOCs and naturally occurring NOx emissions from soils. Because
O3 does not typically penetrate the leaf's cuticle, it must
reach the stomatal openings in the leaf for absorption to occur. The
[[Page 3001]]
movement of O3 and other gases such as CO2 into
and out of leaves is controlled by stomatal guard cells that regulate
the size of the stomatal apertures. These guard cells respond to a
variety of internal species-specific factors as well as external site
specific environmental factors such as light, temperature, humidity,
CO2 concentration, soil fertility, water status, and in some
cases, the presence of air pollutants, including O3. These
modifying factors produce stomatal conductances that vary between
leaves of the same plant, individuals and genotypes within a species as
well as diurnally and seasonally.
b. Cellular to Systemic Response
Once inside the leaf, O3 can react with a variety of
biochemical compounds that are exposed to the air spaces within the
leaf or it can be dissolved into the water lining the cell wall of the
air spaces. Once in the aqueous phase, O3 can be rapidly
altered to form oxidative products that can diffuse more readily into
and through the cell and react with many biochemical compounds. Early
steps in a series of O3-induced events that can lead to leaf
injury seems to involve alteration in cell membrane function, including
membrane transport properties (EPA, 2006a) and/or reactions with
organic molecules that in certain circumstances result in the
generation of signaling compounds. The generation of such signaling
compounds can lead to a cascade of events. One such signaling molecule
is hydrogen peroxide (H2O2). The presence of
higher-than-normal levels of H2O2 within the leaf
is a potential trigger for a set of metabolic reactions that include
those typical of the well documented ``wounding'' response or pathogen
defense pathway generated by cutting of the leaf or by pathogen/insect
attack. Ethylene is another compound produced when plants are subjected
to biotic or abiotic stressors. Increased ethylene production by plants
exposed to O3 stress was identified as a consistent marker
for O3 exposure in studies conducted decades ago (Tingey et
al., 1976).
c. Compensation and Detoxification
Ozone injury will not occur if (1) the rate and amount of
O3 uptake is small enough for the plant to detoxify or
metabolize O3 or its metabolites or (2) the plant is able to
repair or compensate for the O3 impacts (Tingey and Taylor,
1982; U.S. EPA, 1996a). With regard to the first, a few studies have
documented direct stomatal closure or restriction in the presence of
O3 in some species, which limits O3 uptake and
potential subsequent injury. This response may be initiated ranging
from within minutes to hours or days of exposure (Moldau et al., 1990;
Dann and Pell, 1989; Weber et al., 1993). However, exclusion of
O3 simultaneously restricts the uptake of CO2,
which also limits photosynthesis and growth. In addition, antioxidants
present in plants can effectively protect tissue against damage from
low levels of oxidants by dissipating excess oxidizing power. Since
1996, the role of detoxification in providing a level of resistance to
O3 has been further investigated. A number of antioxidants
have been found in plants. However, the pattern of changes in the
amounts of these antioxidants varies greatly among different species
and conditions. Most recent reports indicate that ascorbate within the
cell wall provides the first significant opportunity for detoxification
to occur. In spite of the new research, however, it is still not clear
as to what extent detoxification protects against O3 injury.
Specifically, data are needed on potential rates of antioxidant
production, sub-cellular location(s) of antioxidants, and whether
generation of these antioxidants in response to O3-induced
stress potentially diverts resources and energy away from other vital
uses. Thus, the 2006 Criteria Document concludes that scientific
understanding of the detoxification mechanisms is not yet complete and
requires further investigation (EPA, 2006a).
Regarding the second, once O3 injury has occurred in
leaf tissue, some plants are able to repair or compensate for the
impacts. In general, plants have a variety of compensatory mechanisms
for low levels of stress including reallocation of resources, changes
in root/shoot ratio, production of new tissue, and/or biochemical
shifts, such as increased photosynthetic capacity in new foliage and
changes in respiration rates, indicating possible repair or replacement
of damaged membranes or enzymes. Since these mechanisms are genetically
determined, not all plants have the same complement of compensatory
mechanisms or degree of tolerance, and these may vary over the life of
the plant as not all stages of a plant's development are equally
sensitive to O3. At higher levels or over longer periods of
O3 stress, some of these compensatory mechanisms, such as a
reallocation of resources away from storage in the roots in favor of
leaves or shoots, could occur at a cost to the overall health of the
plant. However, it is not yet clear to what degree or how the use of
plant resources for repair or compensatory processes affects the
overall carbohydrate budget or subsequent plant response to
O3 or other stresses (EPA, 1996a, EPA, 2006a).
d. Changes to Plant Metabolism
Ozone inhibits photosynthesis, the process by which plants produce
energy rich compounds (e.g., carbohydrates) in the leaves. This
impairment can result from direct impact to chloroplast function and/or
O3-induced stomatal closure resulting in reduced uptake of
CO2. A large body of literature published since 1996 has
further elucidated the mechanism of effect of O3 within the
chloroplast. Pell et al. (1997) showed that O3 exposure
results in a loss of the central carboxylating enzyme that plays an
important role in the production of carbohydrates. Due to its central
importance, any decrease in this enzyme may have severe consequences
for the plant's productivity. Several recent studies have found that
O3 has a greater effect as leaves age, with the greatest
impact of O3 occurring on the oldest leaves (Fiscus et al.,
1997; Reid and Fiscus, 1998; Noormets et al., 2001; Morgan et al.,
2004). The loss of this key enzyme as a function of increasing
O3 exposure is also linked to an early senescence or a
speeding up of normal development leading to senescence. If total plant
photosynthesis is sufficiently reduced, the plant will respond by
reallocating the remaining carbohydrate at the level of the whole
organism (EPA, 1996a, 2006a). This reallocation of carbohydrate away
from the roots into above ground vegetative components can have serious
implications for perennial species, as discussed below.
e. Plant Response to Chronic Ozone Exposures
Though many changes that occur with O3 exposure can be
observed within hours, or perhaps days, of the exposure, including
those connected with wounding, other effects take longer to occur and
tend to become most obvious after chronic seasonal exposures to low
O3 concentrations. These lower chronic exposures have been
linked to senescence or some other physiological response very closely
linked to senescence. In perennial plant species, a reduction in
carbohydrate storage in one year may result in the limitation of growth
the following year (Andersen et al., 1997). Such ``carry-over'' effects
have been documented in the growth of tree seedlings (Hogsett et al.,
1989; Sasek et al., 1991; Temple et al., 1993; EPA, 1996a) and in roots
(Andersen et al., 1991; EPA, 1996a). Though it is not fully understood
how chronic seasonal O3 exposure affects long-term growth
and resistance to other biotic and abiotic
[[Page 3002]]
insults in long-lived trees, accumulation of these carry-over effects
over time could affect survival and reproduction.
2. Nature of Effects
Ozone injury at the cellular level can accumulate sufficiently to
induce effects at the level of a whole leaf or plant. These larger
scale effects can include: Reduced carbohydrate production and/or
reallocation; reduced growth and/or reproduction; visible foliar injury
and/or premature senescence; and reduced plant vigor. Much of what is
now known about these O3-related effects, as summarized
below, is based on research that was available in the 1997 review.
Studies available in the 2008 rulemaking continue to support and expand
this knowledge (EPA, 2006a).
a. Carbohydrate Production and Allocation
When total plant photosynthesis is sufficiently reduced, the plant
will respond by reallocating the remaining carbohydrate at the level of
the whole organism. Many studies have demonstrated that root growth is
more sensitive to O3 exposure than stem or leaf growth (EPA,
2006a). When fewer carbohydrates are present in the roots, less energy
is available for root-related functions such as acquisition of water
and nutrients. In addition, by inhibiting photosynthesis and the amount
of carbohydrates available for transfer to the roots, O3 can
disrupt the association between soil fungi and host plants. Fungi in
the soil form a symbiotic relationship with many terrestrial plants.
For host plants, these fungi improve the uptake of nutrients, protect
the roots against pathogens, produce plant growth hormones, and may
transport carbohydrates from one plant to another (EPA, 1996a). These
below ground effects have recently been documented in the field (Grulke
et al., 1998; Grulke and Balduman, 1999). Data from a long-studied
pollution gradient in the San Bernardino Mountains of southern
California suggest that O3 substantially reduces root growth
in natural stands of Ponderosa pine (Pinus ponderosa). Root growth in
mature trees was decreased at least 87 percent in a high-pollution site
as compared to a low-pollution site (Grulke et al., 1998), and a
similar pattern was found in a separate study with whole-tree harvest
along this gradient (Grulke and Balduman, 1999). Though effects on
other ecosystem components were not examined, a reduction of root
growth of this magnitude could have significant implications for the
below-ground communities at those sites. Because effects on leaf and
needle carbohydrate content under O3 stress can range from a
reduction (Barnes et al., 1990; Miller et al., 1989), to no effect
(Alscher et al., 1989), to an increase (Luethy-Krause and Landolt,
1990), studies that examine only above-ground vegetative components may
miss important O3-induced changes below ground. These below-
ground changes could signal a shift in nutrient cycling with
significance at the ecosystem level (Young and Sanzone, 2002).
b. Growth Effects on Trees
Studies comparing the O3-related growth response of
different vegetation types (coniferous and deciduous) and growth stages
(e.g., seedling and mature) have established that on average,
individual coniferous trees are less sensitive than deciduous trees,
and deciduous trees are generally less sensitive to O3 than
most annual plants, with the exception of a few fast growing deciduous
tree species (e.g., quaking aspen, black cherry, and cottonwood), which
are highly sensitive and, in some cases, as much or more sensitive to
O3 than sensitive annual plants. In addition, studies have
shown that the relationship between O3 sensitivity in
seedling and mature growth stages of trees can vary widely, with
seedling growth being more sensitive to O3 exposures in some
species, while in others, the mature growth stage is the more
O3 sensitive. In general, mature deciduous trees are likely
to be more sensitive to O3 than deciduous seedlings, and
mature evergreen trees are likely to be less sensitive to O3
than their seedling counterparts. Based on these results, stomatal
conductance, O3 uptake, and O3 effects cannot be
assumed to be equivalent in seedlings and mature trees.
In the 1997 review (EPA, 1996b), analyses of the effects of
O3 on trees were limited to 11 tree species for which
concentration-response (C-R) functions for the seedling growth stage
had been developed from OTC studies conducted by the National Health
and Environmental Effects Research Lab, Western Ecology Division
(NHEERL-WED). A number of replicate studies were conducted on these
species, leading to a total of 49 experimental cases. The 2007 Staff
Paper presented a graph of the composite regression equation that
combines the results of the C-R functions developed for each of the 49
cases. The NHEERL-WED study predicted relative biomass loss at various
exposure levels in terms of a 12-hour W126. For example, 50 percent of
the tree seedling cases would be protected from greater than 10 percent
biomass loss at a 3-month, 12-hour W126 of approximately 24 ppm-hour,
while 75 percent of cases would be protected from 10 percent biomass
loss at a 3-month, 12-hour W126 level of approximately 16 ppm-hour.
Since the 1997 review, only a few studies have developed C-R
functions for additional tree seedling species (EPA, 2006a). One such
study is of particular importance because it documented growth effects
in the field of a similar magnitude as those previously seen in OTC
studies but without the use of chambers or other fumigation methods
(Gregg et al., 2003). This study placed eastern cottonwood (Populus
deltoides) saplings at sites along a continuum of ambient O3
exposures that gradually increased from urban to rural areas in the New
York City area (Gregg et al., 2003). Eastern cottonwood is a fast
growing O3 sensitive tree species that is important
ecologically along streams and commercially for pulpwood, furniture
manufacturing, and as a possible new source for energy biomass (Burns
and Hankola, 1990). Gregg et al. (2003) found that the cottonwood
saplings grown in urban New York City grew faster than saplings grown
in downwind rural areas. Because these saplings were grown in pots with
carefully controlled soil nutrient and moisture levels, the authors
were able to control for most of the differences between sites. After
carefully considering these and other factors, the authors concluded
the primary explanation for the difference in growth was the gradient
of cumulative O3 exposures that increased as one moved
downwind from urban to less urban and more rural sites. It was
determined that the lower O3 exposure within the city center
was due to NOX titration reactions which removed
O3 from the ambient air. The authors were able to reproduce
the growth responses observed in the field in a companion OTC
experiment, confirming O3 as the stressor inducing the
growth loss response (Gregg et al., 2003).
Another recent set of studies employed a modified Free Air
CO2 Enrichment (FACE) methodology to expose vegetation to
elevated O3 without the use of chambers. This exposure
method was originally developed to expose vegetation to elevated levels
of CO2, but was later modified to include O3
exposure in Illinois (SoyFACE) and Wisconsin (AspenFACE) for soybean
and deciduous trees, respectively (Dickson et al., 2000; Morgan et al.,
2004). The FACE method releases gas (e.g., CO2,
O3) from a series of orifices placed along the length of the
vertical pipes surrounding a circular field plot and uses the
[[Page 3003]]
prevailing wind to distribute it. This exposure method has many
characteristics that differ from those associated with the OTC. Most
significantly, this exposure method more closely replicates conditions
in the field than do OTCs. This is because, except for O3
levels which are varied across co-located plots, plants are exposed to
the same ambient growing conditions that occur naturally in the field
(e.g., location-specific pollutant mixtures; climate conditions such as
light, temperature and precipitation; insect pests, pathogens). By
using one of several co-located plots as a control (e.g., receives no
additional O3), and by exposing the other rings to differing
levels of elevated O3, the growth response signal that is
due solely to the change in O3 exposure can be clearly
determined. Furthermore, the FACE system can expand vertically with the
growth of trees, allowing for exposure experiments to span numerous
years, an especially useful capability in forest research.
On the other hand, the FACE methodology also has the undesirable
characteristic of potentially creating hotspots near O3 gas
release orifices or gradients of exposure in the outer ring of trees
within the plots, such that averaging results across the entire ring
potentially overestimates the response. In recognition of this
possibility, researchers at the AspenFACE experimental site only
measured trees in the center core of each ring, (e.g., at least 5-6
meters away from the emission sites of O3) (Dickson et al.,
2000, Karnosky et al., 2005). By taking this precaution, it is unlikely
that their measurements were influenced by any potential hotspots or
gradients of exposure within the FACE rings. Taking all of the above
into account, results from the Wisconsin FACE site on quaking aspen
appear to demonstrate that the detrimental effects of O3
exposure seen on tree growth and symptom expression in OTCs can be
observed in the field using this exposure method (Karnosky et al.,
1999; 2005).
The 2007 Staff Paper thus concluded that the combined evidence from
the AspenFACE and Gregg et al. (2003) field studies provide compelling
and important support for the appropriateness of continued use of the
C-R functions derived using OTC from the NHEERL-WED studies to estimate
risk to these tree seedlings under ambient field exposure conditions.
These studies make a significant contribution to the coherence of the
weight of evidence available in this review and provide additional
evidence that O3-induced effects observed in chambers also
occur in the field.
Trees and other perennials, in addition to cumulating the effects
of O3 exposures over the annual growing season, can also
cumulate effects across multiple years. It has been reported that
effects can ``carry over'' from one year to another (EPA, 2006a).
Growth affected by a reduction in carbohydrate storage in one year may
result in the limitation of growth in the following year (Andersen et
al., 1997). Carry-over effects have been documented in the growth of
some tree seedlings (Hogsett et al., 1989; Simini et al., 1992; Temple
et al., 1993) and in roots (Andersen et al., 1991; EPA, 1996a). On the
basis of past and recent OTC and field study data, ambient
O3 exposures that occur during the growing season in the
United States are sufficient to potentially affect the annual growth of
a number of sensitive seedling tree species. However, because most
studies do not take into account the possibility of carry over effects
on growth in subsequent years, the true implication of these annual
biomass losses may be missed. It is likely that under ambient exposure
conditions, some sensitive trees and perennial plants could experience
compounded impacts that result from multiple year exposures.
c. Visible Foliar Injury
Cellular injury to leaves due to exposure to O3 can and
often does become visible. Acute injury usually appears within 24 hours
after exposure to O3 and, depending on species, can occur
under a range of exposures and durations from 0.040 ppm for a period of
4 hours to 0.410 ppm for 0.5 hours for crops and 0.060 ppm for 4 hours
to 0.510 ppm for 1 hour for trees and shrubs (Jacobson, 1977). Chronic
injury may be mild to severe. In some cases, cell death or premature
leaf senescence may occur. The significance of O3 injury at
the leaf and whole plant levels depends on how much of the total leaf
area of the plant has been affected, as well as the plant's age, size,
developmental stage, and degree of functional redundancy among the
existing leaf area. As a result, it is not presently possible to
determine, with consistency across species and environments, what
degree of injury at the leaf level has significance to the vigor of the
whole plant.
The presence of visible symptoms due to O3 exposures
can, however, by itself, represent an adverse impact to the public
welfare. Specifically, it can reduce the market value of certain leafy
crops (such as spinach, lettuce), impact the aesthetic value of
ornamentals (such as petunia, geranium, and poinsettia) in urban
landscapes, and affect the aesthetic value of scenic vistas in
protected natural areas such as national parks and wilderness areas.
Many businesses rely on healthy looking vegetation for their
livelihoods (e.g., horticulturalists, landscapers, Christmas tree
growers, farmers of leafy crops) and a variety of ornamental species
have been listed as sensitive to O3 (Abt Associates Inc.,
1995). Though not quantified, there is likely some level of economic
impact to businesses and homeowners from O3-related injury
on sensitive ornamental species due to the cost associated with more
frequent replacement and/or increased maintenance (fertilizer or
pesticide application). In addition, because O3 not only
results in discoloration of leaves but can lead to more rapid
senescence (early shedding of leaves) there potentially could be some
lost tourist dollars at sites where fall foliage is less available or
attractive.
The use of sensitive plants as biological indicators to detect
phytotoxic levels of O3 is a longstanding and effective
methodology (Chappelka and Samuelson, 1998; Manning and Krupa, 1992).
Each bioindicator exhibits typical O3 injury symptoms when
exposed under appropriate conditions. These symptoms are considered
diagnostic as they have been verified in exposure-response studies
under experimental conditions. In recent years, field surveys of
visible foliar injury symptoms have become more common, with greater
attention to the standardization of methods and the use of reliable
indicator species (Campbell et al., 2000; Smith et al., 2003).
Specifically, the United States Forest Service (USFS) through the
Forest Health Monitoring Program (FHM) (1990-2001) and currently the
Forest Inventory and Analysis (FIA) Program collects data regarding the
incidence and severity of visible foliar injury on a variety of
O3 sensitive plant species throughout the U.S. (Coulston et
al., 2003, 2004; Smith et al., 2003).
Since the conclusion of the 1997 review, the FIA monitoring program
network and database has continued to expand. This network continues to
document foliar injury symptoms in the field under ambient exposure
conditions. Recent survey results show that O3-induced
foliar injury incidence is widespread across the country. The visible
foliar injury indicator has been identified as a means to track
O3 exposure stress trends in the nation's natural plant
communities as highlighted in EPA's most recent Report on the
Environment (EPA, 2003a; http://www.epa.gov/indicators/roe).
[[Page 3004]]
Previous Criteria Documents have noted the difficulty in relating
visible foliar injury symptoms to other vegetation effects such as
individual tree growth, stand growth, or ecosystem characteristics
(EPA, 1996a) and this difficulty remains to the present day (EPA,
2006a). It is important to note that direct links between O3
induced visible foliar injury symptoms and other adverse effects are
not always found. Therefore, visible foliar injury cannot serve as a
reliable surrogate measure for other O3-related vegetation
effects because other effects (e.g., biomass loss) have been reported
with and without visible injury. In some cases, visible foliar symptoms
have been correlated with decreased vegetative growth (Karnosky et al.,
1996; Peterson et al., 1987; Somers et al., 1998) and with impaired
reproductive function (Black et al., 2000; Chappelka, 2002). Therefore,
the lack of visible injury should not be construed to indicate a lack
of phytotoxic concentrations of O3 nor absence of other non-
visible O3 effects.
d. Reduced Plant Vigor
Though O3 levels over most of the U.S. are not high
enough to kill vegetation directly, current levels have been shown to
reduce the ability of many sensitive species and genotypes within
species to adapt to or withstand other environmental stresses. These
O3 effects may include increased susceptibility to freezing
temperatures, increased vulnerability to pest infestations and/or root
disease, and compromised ability to compete for available resources. As
an example of the latter, when species with differing O3-
sensitivities occur together, O3-sensitive species may
experience a greater reduction in growth than more O3-
tolerant species, which then can better compete for available
resources. The result of such above effects can produce a loss in plant
vigor in O3-sensitive species that over time may lead to
premature plant death.
e. Ecosystems
Ecosystems are comprised of complex assemblages of organisms and
the physical environment with which they interact. Each level of
organization within an ecosystem has functional and structural
characteristics. At the ecosystem level, functional characteristics
include, but are not limited to, energy flow; nutrient, hydrologic, and
biogeochemical cycling; and maintenance of food chains. The sum of the
functions carried out by ecosystem components provides many benefits to
humankind, as in the case of forest ecosystems (Smith, 1992). Some of
these benefits, also termed ``ecosystem goods and services'', include
food, fiber production, aesthetics, genetic diversity, maintenance of
water quality, air quality, and climate, and energy exchange. A
conceptual framework for discussing the effects of stressors, including
air pollutants such as O3, on ecosystems was developed by
the EPA Science Advisory Board (Young and Sanzone, 2002). In this
report, the authors identify six essential ecological attributes (EEAs)
of ecosystems including landscape condition, biotic condition,
chemical/physical condition, ecological processes, hydrology/
geomorphology, and natural disturbance regime. Each EEA is depicted as
one of six triangles that together build a hexagon. On the outside of
each triangle is a list of stressors that can act on the EEA.
Tropospheric O3 is listed as a stressor of both biotic
condition and the chemical/physical condition of ecosystems. As each
EEA is linked to all the others, it is clearly envisioned in this
framework that O3 could either directly or indirectly impact
all of the EEAs associated with an ecosystem that is being stressed by
O3.
Vegetation often plays an influential role in defining the
structure and function of an ecosystem, as evidenced by the use of
dominant vegetation forms to classify many types of natural ecosystems,
e.g., tundra, wetland, deciduous forest, and conifer forest. Plants
simultaneously inhabit both above-and below-ground environments,
integrating and influencing key ecosystem cycles of energy, water, and
nutrients. When a sufficient number of individual plants within a
community have been affected, O3-related effects can be
propagated up to ecosystem-level effects. Thus, through its impact on
vegetation, O3 can be an important ecosystem stressor.
i. Potential Ozone Alteration of Ecosystem Structure and Function
The 2006 Criteria Document outlines seven case studies where
O3 effects on ecosystems have either been documented or are
suspected. The oldest and clearest example involves the San Bernardino
Mountain forest ecosystem in California. This system experienced
chronic high O3 exposures over a period of 50 or more years.
The O3-sensitive and co-dominant species of ponderosa and
Jeffrey pine demonstrated severe levels of foliar injury, premature
senescence, and needle fall that decreased the photosynthetic capacity
of stressed pines and reduced the production of carbohydrates resulting
in a decrease in radial growth and in the height of stressed trees. It
was also observed that ponderosa and Jeffrey pines with slight to
severe crown injury lost basal area in relation to competing species
that are more tolerant to O3. Due to a loss of vigor, these
trees eventually succumbed to the bark beetle, leading to elevated
levels of tree death. Increased mortality of susceptible trees shifted
the community composition towards white fir and incense cedar,
effectively reversing the development of the normal fire climax mixture
dominated by ponderosa and Jeffrey pines, and leading to increased fire
susceptibility. At the same time, numerous other organisms and
processes were also affected either directly or indirectly, including
successional patterns of fungal microflora and their relationship to
the decomposer community. Nutrient availability was influenced by the
heavy litter and thick needle layer under stands with the most severe
needle injury and defoliation. In this example, O3 appeared
to be a predisposing factor that led to increased drought stress,
windthrow, root diseases, and insect infestation (Takemoto et al.,
2001). Thus, through its effects on tree water balance, cold hardiness,
tolerance to wind, and susceptibility to insect and disease pests,
O3 potentially impacted the ecosystem-related EEA of natural
disturbance regime (e.g., fire, erosion). Although the role of
O3 was extremely difficult to separate from other
confounding factors, such as high nitrogen deposition, there is
evidence that this shift in species composition has altered the
structure and dynamics of associated food webs (Pronos et al., 1999)
and carbon (C) and nitrogen (N) cycling (Arbaugh et al., 2003). Ongoing
and new research in this important ecosystem is needed to reveal the
extent to which ecosystem services have been affected and to what
extent strong causal linkages between historic and/or current ambient
O3 exposures and observed ecosystem-level effects can be
made.
Ozone has also been reported to be a selective pressure among
sensitive tree species (e.g., eastern white pine) in the east. The
nature of community dynamics in eastern forests is different, however,
than in the west, consisting of a wider diversity of species and uneven
aged stands, and the O3 levels are less severe. Therefore,
lower level chronic O3 stress in the east is more likely to
produce subtle long-term forest responses such as shifts in species
composition, rather than wide-spread community degradation.
Some of the best-documented studies of population and community
response
[[Page 3005]]
to O3 effects are the long-term studies of common plantain
(Plantago major) in native plant communities in the United Kingdom
(Davison and Reiling, 1995; Lyons et al., 1997; Reiling and Davison,
1992c). Elevated O3 significantly decreased the growth of
sensitive populations of common plantain (Pearson et al., 1996; Reiling
and Davison, 1992a, b; Whitfield et al., 1997) and reduced its fitness
as determined by decreased reproductive success (Pearson et al., 1996;
Reiling and Davison, 1992a). While spatial comparisons of population
responses to O3 are complicated by other environmental
factors, rapid changes in O3 resistance were imposed by
ambient levels and variations in O3 exposure (Davison and
Reiling, 1995). Specifically, in this case study, it appeared that
O3-sensitive individuals are being removed by O3
stress and the genetic variation represented in the population could be
declining. If genetic diversity and variation is lost in ecosystems,
there may be increased vulnerability of the system to other biotic and
abiotic stressors, and ultimately a change in the EEAs and associated
services provided by those ecosystems.
Recent free-air exposure experiments have also provided new insight
into how O3 may be altering ecosystem structure and function
(Karnosky et al., 2005). For example, a field O3 exposure
experiment at the AspenFACE site in Wisconsin (described in section
IV.A.2.b. above) was designed to examine the effects of both elevated
CO2 and O3 on mixed stands of aspen (Populus
tremuloides), birch (Betula papyrifera), and sugar maple (Acer
saccharum) that are characteristic of Great Lakes aspen-dominated
forests (Karnosky et al., 2003; Karnosky et al., 1999). They found
evidence that the effects on above- and below-ground growth and
physiological processes have cascaded through the ecosystem, even
affecting microbial communities (Larson et al., 2002; Phillips et al.,
2002). This study also confirmed earlier observations of O3-
induced changes in trophic interactions involving keystone tree
species, as well as important insect pests and their natural enemies
(Awmack et al., 2004; Holton et al., 2003; Percy et al., 2002).
Collectively these examples suggest that O3 is an
important stressor in natural ecosystems, but it is difficult to
quantify the contribution of O3 due to the combination of
other stresses present in ecosystems. In most cases, because only a few
components in each of these ecosystems have been examined and
characterized for O3 effects, the full extent of ecosystem
changes in these example ecosystems is not fully understood. Clearly,
there is a need for highly integrated ecosystem studies that
specifically investigate the effect of O3 on ecosystem
structure and function in order to fully determine the extent to which
O3 is altering ecosystem services. Continued research,
employing new approaches, will be necessary to fully understand the
extent to which O3 is affecting ecosystem services.
ii. Effects on Ecosystem Services and Carbon Sequestration
Since it has been established that O3 affects
photosynthesis and growth of plants, O3 is most likely
affecting the productivity of forest ecosystems. Therefore, it is
desirable to link effects on growth and productivity to essential
ecosystem services. However, it is very difficult to quantify
ecosystem-level productivity losses because of the amount of complexity
in scaling from the leaf-level or individual plant to the ecosystem
level, and because not all organisms in an ecosystem are equally
affected by O3.
Terrestrial ecosystems are important in the Earth's carbon (C)
balance and could help offset emissions of CO2 by humans if
anthropogenic C is sequestered in vegetation and soils. The annual
increase in atmospheric CO2 is less than the total inputs
from fossil fuel burning and land use changes (Prentice et al., 2001),
and much of this discrepancy is thought to be attributable to
CO2 uptake by plant photosynthesis (Tans & White, 1998).
Temperate forests of the northern hemisphere have been estimated to be
a net sink of about 0.6 to 0.7 petagrams (Pg) C per year (Goodale et
al. 2002). Ozone interferes with photosynthesis, causes some plants to
senesce leaves prematurely, and in some cases, reduces allocation to
stem and root tissue. Thus, O3 decreases the potential for C
sequestration. For the purposes of this discussion, C sequestration is
defined as the net exchange of carbon by the terrestrial biosphere.
However, long-term storage in the soil organic matter is considered to
be the most stable form of C storage in ecosystems.
In a study including all ecosystem types, Felzer et al. (2004),
estimated that U.S. net primary production (net flux of C into an
ecosystem) was decreased by 2.6-6.8 percent due to O3
pollution in the late 1980s to early 1990s. Ozone not only reduces C
sequestration in existing forests, it can also affect reforestation
projects (Beedlow et al. 2004). This effect, in turn, has been found to
ultimately inhibit C sequestration in forest soils which act as long-
term C storage (Loya et al., 2003; Beedlow et al. 2004). The
interaction of rising O3 pollution and rising CO2
concentrations in the coming decades complicates predictions of future
sequestration potential. Models generally predict that, in the future,
C sequestration will increase with increasing CO2, but often
do not account for the decrease in productivity due to the local
effects of current or potentially increasing levels of tropospheric
O3. In the presence of high O3 levels, the
stimulatory effect of rising CO2 concentrations on forest
productivity has been estimated to be reduced by more that 20 percent
(Tingey et al., 2001; Ollinger et al. 2002; Karnosky et al., 2003).
In summary, it would be anticipated that meeting lower
O3 standards would increase the amount of CO2
uptake by many ecosystems in the U.S. However, the amount of this
improvement would be heavily dependent on the species composition of
those ecosystems. Many ecosystems in the U.S. do have O3
sensitive plants. For example, forest ecosystems with dominant species
such as aspen or ponderosa pine would be expected to increase
CO2 uptake more with lower O3 than forests with
more O3 tolerant species.
A recent critique of the secondary NAAQS review process published
in the report by the National Academy of Sciences on Air Quality
Management in the United States (NRC, 2004) stated that ``EPA's current
practice for setting secondary standards for most criteria pollutants
does not appear to be sufficiently protective of sensitive crops and
ecosystems * * *'' This report made several specific recommendations
for improving the secondary NAAQS process and concluded that ``There is
growing evidence that tighter standards to protect sensitive ecosystems
in the United States are needed. * * *'' An effort has been recently
initiated within the Agency to identify indicators of ecological
condition whose responses can be clearly linked to changes in air
quality that are attributable to Agency environmental programs. Using a
single indicator to represent the complex linkages and dynamic cycles
that define ecosystem condition will always have limitations. With
respect to O3-related impacts on ecosystem condition, only
two candidate indicators, foliar injury (as described above) and radial
growth in trees, have been suggested. Thus, while at the present time,
most O3-related effects on ecosystems must be inferred from
observed or predicted O3-related effects on individual
plants, additional research at the ecosystem level could identify new
indicators and/or establish stronger causal linkages
[[Page 3006]]
between O3-induced plant effects and ecosystem condition.
f. Yield Reductions in Crops
Ozone can interfere with carbon gain (photosynthesis) and
allocation of carbon with or without the presence of visible foliar
injury. As a result of decreased carbohydrate availability, fewer
carbohydrates are available for plant growth, reproduction, and/or
yield. Recent studies have further confirmed and demonstrated
O3 effects on different stages of plant reproduction,
including pollen germination, pollen tube growth, fertilization, and
abortion of reproductive structures, as reviewed by Black et al.
(2000). For seed-bearing plants, these reproductive effects will
culminate in reduced seed production or yield.
As described in the 1997 review and again in the 2006 Criteria
Document and 2007 Staff Paper, the National Crop Loss Assessment
Network (NCLAN) studies undertaken in the early to mid-1980s provide
the largest, most uniform database on the effects of O3 on
agricultural crop yields. The NCLAN protocol was designed to produce
crop exposure-response data representative of the areas in the U.S.
where the crops were typically grown. In total, 15 species (e.g., corn,
soybean, winter wheat, tobacco, sorghum, cotton, barley, peanuts, dry
beans, potato, lettuce, turnip, and hay [alfalfa, clover, and fescue]),
accounting for greater than 85 percent of U.S. agricultural acreage
planted at that time, were studied. Of these 15 species, 13 species
including 38 different cultivars were combined in 54 cases representing
unique combinations of cultivars, sites, water regimes, and exposure
conditions. Crops were grown under typical farm conditions and exposed
in open-top chambers to ambient O3, sub-ambient
O3, and above ambient O3. Robust C-R functions
were developed for each of these crop species. These results showed
that 50 percent of the studied cases would be protected from greater
than 10 percent yield loss at a W126 level of 21 ppm-hour, while a W126
of 13 ppm-hour would provide protection for 75 percent of the cases
studied from greater than 10 percent yield loss.
Recent studies continue to find yield loss levels in crop species
studied previously under NCLAN that reflect the earlier findings. In
other words, there has been no evidence that crops are becoming more
tolerant of O3 (EPA, 2006a). For cotton, some newer
varieties have been found to have higher yield loss due to
O3 compared to older varieties (Olszyk et al., 1993, Grantz
and McCool, 1992). In a meta-analysis of 53 studies, Morgan et al.
(2003) found consistent deleterious effects of O3 exposures
on soybean from studies published between 1973 and 2001. Further, early
results from the field-based exposure experiment SoyFACE in Illinois
indicate a lack of any apparent difference in the O3
tolerance of old and recent cultivars of soybean in a study of 22
soybean varieties (Long et al., 2002). Thus, the 2007 Staff Paper
concluded that the recent scientific literature continues to support
the conclusions of the 1996 Criteria Document that ambient
O3 concentrations are reducing the yield of major crops in
the U.S.
In addition to the effects described on annual crop species,
several studies published since the 1997 review have focused on
perennial forage crops (EPA, 2006a). These recent results confirm that
O3 is also impacting yields and quality of multiple-year
forage crops at sufficient magnitude to have nutritional and possibly
economic implications to their use as ruminant animal feed at
O3 exposures that occur in some years over large areas of
the U.S.
3. Adversity of Effects
The 2007 Staff Paper recognized that the statute requires that a
secondary standard be protective against ``adverse'' O3
effects, not all identifiable O3-induced effects. In
considering what constitutes a vegetation effect that is adverse to the
public welfare, the 2007 Staff Paper recognizes that O3 can
cause a variety of vegetation effects, beginning at the level of the
individual cell and accumulating up to the level of whole leaves,
plants, plant populations, communities and whole ecosystems, not all of
which have been classified in past reviews as ``adverse'' to public
welfare.
Previous reviews have classified O3 vegetation effects
as either ``injury'' or ``damage'' to help in determining adversity.
Specifically, ``injury'' is defined as encompassing all plant
reactions, including reversible changes or changes in plant metabolism
(e.g., altered photosynthetic rate), altered plant quality, or reduced
growth, that does not impair the intended use or value of the plant
(Guderian, 1977). In contrast, ``damage'' has been defined to include
those injury effects that reach sufficient magnitude as to also reduce
or impair the intended use or value of the plant. Examples of effects
that are classified as damage include reductions in aesthetic values
(e.g., foliar injury in ornamental species) as well as losses in terms
of weight, number, or size of the plant part that is harvested (reduced
yield or biomass production). Yield loss also may include changes in
crop quality, i.e., physical appearance, chemical composition, or the
ability to withstand storage, while biomass loss includes slower growth
in species harvested for timber or other fiber uses. While this
construct has proved useful in the past, it appears to be most useful
in the context of evaluating effects on single plants or species grown
in monocultures such as agricultural crops or managed forests. It is
less clear how it might apply to potential effects on natural forests
or entire ecosystems when O3-induced species level impacts
lead to shifts in species composition and/or associated ecosystem
services such as nutrient cycling or hydrologic cycles, where the
intended use or value of the system has not been specifically
identified.
A more recent construct for assessing risks to forests described in
Hogsett et al. (1997) suggests that ``adverse effects could be
classified into one or more of the following categories: (1) Economic
production, (2) ecological structure, (3) genetic resources, and (4)
cultural values.'' This approach expands the context for evaluating the
adversity of O3-related effects beyond the species level.
Another recent publication, A Framework for Assessing and Reporting on
Ecological Condition: An SAB report (Young and Sanzone, 2002), provides
additional support for expanding the consideration of adversity beyond
the species level by making explicit the linkages between stress-
related effects (e.g., O3 exposure) at the species level and
at higher levels within an ecosystem hierarchy. Taking this recent
literature into account, the 2007 Staff Paper concludes that a
determination of what constitutes an ``adverse'' welfare effect in the
context of the secondary NAAQS review can appropriately occur within
this broader paradigm.
B. Biologically Relevant Exposure Indices
The 2006 Criteria Document concluded that O3 exposure
indices that cumulate differentially weighted hourly concentrations are
the best candidates for relating exposure to plant growth responses.
This conclusion follows from the extensive evaluation of the relevant
studies in the 1996 Criteria Document (EPA, 1996a) and the recent
evaluation of studies that have been published since that time. The
following selections, taken from the 1996 Criteria Document (EPA,
1996a, section 5.5), further elucidate the depth and strength of these
conclusions. Specifically, with respect to the importance of taking
into account exposure duration, the 1996 Criteria Document stated,
``when O3 effects are the primary cause of variation
[[Page 3007]]
in plant response, plants from replicate studies of varying duration
showed greater reductions in yield or growth when exposed for the
longer duration'' and ``the mean exposure index of unspecified duration
could not account for the year-to-year variation in response'' (EPA,
1996a, pg. 5-96). Further, ``because the mean exposure index treats all
concentrations equally and does not specifically include an exposure
duration component, the use of a mean exposure index for characterizing
plant exposures appears inappropriate for relating exposure with
vegetation effects'' (EPA, 1996a, pg. 5-88). Regarding the relative
importance of higher concentrations than lower in determining plant
response, the 1996 Criteria Document concluded that ``the ultimate
impact of long-term exposures to O3 on crops and seedling
biomass response depends on the integration of repeated peak
concentrations during the growth of the plant'' (EPA, 1996a, pg. 5-
104). Further, ``at this time, exposure indices that weight the hourly
O3 concentrations differentially appear to be the best
candidates for relating exposure with predicted plant response'' (EPA,
1996a, pgs. 5-136).
At the conclusion of the 1997 review, the biological basis for a
cumulative, seasonal form was not in dispute. There was general
agreement between EPA and CASAC, based on their review of the air
quality criteria, that a cumulative, seasonal form was more
biologically based than the then current 1-hour and newly proposed 8-
hour average form. However, in selecting a specific form appropriate
for a secondary standard, there was less agreement. An evaluation of
the performance of several cumulative seasonal forms in predicting
plant response data taken from OTC experiments had found that all
performed about equally well and was unable to distinguish between them
(EPA, 1996a). In selecting between two of these cumulative forms, the
SUM06 \54\ and W126, in the absence of biological evidence to
distinguish between them, EPA based its decision on both science and
policy considerations. Specifically, these were: (1) All cumulative,
peak-weighted exposure indices considered, including W126 and SUM06,
were about equally good as exposure measures to predict exposure-
response relationships reported in the NCLAN crop studies; and (2) the
SUM06 form would not be influenced by PRB O3 concentrations
(defined at the time as 0.03 to 0.05 ppm) under many typical air
quality distributions. On the basis of these considerations, EPA chose
the SUM06 as the most appropriate cumulative, seasonal form to consider
when proposing an alternative secondary standard form (61 FR 65716).
---------------------------------------------------------------------------
\54\ The SUM06 index is defined as the sum of all hourly
O3 concentrations greater or equal to 0.06 ppm over a
specified time.
---------------------------------------------------------------------------
Though the scientific justification for a cumulative, seasonal form
was generally accepted in the 1997 review, an analysis undertaken by
EPA at that time had shown that there was considerable overlap between
areas that would be expected not to meet the range of alternative 8-
hour standards being considered for the primary NAAQS and those
expected not to meet the range of values (expressed in terms of the
seasonal SUM06 index) of concern for vegetation. This result suggested
that improvements in national air quality expected to result from
attaining an 8-hour primary standard within the recommended range of
levels would also be expected to significantly reduce levels of concern
for vegetation in those same areas. Thus, in the 1996 proposed rule,
EPA proposed two alternatives for consideration: one alternative was to
make the secondary standard equal in every way to the proposed 8-hour,
0.08 ppm primary standard; and the second was to establish a
cumulative, seasonal secondary standard in terms of a SUM06 form as
also appropriate to protect public welfare from known or anticipated
adverse effects given the available scientific knowledge and that such
a seasonal standard ``* * * is more biologically relevant * * *'' (61
FR 65716).
In the 1997 final rule, EPA decided to make the secondary standard
identical to the primary standard. The EPA acknowledged, however, that
``it remained uncertain as to the extent to which air quality
improvements designed to reduce 8-hr average O3
concentrations averaged over a 3-year period would reduce O3
exposures measured by a seasonal SUM06 index.'' (62 FR 38876) In other
words, it was uncertain as to whether the 8-hour average form would, in
practice, provide sufficient protection for vegetation from the
cumulative, seasonal and concentration-weighted exposures described in
the scientific literature as of concern.
On the basis of that history, the 2007 Staff Paper (chapter 7)
revisited the issue of whether the SUM06 was still the most appropriate
choice of cumulative, seasonal form for a secondary standard to protect
the public welfare from known and anticipated adverse vegetation
effects in light of the new information available in this review.
Specifically, the 2007 Staff Paper considered: (1) The continued lack
of evidence within the vegetation effects literature of a biological
threshold for vegetation exposures of concern; and (2) new estimates of
PRB that were lower than in the 1997 review. The W126 form, also
evaluated in the 1997 review, was again selected for comparison with
the SUM06 form. Regarding the first consideration, the 2007 Staff Paper
noted that the W126 form, by its incorporation of a continuous
sigmoidal weighting scheme, does not create an artificially imposed
concentration threshold, yet also gives proportionally more weight to
the higher and typically more biologically potent concentrations, as
supported by the scientific evidence. Second, the index value is not
significantly influenced by O3 concentrations within the
range of estimated PRB, as the weights assigned by the sigmoidal
weighting scheme to concentrations in this range are near zero. Thus,
it would also provide a more appropriate target for air quality
management programs designed to reduce emissions from anthropogenic
sources contributing to O3 formation. On the basis of these
considerations, the 2007 Staff Paper concluded that the W126 form was
the most biologically-relevant cumulative, seasonal form appropriate to
consider in the context of the 2008 rulemaking.
C. Vegetation Exposure and Impact Assessment
The vegetation exposure and impact assessment conducted for the
2008 rulemaking and described in the 2007 Staff paper, consisted of
exposure, risk and benefits analyses and improved and built upon
similar analyses performed in the 1997 review (EPA 1996b). The
vegetation exposure assessment was performed using interpolation and
included information from ambient monitoring networks and results from
air quality modeling. The vegetation risk assessment included both tree
and crop analyses. The tree risk analysis includes three distinct lines
of evidence: (1) Observations of visible foliar injury in the field
linked to monitored O3 air quality for the years 2001-2004;
(2) estimates of seedling growth loss under then current and
alternative O3 exposure conditions; and (3) simulated mature
tree growth reductions using the TREGRO model to simulate the effect of
meeting alternative air quality standards on the predicted annual
growth of a single western species (ponderosa pine) and two eastern
species (red maple and tulip poplar). The crop analysis includes
estimates of the risks to crop yields from then current and alternative
[[Page 3008]]
O3 exposure conditions and the associated change in economic
benefits expected to accrue in the agriculture sector upon meeting the
levels of various alternative standards. Each element of the assessment
is described below, including discussions of known sources and ranges
of uncertainties associated with the elements of this assessment.
1. Exposure Characterization
Though numerous effects of O3 on vegetation have been
documented as discussed above, it is important in considering risk to
examine O3 air quality patterns in the U.S. relative to the
location of O3 sensitive species that have a known
concentration-response in order to predict whether adverse effects are
occurring at current levels of air quality, and whether they are likely
to occur under alternative standard forms and levels.
The most important information about exposure to vegetation comes
from the O3 monitoring data that are available from two
national networks: (1) Air Quality System (AQS; http://www.epa.gov/ttn/airs/airsaqs) and (2) Clean Air Status and Trends Network (CASTNET;
http://www.epa.gov/castnet/). The AQS monitoring network currently has
over 1100 active O3 monitors which are generally sited near
population centers. However, this network also includes approximately
36 monitors located in national parks. CASTNET is the nation's primary
source for data on dry acidic deposition and rural, ground-level
O3. It consists of over 80 sites across the eastern and
western U.S. and is cooperatively operated and funded with the National
Park Service. In the 1997 O3 NAAQS final rule, it was
acknowledged that because the national air quality surveillance network
for O3 was designed principally to monitor O3
exposure in populated areas, there was limited measured data available
to characterize O3 air quality in rural and remote sites.
Since the 1997 review, there has been a small increase in the number of
CASTNET sites (from approximately 52 sites in 1992 to 84 sites in
2004), however these monitors are not used for attainment designations.
National parks represent areas of nationally recognized ecological
and public welfare significance, which have been afforded a high level
of protection by Congress. Two recent reports presented some discussion
of O3 trends in a subset of national parks: The Ozone
Report: Measuring Progress Through 2003 (EPA, 2004), and 2005 Annual
Performance and Progress Report: Air Quality in National Parks (NPS,
2005). Unfortunately, much of this information is presented only in
terms of the current 8-hr average form. The 2007 Staff Paper analyzed
available air quality data in terms of the cumulative 12-hour W126 form
from 2001 to 2005 for a subset of national parks and other significant
natural areas representing 4 general regions of the U.S. Many of these
national parks and natural areas have monitored O3 levels
above concentrations that have been shown to decrease plant growth and
above the 12-hour W126 levels analyzed in this review. For example, the
Great Smokey Mountain, Rocky Mountain, Grand Canyon, Yosemite and
Sequoia National Parks all had more than one year within the 2001-2005
period with a 12-hour W126 above 21 ppm-hour. This level of exposure
has been associated with approximately no more than 10 percent biomass
loss in 50 percent of the 49 tree seedling cases studied in the NHEERL-
WED experiments (Lee and Hogsett, 1996). Black cherry (Prunus
serotina), an important O3-sensitive tree species in the
eastern U.S., occurs in the Great Smoky Mountain National Park and is
estimated to have O3-related seedling biomass loss of
approximately 40 percent when exposed to a 3 month, 12-hour W126
O3 level greater than 21 ppm-hour. Ponderosa pine (Pinus
ponderosa) which occurs in the Grand Canyon, Yosemite and Sequoia
National Parks has been reported to have approximately 10 percent
biomass losses at 3 month, 12 hour W126 O3 levels as low as
17 ppm-hour (Lee and Hogsett, 1996). Impacts on seedlings may
potentially affect long-term tree growth and survival, ultimately
affecting the competitiveness of O3-sensitive tree species
and genotypes within forest stands.
In order to characterize exposures to vegetation at the national
scale, however, the 2007 Staff Paper concluded that it could not rely
solely on limited site-specific monitoring data, and that it was
necessary to select an interpolation method that could be used to
characterize O3 air quality over broad geographic areas. The
2007 Staff Paper therefore investigated the appropriateness of using
the O3 outputs from the EPA/NOAA Community Multi-scale Air
Quality (CMAQ) \55\ model system (http://www.epa.gov/asmdnerl/CMAQ,
Byun and Ching, 1999; Arnold et al. 2003, Eder and Yu, 2005) to improve
spatial interpolations based solely on existing monitoring networks.
Due to the significant resources required to run CMAQ, model outputs
were only available for a limited number of years. For the 2008
rulemaking, the most recent outputs available at the time from CMAQ
version 4.5 were for the year 2001.
---------------------------------------------------------------------------
\55\ The CMAQ model is a multi-pollutant, multiscale air quality
model that contains state-of-the-science techniques for simulating
atmospheric and land processes that affect the transport,
transformation, and deposition of atmospheric pollutants and/or
their precursors on both regional and urban scales. It is designed
as a science-based modeling tool for handling many major pollutants
(including photochemical oxidants/O3, particulate matter,
and nutrient deposition) holistically. The CMAQ model can generate
estimates of hourly O3 concentrations for the contiguous
U.S., making it possible to express model outputs in terms of a
variety of exposure indices (e.g., W126, 8-hour average).
---------------------------------------------------------------------------
Based on the significant difference in monitor network density
between the eastern and western U.S., the 2007 Staff Paper concluded
that it was appropriate to use separate interpolation techniques in
these two regions. Only AQS and CASTNET monitoring data were used for
the eastern interpolation, since it was determined that enhancing the
interpolation with CMAQ data did not add much information to the
eastern U.S. interpolation. In the western U.S., however, where rural
monitoring is more sparse, O3 values generated by the CMAQ
model were used to develop scaling factors to augment the
interpolation.
In order to characterize uncertainties associated with the
interpolation method, monitored O3 concentrations were
systematically compared to interpolated O3 concentrations in
areas where monitors were located. In general, the interpolation method
used in the current review performed well in many areas in the U.S.,
although it under-predicted higher 12-hour W126 exposures in rural
areas. Due to the important influence of higher exposures in
determining risks to plants, this feature of the interpolated surface
could result in an under-estimation of risks to vegetation in some
areas. Taking these uncertainties into account, and given the absence
of more complete rural monitoring data, this approach was used in
developing national vegetation exposure and risk assessments that
estimate relative changes in risk for the various alternative standards
analyzed.
To evaluate changing vegetation exposures and risks under selected
air quality scenarios, the 2007 Staff Paper utilized 2001 base year
O3 air quality distributions that had been adjusted with a
rollback method (Horst and Duff, 1995; Rizzo, 2005, 2006) to reflect
meeting the then current and alternative secondary standard options.
This technique combines both linear and quadratic elements to reduce
higher O3
[[Page 3009]]
concentrations more than lower ones. In this regard, the rollback
method attempts to account for reductions in emissions without greatly
affecting lower concentrations. The following O3 air quality
scenarios were analyzed: (1) 4th-highest daily maximum 8-hour average:
0.084 ppm (the effective level of the then current standard) and 0.070
ppm levels; (2) 3-month, 12-hour. SUM06: 25 ppm-hour (proposed in the
1997 review) and 15 ppm-hour levels; and (3) 3-month, 12-hour W126: 21
ppm-hour and 13 ppm-hour levels.
The two 8-hour average levels were chosen as possible alternatives
of the then current form for comparison with the cumulative, seasonal
alternative forms. The SUM06 scenarios were very similar to the W126
scenarios. Since the W126 was judged to be the more biologically-
relevant cumulative, seasonal form, only the results for the W126
scenarios are summarized below. For the W126 form, the two levels were
selected on the basis of the associated levels of tree seedling biomass
loss and crop yield loss protection identified in the NHEERL-WED and
NCLAN studies, respectively. Specifically, the upper level of W126 (21
ppm-hour) was associated with a level of tree and crop protection of
approximately no more than 10 percent growth or yield loss in 50
percent of cases studied. Alternatively, the lower level of W126 (13
ppm-hour) was associated with a level of tree seedling and crop
protection of approximately no more than 10 percent growth or yield
loss in 75 percent of studied cases.
The following discussion highlights key observations drawn from
comparing predicted changes in interpolated air quality under each
alternative standard form and level scenario for the base year, 2001:
(1) Under the base year (2001) ``as is'' air quality, a large
portion of California had 12-hr W126 O3 levels above 31 ppm-
hour, which has been associated with approximately no more than 14
percent biomass loss in 50 percent of tree seedling cases studies.
Broader multi-state regions in the east (NC, TN, KY, IN, OH, PA, NJ,
NY, DE, MD, VA) and west (CA, NV, AZ, OK, TX) are predicted to have
levels of air quality above the W126 level of 21 ppm-hour, which is
approximately equal to the secondary standard proposed in 1996 and is
associated with approximately no more than 10 percent biomass loss in
50 percent of tree seedling cases studied. Much of the east and Arizona
and California have 12-hour W126 O3 levels above 13 ppm-
hour, which has been associated with approximately no more than 10
percent biomass loss in 75 percent of tree seedling cases studied. The
results of the exposure assessment indicate that current air quality
levels could result in significant impacts to vegetation in some areas.
(2) When 2001 air quality was rolled back to meet the then current
8-hour, 0.084 ppm secondary standard, the overall 3-month 12-hour W126
O3 levels were somewhat improved, but not substantially.
Under this scenario, there were still many areas in California with 12-
hour W126 O3 levels above 31 ppm-hour. A broad multi-state
region in the east (NC, TN, KY, IN, OH, PA, MD) and west (CA, NV, AZ,
OK, TX) were still predicted to have O3 levels above the
W126 level of 21 ppm-hour.
(3) Exposures generated for just meeting a 0.070 ppm, 4th-highest
maximum 8-hour average alternative standard showed substantially
improved O3 air quality when compared to just meeting the
then current 8-hour standard. Most areas were predicted to have
O3 levels below the W126 level of 21 ppm-hour, although some
areas in the east (KY, TN, MI, AR, MO, IL) and west (CA, NV, AZ, UT,
NM, CO, OK, TX) were still predicted to have O3 levels above
the W126 level of 13 ppm-hour.
These results suggest that meeting a 0.070 ppm, 8-hour secondary
standard would provide substantially improved protection in some areas
for vegetation from seasonal O3 exposures of concern. The
2007 Staff Paper recognizes, however, that some areas meeting a 0.070
ppm 8-hour standard could continue to have elevated seasonal exposures,
including forested park lands and other natural areas, and Class I
areas which are federally mandated to preserve certain air quality
related values. This is especially important in the high elevation
forests in the Western U.S. where there are few O3 monitors.
This is because the air quality patterns in remote areas can result in
relatively low 8-hour averages while still experiencing relatively high
cumulative exposures.
To further characterize O3 air quality in terms of
various secondary standard forms, an analysis was performed in the 2007
Staff Paper to evaluate the extent to which county-level O3
air quality measured in terms of various levels of the current 8-hour
average form overlapped with that measured in terms of various levels
of the 12-hour W126 cumulative, seasonal form. The 2007 Staff Paper
presented this analysis using 2002-2004 \56\ county-level O3
air quality data from AQS sites and the subset of CASTNET sites having
the highest O3 levels for the counties in which they are
located. Since the current 8-hour average secondary form is a 3-year
average, the analysis initially compared the 3-year averages of both
the 8-hour and W126 forms. In addition, recognizing that some
vegetation effects (e.g. crop yield loss and foliar injury) are driven
solely by annual O3 exposures and are typically evaluated
with respect to exposures within the annual growing season, the 2007
Staff Paper also presented a comparison of the current 3-year average
8-hour form to the annual W126 form for the individual years, 2002 and
2004.
---------------------------------------------------------------------------
\56\ This analysis was updated using 2003-2005 air quality as it
became available, finding similar results.
---------------------------------------------------------------------------
Results of the 3-year average comparisons showed that of the
counties with air quality meeting the 3-year average form of a 0.084
ppm, 8-hour average standard, 7 counties showed 3-year average W126
values above the 21 ppm-hour level. At the lower W126 level of 13 ppm-
hour, 135 counties with air quality meeting the 3-year average form of
a 0.084 ppm, 8-hour average standard, would be above this W126 level.
In addition, when the 3-year average of an 8-hour form was compared to
annual W126 values, further variability in the degree of overlap
between the 8-hour form and W126 form became apparent. For example, the
relatively high 2002 O3 air quality year showed a greater
degree of overlap between those areas that would meet the levels
analyzed for the current 8-hour and alternative levels of the W126 form
than did the relatively low O3 2004 air quality year. This
lack of a consistent degree of overlap between the two forms in
different air quality years demonstrates that annual vegetation would
be expected to receive widely differing degrees of protection from
cumulative seasonal exposures in some areas from year to year, even
when the 3-year average of the 8-hour form was consistently met.
It is clear that this analysis is limited by the lack of monitoring
in rural areas where important vegetation and ecosystems are located,
especially at higher elevation sites. This is because O3 air
quality distributions at high elevation sites often do not reflect the
typical urban and near-urban pattern of low morning and evening
O3 concentrations with a high mid-day peak, but instead
maintain relatively flat patterns with many concentrations in the mid-
range (e.g., 0.05-0.09 ppm) for extended periods. These conditions can
lead to relatively low daily maximum 8-hour averages concurrently with
high cumulative values so that there is potentially less overlap
between an 8-
[[Page 3010]]
hour average and a cumulative, seasonal form at these sites. The 2007
Staff Paper concluded that it is reasonable to anticipate that
additional unmonitored rural high elevation areas important for
vegetation may not be adequately protected even with a lower level of
the 8-hour form.
The 2006 Criteria Document discusses policy relevant background
(PRB) levels for high elevation sites and makes the following
observations: (1) PRB concentrations of 0.04 to 0.05 ppm occur
occasionally at high-elevation sites (e.g., > 1.5 km) in the spring due
to the free-tropospheric influence, including some limited contribution
from hemispheric pollution (O3 produced from anthropogenic
emissions outside North America); and (2) while stratospheric
intrusions might occasionally elevate O3 at high-altitude
sites, these events are rare at surface sites. Therefore, the 2007
Staff Paper concluded that springtime PRB levels in the range
identified above and rare stratospheric intrusions of O3 are
unlikely to be a major influence on 3-month cumulative seasonal W126
values.
It further remains uncertain as to the extent to which air quality
improvements designed to reduce 8-hour O3 average
concentrations would reduce O3 exposures measured by a
seasonal, cumulative W126 index. The 2007 Staff Paper indicated this to
be an important consideration because: (1) The biological database
stresses the importance of cumulative, seasonal exposures in
determining plant response; (2) plants have not been specifically
tested for the importance of daily maximum 8-hour O3
concentrations in relation to plant response; and (3) the effects of
attainment of a 8-hour standard in upwind urban areas on rural air
quality distributions cannot be characterized with confidence due to
the lack of monitoring data in rural and remote areas. These factors
are important considerations in determining whether the current 8-hour
form can appropriately provide requisite protection for vegetation.
2. Assessment of Risks to Vegetation
The 2007 Staff Paper presents results from quantitative and
qualitative risk assessments of O3 risks to vegetation (EPA,
2007). In the 1997 review, crop yield and seedling biomass loss OTC
data provided the basis for staff analyses, conclusions, and
recommendations (EPA, 1996b). Since then, several additional lines of
evidence have progressed sufficiently to provide staff with a more
complete and coherent picture of the scope of O3-related
vegetation risks, especially those faced by seedling, sapling and
mature tree species growing in field settings, and indirectly, forested
ecosystems. Specifically, research published after the 1997 review
reflects an increased emphasis on field-based exposure methods (e.g.,
free air exposure and ambient gradient), improved field survey
biomonitoring techniques, and mechanistic tree process models. Findings
from each of these research areas are discussed separately below. In
conducting these assessments, the Staff Paper analyses relied on both
measured and modeled air quality information. For some effects, like
visible foliar injury and modeled mature tree growth response, only
monitored air quality information was used. For other effects
categories (e.g., crop yield and tree seedling growth), staff relied on
interpolated O3 exposures.
a. Visible Foliar Injury
As discussed above (section IV.A.2.c), systematic injury surveys
have documented visible foliar injury symptoms diagnostic of phytotoxic
O3 exposures on sensitive bioindicator plants. These surveys
have produced more expansive evidence than that available at the time
of the 1997 review that visible foliar injury is occurring in many
areas of the U.S. under current ambient conditions. The 2007 Staff
Paper presents an assessment combining recent U.S. Forest Service
Forest Inventory and Analysis (FIA) biomonitoring site data with the
county level air quality data for those counties containing the FIA
biomonitoring sites. This assessment showed that incidence of visible
foliar injury ranged from 21 to 39 percent during the four-year period
(2001-2004) across all counties with air quality levels at or below
that of a 0.084 ppm, 8-hour standard. Of the counties that met an 8-
hour level of 0.070 ppm in those years, 11 to 30 percent still had
incidence of visible foliar injury. The magnitude of these percentages
suggests that phytotoxic exposures sufficient to induce visible foliar
injury would still occur in many areas after meeting the level of a
0.084 ppm secondary standard or alternative 0.070 ppm 8-hour standard.
Additionally, the data showed that visible foliar injury occurrence was
geographically widespread and occurring on a variety of plant species
in forested and other natural systems. Linking visible foliar injury to
other plant effects is still problematic. However, its presence
indicates that other O3-related vegetation effects could
also be present.
b. Seedling and Mature Tree Biomass Loss
In the 1997 review, analyses of the effects of O3 on
trees were limited to 11 tree species for which C-R functions for the
seedling growth stage had been developed from OTC studies conducted by
the NHEERL-WED. Important tree species such as quaking aspen, ponderosa
pine, black cherry, and tulip poplar were found to be sensitive to
cumulative seasonal O3 exposures. Work done since the 1997
review at the AspenFACE site in Wisconsin on quaking aspen (Karnosky et
al., 2005) and a gradient study performed in the New York City area
(Gregg et al. 2003) has confirmed the detrimental effects of
O3 exposure on tree growth in field studies without chambers
and beyond the seedling stage (King et al. 2005). These field studies
are discussed above in section IV.A.
To update the seedling biomass loss risk analysis, C-R functions
for biomass loss for available seedling tree species taken from the
2006 Criteria Document and information on tree growing regions derived
from the U.S. Department of Agriculture's Atlas of United States Trees
were combined with projections of O3 air quality based on
2001 interpolated exposures, to produce estimated biomass loss for each
of the seedling tree species individually. Maps of these biomass loss
projections are presented in the 2007 Staff Paper. For example, quaking
aspen had a wide range of O3 exposures across its growing
range and therefore, showed significant variability in percentages of
projected seedling biomass loss across its range. Quaking aspen
seedling biomass loss was projected to be greater than 4 percent over
much of its geographic range, though it can reach above 10 percent in
areas of Ohio, Pennsylvania, New York, New Jersey and California.
Biomass loss for black cherry was projected to be greater than 20
percent in approximately half its range. Greater than 30 percent
biomass loss for black cherry was projected in North Carolina,
Tennessee, Indiana, Ohio, Pennsylvania, Arizona, Michigan, New York,
New Jersey, Maryland and Delaware. For ponderosa pine, an important
tree species in the western U.S., biomass loss was projected to be
above 10 percent in much of its range in California. Biomass loss still
occurred in many tree species when O3 air quality was
adjusted to meet the then current 8-hour standard of 0.084 ppm. For
instance, black cherry, ponderosa pine, eastern white pine, and aspen
had estimated median seedling biomass losses over portions of their
growing
[[Page 3011]]
range as high as 24, 11, 6, and 6 percent, respectively, when
O3 air quality was rolled back to just meet a 0.084 ppm, 8-
hour standard. The 2007 Staff Paper noted that these results are for
tree seedlings and that mature trees of the same species may have more
or less of a response to O3 exposure. Due to the potential
for compounding effects over multiple years, experts at a consensus
workshop on O3 vegetation effects and secondary standards,
hereinafter referred to as the 1996 Consensus Workshop, reported in a
subsequent 1997 Workshop Report, that a biomass loss greater than 2
percent annually can be significant (Heck and Cowling, 1997). Decreased
seedling root growth and survivability could affect overall stand
health and composition in the long term.
In addition to the estimation of O3 effects on seedling
growth, recent work available in the 2008 rulemaking has enhanced our
understanding of risks beyond the seedling stage. In order to better
characterize the potential O3 effects on mature tree growth,
a tree growth model (TREGRO) was used as a tool to evaluate the effect
of changing O3 air quality under just meet scenarios for
selected alternative O3 standards on the growth of mature
trees. TREGRO is a process-based, individual tree growth simulation
model (Weinstein et al, 1991). This model has been used to evaluate the
effects of a variety of O3 exposure scenarios on several
species of trees by incorporating concurrent climate data in different
regions of the U.S. to account for O3 and climate/
meteorology interactions (Tingey et al., 2001; Weinstein et al., 1991;
Retzlaff et al., 2000; Laurence et al., 1993; Laurence et al., 2001;
Weinstein et al., 2005). The model provides an analytical framework
that accounts for the nonlinear relationship between O3
exposure and response. The interactions between O3 exposure,
precipitation and temperature are integrated as they affect vegetation,
thus providing an internal consistency for comparing effects in trees
under different exposure scenarios and climatic conditions. An earlier
assessment of the effectiveness of national ambient air quality
standards in place since the early 1970s took advantage of 40 years of
air quality and climate data for the Crestline site in the San
Bernardino Mountains of California to simulate ponderosa pine growth
over time with the improving air quality using TREGRO (Tingey et al.,
2004).
The TREGRO model was used to assess growth of Ponderosa pine in the
San Bernardino Mountains of California (Crestline) and the growth of
yellow poplar and red maple in the Appalachian mountains of Virginia
and North Carolina, Shenandoah National Park (Big Meadows) and Linville
Gorge Wilderness Area (Cranberry), respectively. Total tree growth
associated with ``as is'' air quality, and air quality adjusted to just
meet alternative O3 standards was assessed. Ponderosa pine
is one of the most widely distributed pines in western North America, a
major source of timber, important as wildlife habitat, and valued for
aesthetics (Burns and Honkala, 1990). Red maple is one of the most
abundant species in the eastern U.S. and is important for its brilliant
fall foliage and highly desirable wildlife browse food (Burns and
Honkala, 1990). Yellow poplar is an abundant species in the southern
Appalachian forest. It is 10 percent of the cove hardwood stands in
southern Appalachians which are widely viewed as some of the country's
most treasured forests because the protected, rich, moist set of
conditions permit trees to grow the largest in the eastern U.S. The
wood has high commercial value because of its versatility and as a
substitute for increasingly scarce softwoods in furniture and framing
construction. Yellow poplar is also valued as a honey tree, a source of
wildlife food, and a shade tree for large areas (Burns and Honkala,
1990).
The 2007 Staff Paper analyses found that just meeting a 0.084 ppm
standard would likely continue to allow O3-related
reductions in annual net biomass gain in these species. This is based
on model outputs that estimate that as O3 levels are reduced
below those of a 0.084 ppm standard, significant improvements in growth
would occur. For instance, estimated growth in red maple increased by 4
and 3 percent at Big Meadows and Cranberry sites, respectively, when
air quality was rolled back to just met a W126 value of 13 ppm-hour.
Yellow poplar was projected to have a growth increase between 0.6 and 8
percent under the same scenario at the two eastern sites.
Though there is uncertainty associated with the above analyses,
this information should be given careful consideration in light of
several other pieces of evidence. Specifically, new evidence from
experimental studies that go beyond the seedling growth stage continues
to show decreased growth under elevated O3 (King et al.
2005). Some mature trees such as red oak have shown an even greater
sensitivity of photosynthesis to O3 than seedlings of the
same species (Hanson et al., 1994). As indicated above, smaller growth
loss increments may be significant for perennial species. The potential
for cumulative ``carry over'' effects as well as compounding also must
be considered. The accumulation of such ``carry-over'' effects over
time may affect long-term survival and reproduction of individuals and
ultimately the abundance of sensitive tree species in forest stands.
c. Crops
As discussed in the 2007 Staff Paper, risk of O3
exposure and associated monetized benefits were estimated for commodity
crops, fruits and vegetables. Similar to the tree seedling analysis,
this analysis combined C-R information on crops, crop growing regions
and interpolated exposures during each crop growing season. NCLAN crop
functions were used for commodity crops. According to USDA National
Agricultural Statistical Survey (NASS) data, the 9 commodity crop
species (e.g., cotton, field corn, grain sorghum, peanut, soybean,
winter wheat, lettuce, kidney bean, potato) included in the 2007 Staff
Paper analysis accounted for 69 percent of 2004 principal crop acreage
planted in the U.S. in 2004.\57\ The C-R functions for six fruit and
vegetable species (tomatoes-processing, grapes, onions, rice,
cantaloupes, Valencia oranges) were identified from the California
fruit and vegetable analysis from the 1997 review (Abt Associates Inc,
1995). The 2007 Staff Paper noted that fruit and vegetable studies were
not part of the NCLAN program and C-R functions were available only in
terms of seasonal 7-hour or 12-hour mean index. This index form is
considered less effective in predicting plant response for a given
change in air quality than the cumulative form used with other crops.
Therefore, the fruit and vegetable C-R functions were considered more
uncertain than those for commodity crops.
---------------------------------------------------------------------------
\57\ Principal crops as defined by the USDA include corn,
sorghum, oats, barley, winter wheat, rye, Durum wheat, other spring
wheat, rice, soybeans, peanuts, sunflower, cotton, dry edible beans,
potatoes, sugar beets, canola, proso millet, hay, tobacco, and
sugarcane. Acreage data for the principal crops were taken from the
USDA NASS 2005 Acreage Report (http://usda.mannlib.cornell.edu/reports/nassr/field/pcp-bba/acrg0605.pdf).
---------------------------------------------------------------------------
Analyses in the 2007 Staff Paper showed that some of the most
important commodity crops such as soybean, winter wheat and cotton had
some projected losses under the 2001 base year air quality. Soybean
yield losses were projected to be 2-4 percent in parts of Pennsylvania,
New Jersey, Maryland and Texas. Winter wheat was projected to have
yield losses of 2-6 percent in parts of California.
[[Page 3012]]
Additionally, cotton was projected to have yield losses of above 6
percent in parts of California, Texas and North Carolina in 2001. The
risk assessment estimated that just meeting the then current 0.084 ppm,
8-hour standard would still allow O3=related yield loss to
occur in some commodity crop species and fruit and vegetable species
currently grown in the U.S. For example, based on median C-R function
response, in counties with the highest O3 levels, potatoes
and cotton had estimated yield losses of 9-15 percent and 5-10 percent,
respectively, when O3 air quality just met the level of a
0.084 ppm, 8-hour standard. Estimated yield improved in these counties
when the alternative W126 standard levels were met. The very important
soybean crop had generally small yield losses throughout the country
under just meeting the then current standard (0-4 percent).
The 2007 Staff Paper also presented estimates of monetized benefits
for crops associated with a 0.084 ppm, 8-hour and alternative
standards. The Agriculture Simulation Model (AGSIM) (Taylor, 1994;
Taylor, 1993) was used to calculate annual average changes in total
undiscounted economic surplus for commodity crops and fruits and
vegetables when the then current and alternative standard levels were
met. Meeting the various alternative standards did show some
significant benefits beyond a 0.084 ppm, 8-hour standard. However, the
2007 Staff Paper recognized that the AGSIM economic benefits estimates
also incorporate several sources of uncertainty, including: (1)
Estimates of economic benefits derived from use of the more uncertain
C-R relationships for fruits and vegetables; (2) uncertain assumptions
about the treatment and effect of government farm payment programs; and
(3) uncertain assumptions about near-term changes in the agriculture
sector due to the increased use of crops as biofuels. Although the
AGSIM model results provided a relative comparison of agricultural
benefits between alternative standards, these uncertainties limited the
utility of the absolute numbers.
D. Reconsideration of Secondary Standard
As discussed above at the beginning of section IV, this
reconsideration of the secondary O3 standard set in the 2008
rulemaking focuses on reconsidering certain elements of the standard,
the form, averaging times, and level. The general approach for setting
a secondary O3 standard used in the 2008 rulemaking, and in
the previous 1997 rulemaking, was to consider two basic policy options:
Setting a distinct secondary standard with a biologically relevant form
and averaging times, or setting a secondary standard identical to the
primary standard. In the 2007 proposed rule, both such options were
evaluated, commented on by CASAC and the public, and proposed, as
discussed below in sections IV.D.1 and IV.D.2, respectively. In the
2008 final rule, EPA decided to set the secondary standard identical to
the revised 8-hour primary standard, as discussed below in section
IV.D.3. Section IV.D.4 summarizes comments received from CASAC
following the 2008 decision. The Administrator's proposed conclusions
based on this reconsideration are presented in section IV.D.5.
1. Considerations Regarding the 2007 Proposed Cumulative Seasonal
Standard
a. Form
The 2006 Criteria Document and 2007 Staff Paper concluded that the
recent vegetation effects literature evaluated in the 2008 rulemaking
strengthened and reaffirmed conclusions made in the 1997 review that
the use of a cumulative exposure index that differentially weights
ambient concentrations is best able to relate ambient exposures to
vegetation response at this time (EPA, 2006a, b; see also discussion in
IV.B above). The 1997 review focused in particular on two of these
cumulative forms, the SUM06 and W126. In the 2008 rulemaking, the 2007
Staff Paper again evaluated these two forms in light of two key pieces
of then recent information: Estimates of PRB that were lower than in
the 1997 review, and continued lack of evidence within the vegetation
effects literature of a biological threshold for vegetation exposures
of concern. On the basis of those policy and science-related
considerations, the 2007 Staff Paper concluded that the W126 form was
more appropriate in the context of the 2008 rulemaking. Specifically,
the W126 form, by its incorporation of a sigmoidal weighting scheme,
does not create an artificially imposed concentration threshold, gives
proportionally more weight to the higher and typically more
biologically potent concentrations, and is not significantly influenced
by O3 concentrations within the range of estimated PRB. The
Staff Paper further concluded that ``it is not appropriate to continue
to use an 8-hour averaging time for the secondary standard'' and that
``the 8-hour average form should be replaced with a cumulative,
seasonal, concentration weighted form'' (EPA, 2007b; pg. 8-25).
The CASAC, based on its assessment of the same vegetation effects
science, agreed with the 2006 Criteria Document and 2007 Staff Paper
and unanimously concluded that it is not appropriate to try to protect
vegetation from the known or anticipated adverse effects of ambient
O3 by continuing to promulgate identical primary and
secondary standards for O3. Moreover, the members of the
CASAC and a substantial majority of the CASAC O3 Panel
agreed with 2007 Staff Paper conclusions and encouraged EPA to
establish an alternative cumulative secondary standard for
O3 and related photochemical oxidants that is distinctly
different in averaging time, form and level from the current or
potentially revised 8-hour primary standard. The CASAC also stated that
``the recommended metric for the secondary ozone standard is the
(sigmoidally-weighted) W126 index'' (Henderson, 2007).
The EPA agreed with the conclusions drawn in the 2006 Criteria
Document, 2007 Staff Paper and by CASAC that the scientific evidence
available in the 2008 rulemaking continued to demonstrate the
cumulative nature of O3-induced plant effects and the need
to give greater weight to higher concentrations. Thus, EPA concluded
that a cumulative exposure index that differentially weights
O3 concentrations represents a reasonable policy choice for
a seasonal secondary standard to protect against the effects of
O3 on vegetation. The EPA further agreed with both the 2007
Staff Paper and CASAC that the most appropriate cumulative,
concentration-weighted form to consider in the 2008 rulemaking was the
sigmoidally weighted W126 form, due to EPA's recognition that there is
no evidence in the literature for an exposure threshold that would be
appropriate across all O3-sensitive vegetation and that this
form is unlikely to be significantly influenced by O3 air
quality within the range of PRB levels identified in this rulemaking.
Thus, in 2007 EPA proposed as one option to replace the then current
0.084 ppm, 8-hour average secondary standard with a standard defined in
terms of the cumulative, seasonal W126 form. The EPA also proposed the
option of making the secondary identical to the proposed revised
primary standard.
b. Averaging Times \58\
---------------------------------------------------------------------------
\58\ While the term ``averaging time'' is used, for the
cumulative, seasonal standard the seasonal and diurnal time periods
at issue are those over which exposures during a specified period of
time are cumulated, not averaged.
---------------------------------------------------------------------------
The 2007 Staff Paper, in addition to form, also considered what
exposure
[[Page 3013]]
periods or durations are most relevant for vegetation, which, unlike
people, is exposed to ambient air continuously throughout its lifespan.
For annual species, this lifespan encompasses a period of only one year
or less; while for perennials, lifespans can range from a few years to
decades or centuries. However, because O3 levels are not
continuously elevated and plants are not equally sensitive to
O3 over the course of a day, season or lifetime, it becomes
necessary to identify periods of exposure that have the most relevance
for plant response. The 2007 Staff Paper discussed exposure periods
relevant for vegetation in terms of a seasonal window and a diurnal
window, and it also discussed defining the standard in terms of an
annual index value versus a 3-year average of annual index values. The
numbered paragraphs below present the 2007 Staff Paper discussions on
these exposure periods, and the annual versus 3-year average index
value, followed by a discussion of CASAC views and EPA proposed
conclusions.
(1) In considering an appropriate seasonal window, the 2007 Staff
Paper recognized that, in general, many annual crops are grown for
periods of a few months before being harvested. In contrast, other
annual and perennial species may be photosynthetically active longer,
and for some species and locations, throughout the entire year. In
general, the period of maximum physiological activity and thus, maximum
potential O3 uptake for annual crops, herbaceous species,
and deciduous trees and shrubs coincides with some or all of the intra-
annual period defined as the O3 season, which varies on a
state-by-state basis. This is because the high temperature and high
light conditions that promote the formation of tropospheric
O3 also promote physiological activity in vegetation.
The 2007 Staff Paper noted that the selection of any single
seasonal exposure period for a national standard would represent a
compromise, given the significant variability in growth patterns and
lengths of growing seasons among the wide range of vegetation species
occurring within the U.S. that may experience adverse effects
associated with O3 exposures. However, the 2007 Staff Paper
further concluded that the consecutive 3-month period within the
O3 season with the highest W126 index value (e.g., maximum
3-month period) would, in most cases, likely coincide with the period
of greatest plant sensitivity on an annual basis. Therefore, the 2007
Staff Paper again concluded, as it did in the 1997 review, that the
annual maximum consecutive 3-month period is a reasonable seasonal time
period, when combined with a cumulative, concentration weighted form,
for protection of sensitive vegetation.
(2) In considering an appropriate diurnal window, the Staff Paper
recognized that over the course of the 24-hour diurnal period, plant
stomatal conductance varies in response to changes in light level, soil
moisture and other environmentally and genetically controlled factors.
In general, stomata are most open during daylight hours in order to
allow sufficient CO2 uptake for use in carbohydrate
production through the light-driven process of photosynthesis. At most
locations, O3 concentrations are also highest during the
daytime, and thus, most likely to coincide with maximum stomatal
uptake. It is also known however, that in some species, stomata may
remain open sufficiently at night to allow for some nocturnal uptake to
occur. In addition, at some rural, high elevation sites, the
O3 concentrations remain relatively flat over the course of
the day, often at levels above estimated PRB. At these sites, nighttime
W126 values can be of similar magnitude as daytime values, though the
significance of these exposures is much less certain. This is because
O3 uptake during daylight hours is known to impair the
light-driven process of photosynthesis, which can then lead to impacts
on carbohydrate production, plant growth, reproduction (yield) and root
function. It is less clear at this time to what extent and by what
mechanisms O3 uptake at night adversely impacts plant
function. In addition, many species have not been shown to take up
O3 at night and/or do not occur in areas with elevated
nighttime O3 concentrations.
In reviewing the information on this topic that became available
after the 1997 review, the 2007 Staff Paper considered the information
compiled in a summary report by Musselman and Minnick (2000). This work
reported that some species take up O3 at night, but that the
degree of nocturnal stomatal conductance varies widely between species
and its relevance to overall O3-induced vegetation effects
remain unclear. In considering this information, the 2007 Staff Paper
concluded that for the vast majority of studied species, daytime
exposures represent the majority of diurnal plant O3 uptake
and are responsible for inducing the plant response of most
significance to the health and productivity of the plant (e.g., reduced
carbohydrate production). Until additional information is available
about the extent to which co-occurrence of sensitive species and
elevated nocturnal O3 exposures exists, and what levels of
nighttime uptake are adverse to affected species, the 2007 Staff Paper
concluded that this information continues to be preliminary, and does
not provide a basis for reaching a different conclusion regarding the
diurnal window at this time. The 2007 Staff Paper further noted that
additional research is needed to address the degree to which a 12-hour
diurnal window may be under-protective in areas where elevated
nighttime levels of O3 co-occur with sensitive species with
a high degree of nocturnal stomatal conductance. Thus, as in the 1997
review, the 2007 Staff Paper again concluded that based on the
available science, the daytime 12-hour window (8 a.m. to 8 p.m.) is the
most appropriate period over which to cumulate diurnal O3
exposures, specifically those most relevant to plant growth and yield
responses.
(3) In considering whether the standard should be defined in terms
of an annual index value or a 3-year average of annual index values,
the 2007 Staff Paper recognized that though most cumulative seasonal
exposure levels of concern for vegetation have been expressed in terms
of the annual timeframe, it may be appropriate to consider a 3-year
average for purposes of standard stability. However, the 2007 Staff
Paper noted that for certain welfare effects of concern (e.g., foliar
injury, yield loss for annual crops, growth effects on other annual
vegetation and potentially tree seedlings), an annual time frame may be
a more appropriate period in which to assess what level would provide
the requisite degree of protection, while for other welfare effects
(e.g., mature tree biomass loss), a 3-year average may also be
appropriate. Thus, the 2007 Staff Paper concluded that it is
appropriate to consider both an annual and a 3-year average. Further,
the 2007 Staff Paper concluded that should a 3-year average of the 12-
hour W126 form be selected, a lower standard level should be considered
to reduce the potential of adverse impacts to annual species from a
single high O3 year that could still occur while attaining a
standard on average over 3 years.
The CASAC, in considering what seasonal, diurnal, and annual or
multiyear time periods are most appropriate when combined with a
cumulative, seasonal form to protect vegetation from exposures of
concern, agreed that the 2007 Staff Paper
[[Page 3014]]
conclusion regarding the 3-month seasonal period and 12-hour daylight
window was appropriate, with the distinction that both of these time
periods likely represents the minimum time periods of importance. In
particular, one O3 Panel member commented that for some
species, additional O3 exposures of importance were
occurring outside the 3-month seasonal and 12-hour diurnal windows.
Further, the CASAC concluded that multi-year averaging to promote a
``stable'' secondary standard is less appropriate for a cumulative,
seasonal secondary standard than for a primary standard based on daily
maximum 8-hour concentrations. The CASAC further concluded that if
multi-year averaging is employed to afford greater stability of the
secondary standard, the level of the standard should be revised
downward to assure that the desired degree of protection is not
exceeded in individual years.
The EPA, in determining which seasonal and diurnal time periods are
most appropriate to propose, took into account the 2007 Staff Paper and
CASAC views. In being careful to consider what is needed to provide the
requisite degree of protection, no more and no less, in 2007 EPA
proposed that the 3-month seasonal period and 12-hour daylight period
are appropriate. Based on the 2007 Staff Paper conclusions discussed
above, EPA was mindful that there is the potential for under-protection
with a 12-hour diurnal window in areas with sufficiently elevated
nighttime levels of O3 where sensitive species with a high
degree of nocturnal stomatal conductance occur. On the other hand, EPA
also recognized that a longer diurnal window (e.g., 24-hour) has the
possibility of over-protecting vegetation in areas where nighttime
O3 levels remain relatively high but where no species having
significant nocturnal uptake exist. In weighing these considerations,
EPA agreed with the 2007 Staff Paper conclusion that until additional
information is available about the extent to which this co-occurrence
of sensitive species and elevated nocturnal O3 exposures
exists, and what levels of nighttime uptake are adverse to affected
species, this information does not provide a basis for reaching a
different conclusion at this time. The EPA also considered to what
extent the 3-month period within the O3 season was
appropriate, recognizing that many species of vegetation have longer
growing seasons. The EPA further proposed that the maximum 3-month
period is sufficient and appropriate to characterize O3
exposure levels associated with known levels of plant response.
Therefore, EPA proposed that the most appropriate exposure periods for
a cumulative, seasonal form is the daytime 12-hour window (8 a.m. to 8
p.m.) during the consecutive 3-month period within the O3
monitoring season with the maximum W126 index value.
The EPA also proposed an annual rather than a multi-year
cumulative, seasonal standard. In proposing this option, EPA also
believed that it was appropriate to consider the benefits to the public
welfare that would accrue from establishing a 3-year average secondary
standard, and solicited comment on this alternative. In so doing, EPA
also agreed with 2007 Staff Paper and CASAC conclusions that should a
3-year standard be finalized, the level of the standard should be set
so as to provide the requisite degree of protection for those
vegetation effects judged to be adverse to the public welfare within a
single annual period.
c. Level
The 2007 Staff Paper, in identifying a range of levels for a 3-
month, 12-hour W126 annual form appropriate to protect the public
welfare from adverse impacts to vegetation from O3
exposures, considered what information from the array of vegetation
effects evidence and exposure and risk assessment results was most
useful. Regarding the vegetation effects evidence, the 2007 Staff Paper
found stronger support than what was available at the time of the 1997
review for an increased level of protection for trees and ecosystems.
Specifically, this expanded body of support includes: (1) Additional
field based data from free air, gradient and biomonitoring surveys
demonstrating adverse levels of O3-induced above and/or
below-ground growth reductions on trees at the seedling, sapling and
mature growth stages and incidence of visible foliar injury occurring
at biomonitoring sites in the field at ambient levels of exposure; (2)
qualitative support from free air (e.g., AspenFACE) and gradient
studies on a limited number of tree species for the continued
appropriateness of using OTC-derived C-R functions to predict tree
seedling response in the field; (3) studies that continue to document
below-ground effects on root growth and ``carry-over'' effects
occurring in subsequent years from O3 exposures; and (4)
increased recognition and understanding of the structure and function
of ecosystems and the complex linkages through which O3, and
other stressors, acting at the organism and species level can influence
higher levels within the ecosystem hierarchy and disrupt essential
ecological attributes critical to the maintenance of ecosystem goods
and services important to the public welfare.
Based on the above observations and on the vegetation effects and
the results of the exposure and impact assessment summarized above, the
2007 Staff Paper concluded that just meeting the then current standard
would still allow adverse levels of tree seedling biomass loss in
sensitive commercially and ecologically important tree species in many
regions of the country. Seedling risk assessment results showed that
some tree seedling species are extremely sensitive (e.g., cottonwood,
black cherry and aspen), with annual biomass losses occurring in the
field of the same or greater magnitude that that of annual crops. Such
information from the tree seedling risk assessment suggests that
O3 levels would need to be substantially reduced to protect
sensitive tree seedlings like black cherry from growth and foliar
injury effects.
In addition to the currently quantifiable risks to trees from
ambient exposures, the 2007 Staff Paper also considered the more subtle
impacts of O3 acting in synergy with other natural and man-
made stressors to adversely affect individual plants, populations and
whole systems. By disrupting the photosynthetic process, decreasing
carbon storage in the roots, increasing early senescence of leaves and
affecting water use efficiency in trees, O3 exposures could
potentially disrupt or change the nutrient and water flow of an entire
system. Weakened trees can become more susceptible to other
environmental stresses such as pest and pathogen outbreaks or harsh
weather conditions. Though it is not possible to quantify all the
ecological and societal benefits associated with varying levels of
alternative secondary standards, the 2007 Staff Paper concluded that
this information should be weighed in considering the extent to which a
secondary standard should be set so as to provide potential protection
against effects that are anticipated to occur.
In addition, the 2007 Staff Paper also recognized that in the 1997
review, EPA took into account the results of a 1996 Consensus Workshop.
At this workshop, a group of independent scientists expressed their
judgments on what standard form(s) and level(s) would provide
vegetation with adequate protection from O3-related adverse
effects. Consensus was reached with respect to selecting appropriate
ranges of levels in terms of a cumulative, seasonal 3-month, 12-hr
SUM06
[[Page 3015]]
standard for a number of vegetation effects endpoints. These ranges are
identified below, with the estimated approximate equivalent W126
standard values shown in parentheses. For growth effects to tree
seedlings in natural forest stands, a consensus was reached that a
SUM06 range of 10 to 15 (W126 range of 7 to 13) ppm-hour would be
protective. For growth effects to tree seedlings and saplings in
plantations, the consensus SUM06 range was 12 to 16 (W126 range of 9 to
14) ppm-hour. For visible foliar injury to natural ecosystems, the
consensus SUM06 range was 8 to 12 (W126 range of 5 to 9) ppm-hour.
Taking these consensus statements into account, EPA stated in the
1997 final rule (62 FR 38856) that ``the report lends important support
to the view that the current secondary standard is not adequately
protective of vegetation * * * [and] * * * foreshadows the direction of
future scientific research in this area, the results of which could be
important in future reviews of the O3 secondary standard''
(62 FR 38856).
Given the importance EPA put on the consensus report in the 1997
review, the 2007 Staff Paper considered to what extent research
published after 1997 provided empirical support for the ranges of
levels identified by the experts as protective of different types of
O3-induced effects. With regard to O3-induced
biomass loss in sensitive tree seedlings/saplings growing in natural
forest stands, the information discussed in the 2007 Staff Paper,
including the evidence from free air and gradient studies, provides
additional direct support for the conclusion that the 1996 Consensus
Workshop approximate W126 range of 7-13 ppm-hour was an appropriate
range to consider in selecting a protective level. With regard to
visible foliar injury, the available evidence, including the 2007 Staff
Paper analysis of incidence in counties with FIA monitoring sites and
air quality data, showed significant levels of county-level visible
foliar injury incidence at the W126 level of 13 ppm-hour. However,
because this analysis did not address risks of this effect at lower
levels of O3 air quality, and because there is a significant
uncertainty in predicting the degree of visible foliar injury symptoms
expected for lower levels of O3 air quality, the evidence
provides less certain but qualitative directional support for the 1996
Consensus Workshop range of 5 to 9 ppm-hour to protect against this
effect. With regard to O3-induced effects on plantation
trees, there is far less direct information available. Though some
forest plantation trees are O3-sensitive, the monoculture
nature of these stands makes uncertain the degree to which competition
for resources might play a role and to what degree the variety of
management practices applied would be expected to mitigate the
O3-induced effects. Thus, it is difficult to distinguish a
protective range of levels for plantation trees from a range of levels
that would be protective of O3-sensitive tree seedlings and
saplings in natural forest stands. Therefore, on the basis of the
strength of the evidence available, the 2007 Staff Paper concluded that
it was appropriate to consider a range for a 3-month, 12-hour, W126
standard that included the 1996 consensus recommendations for growth
effects in tree seedlings in natural forest stands (i.e., 7-13 ppm-hour
in terms of a W126 form).
In considering the available information on O3-related
effects on crops in the 2008 rulemaking, the 2007 Staff Paper observed
the following regarding the strength of the underlying crop science:
(1) Nothing in the recent literature points to a change in the
relationship between O3 exposure and crop response across
the range of species and/or cultivars of commodity crops currently
grown in the U.S. that could be construed to make less appropriate the
use of commodity crop C-R functions developed in the NCLAN program; (2)
new field-based studies (e.g., SoyFACE) provide qualitative support in
a few limited cases for the appropriateness of using OTC-derived C-R
functions to predict crop response in the field; and (3) refinements in
the exposure, risk and benefits assessments in this review reduce some
of the uncertainties present in the 1997 review. On the basis of these
observations, the 2007 Staff Paper concluded that nothing in the newly
assessed information called into question the strength of the
underlying science upon which EPA based its proposed decision in the
1997 review to select a level of a cumulative, seasonal form associated
with protecting 50 percent of crop cases from no more than 10 percent
yield loss as providing the requisite degree of protection for
commodity crops.
The 2007 Staff Paper then considered whether any additional
information is available to inform judgments as to the adversity of
various O3-induced levels of crop yield loss to the public
welfare. As noted above, the 2007 Staff Paper observed that
agricultural systems are heavily managed, and that in addition to
stress from O3, the annual productivity of agricultural
systems is vulnerable to disruption from many other stressors (e.g.,
weather, insects, disease), whose impact in any given year can greatly
outweigh the direct reduction in annual productivity resulting from
elevated O3 exposures. On the other hand, O3 can
also more subtly impact crop and forage nutritive quality and
indirectly exacerbate the severity of the impact from other stressors.
Though these latter effects currently cannot be quantified, they should
be considered in judging to what extent a level of protection selected
to protect commodity crops should be precautionary.
Based on the above considerations, the 2007 Staff Paper concluded
that the level of protection (no more than 10% yield or biomass loss in
50% of studied cases) judged requisite in the 1997 review to protect
the public welfare from adverse levels of O3-induced
reductions in crop yields and tree seedling biomass loss, as provided
by a W126 level of 21 ppm-hour, remains appropriate for consideration
as an upper bound of a range of appropriate levels.
Thus, the 2007 Staff Paper concluded, based on all the above
considerations, that an appropriate range of 3-month, 12-hour W126
levels was 7 to 21 ppm-hour, recognizing that the level selected is
largely a policy judgment as to the requisite level of protection
needed. In determining the requisite level of protection for crops and
trees, and indirectly, ecosystems, the 2007 Staff Paper recognized that
it is appropriate to weigh the importance of the predicted risks of
these effects in the overall context of public welfare protection,
along with a determination as to the appropriate weight to place on the
associated uncertainties and limitations of this information.
The CASAC, in its final letter to the Administrator (Henderson,
2007), agreed with the 2007 Staff Paper recommendations that the lower
bound of the range within which a seasonal W126 welfare-based
(secondary) O3 standard should be considered is
approximately 7 ppm-hour; however, it did not agree with staff's
recommendation that the upper bound of the range for consideration
should be as high as 21 ppm-hour. Rather, CASAC recommended that the
upper bound of the range considered should be no higher than 15 ppm-
hour, which is just above the upper ends of the ranges identified in
the 1996 Consensus Workshop as being protective of tree seedlings and
saplings grown in natural forest stands and in plantations. The lower
end of this range (7 ppm-hour) is the same as the lower end of the
range identified in the 1996 Consensus Workshop as protective of tree
seedlings
[[Page 3016]]
in natural forest stands from growth effects.
In the 2007 proposed rule, taking 2007 Staff Paper and CASAC views
into account, EPA proposed a range of levels for a cumulative, seasonal
secondary standard as expressed in terms of the maximum 3 month, 12-
hour W126 form, in the range of 7 to 21 ppm-hour. This range
encompasses the range of levels recommended by CASAC, and also includes
a higher level as recommended for consideration in the 2007 Staff
Paper. Given the uncertainty in determining the risk attributable to
various levels of exposure to O3, EPA believed, as a public
welfare policy judgment, that this was a reasonable range to propose.
2. Considerations Regarding the 2007 Proposed 8-Hour Standard
In the 1997 review, the 1996 Staff Paper included an analysis to
compare the degree of overlap between areas that would be expected not
to meet the range of alternative 8-hour standards being considered for
the primary NAAQS and those expected not to meet the range of values
(expressed in terms of the seasonal SUM06 index) of concern for
vegetation. This result suggested that improvements in national air
quality expected to result from attaining an 8-hour primary standard
within the recommended range of levels would also be expected to reduce
levels of concern for vegetation in those same areas. In the 1997 final
rule, the decision was made, on the basis of both science and policy
considerations, to make the secondary identical to the primary
standard. It acknowledged, however, that uncertainties remained ``as to
the extent to which air quality improvements designed to reduce 8-hour
average O3 concentrations averaged over a 3-year period
would reduce O3 exposures measured by a seasonal SUM06
index'' (62 FR 38876).
On the basis of that history, the 2007 Staff Paper analyzed the
degree of overlap expected between alternative 8-hour and cumulative
seasonal secondary standards (as discussed above in section IV.C.1)
using then recent air quality. Based on the results, the 2007 Staff
Paper concluded that the degree to which the then current 8-hour
standard form and level would overlap with areas of concern for
vegetation expressed in terms of the 12-hour W126 standard is
inconsistent from year to year and would depend greatly on the level of
the 12-hour W126 and 8-hour standards selected and the distribution of
hourly O3 concentrations within the annual and/or 3-year
average period.
Thus, though the 2007 Staff Paper recognized again that meeting the
current or alternative levels of the 8-hour average standard could
result in air quality improvements that would potentially benefit
vegetation in some areas, it urged caution be used in evaluating the
likely vegetation impacts associated with a given level of air quality
expressed in terms of the 8-hour average form in the absence of
parallel W126 information. This caution was due to the concern that the
analysis in the 2007 Staff Paper may not be an accurate reflection of
the true situation in non-monitored, rural counties due to the lack of
more complete monitor coverage in many rural areas. Further, of the
counties that did not show overlap between the two standard forms, most
were located in rural/remote high elevation areas which have
O3 air quality patterns that are typically different from
those associated with urban and near urban sites at lower elevations.
Because the majority of such areas are currently not monitored, it is
believed there are likely to be additional areas that have similar air
quality distributions that would lead to the same disconnect between
forms. Thus, the 2007 Staff Paper concluded that it remained
problematic to determine the appropriate level of protection for
vegetation using an 8-hour average form.
The CASAC recognized that an important difference between the
effects of acute exposures to O3 on human health and the
effects of O3 exposures on welfare is that vegetation
effects are more dependent on the cumulative exposure to, and uptake
of, O3 over the course of the entire growing season
(Henderson, 2006c). The CASAC O3 Panel members were
unanimous in concluding the protection of natural terrestrial
ecosystems and managed agricultural crops requires a secondary
O3 standard that is substantially different from the primary
O3 standard in averaging time, level, and form (Henderson,
2007).
In considering the appropriateness of proposing a revised secondary
standard that would be identical to the proposed primary standard, EPA
took into account the approach used by the Agency in the 1997 review,
the conclusions of the 2007 Staff Paper, CASAC advice, and the views of
public commenters. The EPA first considered the 2007 Staff Paper
analysis of the projected degree of overlap between counties with air
quality expected to meet various alternative levels of an 8-hour
standard and alternative levels of a W126 standard based on monitored
air quality data. This analysis showed significant overlap within the
proposed range of the primary 8-hour form and selected levels of the
W126 standard form being considered, with the degree of overlap between
these two forms depending greatly on the levels selected and the
distribution of hourly O3 concentrations within the annual
and/or 3-year average period. On this basis, EPA concluded that a
secondary standard set identical to the proposed primary standard would
provide a significant degree of additional protection for vegetation as
compared to that provided by the current secondary standard. The EPA
also recognized that lack of rural monitoring data made uncertain the
degree to which the proposed 8-hour or W126 alternatives would be
protective, and that there would be the potential for not providing the
appropriate degree of protection for vegetation in areas with air
quality distributions that result in a high cumulative, seasonal
exposure but do not result in high 8-hour average exposures. While this
potential for under-protection using an 8-hour standard was clear, the
number and size of areas at issue and the degree of risk was hard to
determine. On the other hand, EPA also considered at that time that
there was a potential risk of over-protection with a cumulative,
seasonal standard given the inherent uncertainties associated with
moving to a new form for the secondary standard, in particular those
associated with predicting exposure and risk patterns based on a
limited rural monitoring network.
The EPA also considered the views and recommendations of CASAC, and
agreed that a cumulative, seasonal standard is the most biologically
relevant way to relate exposure to plant growth response. However, as
reflected in the public comments, EPA also recognized that there
remained significant uncertainties in determining or quantifying the
degree of risk attributable to varying levels of O3
exposure, the degree of protection that any specific cumulative,
seasonal standard would produce, and the associated potential for error
in determining the standard that will provide a requisite degree of
protection--i.e., sufficient but not more than what is necessary. Given
this uncertainty, EPA also believed it was appropriate to consider the
degree of protection that would be afforded by a secondary standard
that was identical to the then proposed primary standard. Based on its
consideration of the full range of views as described above, and in the
2007 proposed rule, EPA proposed as a second option to revise
[[Page 3017]]
the secondary standard to be identical in every way to the then
proposed primary standard.
3. Basis for 2008 Decision on the Secondary Standard
In the 2008 final rule, EPA noted that deciding on the appropriate
secondary standard involved making a choice between two possible
alternatives, each with their strengths and weaknesses. The 2008 final
rule reported that within the Administration at that time there had
been a robust discussion of the same strengths and weaknesses
associated with each option that were identified earlier. The process
by which EPA reached its final conclusion is described in the final
rule (73 FR 16497). The rationale for the 2008 decision presented in
the final rule (73 FR 16499-16500) is described below.
In considering the appropriateness of establishing a new standard
defined in terms of a cumulative, seasonal form, or revising the then
current secondary standard by making it identical to the revised
primary standard, EPA took into account the approach used by the Agency
in the 1997 review, the conclusions of the 2007 Staff Paper, CASAC
advice, and the views of public commenters. In giving consideration to
the approach taken in the 1997 review, EPA first considered the 2007
Staff Paper analysis of the projected degree of overlap between
counties with air quality expected to meet the revised 8-hour primary
standard, set at a level of 0.075 ppm, and alternative levels of a W126
standard based on currently monitored air quality data. This analysis
showed significant overlap between the revised 8-hour primary standard
and selected levels of the W126 standard form being considered, with
the degree of overlap between these alternative standards depending
greatly on the W126 level selected and the distribution of hourly
O3 concentrations within the annual and/or 3-year average
period.\59\ On this basis, as an initial matter, EPA concluded that a
secondary standard set identical to the proposed primary standard would
provide a significant degree of additional protection for vegetation as
compared to that provided by the then current 0.084 ppm secondary
standard. In further considering the significant uncertainties that
remain in the available body of evidence of O3-related
vegetation effects and in the exposure and risk analyses conducted for
the 2008 rulemaking, and the difficulty in determining at what point
various types of vegetation effects become adverse for sensitive
vegetation and ecosystems, EPA focused its consideration on a level for
an alternative W126 standard at the upper end of the proposed range
(i.e., 21 ppm-hour). The 2007 Staff Paper analysis showed that at that
W126 standard level, there would be essentially no counties with air
quality that would be expected both to exceed such an alternative W126
standard and to meet the revised 8-hour primary standard--that is,
based on this analysis of currently monitored counties, a W126 standard
would be unlikely to provide additional protection in any monitored
areas beyond that likely to be provided by the revised primary
standard.
---------------------------------------------------------------------------
\59\ Prior to publication of the 2008 final rule, EPA did
further analysis of the degree of overlap to extend the 2007 Staff
Paper analyses, and that analysis was available in the docket.
---------------------------------------------------------------------------
The EPA also recognized that the general lack of rural monitoring
data made uncertain the degree to which the revised 8-hour standard or
an alternative W126 standard would be protective in those areas, and
that there would be the potential for not providing the appropriate
degree of protection for vegetation in areas with air quality
distributions that result in a high cumulative, seasonal exposure but
do not result in high 8-hour average exposures. While this potential
for under-protection using an 8-hour standard was clear, the number and
size of areas at issue and the degree of risk was hard to determine.
However, EPA concluded at that time that an 8-hour standard would also
tend to avoid the potential for providing more protection than is
necessary, a risk that EPA concluded would arise from moving to a new
form for the secondary standard despite significant uncertainty in
determining the degree of risk for any exposure level and the
appropriate level of protection, as well as uncertainty in predicting
exposure and risk patterns.
The EPA also considered the views and recommendations of CASAC, and
agreed that a cumulative, seasonal standard was the most biologically
relevant way to relate exposure to plant growth response. However, as
reflected in some public comments, EPA also judged that there remained
significant uncertainties in determining or quantifying the degree of
risk attributable to varying levels of O3 exposure, the
degree of protection that any specific cumulative, seasonal standard
would produce, and the associated potential for error in determining
the standard that will provide a requisite degree of protection--i.e.,
sufficient but not more than what is necessary. Given these significant
uncertainties, EPA concluded at that time that establishing a new
secondary standard with a cumulative, seasonal form would result in
uncertain benefits beyond those afforded by the revised primary
standard and therefore may be more than necessary to provide the
requisite degree of protection.
Based on its consideration of the views discussed above, EPA judged
in the 2008 rulemaking that the appropriate balance to be drawn was to
revise the secondary standard to be identical in every way to the
revised primary standard. The EPA believed that such a standard would
be sufficient to protect public welfare from known or anticipated
adverse effects, and did not believe that an alternative cumulative,
seasonal standard was needed to provide this degree of protection. The
EPA believed that this judgment appropriately considered the
requirement for a standard that is neither more nor less stringent than
necessary for this purpose.
For the reasons discussed above, and taking into account
information and assessments presented in the 2006 Criteria Document and
2007 Staff Paper, the advice and recommendations of the CASAC Panel,
and the public comments to date, EPA decided to revise the existing 8-
hour secondary standard. Specifically, EPA revised the then current 8-
hour average 0.084 ppm secondary standard by making it identical to the
revised 8-hour primary standard set at a level of 0.075 ppm.
4. CASAC Views Following 2008 Decision
Following the 2008 decision on the O3 standards, serious
questions were raised as to whether the standards met the requirements
of the CAA. In April 2008, the members of the CASAC Ozone Review Panel
sent a letter to EPA stating ``In our most-recent letters to you on
this subject--dated October 2006 and March 2007--* * * the Committee
recommended an alternative secondary standard of cumulative form that
is substantially different from the primary Ozone NAAQS in averaging
time, level and form--specifically, the W126 index within the range of
7 to 15 ppm-hour, accumulated over at least the 12 ``daylight'' hours
and the three maximum ozone months of the summer growing season''
(Henderson, 2008). The letter continued: ``The CASAC now wishes to
convey, by means of this letter, its additional, unsolicited advice
with regard to the primary and secondary Ozone NAAQS. In doing so, the
participating members of the CASAC Ozone Review Panel are unanimous in
strongly urging you or your successor as EPA Administrator to
[[Page 3018]]
ensure that these recommendations be considered during the next review
cycle for the Ozone NAAQS that will begin next year'' (id.). The letter
further stated the following views:
The CASAC was * * * greatly disappointed that you failed to
change the form of the secondary standard to make it different from
the primary standard. As stated in the preamble to the Final Rule,
even in the previous 1996 ozone review, ``there was general
agreement between the EPA staff, CASAC, and the Administrator, * * *
that a cumulative, seasonal form was more biologically relevant than
the previous 1-hour and new 8-hour average forms (61 FR 65716)'' for
the secondary standard. Therefore, in both the previous review and
in this review, the Agency staff and its advisors agreed that a
change in the form of the secondary standard was scientifically
well-justified.
* * * * *
Unfortunately, this scientifically-sound approach of using a
cumulative exposure index for welfare effects was not adopted, and
the default position of using the primary standard for the secondary
standard was once again instituted. Keeping the same form for the
secondary Ozone NAAQS as for the primary standard is not supported
by current scientific knowledge indicating that different indicator
variables are needed to protect vegetation compared to public
health. The CASAC was further disappointed that a secondary standard
of the W126 form was not considered from within the Committee's
previously-recommended range of 7 to 15 ppm-hour. The CASAC
sincerely hopes that, in the next round of Ozone NAAQS review, the
Agency will be able to support and establish a reasonable and
scientifically-defensible cumulative form for the secondary
standard. (Henderson, 2008)
5. Administrator's Proposed Conclusions
For the reasons discussed below, the Administrator proposes to set
a cumulative seasonal standard expressed as an annual index of the sum
of weighted hourly concentrations (i.e., the W126 form), cumulated over
12 hours per day (8 am to 8 pm) during the consecutive 3-month period
within the O3 season with the maximum index value, set at a
level within the range of 7 to 15 ppm-hour. This proposed decision
takes into account the information and assessments presented in the
2006 Criteria Document and the 2007 Staff Paper and related technical
support documents, the advice and recommendations of CASAC both during
and following the 2008 rulemaking, and public comments received in
conjunction with review of drafts of these documents and on the 2007
proposed rule.
a. Form
As discussed above in section IV.B, the 2006 Criteria Document and
2007 Staff Paper concluded that the recent vegetation effects
literature evaluated in the 2008 rulemaking strengthens and reaffirms
conclusions made in the 1997 review that the use of a cumulative
exposure index that differentially weights ambient concentrations is
best able to relate ambient exposures to vegetation response. The 1997
review focused in particular on two of these cumulative forms, the
SUM06 and W126 (EPA, 1996). Given that the data available at that time
were unable to distinguish between these forms, the EPA, based on the
policy consideration of not including O3 concentrations
considered to be within the PRB, estimated at that time to be between
0.03 and 0.05 ppm, concluded that the SUM06 form would be the more
appropriate choice for a cumulative, exposure index for a secondary
standard.
In the 2008 rulemaking, the 2007 Staff Paper evaluated the
continued appropriateness of the SUM06 form in light of new estimates
of PRB that were lower than in the 1997 review, and the continued lack
of evidence within the vegetation effects literature of a biological
threshold for vegetation exposures of concern. On the basis of these
policy and science-related considerations, the 2007 Staff Paper
concluded that the W126 form was the more appropriate cumulative,
concentration-weighted form. Specifically, the W126, by its
incorporation of a sigmoidal weighting scheme, does not create an
artificially imposed concentration threshold, gives proportionally more
weight to the higher and typically more biologically potent
concentrations, and is not significantly influenced by O3
concentrations within the range of estimated PRB.
As discussed above, the CASAC, based on its assessment of the same
vegetation effects science, agreed with the 2006 Criteria Document and
2007 Staff Paper and unanimously concluded that protection of
vegetation from the known or anticipated adverse effects of ambient
O3 ``requires a secondary standard that is substantially
different from the primary standard in averaging time, level, and
form,'' i.e. not identical to the primary standard for O3
(Henderson, 2007). Moreover, the members of CASAC and a substantial
majority of the other CASAC Panel members agreed with 2007 Staff Paper
conclusions and encouraged EPA to establish an alternative cumulative
secondary standard for O3 and related photochemical oxidants
that is distinctly different in averaging time, form and level from the
then current or potentially revised 8-hour primary standard (Henderson,
2006c). The CASAC Panel also stated that ``the recommended metric for
the secondary ozone standard is the (sigmoidally weighted) W126 index''
(Henderson, 2007).
In reconsidering the 2008 final rule, the Administrator agrees with
the conclusions drawn in the 2006 Criteria Document, 2007 Staff Paper
and by CASAC that the scientific evidence available in the 2008
rulemaking continues to demonstrate the cumulative nature of
O3-induced plant effects and the need to give greater weight
to higher concentrations. Thus, the Administrator concludes that a
cumulative exposure index that differentially weights O3
concentrations represents a reasonable policy choice for a secondary
standard to protect against the effects of O3 on vegetation.
The Administrator further agrees with both the 2007 Staff Paper and
CASAC that the most appropriate cumulative, concentration-weighted form
to consider is the sigmoidally weighted W126 form.
The Administrator notes that in the 2007 proposed rule, EPA
proposed a second option of revising the then current 8-hour average
secondary standard by making it identical to the proposed 8-hour
primary standard. The 2007 Staff Paper analyzed the degree of overlap
expected between alternative 8-hour and cumulative seasonal secondary
standards using recent air quality monitoring data. Based on the
results, the 2007 Staff Paper concluded that the degree to which the
current 8-hour standard form and level would overlap with areas of
concern for vegetation expressed in terms of the 12-hour W126 standard
is inconsistent from year to year and would depend greatly on the level
of the 12-hour W126 and 8-hour standards selected and the distribution
of hourly O3 concentrations within the annual and/or 3-year
average period. The 2007 Staff Paper also recognized that meeting the
then current or alternative levels of the 8-hour average standard could
result in air quality improvements that would potentially benefit
vegetation in some areas, but urged caution be used in evaluating the
likely vegetation impacts associated with a given level of air quality
expressed in terms of the 8-hour average form in the absence of
parallel W126 information. This caution was due to the concern that the
analysis in the 2007 Staff Paper may not be an accurate reflection of
the true situation in non-monitored, rural counties due to the lack of
more complete monitor coverage in many rural areas. Further, of
[[Page 3019]]
the counties that did not show overlap between the two standard forms,
most were located in rural/remote high elevation areas which have
O3 air quality patterns that are typically different from
those associated with urban and near urban sites at lower elevations.
Because the majority of such areas are currently not monitored, there
are likely to be additional areas that have similar air quality
distributions that would lead to the same disconnect between forms.
Thus, the 2007 Staff Paper concluded that it remains problematic to
determine the appropriate level of protection for vegetation using an
8-hour average form.
The Administrator also notes that CASAC recognized that an
important difference between the effects of acute exposures to
O3 on human health and the effects of O3
exposures on welfare is that vegetation effects are more dependent on
the cumulative exposure to, and uptake of, O3 over the
course of the entire growing season (Henderson, 2006c). The CASAC
O3 Panel members were unanimous in concluding the protection
of natural terrestrial ecosystems and managed agricultural crops
requires a secondary O3 standard that is substantially
different from the primary O3 standard in form, averaging
time, and level (Henderson, 2007).
In reaching her proposed decision in this reconsideration of the
2008 final rule, the Administrator has considered the comments received
on the 2007 proposed rule regarding revising the secondary standard
either to reflect a new, cumulative form or by remaining equal to a
revised primary standard. The commenters generally fell into two
groups.
One group of commenters, including environmental organizations,
strongly supported the proposed option of moving to a cumulative,
seasonal standard, generally based on the reasoning explained in the
2007 proposal. Commenters in this group also expressed serious concerns
with the other proposed option of setting a secondary O3
standard in terms of the same form and averaging time (i.e., daily
maximum 8-hour average O3 concentration) as the primary
standard. These commenters expressed the view that such a standard
would fail to protect public welfare because the maximum daily 8-hour
average O3 concentration failed to adequately characterize
harmful O3 exposures to vegetation. This view was generally
based on the observation that there is no consistent relationship in
areas across the U.S. between 8-hour peak O3 concentrations
and the longer-term cumulative exposures aggregated over a growing
season that are biologically relevant in characterizing O3-
related effects on sensitive vegetation. Thus, as EPA noted in the 2007
proposed rule, there is a lack of a rational connection between the
level of an 8-hour standard and the requisite degree of protection
required for a secondary O3 NAAQS.
Another group of commenters, including industry organizations,
agreed that a cumulative form of the standard may better match the
underlying data, but expressed the view that remaining uncertainties
associated with the vegetation effects evidence and/or EPA's exposure,
risk and benefits assessments were so great that the available
information did not provide an adequate basis to adopt a standard with
a level based on a cumulative, seasonal form. These commenters asserted
that because of the substantial uncertainties remaining at the time of
the 2008 rulemaking, the benefits of changing to a W126 form were too
uncertain to warrant revising the form of the standard at that time.
The Administrator notes that in both the 1997 and the 2008
decisions, EPA recognized that the risk to vegetation from
O3 exposures comes from cumulative exposures over a season
or seasons. The CASAC has fully endorsed this view based on the
available scientific evidence and assessments, and there is no
significant disagreement on this issue by commenters. Thus, it is clear
that the purpose of the secondary O3 NAAQS should be to
provide an appropriate degree of protection against cumulative,
seasonal exposures to O3 that are known or anticipated to
harm sensitive vegetation or ecosystems. In reconsidering the 2008
final rule, the Administrator recognizes that the issue before the
Agency is what form of the standard is most appropriate to perform that
function.
Within this framework, the Administrator recognizes that it is
clear that a cumulative, seasonal form has a distinct advantage in
protecting against cumulative, seasonal exposures. Such a form is
specifically designed to measure directly the kind of O3
exposures that can cause harm to vegetation. In contrast, an 8-hour
standard does not measure cumulative, seasonal exposures directly, and
can only indirectly afford some degree of protection against such
exposures. To the extent that clear relationships exist between 8-hour
daily peak O3 concentrations and cumulative, seasonal
exposures, the 8-hour form and averaging time would have the potential
to be effective as an indirect surrogate. However, as discussed in the
2007 proposed rule and the 2008 final rule, the evidence shows that
there are known types of O3 air quality patterns that can
lead to high levels of cumulative, seasonal O3 exposures
without the occurrence of high daily 8-hour peak O3
concentrations. An 8-hour form and averaging time is an indirect way to
measure biologically relevant exposure patterns, is poorly correlated
with such exposure patterns, and therefore is less likely to identify
and protect against the kind of cumulative, seasonal exposure patterns
that have been determined to be harmful.
Past arguments or reasons for not moving to a cumulative, seasonal
form, with appropriate exposure periods, have not been based on
disagreement over the biological relevance of the cumulative, seasonal
form, or the recognized disadvantages of an 8-hour standard in
measuring and identifying a specified cumulative, seasonal exposure
pattern. The reasons for not moving to such a form have been based on
concerns over whether EPA has an adequate basis to identify the nature
and magnitude of cumulative, seasonal exposure patterns that the
standard should be designed to protect against, given the various
uncertainties in the evidence and the lack of rural O3
monitoring data. This most directly translates into a concern over
whether EPA has an adequate basis to determine an appropriate level for
a cumulative, seasonal secondary standard.
The Administrator has also considered issues associated with
selection of the W126 cumulative form, as reflected in the following
assertions made by some commenters on the 2007 proposed rule: (1) The
W126 form lacks a biological basis, since it is merely a mathematical
expression of exposure that has been fit to specific responses in OTC
studies, such that its relevance for real world biological responses is
unclear; (2) a flux-based model would be a better choice than a
cumulative metric because it is an improvement over the many
limitations and simplifications associated with the cumulative form;
however, there is insufficient data to apply such a model at present;
(3) the European experience with cumulative O3 metrics has
been disappointing and now Europeans are working on their second level
approach, which will be flux-based; and (4) a second index that
reflects the accumulation of peaks at or above 0.10 ppm (called N100)
should be added to a W126 index to achieve appropriate protection.
With regard to whether the W126 index lacks a biological basis, the
Administrator finds no basis for reaching such a conclusion. As
discussed above in section IV.B, the
[[Page 3020]]
vegetation effects science is clear that exposures of concern to plants
are not based on one discrete 8-hour period but on the repeated
occurrence of elevated O3 levels throughout the plant's
growing season. The cumulative nature of the W126 is supported by the
basic biological understanding that plants in the U.S. are generally
most biologically active during the warm season and are exposed to
ambient O3 throughout this biologically active period. In
addition, it has been shown in the scientific literature that all else
being equal, plants respond more to higher O3
concentrations, with no evidence of an exposure threshold for
vegetation effects. The W126 sigmoidal weighting function reflects both
of these understandings, by not including a threshold below which
concentrations are not included, and by differentially weighting
concentrations to give greater weight to higher concentrations and less
weight to lower ones.
With regard to whether a flux-based model would be a better choice,
the 2007 Staff Paper acknowledged that flux models may produce a more
accurate calculation of dose to a specific plant species in a specific
area. However, dose-response relationships have not been developed for
these flux calculations for plants growing in the U.S. Further, flux
calculations require large amounts of data for the physiology of each
plant species and the local conditions for the growing range of each
plant species. These exercises may be useful for limited small-scale
risk assessments, but do not provide an appropriate basis for a
national standard at this time.
With regard to dissatisfaction with the performance of a particular
cumulative index in use in Europe,\60\ and growing interest in
development of flux-based models, the 2007 Staff Paper (Appendix 7A)
noted that ``because of a lack of flux-response data, a cumulative,
cutoff concentration based (e.g., AOT40) exposure index will remain in
use in Europe for the near future for most crops and for forests and
semi-natural herbaceous vegetation (Ashmore et al., 2004a).'' Further,
like the SUM06 index, the AOT40 index incorporates a threshold below
which concentrations are not considered. Though the AOT40 threshold is
lower than the threshold value in SUM06, the 2007 Staff Paper concluded
that the vegetation effects information does not provide evidence of an
effects threshold that applies to all species. Thus, the Administrator
concludes neither of these forms is as biologically relevant as the
W126 form.
---------------------------------------------------------------------------
\60\ The AOT40 index used in Europe is a cumulative index that
incorporates a threshold at 0.04 ppm (40 ppb). This index is
calculated as the area over the threshold (AOT) by subtracting 40
ppb from the value of each hourly concentration above that threshold
and then cumulating each hourly difference over a specified window.
---------------------------------------------------------------------------
With regard to consideration of coupling a W126 form with a
separate N100 index, there was very little research on the N100 index
or a coupled approach to be evaluated in the 2008 rulemaking. The
CASAC, after reviewing all the information in the 2006 Criteria
Document and the 2007 Staff Paper, did not recommend an additional N100
index for consideration. Therefore, there is no basis at this time to
judge the extent to which such a coupled W126-N100 form would be a
better choice than the proposed W126 form. Further, the W126 form
incorporates a weighting scheme that places greater weight on
increasing concentrations and gives every concentration of 0.10 ppm and
above an equal weight of 1, which is the highest weight in this
sigmoidal weighting function.
In summary, having considered the scientific information and
assessment results available in the 2008 rulemaking as discussed above
in this proposal notice, as well as the recommendations of the staff
and CASAC, and having taken into consideration issues raised in public
comments received as part of the 2008 rulemaking, and recognizing the
determinations made below in section IV.D.5.c on level, the
Administrator concludes that it is appropriate to set the secondary
standard using a cumulative, seasonal form. The Administrator also
concludes that the W126 form is best suited to reflect the biological
impacts of O3 exposure on vegetation, and that there is
adequate certainty in the information available in the 2008 rulemaking
to support such a change in form. Thus, the Administrator proposes to
set the secondary standard using a cumulative, seasonal W126 form.
b. Averaging Times \61\
---------------------------------------------------------------------------
\61\ While the term ``averaging time'' is used, for the
cumulative, seasonal standard the seasonal and diurnal time periods
at issue are those over which exposures during a specified period of
time are cumulated, not averaged.
---------------------------------------------------------------------------
The Administrator, in addition to reconsidering what form of a
secondary standard is most appropriate for protecting vegetation, is
also reconsidering what exposure periods (e.g., seasonal window,
diurnal window), and what standard index, in terms of an annual index
value versus a 3-year average of annual index values, are most
appropriate when used in conjunction with the W126 cumulative seasonal
form. Based on the information set forth in the 2007 Staff Paper, as
well as CASAC views, as discussed above in section IV.D.1.b, the
Administrator has reached conclusions regarding exposure periods, and
the annual versus 3-year average index, that have the most biological
relevance for plant response, as discussed below.
In considering an appropriate seasonal window, the Administrator
notes that the 2007 Staff Paper concluded that the consecutive 3-month
period within the O3 season with the highest W126 index
value (e.g., maximum 3-month period) was a reasonable seasonal time
period to consider. The Administrator further notes that the 2007 Staff
Paper acknowledged that the selection of any single seasonal exposure
period for a national standard would necessarily represent a
compromise, given the significant variability in growth patterns and
lengths of growing seasons among the wide range of sensitive vegetation
species occurring within the U.S. However, the Administrator also
considered the Staff Paper conclusion that the period of maximum
potential plant uptake of O3 would also likely coincide with
the period of highest O3 occurring within the intra-annual
period defined as the O3 season, since the high temperature
and light conditions conducive to O3 formation are also
conducive for plant activity. The Administrator also observes that the
CASAC panel was supportive of the Staff Paper views, while recognizing
that 3 months likely represented the minimum timeframe appropriate to
consider. Therefore, the Administrator concludes, on these bases, that
the consecutive 3-month period within the O3 season with the
highest W126 index value (e.g., maximum 3-month period) remains an
appropriate seasonal window to propose for the protection of sensitive
vegetation.
With regard to consideration of an appropriate diurnal window, the
Administrator has taken into account the 2007 Staff Paper conclusion
that for the vast majority of studied species, daytime exposures
represent the majority of diurnal plant O3 uptake and are
responsible for inducing the plant response of most significance to the
health and productivity of the plant (e.g., reduced carbohydrate
production). The Administrator is also aware, based on discussions in
the 2007 Staff Paper that there are some number of species that show
non-negligible amounts of O3 uptake at night due to
incomplete stomatal closure. In reaching her conclusion that the 2007
Staff Paper recommendation of a 12-hour daytime
[[Page 3021]]
window (8 a.m. to 8 p.m.) remains the most appropriate period over
which to cumulate diurnal O3 exposures, specifically those
most relevant to plant growth and yield responses, the Administrator
places weight on the fact that the CASAC comments were also supportive
of this diurnal window, recognizing again that it likely represents a
minimum period over which plants can be vulnerable to O3
uptake. Therefore, the Administrator is again proposing the 12-hour
daytime window (8 a.m. to 8 p.m.) as an appropriate diurnal window to
protect against O3-induced plant effects.
Lastly, in considering whether an annual or a 3-year average index
is more appropriate, the Administrator notes that in addition to the
available scientific evidence regarding plant effects that can be
brought to bear, there are also other public welfare considerations
that may be appropriate to consider. In taking this view, the
Administrator notes that the 2007 Staff Paper recognized that though
most cumulative seasonal exposure levels of concern for vegetation have
been expressed in terms of the annual timeframe, it may be appropriate
to consider a 3-year average for purposes of standard stability. The
Administrator has considered that while the 2007 Staff Paper notes that
for certain welfare effects of concern (e.g., foliar injury, yield loss
for annual crops, growth effects on other annual vegetation and
potentially tree seedlings), an annual time frame may be a more
appropriate period in which to assess what level would provide the
requisite degree of protection, for other welfare effects (e.g., mature
tree biomass loss), it also points out that a 3-year average may also
be appropriate. The Administrator further observes that in concluding
that it was appropriate to consider both an annual and a 3-year
average, the 2007 Staff Paper also concluded that should a 3-year
average of the 3-month, 12-hour W126 form be selected, a potentially
lower level should be considered to reduce the potential of adverse
impacts to annual species from a single high O3 year that
could still occur while attaining a standard on average over 3-years.
The Administrator also took note that the CASAC Panel, in addressing
this issue of annual versus 3-year average concluded that multi-year
averaging to promote a ``stable'' secondary standard is less
appropriate for a cumulative, seasonal secondary standard than for a
primary standard based on maximum 8-hour concentrations, and further
concluded that if multi-year averaging is employed to increase the
stability of the secondary standard, the level of the standard should
be revised downward to assure that the desired degree of protection is
not exceeded in individual years. The Administrator, in considering the
merits of both the annual and 3-year average, and taking into account
both the 2007 Staff Paper and CASAC views, concludes that it is
important to place more weight on the public welfare benefit in having
a stable standard, and that appropriate protection for vegetation can
be achieved using a 3-year average form. The Administrator is thus
proposing a 3-year average. However, given the uncertain nature of the
evidence and potential concerns with using a 3-year average form, the
Administrator is proposing to take comment on the appropriateness of
the specific seasonal and diurnal exposure periods proposed, as well as
the use of a 3-year average, and, as discussed below, the impact that
selection of these proposed seasonal and diurnal exposure periods would
have, in conjunction with a 3-year average form, on the appropriateness
of the proposed range of levels.
c. Level
i. Considerations Regarding 2007 Proposed Range of Levels
The 2007 Staff Paper, in identifying a range of levels for a 3-
month, 12-hour (daytime) W126 standard appropriate for the
Administrator to consider in protecting the public welfare from known
or anticipated adverse effects to vegetation from O3
exposures, considered what information from the array of vegetation
effects evidence and exposure and risk assessment results was most
useful. With respect to the vegetation effects evidence, the 2007 Staff
Paper found stronger support than what was available at the time of the
1997 review for an increased level of protection for trees and forested
ecosystems. Specifically, the expanded body of evidence included: (1)
Additional field based data from free air, gradient and biomonitoring
surveys demonstrating adverse levels of O3-induced growth
reductions on trees at the seedling, sapling and mature growth stages
and incidence of visible foliar injury occurring at biomonitoring sites
in the field at ambient levels of exposure; (2) qualitative support
from free air (e.g., AspenFACE) and gradient studies on a limited
number of tree species for the continued appropriateness of using OTC-
derived C-R functions to predict tree seedling response in the field;
(3) studies that continued to document below-ground effects on root
growth and ``carry-over'' effects occurring in subsequent years from
O3 exposures; and (4) increased recognition and
understanding of the structure and function of ecosystems and the
complex linkages through which O3, and other stressors,
acting at the organism and species level can influence higher levels
within the ecosystem hierarchy and disrupt essential ecological
attributes critical to the maintenance of ecosystem goods and services
important to the public welfare.
Based on the above sources of vegetation effects information and
the results of the exposure and risk assessments summarized above, the
2007 Staff Paper concluded that just meeting the then current 0.084
ppm, 8-hour average standard would continue to allow adverse levels of
O3-induced effects to occur in sensitive commercially and
ecologically important tree species in many regions of the country. The
2007 Staff Paper further concluded that air quality levels would need
to be substantially reduced to protect sensitive tree seedlings, such
as black cherry, aspen, and cottonwood, from these growth and foliar
injury effects.
In addition to the currently quantifiable risks to trees from
ambient exposures, the 2007 Staff Paper also considered the more subtle
impacts of O3 acting in synergy with other natural and man-
made stressors to adversely affect individual plants, populations and
whole systems. By disrupting the photosynthetic process, decreasing
carbon storage in the roots, increasing early senescence of leaves and
affecting water use efficiency in trees, O3 exposures could
potentially disrupt or change the nutrient and water flow of an entire
system. Weakened trees can become more susceptible to other
environmental stresses such as pest and pathogen outbreaks or harsh
weather conditions. Though it is not possible to quantify all the
ecological and societal benefits associated with varying levels of
alternative secondary standards, the 2007 Staff Paper concluded that
this information should be weighed in considering the extent to which a
secondary standard should be set so as to provide potential protection
against effects that are anticipated to occur.
The 2007 Staff Paper also recognized that in the 1997 review, EPA
took into account the results of a 1996 Consensus Workshop. At this
workshop, a group of independent scientists expressed their judgments
on what standard form(s) and level(s) would provide vegetation with
adequate protection from O3-related adverse effects.
Consensus was reached
[[Page 3022]]
on protective ranges of levels in terms of a cumulative, seasonal 3-
month, 12-hr SUM06 standard for a number of vegetation effects
endpoints. These ranges are identified below, with the estimated
approximate equivalent W126 standard levels shown in parentheses. For
growth effects to tree seedlings in natural forest stands, a consensus
was reached that a SUM06 range of 10 to 15 (W126 range of 7 to 13) ppm-
hour would be protective. For growth effects to tree seedlings and
saplings in plantations, the consensus SUM06 range was 12 to 16 (W126
range of 9 to 14) ppm-hour. For visible foliar injury to natural
ecosystems, the consensus SUM06 range was 8 to 12 (W126 range of 5 to
9) ppm-hour.
The 2007 Staff Paper then considered to what extent recent research
provided empirical support for the ranges of levels identified by the
experts as protective of different types of O3-induced
effects. As discussed above in section IV.D.1.c, the 2007 Staff Paper
concluded on the basis of the available evidence that it was
appropriate to consider a range for a 3-month, 12-hour, W126 standard
level that included the 1996 Consensus Workshop recommendations
regarding a range of levels protective against O3-induced
growth effects in tree seedlings in natural forest stands (i.e., 7-13
ppm-hour in terms of a W126 form).
In considering the newly available information on O3-
related effects on crops in this review, the 2007 Staff Paper observed
the following regarding the strength of the underlying crop science:
(1) Nothing in the recent literature points to a change in the
relationship between O3 exposure and crop response across
the range of species and/or cultivars of commodity crops currently
grown in the U.S. that could be construed to make less appropriate the
use of commodity crop C-R functions developed in the NCLAN program; (2)
new field-based studies (e.g., SoyFACE) provide qualitative support in
a few limited cases for the appropriateness of using OTC-derived C-R
functions to predict crop response in the field; and (3) refinements in
the exposure, risk and benefits assessments in this review reduce some
of the uncertainties present in 1996. On the basis of these
observations, the 2007 Staff Paper concluded that nothing in the newly
assessed information calls into question the strength of the underlying
science upon which EPA based its proposed decision in the last review
to select a level of a cumulative, seasonal form associated with
protecting 50 percent of crop cases from no more than 10 percent yield
loss as providing the requisite degree of protection for commodity
crops.
The 2007 Staff Paper then considered whether any additional
information was available to inform judgments as to the adversity of
various O3-induced levels of crop yield loss to the public
welfare. As noted above, the 2007 Staff Paper observed that
agricultural systems are heavily managed, and that in addition to
stress from O3, the annual productivity of agricultural
systems is vulnerable to disruption from many other stressors (e.g.,
weather, insects, disease), whose impact in any given year can greatly
outweigh the direct reduction in annual productivity resulting from
elevated O3 exposures. On the other hand, O3 can
also more subtly impact crop and forage nutritive quality and
indirectly exacerbate the severity of the impact from other stressors.
Since these latter effects could not be quantified at that time, they
could only be considered qualitatively in reaching judgments about an
appropriate degree of protection for commodity crops from
O3-related effects.
Based on the above considerations, the 2007 Staff Paper concluded
that the level of protection judged requisite in the 1997 review to
protect the public welfare from adverse levels of O3-induced
reductions in crop yields and tree seedling biomass loss, as
approximately provided by a W126 level of 21 ppm-hour, remained
appropriate for consideration as an upper bound of a range of
appropriate levels. The 2007 Staff Paper also recognized that a
standard set at this level would not protect the most sensitive species
or individuals within a species from all potential effects related to
O3 exposures and further, that this level derives from the
extensive and quantitative historic and recent crop effects database,
as well as current staff exposure and risk analyses (EPA, 2007, pg. 8-
22).
In identifying a lower bound for the range of alternative standard
levels appropriate for consideration, staff concluded that several
lines of evidence pointed to the need for greater protection for tree
seedlings, mature trees, and associated forested ecosystems. Staff
believed that tree growth was an important endpoint to consider because
it is related to other aspects of societal welfare such as sustainable
production of timber and related goods, recreation, and carbon
(CO2) sequestration. Impacts on tree growth can also affect
ecosystems through shifts in species composition and the loss of
genetic diversity due to the loss of O3 sensitive
individuals or species. In selecting an appropriate level of protection
for trees, staff considered the results of the 1996 Consensus Workshop
which identified the SUM06 range of 10 to 15 (W126 of 7 to 13) ppm-hour
for growth effects to tree seedlings in natural forest stands.
Because staff believed that O3-related effects on forest
tree species are important public welfare effects of concern, it
therefore concluded, based on the above, that it was appropriate to
include 7 ppm-hour as the lower bound of the recommended range, the
lower end of the approximate range recommended by CASAC (Henderson,
2006c) and identified by the 1996 Consensus Workshop participants as
protective of forest trees. At this lower end of the range, staff
anticipated, based on its analyses of risks of tree seedling biomass
loss and mature tree growth reductions and on the basis of the
scientific effects literature, that adverse effects of O3 on
forested ecosystems would be substantially reduced. Further, staff
anticipated that the lower end of this range would provide increased
protection from the more subtle impacts of O3 acting in
synergy with other natural and man-made stressors to adversely affect
individual plants, populations and whole systems. Staff also noted that
by disrupting the photosynthetic process, decreasing carbon storage in
the roots, increasing early senescence of leaves and affecting water
use efficiency in trees, O3 exposure could potentially
disrupt or change the nutrient and water flow of an entire system. Such
weakened trees can become more susceptible to other environmental
stresses such as pest and pathogen outbreaks or harsh weather
conditions. While recognizing that it is not possible to quantify all
the ecological and societal benefits associated with varying levels of
alternative secondary standards, staff believed that this information
should be weighed in considering the extent to which a secondary
standard should be precautionary in nature in protecting against
effects that have not yet been adequately studied and evaluated.
Thus, the 2007 Staff Paper concluded, based on all the above
considerations, that an appropriate range of levels, for an annual
standard using a 3-month, 12-hour W126 form, for the Administrator to
consider was 7 to 21 ppm-hour, recognizing that the level selected is
largely a policy judgment as to the requisite level of protection
needed. In determining the requisite level of protection for crops and
trees, the 2007 Staff Paper recognized that it was appropriate to weigh
the importance of the predicted risks of these effects in the overall
context of
[[Page 3023]]
public welfare protection, along with a determination as to the
appropriate weight to place on the associated uncertainties and
limitations of this information.
ii. CASAC and Public Comments Prior to 2008 Decision
In considering the evidence described in both the 2006 Criteria
Document and 2006 draft Staff Paper, CASAC, in its October 24, 2006
letter to the Administrator, expressed its view regarding the
appropriate form and range of levels for the Administrator to consider.
The CASAC preferred a seasonal 3-month W126 standard in a range that is
the approximate equivalent of the SUM06 at 10 to 20 ppm-hour. Following
the 2007 proposal, EPA received additional CASAC and public comments
regarding an appropriate range of levels of a W126 form for the
Administrator to consider in finalizing a revised secondary NAAQS for
O3. The CASAC, in its final letter to the Administrator
(Henderson, 2007), agreed with the 2007 Staff Paper recommendations
that the lower bound of the range within which a seasonal W126
secondary O3 standard should be considered is approximately
7 ppm-hour; however, it did not agree with staff's recommendation that
the upper bound of the range should be as high as 21 ppm-hour. Rather,
as discussed above in section IV.D.1.c, the CASAC Panel recommended
that the upper bound of the range considered should be no higher than a
W126 of 15 ppm-hour for an annual standard.
The comments received from the public fell into two groups. One
group of commenters supported the CASAC recommended range of 7-15 ppm-
hour for a W126 standard. Many of these same commenters further
emphasized the lower end of the proposed range as necessary to provide
adequate protection for sensitive species. These commenters based their
recommendation primarily on four sources of information: (1) Field-
based evidence of foliar injury occurring on sensitive species at air
quality levels well below that of the current standard; (2) the 1996
Consensus Workshop recommendations for protective levels in terms of
cumulative exposures for different vegetation types; (3) CASAC advice
and recommendations; and (4) studies published after the close of the
2006 Criteria Document that potentially strengthen the link between
species level impacts and ecosystem response.
The other group of commenters did not support revising the current
secondary standard. These commenters primarily focused on uncertainties
regarding the sources of information relied upon by the first group of
commenters as support for a level within the range of levels
recommended by CASAC. These uncertainties included: (1) potential
confounders, such as soil moisture, on visible foliar injury and the
lack of a clear relationship between visible foliar injury symptoms and
other vegetation effects; (2) lack of documentation of the basis for
the recommendations from the 1996 Consensus Workshop in selecting a
range of levels, indicating that these recommendations should be used
with great caution; (3) failure of CASAC and EPA to take into account
the monitor height measurement gradient when making their
recommendations concerning the level of the secondary standard; and (4)
inability to quantitatively estimate ecosystem effects of O3
or to extrapolate meaningfully from effects on individual plants to
ecosystem effects due to inadequate data.
iii. Conclusions on Level
The Administrator is proposing to set a cumulative, seasonal
standard expressed in terms of the maximum 3-month, 12-hour W126 form,
in the range of 7 to 15 ppm-hour. In reaching this proposed decision
about an appropriate range of levels for the secondary standard, the
Administrator has considered the following: the evidence described in
the 2006 Criteria Document and the 2007 Staff Paper; the results of the
vegetation exposure and risk assessments discussed above and in the
2007 Staff Paper, giving weight to the assessments as judged
appropriate; the CASAC Panel's advice and recommendations in the
CASAC's letters to the Administrator; EPA staff recommendations; and
public comments received during the development of these documents,
either in connection with CASAC meetings or separately. In considering
what range of levels of a cumulative 3-month standard to propose, the
Administrator notes that this choice requires judgment as to what
standard will protect the public welfare from any known or anticipated
adverse effects. This choice must be based on an interpretation of the
evidence and other information, such as the exposure and risk
assessments, that neither overstates nor understates the strength and
limitations of the evidence and information nor the appropriate
inferences to be drawn. In taking all of the above into consideration,
the Administrator also notes that there is no bright line clearly
directing the choice of level for any of the effects of concern, and
the choice of what is appropriate is clearly a public welfare policy
judgment entrusted to the Administrator.
In particular, the Administrator has given careful consideration to
the following: (1) The nature and degree of effects of O3 to
the public welfare, including what constitutes an adverse effect; (2)
the strengths and limitations of the evidence that is available
regarding known or anticipated adverse effects from cumulative,
seasonal exposures, and its usefulness in informing selection of a
proposed range; and (3) CASAC's views regarding the strength of the
evidence and its adequacy to inform a range of levels. Each of these
topics is discussed in turn below.
In determining the nature and degree of effects of O3 on
the public welfare, the Administrator recognizes that the significance
to the public welfare of O3-induced effects on sensitive
vegetation growing within the U.S. can vary, depending on the nature of
the effect, the intended use of the sensitive plants or ecosystems, and
the types of environments in which the sensitive vegetation and
ecosystems are located. Any given O3-related effect on
vegetation and ecosystems (e.g., biomass loss, foliar injury),
therefore, may be judged to have a different degree of impact on the
public depending, for example, on whether that effect occurs in a Class
I area, a city park, or commercial cropland. In her judgment, it is
appropriate that this variation in the significance of O3-
related vegetation effects should be taken into consideration in
judging the level of ambient O3 that is requisite to protect
the public welfare from any known or anticipated adverse effects. In
this regard, the Administrator agrees with the definition of adversity
as described above in section IV.A.3 and in the 2008 rulemaking. As a
result, the Administrator concludes that of those known and anticipated
O3-related vegetation and ecosystem effects identified and
discussed in this reconsideration, the highest priority and
significance should be given to those that occur on sensitive species
that are known to or are likely to occur in federally protected areas
such as Class I areas \62\ or on lands set aside by States, Tribes and
public interest groups to provide similar benefits to the public
[[Page 3024]]
welfare, for residents on those lands, as well as visitors to those
areas.
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\62\ For example, the level of protection granted by Congress
under the Wilderness Act of 1964 for designated ``wilderness areas''
requires that these areas ``shall be administered for the use and
enjoyment of the American people in such manner as will leave them
unimpaired for future use as wilderness, and so as to provide for
the protection of these areas, the preservation of their wilderness
character'' (The Wilderness Act, 1964).
---------------------------------------------------------------------------
Likewise, the Administrator also notes that the same known or
anticipated O3-induced effects, occurring in other areas may
call for less protection. For example, the maintenance of adequate
agricultural crop yields is extremely important to the public welfare
and is currently achieved through the application of intensive
management practices, including in some cases, genetic engineering.
These management practices, in conjunction with market forces and
government programs, assure an appropriate balance is reached between
costs of production and market availability. Thus, while research on
agricultural crop species remains useful in illuminating mechanisms of
action and physiological processes, information from this sector on
O3-induced effects is considered less useful in informing
judgments on what level(s) would be sufficient but not more than
necessary to protect the public welfare. With respect to commercial
production of commodities, the Administrator notes that judgments about
the extent to which O3-related effects on commercially
managed vegetation are adverse from a public welfare perspective are
particularly difficult to reach, given that what is known about the
relationship between O3 exposures and agricultural crop
yield response derives largely from data generated almost 20 years ago.
The Administrator recognizes that there is substantial uncertainty at
this time as to whether these data remain relevant to the majority of
species and cultivars of crops being grown in the field today. In
addition, the extensive management of such vegetation may to some
degree mitigate potential O3-related effects. The management
practices used on these lands are highly variable and are designed to
achieve optimal yields, taking into consideration various environmental
conditions. Thus, the Administrator concludes there is no need for such
additional protection for agricultural crops through the NAAQS.
The Administrator also recognizes that O3-related
effects on sensitive vegetation can occur in other areas that have not
been afforded special Federal protections, ranging from effects on
vegetation growing in residential or commercial settings, such as
ornamentals used in urban/suburban landscaping, to vegetation grown in
land use categories that are heavily managed for commercial production
of commodities such as timber. For vegetation used for residential or
commercial ornamental purposes, such as urban/suburban landscaping, the
Administrator believes that there is not adequate information at this
time to establish a secondary standard based specifically on impairment
of urban/suburban landscaping and other uses of ornamental vegetation,
but notes that a secondary standard revised to provide protection for
sensitive natural vegetation and ecosystems would likely also provide
some degree of protection for such ornamental vegetation.
Based on the above, the Administrator finds that the types of
information most useful in informing the selection of an appropriate
range of protective levels is appropriately focused on information
regarding exposures and responses of sensitive trees and other native
species known or anticipated to occur in protected areas such as Class
I areas or on lands set aside by States, Tribes and public interest
groups to provide similar benefits to the public welfare, for residents
on those lands, as well as visitors to those areas.
With regard to the available evidence, the Administrator finds the
coherence and strength of the weight of evidence from the large body of
available literature compelling. This evidence addresses a broad array
of O3-induced effects on a variety of tree species across a
range of growth stages (i.e., seedlings, saplings and mature trees)
using diverse field-based (e.g. free air, gradient and ambient) and OTC
exposure methods. It demonstrates that significant numbers of forest
tree species are potentially experiencing O3-induced stress
under levels of ambient air quality, both at and below the level of the
1997 standard.
In particular, the Administrator notes the evidence from recent
field-based studies and a gradient study of eastern cottonwood saplings
(Gregg et al., 2003). She observes that this study found that
cottonwood saplings grown in urban New York City grew faster than
saplings grown in downwind rural areas where cumulative O3
exposures were higher, and the difference in biomass production between
the urban site with the lowest cumulative exposure and the rural site
with the highest cumulative exposure is dramatic (Figure 7-17 in the
2007 Staff Paper). The Administrator further notes that cottonwood is
one of the most sensitive tree species studied to date and it is also
important both from an ecological and public welfare perspective, as
discussed above in section IV.A.2.b and in the 2007 Staff Paper.
The Administrator also notes the evidence related to the
O3-induced effect of visible foliar injury. The
Administrator observes that the visible foliar injury database created
from the ambient field-based monitoring network managed by the Unites
States Forest Service (USFS) Forest Inventory and Analysis (FIA)
Program has continued to expand since the conclusion of the 1997
review. In utilizing this dataset, EPA staff collaborated with FIA
staff to compare the incidence of visible foliar injury at different
levels of air quality by county throughout the U.S. in counties with
FIA monitoring sites. In considering the results of this analysis,
depicted in Table 7-4 of the 2007 Staff Paper, the Administrator notes
that for the 2001-2004 period, the percent of counties with documented
foliar injury at a level approximately equivalent to the W126 of 21
ppm-hour, was 26 to 49 percent, while at the lower level approximately
equivalent to a W126 of 13 ppm-hour, incidence values ranged from 12 to
35 percent. The Administrator believes it likely that some sensitive
species occurring in specially protected areas would also exhibit
visible foliar injury symptoms to a similar degree at these exposure
levels. She further notes that while direct links between O3
induced visible foliar injury symptoms and other adverse effects (e.g.,
biomass loss) are not always found, visible foliar injury in itself is
considered by the National Park Service (NPS) to affect adversely air
quality related values (AQRV) in Class I areas.
The Administrator places significant weight on the judgments of
CASAC. In so doing, the Administrator has carefully considered its
stated views and the basis for the range of levels the CASAC
O3 Panel recommended. In its 2007 letter to the
Administrator, the CASAC O3 Panel agreed with EPA staff
recommendations that the lower bound of the range within which a
seasonal W126 O3 standard should be considered is
approximately 7 ppm-hour. However, ``it does not agree with Staff's
recommendations that the upper bound of the range should be as high as
21 ppm-hour. Rather, the Panel recommends that the upper bound of the
range considered should be no higher than 15 ppm-hour, which the Panel
estimates is approximately equivalent to a seasonal 12-hour SUM06 level
of 20 ppm-hour'' (Henderson, 2007). The Administrator notes that CASAC
views concerning an appropriate range of levels for the Administrator
to consider were presented after CASAC had considered the entire body
of evidence presented in both the 2006 Criteria Document and 2007 Staff
Paper, and are generally consistent with the 1996 Consensus Workshop
recommendations.
[[Page 3025]]
In considering the issues raised by commenters on the 2007 proposed
rule, the Administrator noted that many public commenters supported the
range of levels recommended by CASAC. The Administrator also considered
the views expressed by the NPS as to what range of levels it identified
as useful in helping it achieve its mandate to protect AQRVs in
national parks and wilderness areas and to provide a level of
protection for its resources in keeping with the Congressional mandate
set forth in The Wilderness Act of 1964. In so doing, the Administrator
notes that the NPS supported the range recommended by CASAC, while
emphasizing that the lower end of the range was more appropriate. The
NPS notes that though some visible foliar injury would still be
expected to occur above the lower end of the CASAC recommended range
(i.e. 7 ppm-hour), the potential for growth impacts at that level would
be very low. It further notes that most of these parks contain aspen,
black cherry, or ponderosa pine, all sensitive species predicted to
have significant growth effects at current W126 levels.
The Administrator also considered those comments that highlighted
sources of uncertainty in the evidence and risk assessments (summarized
above in section IV.D.5.c.ii) to inform her judgments on how much
weight to place on these associated uncertainties, as discussed below.
With regard to the issue of possible confounders of foliar injury
information, the Administrator recognizes that visible foliar injury,
like other O3-induced plant effects, is moderated by
environmental factors other than O3 exposure. However, the
Administrator also notes that the O3-related visible foliar
injury effect persisted across a four year period (2001-2004), despite
year-to-year variability in meteorology and other environmental factors
(see Table 7-4 in the 2007 Staff Paper). She also notes that
approximately 26 to 49 percent of counties had visible foliar injury
incidence at the approximate W126 level of 21 ppm-hour, while at a W126
level of 13 ppm-hour, this range of percentages dropped to
approximately 12 to 23 percent. In an area such as a national park,
where visitors come in part for the aesthetic quality of the landscape,
the Administrator recognizes that visible foliar injury incidence is an
important welfare effect which should be considered in determining an
appropriately protective standard level.
With regard to the issues of what weight to place on the
recommendations from the 1996 Consensus Workshop in selecting a range
of levels, as the 1997 Workshop Report did not clearly document the
basis for its recommendations, the Administrator recognizes that the
absence of such documentation does call for care in placing weight on
such recommendations. However, the Administrator notes that the
workshop participants were asked to review both the 1996 O3
Criteria Document and Staff Paper, representing the most up to date
compilation of the state of the science available at that time, in
order to ensure that their expert judgments made were also informed by
the latest science. She also notes that another group of experts, the
CASAC O3 Panel, reached a similar consensus based upon an
expanded body of scientific evidence. In addition, the 2007 Staff Paper
evaluated the same recommendations in the context of subsequent
empirical evidence, and reached similar views, with the exception of
the upper end of the recommended range, which in the 2007 Staff Paper
was based on effects on commercial crops that had been considered in
the 1997 review. While it would always be more useful to have
documentation of the reasoning and basis for an expert's advice, in
this case the Administrator judges that the 1996 Consensus Workshop
recommendations should be given substantial weight.
With regard to other issues raised by some commenters related to
uncertainties in the technical evidence and analyses, the Administrator
notes that such issues had been addressed in the 2007 Staff Paper that
reflected CASAC's advice on such issues. For example, while the
Administrator recognizes that uncertainty remains as to what level of
annual tree seedling biomass loss when compounded over multiple years
should be judged adverse to the public welfare, she believes that the
potential for such anticipated effects should be considered in judging
to what degree a standard should be precautionary.
In considering all of the issues discussed above, the Administrator
has decided to propose a range of 7-15 ppm-hour. In selecting as an
upper bound a level of 15 ppm-hour, the Administrator notes that this
level was specifically supported by the CASAC O3 Panel and
is just above the range identified in the 1996 Consensus Workshop
report as needed to provide adequate protection for trees growing in
natural areas. In addition, the NPS, along with many public commenters,
were in support of the CASAC range, including the upper bound of 15
ppm-hour, and indicated that lower values within this range would be
more protective for sensitive trees in protected areas from biomass
loss and visible foliar injury symptoms.
While the upper end of this range is lower than the upper end of 21
ppm-hour recommended in the 2007 Staff Paper, this upper level of 21
ppm-hour was originally put forward in the 1997 review in terms of a
SUM06 of 25 ppm-hour (W126 of 21 ppm-hour) and was justified on the
basis that it was predicted to allow up to 10% biomass loss annually in
50% of studied commercial crops and tree seedling species. Recognizing
the significant uncertainties that are associated with evaluating
effects on commercial crops from a public welfare perspective, the
Administrator now concludes that commercial crop data are no longer
useful for setting the upper level of the range for proposal.
With regard to her selection of a proposed range, the Administrator
has considered that the direction from Congress to provide a high
degree of protection in Class I areas creates a clearer target for
gauging what types and magnitudes of effects would be known or
anticipated to affect the intended use of these and other similarly
protected areas, that would thus be considered adverse to the public
welfare. Such similar areas include lands set aside by States, Tribes
and public interest groups to provide similar benefits to the public
welfare, for residents on those lands, as well as visitors to those
areas. The Administrator also believes that in order to preserve
wilderness areas in an unimpaired state for future generations, she
must consider a level that affords substantial protection from known
adverse O3-related effects of biomass loss and foliar injury
on sensitive tree species, as well as a level that takes into account
potential ``anticipated'' adverse O3-related effects,
including effects that result in continued impairment in the year
following O3 exposure (i.e., carry-over effects), below
ground impacts, ecosystem level impacts, and reduced CO2
sequestration
While the Administrator acknowledges that growth effects and
visible foliar injury can still occur in sensitive species at levels
below the upper bound of the proposed range, the Administrator also
recognizes that some significant uncertainties remain regarding the
risk of these effects, as discussed above. For example, the
Administrator concludes that remaining uncertainties make it difficult
to judge the point at which visible foliar injury becomes adverse to
the public welfare in various types of specially protected areas.
Uncertainties associated with monitoring ambient exposures must be
[[Page 3026]]
considered in evaluating the strength of predictions regarding the
degree of tree seedling growth impairment estimated to occur at varying
ambient exposures. These uncertainties add to the challenge of judging
which exposure levels are expected to be associated with levels of tree
seedling growth effects considered adverse to public welfare The
Administrator believes that it is important to consider these
uncertainties, and the weight to place on such uncertainties, in
selecting a range of standard levels to propose. Establishing 15 ppm-
hour as the upper end of the proposed range reflects her judgment
regarding the appropriate weight to place on these uncertainties in
determining the degree of protection that is warranted for known and
anticipated adverse effects.
With regard to her selection of a lower bound for the proposed
range, the Administrator believes that if weight is placed on taking a
more precautionary approach, recognizing that the real world impacts on
trees and ecosystems could, in some cases, be greater than predicted,
then the lower end of the range of 7 ppm-hour could be warranted. There
is clear evidence that higher cumulative exposures can occur in rural
areas downwind of urban areas and potentially in Class I areas.
Unmonitored high elevation sites would also likely have higher
cumulative exposures than lower elevation sites that are currently
monitored. All of these considerations lead the Administrator to
propose 7 ppm-hour as the low end of the proposed range.
As discussed above in section IV.D.5.a, the main opposition to
changing to a secondary standard with a cumulative, seasonal form has
been the view that EPA does not have an adequate basis to identify the
kinds and types of cumulative, seasonal exposure patterns that the
standard should be designed to protect against, given the various
uncertainties in the evidence, and whether EPA has an adequate basis to
determine an appropriate level for a cumulative, seasonal secondary
standard. While EPA agreed with this position in the 1997 review, the
Administrator believes that the evidence before her appropriately
supports a secondary standard that is distinctly different in form and
averaging time from the 8-hour primary standard, and that such a
standard is necessary to provide sufficient protection from cumulative,
seasonal exposures to O3.
While a different conclusion on this issue was reached in the 1997
review, the current conclusion that an exposure index that is
cumulative and seasonal in nature, and therefore that setting a
standard based on such a form is necessary and appropriate, is based on
information newly available in the 2008 rulemaking, which strengthens
the information available in the 1997 review and reduces remaining
uncertainties.
Such newly available information includes quantitative information
for a broader array of vegetation effects (extending to sapling and
mature tree growth stages) obtained using a more diverse set of field-
based research study designs and improved analytical methods for
assessing O3-related exposures and risks as discussed above
in sections IV.A-C.
These newly available studies also provide important support to the
quantitative estimates of impaired tree growth based on earlier studies
available in the 1997 review and address one of the key data gaps cited
in the 1997 review. Additional qualitative information is also
available regarding improved understanding of linkages between stress-
related effects of O3 exposures at the species level and
those at higher levels within ecosystems. Finally, this information
includes the use of new analytical methods, including a new multi-
pollutant, multi-scale air quality model used to characterize exposures
of O3-sensitive tree and crop species further address
uncertainties in the assessments done in the 1997 review. In total,
this newly available information increases the Administrator's
confidence in important aspects of this rulemaking
The decision in 2008 to set the secondary O3 standard
identical to the 8-hour primary standard largely mirrored the decision
in 1997, but failed to account for this significant increase in the
body of knowledge available to support the 2008 rulemaking. This body
of knowledge, while continuing to reflect significant uncertainties,
provides an appropriate basis for determining a level of a cumulative,
seasonal standard that, in the judgment of the Administrator, provides
sufficient but not more than necessary protection from cumulative,
seasonal exposures to O3. This is clearly so when compared
to a standard that uses an indirect form that is not biologically
relevant, an 8-hour average standard aimed at peak daily exposures.
This judgment is fully consistent with the advice provided by CASAC.
After carefully taking the above considerations into account, and
giving significant weight to the views of CASAC, the Administrator has
decided to propose a range of levels of 7-15 ppm-hour for a cumulative,
seasonal secondary O3 standard expressed as an index of the
annual sum of weighted hourly concentrations (i.e., the W126 form),
cumulated over 12 hours per day during the consecutive 3-month period
within the O3 season with the maximum index value, averaged
over three years. In the Administrator's judgment, based on the
information available in the 2008 rulemaking, a standard could be set
within this range that would be requisite to protect public welfare
from known or anticipated adverse effects to O3-sensitive
vegetation and ecosystems. In the Administrator's judgment, a standard
set at a level below the lower end of the range is not now supported by
the weight of evidence and would not give sufficient weight to the
important uncertainties and limitations inherent in the available
scientific evidence and in the quantitative assessments conducted for
the 2008 rulemaking. A standard set at a level above the upper end of
the range is also not now supported by the weight of evidence and would
not give sufficient weight to the credible inferences that the Agency
has drawn from the scientific evidence nor to the quantitative
assessments conducted for the 2008 rulemaking. The Administrator judges
that the appropriate balance to be drawn, based on the entire body of
evidence and information available in the 2008 rulemaking, is a range
between 7 and 15 ppm-hour. On balance, the Administrator believes that
a standard could be set within this range that would be sufficient but
not more than necessary to protect public welfare from known or
anticipated adverse effects due to O3.
In reaching this proposed decision, as discussed above, the
Administrator has focused on the nature of the benefits associated with
setting a distinct secondary standard with a cumulative, seasonal form
relative to a standard with a peak daily 8-hour average form, as well
as on assessments that quantify the degree of protection likely to be
afforded by such standards. In so doing, the Administrator has
acknowledged limitations in quantifying the expected benefits
associated with the proposed cumulative seasonal standard relative to
the secondary standard set in 2008. Having considered the public
comments received on the 2007 proposed rule in reaching this proposed
decision, the Administrator is interested in again receiving public
comment on the benefits to public welfare associated with the proposed
cumulative seasonal standard set at specific levels within the proposed
range relative to the standard set in 2008.
[[Page 3027]]
E. Proposed Decision on the Secondary O3 Standard
For the reasons discussed above, and taking into account
information and assessments presented in the 2006 Criteria Document and
2007 Staff Paper, the advice and recommendations of CASAC, and the
public comments received in conjunction with the 2008 rulemaking, the
Administrator has decided to propose to set a new cumulative, seasonal
secondary O3 standard with a form expressed as an index of
the annual sum of weighted hourly concentrations (i.e., the W126 form),
cumulated over 12 hours per day (8 a.m. to 8 p.m.) during the
consecutive 3-month period within the O3 season with the
maximum index value, averaged over three years, set within a range of 7
to 15 ppm-hour. The Administrator solicits comment on the weight that
is appropriately placed on the various types of evidence and analyses
upon which this proposed standard is based, and on the appropriate
weight to be placed on the uncertainties in this information, as well
as on the benefits to public welfare associated with the proposed
standard relative to the benefits associated with the standard set in
2008.
Data handling conventions for the proposed new secondary
O3 standard are specified in the proposed addition of a new
section to 40 CFR 50 Appendix P, as discussed in section V below.
Issues related to monitoring requirements for the proposed new
secondary O3 standard are discussed below in section VI.
V. Interpretation of the NAAQS for O3 and Proposed Revisions
to the Exceptional Events Rule
Appendix P to 40 CFR part 50, Interpretation of the Primary and
Secondary National Ambient Air Quality Standards for Ozone, addresses
data completeness requirements, data reporting, handling, and rounding
conventions, and example calculations. The current Appendix P explains
the computations necessary for determining when the current identical
primary and secondary standards are met. The EPA is proposing to revise
Appendix P to reflect the proposed revisions to the primary and
secondary O3 NAAQS discussed above and to make other changes
described below.
As discussed below, the proposed revisions to Appendix P include
the following: The addition of data interpretation procedures
applicable to the proposed cumulative, seasonal secondary NAAQS (see
section V.B); clarification of certain language in the current
provisions applicable to the primary NAAQS to reduce potential
confusion (section V.C); revisions to the provisions regarding the use
of incomplete data sets for purposes of the primary NAAQS and the data
completeness requirements across three years (sections V.D and V.E);
the addition of a provision providing the Administrator discretion to
use incomplete data as if it were complete, for the purpose of the
primary NAAQS (section V.F); a change from truncation to rounding of
multi-hour and multi-year average O3 concentrations for the
purposes of the primary standard (section V.G); and the addition of
provisions addressing data to be used in making comparisons to the
NAAQS (section V.H). The proposed revisions also include changes in
organization for greater clarity and consistency with other data
interpretation appendices to 40 CFR part 50, which are not further
described in this preamble.
The EPA is also proposing changes to the O3-specific
deadlines, in 40 CFR 50.14, by which states must flag ambient air data
that they believe have been affected by exceptional events and submit
initial descriptions of those events, and the deadlines by which states
must submit detailed justifications to support the exclusion of that
data from EPA determinations of attainment or nonattainment with the
NAAQS. The O3-specific deadlines in the current 40 CFR 50.14
would not be appropriate given the anticipated schedule for the
designations of areas under the proposed revised O3 NAAQS.
A. Background
The purpose of a data interpretation appendix in general is to
provide the practical details on how to make a comparison between
multi-day and possibly multi-monitor ambient air concentration data and
the level of the NAAQS, so that determinations of compliance and
violation are as objective as possible. Data interpretation guidelines
also provide criteria for determining whether there are sufficient data
to make a NAAQS level comparison at all. Appendix P was promulgated in
March 2008 along with the most recent revisions to the primary and
secondary O3 NAAQS. It is very similar to Appendix I,
Interpretation of the 8-Hour Primary and Secondary National Ambient Air
Quality Standards for Ozone, which was adopted in 1997 when the
O3 NAAQS were first revised to have an 8-hour averaging
period rather than the earlier 1-hour averaging period, along with
other changes in form and level. The only substantive difference
between Appendix I and the current version of Appendix P is that
Appendix P contains truncation procedures consistent with the
additional decimal digit used to express the level of the 2008 NAAQS in
parts per million (0.075 ppm) compared to the 1997 NAAQS (0.08 ppm). In
July 2007, EPA had also proposed to include in Appendix P data
interpretation procedures for the proposed cumulative, seasonal
secondary O3 NAAQS, but these procedures were not finalized
given that the final secondary NAAQS was identical in all respects to
the final primary NAAQS.
An exceptional event is defined in 40 CFR 50.1 as an event that
affects air quality, is not reasonably controllable or preventable, is
an event caused by human activity that is unlikely to recur at a
particular location or a natural event, and is determined by the
Administrator in accordance with 40 CFR 50.14 to be an exceptional
event. Air quality data that are determined to have been affected by an
exceptional event under the procedural steps and substantive criteria
specified in section 50.14 may be excluded from consideration when EPA
makes a determination that an area is meeting or violating the
associated NAAQS. The key procedural deadlines in section 50.14 are
that a state must notify EPA that data have been affected by an event,
i.e., ``flag'' the data in the Air Quality Systems (AQS) database, and
provide an initial description of the event by July 1 of the year after
the data are collected, and that the State must submit the full
justification for exclusion within 3 years after the quarter in which
the data were collected. However, if a regulatory decision based on the
data, for example a designation action, is anticipated, the schedule is
shortened and all information must be submitted to EPA no later than a
year before the decision is to be made. This generic schedule presents
problems when a NAAQS has been recently revised, as discussed in
section V.I below. On May 15, 2009, EPA finalized a set of
O3-specific deadlines that corrected these problems at the
time with respect to the 2008 NAAQS revisions (74 FR 23307). However,
because of the anticipated effect of the current reconsideration on the
schedule for O3 designations, the schedule problems will
resurface unless the deadlines are adjusted again.
B. Interpretation of the Secondary O3 Standard
The EPA is proposing data interpretation procedures for the
proposed secondary O3 NAAQS, which is defined in terms of a
specific cumulative, seasonal form, commonly
[[Page 3028]]
referred to as the W126 form, as described above in section IV. The
proposed new section 4 of Appendix P on data interpretation for the
secondary standard contains the following main features.
The ``design value'' for the secondary standard, the statistic for
a monitoring site which would be compared to the level of the secondary
standard to determine if the site meets the standard, would be the
average of the annual maximum values of the three-month index value
from three calendar years.
The new section would provide clear directions and examples for the
calculation of the daily index value, the monthly cumulative index
value, the annual maximum index value for a year, and the design value
itself.
Only the data from the required O3 monitoring season
would be examined to determine the annual maximum index value; any
additional period of monitoring undertaken voluntarily by a state would
not be considered. The EPA believes that because of the recently
proposed extension of the required monitoring seasons in many states
(74 FR 34525, July 16, 2009), as discussed below in section VI, such a
period of voluntary monitoring would be unlikely to have such high
index values as to affect the annual maximum index value. Moreover, the
proposed required monitoring season may encompass the most active
growing season in many areas. The EPA invites comment on whether
instead the entire actual O3 monitoring period should be
considered, to eliminate any possibility that the highest cumulative
index value that can be determined with available data might be missed.
For each month in a three-month period, O3 data would
have to be available for at least 75 percent of daylight hours (defined
for this purpose as 8 a.m.-7:59 p.m. LST). If data are available for at
least 75 percent but fewer than 100 percent of these daylight hours in
a month, the cumulative index value calculated from the available
daylight hours in the month would be increased to compensate for the
missing hours, based on an assumption that the missing hours would have
the same distribution of O3 concentrations as the available
hours. A substitution test is also proposed, by which months in which
fewer than 75 percent of daylight hours have O3
concentration data might also be useable for calculating a valid
cumulative index value. Such months would be used if the available
O3 concentrations are so high that even substituting low
concentration values for enough missing data to meet the 75 percent
requirement would result in a design value greater than the level of
the standard. The low value that would be substituted would be the
lowest 1-hour O3 concentration observed at the monitoring
site during daylight hours during the required O3 monitoring
season, in that calendar year, or one-half the method detection limit
(MDL) of the ozone instrument, whichever is higher.\63\
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\63\ Because only enough missing 1-hour ozone values would be
substituted as needed to meet the 75 percent completeness
requirement, to avoid unreasonable underestimation of the true W126
index, tying the the selection of the substitution value to the hour
of the missing value, as is proposed for data substitution for the
purpose of the primary standard (see section V.D), would introduce
considerable complexity by requiring an algorithm for determining
which specific missing values would be substituted. Therfore, EPA is
proposing this simpler substitution approach for the secondary
standard.
---------------------------------------------------------------------------
The EPA notes that while this proposed approach to identifying the
substitution value for the secondary standard is technically
appropriate, it would necessitate data processing efforts during
implementation that might be avoidable via some other approach that is
also technically reasonable. We therefore invite comment on such
alternative approaches, and we may adopt another approach in the final
rule. For example, for simplicity the substituted 1-hour O3
concentration value could instead simply always be zero or one-half the
MDL of the O3 instrument, noting that because of the
sigmoidal weighting factor the exact magnitude of the low substitution
value may typically make very little difference to the annual index
value. Also, using the previous calendar year as the source of the
substitution value instead of the current calendar year would have the
advantage of allowing all parties to know early in each year what the
substitution value will be.
The EPA is proposing that all decimal digits be retained in
intermediate steps of the calculation of the cumulative index, with the
result rounded to have no decimal digits when expressed in ppm-hours
before comparison the level of the secondary NAAQS.
EPA expects that the three months over which the cumulative
weighted index value is highest will generally occur in the middle of
each year. Therefore, the proposed new section 4 of Appendix P presumes
this, and does not address a situation in which the three months of
maximum cumulative index spans two calendar years, for example December
to February. The EPA invites comment on whether a provision addressing
such a remote possibility is needed and what its terms should be. For
example, the process of checking each three month period in a calendar
year to determine which gives the highest index value could include the
combinations of December/January/February and November/December/January
within one calendar year.
C. Clarifications Related to the Primary Standard
The EPA is proposing two clarifying changes to Appendix P to make
unambiguous two aspects of data interpretation for the primary 8-hour
standard. The first change clarifies that the standard data
completeness requirement that valid daily maximum 8-hour values exist
for 75 percent of all days refers to days within the required
O3 monitoring season only. The current wording of Appendix P
is somewhat open to a reading that the requirement applies to all days
in the actual monitoring record for the site in question, which could
be longer than the required season if a state voluntarily monitors on
additional days, or shorter than the required season if a monitor has
started or ceased operation sometime during the required season. The
O3 data completeness requirement is intended to avoid a
determination that an area has met the NAAQS when in fact more than a
reasonable number of days with high O3 potential were not
successfully monitored. This purpose can be served if the data within
the required O3 monitoring season only are reasonably
complete, because as mentioned above EPA has proposed to revise the
required O3 seasons so that they encompass all days with
potential for an exceedance of even the lowest proposed level for the
primary standard. Unsuccessful monitoring outside the required season
should not be an obstacle to a finding of attainment. However, if an
O3 monitor has missed more than 25 percent of the required
O3 monitoring season, for example because it started or
stopped operation mid-season, this should prevent a finding of
attainment based on a three-year period that includes that season. The
proposed clarifying language reflects EPA's actual intention and our
past practice in applying Appendix P for regulatory purposes, and
Appendix I as well.\64\
---------------------------------------------------------------------------
\64\ At present, EPA's Air Quality System (AQS) for storing and
reporting air quality data provides a completeness report that is
based on yet a third approach, in which the period for reporting
data completeness is the required monitoring season plus any
extension needed to encompass any exceedances that may have occurred
outside the required season. However, EPA's practice for regulatory
purposes has been to consider completeness only over the required
ozone monitoring season.
---------------------------------------------------------------------------
[[Page 3029]]
The second proposed clarifying change would make it clear that when
determining the fourth-highest daily maximum 8-hour O3
concentration for a year, all days with monitoring data are to be
considered, not just days within the required O3 monitoring
season. This proposed clarifying language also reflects EPA's actual
intention and our past practice in applying Appendix P, and Appendix I
as well. While EPA believes it to be quite unlikely that an exceedance
will occur outside the proposed revised required O3
monitoring seasons and have a high enough concentration to affect the
selection of the fourth-highest concentration for the year, when and if
such an occurrence does happen, the data should not be ignored.
D. Revision to Exceptions From Standard Data Completeness Requirements
for the Primary Standard
The EPA is proposing to revise portions of Appendix P that describe
certain exceptions to the standard data completeness requirements,
under which a monitoring site can in some cases be determined to be
meeting or violating the primary NAAQS despite not meeting the standard
data completeness requirements. These changes would make Appendix P
more logical in certain types of cases with incomplete data. While the
particular types of cases whose outcome would be different with these
changes have been rare historically, there may be more such affected
cases in the future in conjunction with a primary O3
standard revised to a level within the range of levels proposed in this
action.
The standard data completeness requirements in Appendix P for the
primary O3 NAAQS apply a 75 percent requirement at each of
three stages of data completeness testing. As discussed below, for each
stage, there is an existing exception to the 75 percent requirement.
In the first stage, an 8-hour period can be considered to have a
valid 8-hour average O3 concentration only if at least 75
percent of the hours, i.e., 6 or more hours, have a valid hourly
O3 value. The provided exception is that if there are 5 or
fewer hours but if substituting a very low value (specifically, one-
half the MDL of the O3 instrument) for all the missing hours
results in a hypothetical 8-hour average that is above the level of the
primary standard, the 8-hour period is considered valid and is assigned
the hypothetical level resulting from the data substitution.\65\ For
example, if the O3 concentration was 0.125 ppm for 5 hours,
substituting a typical MDL/2 value of 0.0025 ppm for three missing
hours would result in an 8-hour average of 0.079 ppm, which is an
exceedance of the current primary standard, so the valid 8-hour average
for the period would be taken to be 0.079 ppm. If this value is higher
than one or more of the highest four daily maximum 8-hour
concentrations otherwise calculated for the year, considering it to be
valid affects the value identified as the fourth-highest for the year
and thus also affects the final design value. The logical problem with
this approach is that it is possible for a hypothetical 8-hour average
with such substitution to be below the level of the NAAQS, thus not
meeting the current condition for the exception, but for it to still
make a critical difference in making the three-year design value be
above the level of the NAAQS, because a three-year design value can
include (and be sensitive to the exact value of) an annual fourth-
highest daily maximum that is not above the level of the NAAQS. This
could be the case if the hypothetical 8-hour average with substitution
is the maximum concentration 8-hour period for its day, and the day is
one of the highest four O3 days of the year. Whether it
actually is the case would further depend on the value of the 8-hour
average itself, the values of the next highest daily maximum 8-hour
average concentration in the year, and the values of the annual fourth-
highest daily maximum 8-hour concentration from the other two years. If
the substituted 8-hour average would make a critical difference, it
should be treated as valid and used in the calculation of the three-
year design value, even if it is not itself above the level of the
standard. Another problem is that one-half of the MDL, which typically
is about 0.0025 ppm, is very likely to be considerably lower than the
actual O3 concentrations that were not successfully
measured. Thus, while the one-half-MDL-substituted value is prevented
from being an overestimate of the actual 8-hour average concentration,
it is an unreasonably low estimate of that concentration which may have
the effect of allowing a site with actual O3 levels above
the standard to be found to meet the standard. The condition in the
exception requiring a one-half-MDL-substituted ``8-hour'' average to be
above the level of the NAAQS is therefore inappropriate.
---------------------------------------------------------------------------
\65\ Actually, it is an interpretation of the text of Appendix
P, section 2.1, that the average resulting from the data
substitution is to be taken as the ``8-hour'' average, rather than
the average of the available 5 or fewer hours of data, which would
be higher. The text is not entirely clear on this point.
---------------------------------------------------------------------------
In the second stage of data completeness testing, 75 percent of the
24 possible 8-hour time blocks, which is 18 or more, must have valid 8-
hour average concentrations values. The intent of this requirement is
to make sure that most of the day was actually monitored, such that the
highest concentration 8-hour period was likely to be captured in the
data. When this is not the case, the day is not considered in selecting
the annual fourth-highest daily maximum 8-hour concentration and no
credit for the day's monitoring is given towards the third stage of
data interpretation (see below). The provided exception in the current
Appendix P is that a day is considered valid if at least one 8-hour
period has an average concentration above the level of the standard.
However, as in the first stage, it is possible for an 8-hour period
with an average concentration at or below the level of the NAAQS to
play a critical role in whether the three-year design value meets the
standard. Invalidating the day could have the effect of causing a lower
value to be selected as the annual fourth-highest daily maximum 8-hour
concentration, leading to a three-year design value that does not
exceed the NAAQS while it would have exceeded if the day and the 8-hour
average value had been treated as valid. The condition in the exception
requiring at least one 8-hour average during the day to be above the
level of the NAAQS is therefore inappropriate.
In the third stage of data completeness testing, a completeness
criterion is applied for the number of days in the required
O3 season that have a valid maximum 8-hour average, i.e.,
days that have met the completeness conditions in the first two stages
or have met the condition for an exception. Specifically, for each of
the three years being used in the design value calculation, the number
of valid days within the required O3 monitoring season (with
no credit for extra days outside the season) must be at least 75
percent of the days in the required O3 season, and the
number of valid days across all three years must be 90 percent of the
days in the three seasons.\66\ The provided exception to the 75/90
percent requirement is that data from a year with less than 75 percent
of seasonal days can nevertheless be used if during the year at least
one day's maximum 8-hour average O3 concentration was
[[Page 3030]]
above the level of the standard and if the three-year design value is
also above the standard.\67\ The problem with this exception, similar
to the problems with the exceptions in the first and second stages of
data completeness testing, is that a daily maximum 8-hour concentration
that is at or below the level of the NAAQS can nevertheless make a
critical difference in making the three-year design value be above the
level of the NAAQS. When it does, an incorrect final result will be
reached if the year of data is not granted an exception to the 75/90
percent requirement. Specifically, there would be no valid three-year
design value and no conclusion would be reached as to attainment or
nonattainment, despite it being clear that the actual situation is
nonattainment, in the sense that successful collection of additional
hours and days of monitoring data could not possibly have resulted in a
passing three-year design value. Moreover, since the three-year design
value is the average of the fourth-highest daily maximum 8-hour
concentration from each year, there is no logical connection between
the design value and the existence of a single daily maximum
concentration greater than the level of the standard, which is the
current condition for the exception for this stage of testing for data
incompleteness.
---------------------------------------------------------------------------
\66\ EPA also is proposing eliminate this 90 percent
requirement, see section V.E. The point made in this paragraph
applies with or without the 90 percent requirement in place.
\67\ EPA notes that in the current versions of Appendix I and P,
it is not explicit that this provided exception also applies in the
case of three years which each have 75 percent or more of days with
valid data but less than 90 percent across three years. Because EPA
is proposing to remove the 90 percent requirement (see section V.E)
this ambiguity does not need correction.
---------------------------------------------------------------------------
EPA proposes to remedy this situation by replacing the three
separate statements of the exceptions to the three standard
completeness requirements with a new data substitution step that
addresses the root cause of the data incompleteness situation: missing
hourly concentrations which make it doubtful whether actual maximum
daily 8-hour concentrations were measured on a reasonably large
percentage of the days during the required O3 monitoring
season of each year. In the event that only 1, 2, 3, 4, or 5 hourly
averages are available for an 8-hour period, a partially substituted 8-
hour average would be computed by substituting for all the hours
without hourly averages a low hourly average value selected as follows,
and then using 8 as the divisor.\68\ For days within the required
O3 monitoring season, the substitution value would be the
lowest hourly average O3 concentration observed for that
hour of the day (local standard time) on any day during the required
O3 monitoring season of that year, or one-half the MDL,
whichever is higher. Using this value makes it highly unlikely that the
resulting partially substituted 8-hour average concentration is higher
than the actual concentration. Therefore, using the partially
substituted 8-hour average in the design value calculation procedure is
highly unlikely to result in an incorrect finding that a site does not
meet the standard, but it may lead to a correct finding that a site
does not meet the standard in some cases in which there would be no
finding possible or an incorrect finding under the current version of
Appendix P. However, the use of the higher of the lowest observed same-
hour concentration or one-half the MDL could be problematic if a robust
set of hourly measurements is not available for the year, for example
if a monitor began operation late in an ozone season. In such a case,
the lowest observed same-hour concentration might not be low enough to
eliminate all possibility that the value used for substitution is
higher than the missing concentration value. To reduce this likelihood
to essentially zero, we are proposing that if the number of same-hour
concentration values available for the required O3
monitoring season for the year is less than 50 percent of the number of
days during the required O3 monitoring season, one-half the
MDL of the O3 instrument would be used in the substitution
instead of the lowest observed concentration. We invite comment on
whether another percentage should be used for this purpose instead of
50 percent.
---------------------------------------------------------------------------
\68\ Appendix P now provides that in the event that only 6 or 7
hourly averages are available, the valid 8-hour average shall be
computed on the basis of the hours available, using 6 or 7 as the
divisor. We are not proposing to change this provision.
---------------------------------------------------------------------------
The EPA notes that while this proposed approach to identifying the
substitution value for the primary standard is technically appropriate,
it would necessitate new data processing efforts during implementation
that might be avoidable via some other approach that is also
technically reasonable. There may also be approaches which are more
technically appropriate. We therefore invite comment on such
alternative approaches, and we may adopt another approach in the final
rule. Examples of simpler approaches would be to identify in the final
rule a fixed substitution value other than one-half the MDL, to accept
as valid 8-hour periods with only five measured hourly concentrations,
to interpret between two hourly concentrations to obtain a substitute
for a single missing hourly concentration, or to use the previous
calendar year as the source of the substitution value instead of the
current calendar year (thereby allowing all parties to know early in
each year what the substitution value will be). Examples of more
complex approaches that might be more technically appropriate include
selecting a low percentile of the available same-hour concentration
data rather than the lowest value to be the substitution value, or
selecting the lowest same-hour value from the same calendar quarter or
month (of the current year or the most recent year) rather than from
the entire required ozone monitoring season. We also invite comment on
whether the proposed approach to substitution should be used at all and
if not what other approach should be used to address the potential
problem just described.
We propose that for simplicity and to further reduce any risk of a
false finding that a site does not meet the standard, for days outside
the required O3 monitoring season, the substitution value
would always be one-half the MDL of the O3 instrument. We
similarly invite comment on this aspect.
There would be no condition that a partially substituted 8-hour
average exceed the level of the standard for it be used in calculating
the design value, unlike is now the case. An 8-hour period with no
available hourly averages at all would not have a valid 8-hour average,
as is now the case.
In addition, to complete the solution to the problems described
above, we are proposing that a design value that is greater than the
level of the primary standard would be valid provided that in each year
there were at least four days with at least one valid 8-hour
concentration.\69\ One or more of these 8-hour average concentrations
could be the partially substituted 8-hour average concentration
resulting from the above described substitution procedure. In such a
case, there is essentially no possibility that more complete monitoring
data would have shown the site to be meeting the NAAQS. It is
appropriate to include all 8-hour averages including those involving
substitution when testing for an exceedance of the standard, because
those averages are extremely unlike to
[[Page 3031]]
be overestimates of actual concentrations.
---------------------------------------------------------------------------
\69\ The requirement that there be at least four days with at
least one hourly measurement is actually redundant and is stated
only for ease of understanding, since there would be no annual
fourth-highest daily maximum 8-hour concentration unless there are
at least four days with monitoring data, and a single hourly data
point is necessary and sufficient (with the proposed substitution
step) to generate a daily maximum 8-hour concentration.
---------------------------------------------------------------------------
Finally, a design value equal to or less than the level of the
standard would be valid only if at least 75 percent of the days in the
required O3 monitoring season of each year have daily
maximum 8-hour concentrations that are based on at least 18 periods
with at least 6 hourly concentrations. This ensures that a site will be
found to meet the standard only when a reasonably high percentage of
the days in the required O3 monitoring season have
reasonably complete hourly data. In this situation, it would be
inappropriate to count the 8-hour periods with five or fewer actual
hourly measurement values towards the 75 percent requirement when
testing for whether a site meets the standard, because those 8-hour
averages will be based on substitution of low values and therefore will
be underestimates of actual concentrations. The only way to be
reasonably certain that no 8-hour period had a high enough
concentration so as to contribute to a design value over the level of
the standard is to have at least 18 periods in which substitution for
missing O3 values was not needed. This provision has the
same effect as several elements of the current Appendix P considered
together, and thus is not a substantive change.
E. Elimination of the Requirement for 90 Percent Completeness of Daily
Data Across Three Years
As stated above in section VI.D, Appendix P currently requires that
in order for a design value equal to or less than the standard to be
valid, at least 75 percent of days in each of three years must have a
valid daily maximum 8-hour average concentration value, i.e., that many
days must have at least 18 8-hour periods with at least 6 reported
hourly concentrations each. Appendix P also requires that the average
of the percentages from three consecutive years be at least 90 percent.
The EPA is proposing to eliminate this 90 percent requirement for the
average of three years and to retain only the requirement that each
individual year have a percentage of at least 75 percent.
The 90 percent requirement was incorporated into Appendix I (the
data interpretation appendix for the 0.08 ppm O3 NAAQS) in
1997 with an explanation that EPA had observed that 90 percent of
O3 monitoring sites routinely achieved 90 percent data
capture. The EPA now notes, however, that while the majority of
monitoring sites do achieve 90 percent or better data capture in any
given year, there are exceptions every year. The 90 percent requirement
applied to the average percentage over three years is quite unforgiving
if there has been one year with relatively low data completeness. For
example, if one year just met the 75 percent requirement, the remaining
two years would have to achieve a 97.5 percent data capture rate in
order for the three years to meet the 90 percent requirement. This
would allow only 4 missed hours of measurements per week, which would
be challenging. The consequences for states could be important, under
the current requirement. One possible result could be that an area
actually in nonattainment with the NAAQS might have to be designated
unclassifiable, although the substitution procedure proposed for cases
of incomplete data, as described above in section VI.D, provides a path
to an appropriate nonattainment finding in at least some cases. Another
possible result is that a nonattainment area which had actually come
into attainment could be unable to receive an attainment determination
until three more years of sufficiently complete data are collected.
This might, for example, result in an area which has achieved needed
emissions reductions by its attainment deadline nevertheless being
bumped up to a higher classification.
The 90 percent requirement over three years has the potential to
treat two areas disparately, for no obvious logical reason. Consider
two areas with identical air quality. Suppose the first area has annual
completeness percentages of 75, 95, and 95 percent (averaging to 85
percent and thus failing the 90 percent requirement) and the second
area has annual completeness percentages of 75, 98, and 98 percent
(averaging to 90 percent). Suppose that the three-year design values in
both areas are below the level of the NAAQS. Practically speaking, the
most important uncertainty about whether each area actually meets the
NAAQS is the low data capture rate in the first year. There is no
obvious logic why the fact that the second area achieves marginally
better data capture in the second and third year should permit it to
receive an attainment finding despite this uncertainty, while the first
area may not.
The EPA also notes that for the other gaseous criteria pollutants--
sulfur dioxide, carbon monoxide and nitrogen dioxide--the completeness
requirement is for 75 percent completeness of hourly measurements in an
individual year.\70\
---------------------------------------------------------------------------
\70\ EPA has recently proposed to amend the completeness
requirements for sulfur dioxide and nitrogen dioxide to add
quarterly 75 percent completeness requirements in connection with
proposals to establish 1-hour primary NAAQS for these pollutants,
still with no requirement for 90 percent completeness across three
years.
---------------------------------------------------------------------------
For these reasons, EPA proposes to eliminate the 90 percent
requirement across three years of data but to retain the 75 percent
requirement for individual years. The EPA notes that as a practical
matter, the current 90 percent requirement in effect requires a minimum
data capture rate somewhat above 75 percent in each year, because if
data capture in any one year were as low as 75 percent the required
data capture in the other years would be very hard to achieve. The
minimum annual data capture rate is effectively somewhere in the range
of 80 percent (implying a requirement to achieve 95 percent data
capture in the two remaining years in order to meet the 90 percent
requirement across three years) and 85 percent (implying a requirement
to achieve 92.5 percent data capture in the two remaining years). The
EPA invites comment on whether instead of retaining the 75 percent
completeness requirement in each individual year, the requirement
should be 80 percent or 85 percent.
F. Administrator Discretion To Use Incomplete Data
The EPA is proposing that the Administrator have general discretion
to use incomplete data to calculate design values that would be treated
as valid for comparison to the NAAQS despite the incompleteness, either
at the request of a state or at her own initiative. Similar provisions
exist already for the PM2.5 and lead NAAQS, and EPA has
recently proposed such provisions to accompany the proposed 1-hour
NO2 and SO2 primary NAAQS. The Administrator
would consider monitoring site closures/moves, monitoring diligence,
and nearby concentrations in determining whether to use such data.
G. Truncation Versus Rounding
Almost all State agencies now report hourly O3
concentrations in parts per million to three decimal places, since the
typical incremental sensitivity of currently used O3
monitors is 0.001 ppm. In the current Appendix P approach, in
calculating 8-hour average O3 concentrations from such
hourly data any calculated digits past the third decimal place are
truncated rather than retained or rounded back to three decimal places.
Also, in calculating 3-year averages of the fourth-highest daily
maximum 8-hour average concentrations, Appendix P currently requires
the result to be reported to the
[[Page 3032]]
third decimal place with digits to the right of the third decimal place
truncated. In this regard, Appendix P follows the precedent of Appendix
I, except that Appendix P is based on a NAAQS level specified to three
decimal places (0.075 ppm) while Appendix I addressed the case of a
NAAQS level specified to only two decimal places (0.08 ppm). In the
rulemaking that concluded in 2008 by establishing the 0.075 ppm level,
EPA noted that the 2007 Staff Paper demonstrated that taking into
account the precision and bias in 1-hour O3 measurements,
the 8-hour design value had an uncertainty of approximately 0.001 ppm.
Thus, EPA considered any value less than 0.001 ppm to be highly
uncertain and, therefore, proposed and adopted truncation to the third
decimal place for reporting 1-hour O3 concentrations and for
both the individual 8-hour averages used to determine the annual fourth
maximum and the 3-year average of the fourth maxima.
The effect of this repeated truncation is that there is a
consistent downward bias in the calculation of the three-year design
value. The size of this bias can be notable. For example, seven hours
with O3 concentrations of 0.076 ppm plus one hour of 0.075
ppm results in an 8-hour average of 0.075 ppm after truncation, nearly
a full 0.001 ppm below the actual 8-hour average of 0.075875 ppm. Seven
hours with O3 concentrations of 0.077 ppm plus one hour of
0.076 ppm results in an 8-hour average of 0.076 ppm after truncation.
One year with the first pattern plus two years with the second pattern
would give a three-year design value of 0.075 ppm, meeting the NAAQS,
even though 23 of the 24 individual 1-hour concentrations involved in
the calculation of the design value were above 0.075 ppm.
The EPA has decided to reconsider this aspect of O3 data
interpretation. Specifically, we are proposing that (1) 1-hour
concentrations continue to be reported to only three decimal places,
the same as is now specified in Appendix P, i.e., that the current
practice of truncation of the 1-hour data to the nearest 0.001 ppm be
retained; (2) all digits resulting from the calculation of 8-hour
averages be retained; and (3) the three-year average of annual fourth-
highest daily maximum 8-hour concentrations be rounded to three decimal
places before comparison to the NAAQS. The EPA continues to believe
that given the uncertainty in individual 1-hour O3
concentration measurements it is appropriate to truncate those
measurements at three decimal places (many O3 instruments
are programmed to only report three digits anyway). However, the
calculations of 8-hour averages and three-year averages are
mathematical steps, not a measurement process subject to uncertainties,
and EPA perceives no logic in having a consistent downward bias by
truncating the results of these mathematical steps. The EPA notes that
the O3 NAAQS is the only NAAQS for which multi-hour, multi-
day, or multi-year averages of concentrations are truncated rather than
rounded. The proposed change will make this aspect of O3
data interpretation consistent with data interpretation procedures for
the other criteria pollutants.
H. Data Selection
The current version of Appendix P does not explicitly address the
issue of what ambient monitoring data for O3 can and must be
compared to the O3 NAAQS. The EPA proposes to add to
Appendix P language addressing this issue. This language is similar to
provisions recently proposed to be included in new data interpretation
appendices for nitrogen dioxide and sulfur dioxide. The new section of
Appendix P would clarify that all quality assured data collected with
approved monitoring methods and known to EPA shall be compared to the
NAAQS, even if not submitted to EPA's Air Quality System. The section
also addresses the question of what O3 data should be used
when two or more O3 monitors have been operating and have
reported data for the same period at one monitoring site.
I. Exceptional Events Information Submission Schedule
States are responsible for identifying air quality data that they
believe warrant special consideration, including data affected by
exceptional events. States identify such data by flagging (making a
notation in a designated field in the electronic data record) specific
values in the Air Quality System (AQS) database. States must flag the
data and submit a justification that the data are affected by
exceptional events if they wish EPA to consider excluding the data in
determining whether or not an area is attaining the new O3
NAAQS.
All states that include areas that could exceed the O3
NAAQS and could therefore be designated as nonattainment for the
O3 NAAQS have the potential to be affected by this
rulemaking. Therefore, this action applies to all states; to local air
quality agencies to which a state has delegated relevant
responsibilities for air quality management including air quality
monitoring and data analysis; and to Tribal air quality agencies where
appropriate. The Exceptional Events Rule preamble describes in greater
detail to whom the rule applies (72 FR 13562-13563, March 22, 2007).
The CAA Section 319(b)(2) authorizes EPA to promulgate regulations
that govern the review and handling of air quality monitoring data
influenced by exceptional events. Under this authority, EPA promulgated
the Exceptional Events Rule (Treatment of Data Influenced by
Exceptional Events (72 FR 13560, March 22, 2007) which sets a schedule
for states to flag monitored data affected by exceptional events in AQS
and for them to submit documentation to demonstrate that the flagged
data values were caused by an exceptional event. Under this schedule, a
state must initially notify EPA that data have been affected by an
exceptional event by July 1 of the year after the data are collected;
this is accomplished by flagging the data in AQS. The state must also
include an initial description of the event when flagging the data. In
addition, the state is required to submit a full demonstration to
justify exclusion of such data within three years after the quarter in
which the data were collected, or if a regulatory decision based on the
data (such as a designation action) is anticipated, the demonstration
must be submitted to EPA no later than one year before the decision is
to be made.
The rule also authorizes EPA to revise data flagging and
documentation schedules for data used in the initial designation of
areas under a new NAAQS. The generic schedule, while appropriate for
the period after initial designations have been made under a NAAQS, may
need adjustment when a new NAAQS is promulgated because until the level
and form of the NAAQS have been promulgated, a state would not have
complete knowledge of the criteria for excluding data. In these cases,
the generic schedule may preclude states from submitting timely flags
and associated documentation for otherwise approvable exceptional
events. This could, if not modified, result in some areas receiving a
nonattainment designation when the NAAQS violations were legitimately
due to exceptional events.
As a result of the Administrator's decision to reconsider the 2008
O3 NAAQS, EPA is proposing to revise the exceptional events
flagging and documentation schedule to correspond to the designations
schedules that EPA is considering for the proposed revisions to the
primary and secondary O3 NAAQS. The designation schedules
[[Page 3033]]
under consideration are discussed in greater detail below in section
VII.A and summarized here. The CAA requires EPA to promulgate the
initial designations for all areas no later than 2 years from the
promulgation of a new NAAQS. Such period may be extended for up to one
year if EPA has insufficient information. (See CAA section 107(d).) For
a new primary O3 standard, EPA intends to issue designations
on an accelerated schedule. For a new seasonal secondary O3
standard, EPA is considering two alternative schedules for initial area
designations.
Primary Standard: If, as a result of the reconsideration, EPA
promulgates a new primary O3 standard on August 31, 2010,
EPA is proposing that state Governors would need to submit their
initial designation recommendations to EPA by January 7, 2011. EPA
would promulgate the final designations in July 2011 to allow
sufficient time for the designations to be published and effective by
August 31, 2011. EPA expects to base the final designations for the
primary O3 standard on three consecutive years of certified
air quality monitoring data from the years 2007-2009 or 2008-2010, if
available. EPA is proposing that for exceptional event claims made for
data years 2007-2009, states must flag and provide an initial
description and detailed documentation by November 1, 2010. For data
collected during data year 2010, EPA is proposing that exceptional
event data that states want EPA to exclude from consideration in the
designations process must be flagged with an initial description and
fully documented by March 1, 2011 or 60 days after the end of the
quarter when the event occurred, whichever date is first. To meet this
proposed 60-day deadline, a state would also have to submit the
O3 concentration data to AQS sooner than the normal deadline
for such submission, which is 90 days after the end of the calendar
quarter. EPA believes this is a reasonable expectation given that most
states currently submit O3 data earlier than the 90-day
deadline.
Secondary Standard: If, as a result of the reconsideration, EPA
promulgates a new seasonal secondary O3 standard by August
31, 2010, EPA is taking comment on two alternative designations
schedules. Under the first alternative, EPA would designate areas for
the secondary standard on the same accelerated schedule discussed above
for the primary standard. Under the second alternative, EPA would
designate areas for the secondary standard on the maximum 2-year
schedule provided under the CAA. Accelerated Schedule: Under the
accelerated schedule for a seasonal secondary O3 NAAQS, EPA
is proposing that for exceptional event claims made for data years
2007-2009, states must flag and provide an initial description and
detailed documentation by November 1, 2010. For data collected during
data year 2010, EPA is proposing that exceptional event data that
states want EPA to exclude from consideration in the designations
process must be flagged with an initial description and fully
documented by March 1, 2011 or 60 days after the end of the quarter
when the event occurred, whichever date is first.
2-year Schedule: Under the 2-year schedule, states would have 1
year, or by August 2011, to submit their designations recommendations
and EPA would finalize designations under the new secondary standard by
August 2012. EPA expects to base final designations for a new seasonal
secondary standard on the most recent three years of certified air
quality monitoring data, which would typically be from the years 2009-
2011 in this case. Exceptional event data claims used from years 2008-
2010 must be flagged with an initial description included in AQS and
submitted with complete documentation supporting such claims by July 1,
2011. Exceptional event data claims from data year 2011 must be flagged
with an initial description and submitted with complete documentation
supporting such claims 60 days after the end of the calendar quarter
when the event occurred or March 1, 2012, whichever occurs first.
Therefore, using the authority provided in CAA section 319(b)(2)
and in the Exceptional Events Rule at 40 CFR 50.14(c)(2)(vi), EPA is
proposing to modify the schedule for data flagging and submission of
demonstrations for exceptional events data considered for initial
designations under the proposed reconsidered O3 primary and
secondary NAAQS, as follows:
Table 1--Schedule for Exceptional Event Flagging and Documentation Submission for Data To Be Used in
Designations Decisions for New NAAQS
----------------------------------------------------------------------------------------------------------------
Air quality
NAAQS Pollutant/standard/(level)/ data collected Event flagging & initial Detailed documentation
promulgation date for calendar description deadline submission deadline
year
----------------------------------------------------------------------------------------------------------------
Primary Ozone/8-Hr Standard (Level TBD)/ 2007-2009 November 1, 2010 \b\...... November 1, 2010.\b\
promulgated by August 31, 2010.
2010 60 Days after the end of 60 Days after the end of
the calendar quarter in the calendar quarter in
which the event occurred which the event occurred
or March 1, 2011, or March 1, 2011,
whichever date occurs whichever date occurs
first.\b\ first.\b\
Secondary Ozone/(Level TBD) Alternative 2008 July 1, 2011\b\........... July 1, 2011.\a\
2-year Schedule--to be promulgated by
August 31, 2010.
2009-2010 July 1, 2011\b\........... July 1, 2011.\b\
2011 60 Days after the end of 60 Days after the end of
the calendar quarter in the calendar quarter in
which the event occurred which the event occurred
or March 1, 2012, or March 1, 2012,
whichever occurs whichever occurs
first.\b\ first.\b\
Secondary Ozone/(Level TBD)--Alternative 2007-2009 November 1, 2010 \b\...... November 1, 2010.\b\
Accelerated Schedule--to be promulgated
by August 31, 2010.
2010 60 Days after the end of 60 Days after the end of
the calendar quarter in the calendar quarter in
which the event occurred which the event occurred
or March 1, 2011, or March 1, 2011,
whichever date occurs whichever date occurs
first.\b\ first.\b\
----------------------------------------------------------------------------------------------------------------
\a\ These dates are unchanged from those published in the original rulemaking.
[[Page 3034]]
\b\ Indicates change from general schedule in 40 CFR 50.14.
Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final
initial designations for new NAAQS. The general schedule applies for all other purposes, most notably, for
data used by EPA for redesignations to attainment.
VI. Ambient Monitoring Related to Proposed O3 Standards
Presently, States (including the District of Columbia, Puerto Rico,
and the Virgin Islands, and including local agencies when so delegated
by the State) are required to operate minimum numbers of EPA-approved
O3 monitors based on the population of each of their
Metropolitan Statistical Areas (MSA) and the most recently measured
O3 levels in each area. Each State (or in some cases
portions of a State) also has a required O3 monitoring
season based on historical experience on when O3 levels are
high enough to be of regulatory or public health concern. These
requirements are contained in 40 CFR part 58 Appendix D, Network Design
Criteria for Ambient Air Quality Monitoring. See section 4.1,
especially Tables D-2 and D-3. These requirements were last revised on
October 17, 2006 as part of a comprehensive review of ambient
monitoring requirements for all criteria pollutants (71 FR 61236).
A. Background
In the 2007 proposed rule for the O3 NAAQS (72 FR
37818), EPA did not propose specific changes to monitoring requirements
to support the proposed NAAQS revisions, but instead solicited comment
on several key matters that were expected to be important issues
affecting the potential redesign of monitoring networks if revisions to
the NAAQS were finalized. These matters included O3
monitoring requirements in urban areas, the potential need for
monitoring to support multiple objectives important to characterization
in non-urban areas including the support of the secondary O3
NAAQS, and the length of the required O3 monitoring seasons.
Comments on these monitoring issues were received during the ensuing
public comment period, and these comments were summarized in the 2008
final rule for the O3 NAAQS (73 FR 16501). As noted in that
action, EPA stated its intention to propose, in a separate rulemaking,
the specific changes to O3 monitoring requirements that were
deemed necessary to support the revised 2008 O3 NAAQS which
set the level of the primary 8-hour O3 standard to 0.075 ppm
and set the secondary standard identical in all respects to the primary
standard. EPA published these proposed changes to O3
monitoring requirements in a proposal dated July 16, 2009, Ambient
Ozone Monitoring Regulations: Revisions to Network Design Requirements
(74 FR 34525). The EPA currently plans to finalize these changes in a
final O3 monitoring rule in 2010, either before or in
conjunction with the final rule on the O3 NAAQS.
In the following sections, the specific provisions of the 2009
O3 monitoring proposal are briefly reviewed, and then
discussed in the context of the proposed revisions of the 2008
O3 NAAQS that have been discussed earlier in this notice.
B. Urban Monitoring Requirements
As noted earlier, current O3 monitoring requirements for
urban areas are based on two factors: MSA population and the most
recent 3-year design value concentrations within each MSA. There are
higher minimum monitoring requirements for areas that have most recent
design values greater than or equal to 85 percent of the NAAQS (i.e.,
design value concentrations that are greater than or equal to 85
percent of the level of the NAAQS), and lower requirements for areas
that have design values less than 85 percent of the NAAQS. These
minimum monitoring requirements for O3 were revised during
the 2006 monitoring rulemaking to ensure that additional monitors would
be required in areas with higher design values and to also ensure that
these requirements would remain applicable through future NAAQS reviews
and potential revisions of the standards. Accordingly, these
requirements do not need to be updated with the revisions of the
O3 NAAQS proposed in this action since the 85 percent
threshold will be applied to the standard levels that are finalized for
the primary and secondary standards.\71\ For example, given the range
of levels of the primary standard being proposed, the level of the 85
percent threshold that requires greater minimum monitoring requirements
ranges from 0.051 ppm (85 percent of 0.060 ppm) to 0.060 ppm (85
percent of 0.070 ppm).
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\71\ The requirements specified in Table D-2 of Appendix D to
part 58, as noted in the third footnote of Table D-2, are applicable
to the levels of the O3 NAAQS as defined in 40 CFR part
50. Accordingly, the 85 percent threshold for requiring higher
minimum monitoring requirements within MSAs would apply to the
proposed levels for the cumulative, seasonal secondary standard as
well as to the proposed levels of the 8-hour primary standard.
---------------------------------------------------------------------------
EPA did propose one change to urban monitoring requirements in the
2009 O3 monitoring proposal. Specifically, EPA proposed to
modify the minimum O3 monitoring requirements to require one
monitor to be placed in MSAs of populations ranging from 50,000 to less
than 350,000 in situations where there is no current monitor and no
history of O3 monitoring within the previous 5 years
indicating a design value of less than 85 percent of the revised
NAAQS.\72\ Since this proposed change to minimum requirements is also
subject to the 85 percent threshold, EPA believes that the proposed
change remains appropriate to support the revisions to the primary and
secondary O3 NAAQS proposed in this action.
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\72\ These MSAs are not currently required to monitor for
O3.
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C. Non-Urban Monitoring Requirements
In the 2007 proposed rule for the O3 NAAQS, EPA
solicited comment on the status of monitoring requirements for non-
urban areas, specifically whether non-urban areas with sensitive
vegetation that are only currently sparsely monitored for O3
could experience undetected violations of the secondary NAAQS as a
result of transport from urban areas with high precursor emissions and/
or O3 concentrations or from formation of additional
O3 from precursors emitted from sources outside urban areas.
Comments that were received in response to the 2009 O3
NAAQS monitoring proposal noted the voluntary nature of most non-urban
O3 monitoring and the resulting relative lack of non-urban
O3 monitors in some areas. These commenters stated that EPA
should consider adding monitoring requirements to support the secondary
NAAQS by requiring O3 monitors in locations that contain
O3-sensitive plants or ecosystems. These commenters also
noted that the placement of current O3 monitors may not be
appropriate for evaluating issues such as vegetation exposure since
many of these monitors were likely located to meet other objectives.
Based on these comments as well as analyses of O3
concentrations from discretionary non-urban monitors located across the
U.S, EPA included new proposed non-urban O3 monitoring
requirements in the 2009 O3 monitoring proposal. These
proposed requirements are intended to satisfy several important
objectives including: (1) Better characterization of O3
concentrations to which O3-sensitive vegetation and
[[Page 3035]]
ecosystems are exposed in rural/remote areas to ensure that potential
secondary NAAQS violations are measured; (2) assessment of
O3 concentrations in smaller communities located outside of
the larger urban MSAs covered by urban monitoring requirements; and (3)
the assessment of the location and severity of maximum O3
concentrations that occur in non-urban areas and may be attributable to
upwind urban sources. For reasons noted below, EPA believes that these
proposed O3 monitoring requirements are sufficient to
support the revisions to the O3 NAAQS proposed in this
action.
With regard to the first objective, we note uncertainties will
remain about the O3 concentrations to which sensitive
natural vegetation and ecosystems are exposed until additional monitors
are sited in National Parks, State and/or tribal areas, wilderness
areas, and other similar locations with sensitive ecosystems that are
set aside to provide similar public welfare benefits. These monitors
would support evaluation of the secondary NAAQS with a more robust data
set than is now available. As noted in the 2009 O3
monitoring proposal, EPA proposed that States operate at least one
monitor to be located in areas such as some Federal, State, Tribal, or
private lands, including wilderness areas that have O3-
sensitive natural vegetation and/or ecosystems. If EPA finalizes a
cumulative, seasonal secondary standard at the lower end of the
proposed range, then it is plausible that additional O3
monitors, above the number required by the monitoring proposal, may be
needed in such areas to provide adequate coverage of locations likely
to experience violations of the revised secondary NAAQS. These
additional monitors could be established through discretionary State
initiatives to supplement minimum monitoring requirements, negotiated
agreements between States and EPA Regional Administrators, or through a
future rulemaking that addresses potential increased O3
monitoring requirements to specifically address the need for additional
monitoring to ensure detection of secondary standard violations.
With regard to the second objective of characterizing elevated
ambient O3 levels to which people are exposed in smaller
communities located outside of the larger urban MSAs, the likelihood of
measuring concentrations that approach or exceed the levels of the
NAAQS due to the transport of O3 from upwind areas and/or
the formation of O3 due to precursor emissions from
industrial sources outside of urban areas is clearly increased due to
the revised NAAQS proposed in this action. Given that the analyses
described in the 2009 O3 monitoring proposal demonstrated
that 50 percent of existing monitors located in such Micropolitan
Statistical Areas \73\ exceeded the current NAAQS and nearly all
monitors recorded design values greater than or equal to 85 percent of
the current NAAQS, the potential for violations in such areas can only
be increased with the NAAQS revisions proposed in this action. As noted
for the first non-urban monitoring objective, it is plausible that
additional O3 monitors, above the number required by the
2009 monitoring proposal may be needed in Micropolitan Statistical
Areas to provide adequate coverage of locations likely to experience
violations of the proposed lower primary NAAQS levels. These additional
monitors could be established through discretionary State initiatives
to supplement minimum monitoring requirements, negotiated requirements
between States and EPA Regional Administrators, or through a future
rulemaking that addresses potential increased O3 monitoring
requirements to specifically address the need for additional monitoring
to ensure detection of primary standard violations in smaller
communities.
---------------------------------------------------------------------------
\73\ Defined as areas having at least one urban cluster of at
least 10,000 but less than a population of 50,000.
---------------------------------------------------------------------------
The third proposed non-urban monitoring objective, requiring
O3 monitors to be located in the area of expected maximum
O3 concentration outside of any MSA, potentially including
the far downwind transport zones of currently well-monitored urban
areas, is not directly related to the level of the O3 NAAQS.
It is instead intended to ensure that all parts of a State meet the
NAAQS and that all necessary emission control strategies have been
included in State Implementation Plans. Accordingly, this proposed
monitoring objective remains applicable independent of revisions to the
O3 NAAQS proposed in this action.
D. Revisions to the Length of the Required O3 Monitoring Seasons
Ozone monitoring is only required during the seasons of the year
that are conducive to O3 formation. These seasons vary in
length as the conditions that determine the likely O3
formation (i.e., seasonally-dependent factors such as ambient
temperature, strength of solar insolation, and length of day) differ by
location. In some locations, conditions conducive to O3
formation are limited to a few summer months of the year while in other
locations these conditions occur year-round. As a result, the length of
currently required O3 monitoring seasons can vary from a
length of 4 months in colder climates to a length of 12 months in
warmer climates.
The 2009 O3 monitoring proposal also addressed the issue
of whether in some areas the required O3 monitoring season
should be made longer. The proposal also addressed the status of any
currently effective Regional Administrator-granted waiver approvals to
O3 monitoring seasons, and the impact of proposed changes to
monitoring requirements on such waiver approvals.
The EPA performed several analyses in support of proposed changes
to the required O3 monitoring seasons. The first analysis
determined the number of observed exceedances of the 0.075 ppm level of
the current 8-hour NAAQS in the months falling outside the currently
required local O3 monitoring season using monitors in areas
that collected O3 data year-round in 2004-2006. The second
analysis examined observed occurrences of daily maximum 8-hour
O3 averages of at least 0.060 ppm. This threshold was chosen
because it represented 80 percent of the current 0.075 ppm NAAQS level
and provides an indicator of ambient conditions that may be conducive
to the formation of O3 concentrations that approach or
exceed the NAAQS. While proposals for revising each State's required
monitoring season were based on observed data in and surrounding each
State, statistically predicted exceedances were also used to validate
conclusions for each State.
The aforementioned analyses provided several results. The analysis
of observed exceedances of the 0.075 ppm level of the current
O3 NAAQS indicated occurrences in eight States during months
outside of the current required monitoring season. The eight States
were Maine, Massachusetts, New Hampshire, New Jersey, New York, South
Carolina, Vermont, and Wyoming. With the exception of Wyoming, these
exceedances occurred in a very limited manner and timeframe, just
before the beginning of these States' required O3 monitoring
season (beginning in these States on April 1). The frequency of
observed occurrences of maximum 8-hour average O3 levels of
at least 0.060 ppm was quite high across the country in months outside
of the current required monitoring season. A total of 32 States
experienced such occurrences; 22 States had such levels only before the
required monitoring season; 9 States had such levels both before and
after the required monitoring
[[Page 3036]]
season; and 1 State had such levels only after the required monitoring
season. In a number of cases, the frequency of such ambient
concentrations was high, with some States experiencing between 31 to 46
out-of-season days during 2004 to 2006 at a high percentage of all
operating year-round O3 monitors.
Based on these analyses, EPA proposed a lengthening of the
O3 monitoring season requirements in many areas. The 2009
proposed changes were based not only on the goal of monitoring out-of-
season O3 NAAQS violations but also on the goal of ensuring
monitoring when ambient O3 levels reach 80 percent of the
NAAQS so that persons unusually sensitive to O3 would be
alerted to potential NAAQS exceedances.
The EPA believes that the factors used to support the 2009 proposed
changes to O3 monitoring seasons are appropriate to support
the revisions of the O3 NAAQS proposed in this action. With
regard to the primary standard, we note that the lower end of the range
being proposed is an 8-hour level of 0.060 ppm, which is identical to
the ambient O3 level that was utilized in one of the
analyses discussed above. Although that level was chosen to provide an
indicator of ambient levels that were below but approaching the level
of the NAAQS and hence to serve as an alert to potential exceedances,
we note that EPA's traditional practice had been to base the length of
required O3 monitoring seasons on the likelihood of
measuring exceedances of the level of the NAAQS. Therefore, if EPA
finalizes the level of the primary standard at the lower end of the
proposed range, the O3 monitoring seasons that have been
proposed as part of the 2009 O3 monitoring proposal would
provide sufficient monitoring coverage to ensure the goal of measuring
potential violations of the primary standard.
One O3 monitoring season issue that was not considered
in the 2009 O3 monitoring proposal was the question of
whether analyses of ambient data based on 8-hour average statistics
would also indicate whether the resulting proposed monitoring seasons
would capture the cumulative maximum consecutive 3-month O3
levels necessary to compute design values based on the secondary NAAQS
proposed in this action, which is defined in terms of a W126 cumulative
peak-weighted index, as discussed above in section IV. If areas
experienced high cumulative index values during months outside of the
required O3 monitoring seasons (based on 8-hour statistics),
then further revisions to the required monitoring seasons might be
necessary to ensure monitoring during all months important to the
calculation of design values for the revised form proposed for the
secondary NAAQS. A related issue is whether such high cumulative
O3 values also occurred during time periods that are
biologically relevant for O3-sensitive vegetation.
The EPA is not proposing additional revisions to O3
monitoring seasons at this time. Additional analyses of the
distribution of elevated cumulative W126 index values will be
conducted, and the biologically relevant seasonal issue will be further
reviewed. Based on the results of these analyses, EPA may consider
proposing further revisions to the O3 monitoring season as
related to the secondary O3 NAAQS.
VII. Implementation of Proposed O3 Standards
A. Designations
After EPA establishes or revises a NAAQS, the CAA directs EPA and
the states to take steps to ensure that the new or revised NAAQS are
met. The first step is to identify areas of the country that do not
meet the new or revised NAAQS. This step is known as the initial area
designations.
The CAA provides that, ``By such date as the Administrator may
reasonably require, but not later than 1 year after promulgation of a
new or revised national ambient air quality standard for any pollutant
under section 109, the Governor of each state shall * * * submit to the
Administrator a list of all areas (or portions thereof) in the state''
that designates those areas as nonattainment, attainment, or
unclassifiable. The CAA specifies that, ``The Administrator may not
require the Governor to submit the required list sooner than 120 days
after promulgating a new or revised national ambient air quality
standard.'' The CAA defines an area as nonattainment if it is violating
the NAAQS or if it is contributing to a violation in a nearby area.
(See CAA section 107(d)(1).)
The CAA further provides, ``Upon promulgation or revision of a
national ambient air quality standard, the Administrator shall
promulgate the designations of all areas (or portions thereof) * * * as
expeditiously as practicable, but in no case later than 2 years from
the date of promulgation of the new or revised national ambient air
quality standard. Such period may be extended for up to one year in the
event the Administrator has insufficient information to promulgate the
designations.'' EPA is required to notify states of any intended
modifications to their recommendations that EPA may deem necessary no
later than 120 days prior to promulgating designations. States then
have an opportunity to demonstrate why any such proposed modification
is inappropriate. Whether or not a state provides a recommendation, EPA
must promulgate the designation that the Agency deems appropriate. (See
CAA section 107(d)(1)(B).)
On September 16, 2009, when the Administrator announced her
decision to reconsider the 2008 O3 NAAQS, she also indicated
that the Agency would work with states to accelerate implementation of
the standards adopted after reconsideration, including the initial area
designations process. Acceleration of designations for the primary
standard would help limit any delays in health protections associated
with the reconsideration of the standards. If a secondary standard
different from the primary standard is adopted, this would be the first
time different primary and secondary standards would be in place for
the O3 standards. While welfare protection is also
important, for the reasons provided below, we are providing alternative
schedules for designating areas for the secondary standard.
If, as a result of the reconsideration, EPA determines that the
record supports a primary standard different from that promulgated in
2008 and promulgates such different primary O3 NAAQS in
2010, EPA intends to promulgate final designations on an accelerated
schedule to allow the designations to be effective in 1 year. In order
to meet such a schedule, EPA is proposing that the deadline for states
to submit their designations recommendations for the revised 2010
primary standard be 129 days after promulgation of that primary
standard. EPA recognizes that the proposed deadline would be an
ambitious schedule. Therefore, EPA intends to provide technical
information and guidance for states as early as possible to facilitate
the development of their recommendations. Many of the areas that would
be violating the proposed primary ozone standard are also violating the
2008 ozone standards. State Governors have provided recommendations on
these areas pursuant to the 2008 standards and recommendations may not
need much further evaluation.
Based on this proposed schedule, if EPA promulgates a new primary
standard on August 31, 2010, state Governors would need to submit their
initial designation recommendations to EPA by January 7, 2011. If the
Administrator intends to modify any state recommendation, EPA would
[[Page 3037]]
notify the Governor no later than March 2011, 120 days prior to
promulgating the final designations. States would then have an
opportunity to comment on EPA's intended designations before EPA
promulgates the final designations. EPA would promulgate the final
designations in July 2011 to allow sufficient time for the designations
to be published and effective by August 31, 2011. EPA expects to base
the final designations for the primary O3 standard on three
consecutive years of certified air quality monitoring data from the
years 2007-2009 or from 2008-2010, if available.
If, as a result of the reconsideration, EPA promulgates a distinct
secondary standard that differs from that promulgated in 2008 and also
differs from the 2010 primary standard, as proposed above, EPA is
proposing two alternative deadlines for states to submit their
designations recommendations. Under the first alternative, EPA would
designate areas for the secondary standard on the same accelerated
schedule discussed above for the primary standard. In order to meet
that schedule, EPA is proposing that states submit their
recommendations for the revised 2010 secondary standard 129 days after
promulgation of that secondary standard. Accordingly, if EPA
promulgates the new secondary standard on August 31, 2010, state
Governors would need to submit their initial designation
recommendations to EPA by January 7, 2011.
Weighing in favor of designating areas for the secondary standard
at the same time as designations for the primary standard is that
planning for both standards would occur on the same schedule. Our
examination of current air quality data from the existing monitoring
network indicates that for levels of the primary and secondary
standards proposed in this action, it is likely that the vast majority
of areas violating the secondary standard would overlap with areas
violating the primary standard. In this case, implementing requirements
for the primary and secondary standards on different schedules could
present resource challenges to state and local agencies by requiring
duplication of effort and hindering consideration of all factors when
deciding which control strategies to adopt for each standard. For
example, if designations for the secondary standard were delayed by a
certain period (e.g., a year) beyond the designations for the primary
standard, then EPA would likely delay submission of attainment SIPs for
the secondary standard for a similar period beyond the proposed date
for submission of the attainment SIPs for the primary standard. In this
case, the initial transportation conformity determination for the
secondary standard would be required later than the initial
determination for the primary standard by the difference in time
between the effective dates of the two designations.
Under the second alternative, EPA would designate areas for the
secondary standard on the maximum 2-year schedule provided under the
CAA. To meet that 2-year schedule, EPA is proposing that states submit
their recommendations for the revised secondary standard no later than
1 year after promulgation of the 2010 secondary standard. Accordingly,
if EPA promulgates a secondary standard on August 31, 2010, that
differs from the primary standard, as proposed, under the alternative
2-year designations schedule, state Governors would need to submit
their initial designation recommendations to EPA by August 31, 2011. If
the Administrator intends to modify any state recommendation, EPA would
notify the Governor no later than May 2012, 120 days prior to the 2-
year deadline for promulgating the final designations. States would
then have an opportunity to comment on EPA's intended designations
before EPA promulgates the final designations. EPA would promulgate the
final designations for the secondary standard by August 31, 2012. EPA
expects to base the final designations in August 2012 for a different
secondary standard on the most recent three consecutive years of
certified air quality monitoring data, which would be from the years
2009-2011.
In the past, EPA has always set the secondary O3
standard to be identical to the primary O3 standard and the
standards have embodied relatively short-term average concentrations
(e.g., 1-hour or 8-hour). In this action, EPA is proposing a
cumulative, seasonal secondary standard that differs from the proposed
primary standard. EPA has not previously set a seasonal secondary
standard for O3. Therefore, EPA and states do not have
experience in implementing this type of secondary O3
standard or in determining what area boundaries would be appropriate.
As we further explore implementation considerations for the secondary
standard, we may encounter unanticipated issues that may require
additional time to address. Thus, EPA is considering whether an
accelerated schedule for a seasonal secondary standard would provide
adequate time for resolving issues that we cannot now anticipate. If
EPA designates areas for the secondary standard on a 2-year schedule,
we note that we expect that accelerated implementation of the health-
based primary standard would also result in accelerated welfare
benefits. EPA requests comment on factors affecting the efficient and
effective implementation of a secondary standard that differs from the
primary standard in the context of establishing designations schedules.
EPA notes, as discussed in greater detail above in section VI, that
it has proposed a monitoring rule that would increase the density of
monitoring in National Parks and other non-urban and lesser populated
areas (July 16, 2009; 74 FR 34525). The proposed requirements are
intended to satisfy several important objectives, including better
characterization of O3 exposures to O3-sensitive
vegetation and ecosystems in rural/remote areas to ensure that
potential secondary NAAQS violations are measured. As proposed, the new
monitors would not be deployed until 2012 or 2013. Therefore, data from
these monitors would not be available for use within the statutory
timeframe for EPA to complete designations for a 2010 secondary
standard regardless of which schedule EPA follows.
While CAA section 107 specifically addresses states, EPA intends to
follow the same process for tribes to the extent practicable, pursuant
to section 301(d) of the CAA regarding tribal authority, and the Tribal
Authority Rule (63 FR 7254; February 12, 1998).
In a separate notice elsewhere in today's Federal Register, EPA is
announcing that it is using its authority under the CAA to extend by 1
year the deadline for promulgating initial area designations for the
O3 NAAQS that were promulgated in March 2008. The new
deadline is March 12, 2011. That notice explains the basis for the
deadline extension. As mentioned above, on September 16, 2009, EPA
notified the Court of its decision to initiate a rulemaking to
reconsider the primary and secondary O3 NAAQS set in March
2008 to ensure they satisfy the requirements of the CAA. In its notice
to the Court, EPA stated that the final rule would be signed by August
31, 2010. Extending the deadline for promulgating designations for the
2008 O3 NAAQS until March 12, 2011 will allow EPA to
complete the reconsideration rulemaking for the 2008 O3
NAAQS before determining whether it is necessary to finalize
designations for those NAAQS or, instead, whether it is necessary to
begin the designation process for different NAAQS promulgated pursuant
to the reconsideration.
[[Page 3038]]
B. State Implementation Plans
The CAA section 110 provides the general requirements for SIPs.
Within 3 years after the promulgation of new or revised NAAQS (or such
shorter period as the Administrator may prescribe) each State must
adopt and submit ``infrastructure'' SIPs to EPA to address the
requirements of section 110(a)(1). Thus, States should submit these
SIPs no later than August 21, 2013, three years after promulgation of
the reconsidered ozone standard in 2010. These ``infrastructure SIPs''
provide assurances of State resources and authorities, and establish
the basic State programs, to implement, maintain, and enforce new or
revised standards.
In addition to the infrastructure SIPs, which apply to all States,
CAA title I, part D outlines the State requirements for achieving clean
air in designated nonattainment areas. These requirements include
timelines for when designated nonattainment areas must attain the
standards, deadlines for developing SIPs that demonstrate how the State
will ensure attainment of the standards, and specific emissions control
requirements. EPA plans to address how these requirements, such as
attainment demonstrations and attainment dates, reasonable further
progress, new source review, conformity, and other implementation
requirements, apply to the O3 NAAQS promulgated pursuant to
the reconsideration in a subsequent rulemaking. Also in that rulemaking
EPA will establish deadlines for submission of nonattainment area SIPs
but anticipates that the deadlines will be no later than the end of
December 2013, or 28 months after final designations.
C. Trans-Boundary Emissions
Cross border O3 contributions from within North America
(Canada and Mexico) entering the U.S. are generally thought to be
small. Section 179B of the Clean Air Act allows designated
nonattainment areas to petition EPA to consider whether such a locality
might have met a clean air standard ``but for'' cross border
contributions. To date, few areas have petitioned EPA under this
authority. The impact of foreign emissions on domestic air quality in
the United States is a challenging and complex problem to assess. EPA
is engaged in a number of activities to improve our understanding of
international transport. As work progresses on these activities, EPA
will be able to better address the uncertainties associated with trans-
boundary flows of air pollution and their impacts.
VIII. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
Under section 3(f)(1) of Executive Order (EO) 12866 (58 FR 51735,
October 4, 1993), the O3 NAAQS action is an ``economically
significant regulatory action'' because it is likely to have an annual
effect on the economy of $100 million or more. Accordingly, EPA
submitted this action to the Office of Management and Budget (OMB) for
review under EO 12866 and any changes made in response to OMB
recommendations have been documented in the docket for this action. In
addition, EPA prepared this regulatory impact analysis (RIA) of the
potential costs and benefits associated with this action. This analysis
is contained in the Regulatory Impact Analysis for the Ozone NAAQS
Reconsideration, October 2009 (henceforth, ``RIA''). A copy of the
analysis is available in the RIA docket (EPA-HQ-OAR-2007-0225) and the
analysis is briefly summarized here. The RIA estimates the costs and
monetized human health and welfare benefits of attaining five
alternative O3 NAAQS nationwide. Specifically, the RIA
examines the alternatives of 0.079 ppm, 0.075 ppm, 0.070 ppm, 0.065
ppm, and 0.060 ppm. The RIA contains illustrative analyses that
consider a limited number of emissions control scenarios that States
and Regional Planning Organizations might implement to achieve these
alternative O3 NAAQS. However, the Clean Air Act (CAA) and
judicial decisions make clear that the economic and technical
feasibility of attaining ambient standards are not to be considered in
setting or revising NAAQS, although such factors may be considered in
the development of State plans to implement the standards. Accordingly,
although an RIA has been prepared, the results of the RIA have not been
considered in issuing this proposed rule.
B. Paperwork Reduction Act
This action does not impose an information collection burden under
the provisions of the Paperwork Reduction Act, 44 U.S.C. 3501 et seq.
There are no information collection requirements directly associated
with the establishment of a NAAQS under section 109 of the CAA.
Burden means the total time, effort, or financial resources
expended by persons to generate, maintain, retain, or disclose or
provide information to or for a Federal agency. This includes the time
needed to review instructions; develop, acquire, install, and utilize
technology and systems for the purposes of collecting, validating, and
verifying information, processing and maintaining information, and
disclosing and providing information; adjust the existing ways to
comply with any previously applicable instructions and requirements;
train personnel to be able to respond to a collection of information;
search data sources; complete and review the collection of information;
and transmit or otherwise disclose the information.
An agency may not conduct or sponsor, and a person is not required
to respond to a collection of information unless it displays a
currently valid OMB control number. The OMB control numbers for EPA's
regulations in 40 CFR are listed in 40 CFR part 9.
C. Regulatory Flexibility Act
The Regulatory Flexibility Act (RFA) generally requires an agency
to prepare a regulatory flexibility analysis of any rule subject to
notice and comment rulemaking requirements under the Administrative
Procedure Act or any other statute unless the agency certifies that the
rule will not have a significant economic impact on a substantial
number of small entities. Small entities include small businesses,
small organizations, and small governmental jurisdictions.
For purposes of assessing the impacts of today's proposed rule on
small entities, small entity is defined as: (1) A small business that
is a small industrial entity as defined by the Small Business
Administration's (SBA) regulations at 13 CFR 121.201; (2) a small
governmental jurisdiction that is a government of a city, county, town,
school district or special district with a population of less than
50,000; and (3) a small organization that is any not-for-profit
enterprise which is independently owned and operated and is not
dominant in its field.
After considering the economic impacts of today's proposed rule on
small entities, I certify that this action will not have a significant
economic impact on a substantial number of small entities. This
proposed rule will not impose any requirements on small entities.
Rather, this rule establishes national standards for allowable
concentrations of O3 in ambient air as required by section
109 of the CAA. See also American Trucking Associations v. EPA. 175 F.
3d at 1044-45 (NAAQS do not have significant impacts upon small
[[Page 3039]]
entities because NAAQS themselves impose no regulations upon small
entities). We continue to be interested in the potential impacts of the
proposed rule on small entities and welcome comments on issues related
to such impacts
D. Unfunded Mandates Reform Act
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public
Law 104-4, establishes requirements for Federal agencies to assess the
effects of their regulatory actions on State, local, and Tribal
governments and the private sector. Under section 202 of the UMRA, EPA
generally must prepare a written statement, including a cost-benefit
analysis, for proposed and final rules with ``Federal mandates'' that
may result in expenditures to State, local, and Tribal governments, in
the aggregate, or to the private sector, of $100 million or more in any
1 year. Before promulgating an EPA rule for which a written statement
is needed, section 205 of the UMRA generally requires EPA to identify
and consider a reasonable number of regulatory alternatives and to
adopt the least costly, most cost-effective or least burdensome
alternative that achieves the objectives of the rule. The provisions of
section 205 do not apply when they are inconsistent with applicable
law. Moreover, section 205 allows EPA to adopt an alternative other
than the least costly, most cost-effective or least burdensome
alternative if the Administrator publishes with the final rule an
explanation why that alternative was not adopted. Before EPA
establishes any regulatory requirements that may significantly or
uniquely affect small governments, including Tribal governments, it
must have developed under section 203 of the UMRA a small government
agency plan. The plan must provide for notifying potentially affected
small governments, enabling officials of affected small governments to
have meaningful and timely input in the development of EPA regulatory
proposals with significant Federal intergovernmental mandates, and
informing, educating, and advising small governments on compliance with
the regulatory requirements.
Today's proposed rule contains no Federal mandates (under the
regulatory provisions of Title II of the UMRA) for State, local, or
Tribal governments or the private sector. The proposed rule imposes no
new expenditure or enforceable duty on any State, local or Tribal
governments or the private sector, and EPA has determined that this
proposed rule contains no regulatory requirements that might
significantly or uniquely affect small governments. Furthermore, as
indicated previously, in setting a NAAQS EPA cannot consider the
economic or technological feasibility of attaining ambient air quality
standards, although such factors may be considered to a degree in the
development of State plans to implement the standards. See also
American Trucking Associations v. EPA, 175 F. 3d at 1043 (noting that
because EPA is precluded from considering costs of implementation in
establishing NAAQS, preparation of a Regulatory Impact Analysis
pursuant to the Unfunded Mandates Reform Act would not furnish any
information which the court could consider in reviewing the NAAQS).
Accordingly, EPA has determined that the provisions of sections 202,
203, and 205 of the UMRA do not apply to this proposed decision. The
EPA acknowledges, however, that any corresponding revisions to
associated SIP requirements and air quality surveillance requirements,
40 CFR part 51 and 40 CFR part 58, respectively, might result in such
effects. Accordingly, EPA will address, as appropriate, unfunded
mandates if and when it proposes any revisions to 40 CFR parts 51 or
58.
E. Executive Order 13132: Federalism
Executive Order 13132, entitled ``Federalism'' (64 FR 43255, August
10, 1999), requires EPA to develop an accountable process to ensure
``meaningful and timely input by State and local officials in the
development of regulatory policies that have federalism implications.''
``Policies that have federalism implications'' is defined in the
Executive Order to include regulations that have ``substantial direct
effects on the States, on the relationship between the national
government and the States, or on the distribution of power and
responsibilities among the various levels of government.''
This proposed rule does not have federalism implications. It will
not have substantial direct effects on the States, on the relationship
between the national government and the States, or on the distribution
of power and responsibilities among the various levels of government,
as specified in Executive Order 13132. The rule does not alter the
relationship between the Federal government and the States regarding
the establishment and implementation of air quality improvement
programs as codified in the CAA. Under section 109 of the CAA, EPA is
mandated to establish NAAQS; however, CAA section 116 preserves the
rights of States to establish more stringent requirements if deemed
necessary by a State. Furthermore, this proposed rule does not impact
CAA section 107 which establishes that the States have primary
responsibility for implementation of the NAAQS. Finally, as noted in
section E (above) on UMRA, this rule does not impose significant costs
on State, local, or Tribal governments or the private sector. Thus,
Executive Order 13132 does not apply to this rule.
However, as also noted in section D (above) on UMRA, EPA recognizes
that States will have a substantial interest in this rule and any
corresponding revisions to associated SIP requirements and air quality
surveillance requirements, 40 CFR part 51 and 40 CFR part 58,
respectively. Therefore, in the spirit of Executive Order 13132, and
consistent with EPA policy to promote communications between EPA and
State and local governments, EPA specifically solicits comment on this
proposed rule from State and local officials.
F. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments
Executive Order 13175, entitled ``Consultation and Coordination
with Indian Tribal Governments'' (65 FR 67249, November 9, 2000),
requires EPA to develop an accountable process to ensure ``meaningful
and timely input by tribal officials in the development of regulatory
policies that have tribal implications.'' This rule concerns the
establishment of O3 NAAQS. The Tribal Authority Rule gives
Tribes the opportunity to develop and implement CAA programs such as
the O3 NAAQS, but it leaves to the discretion of the Tribe
whether to develop these programs and which programs, or appropriate
elements of a program, they will adopt.
This proposed rule does not have Tribal implications, as specified
in Executive Order 13175. It does not have a substantial direct effect
on one or more Indian Tribes, since Tribes are not obligated to adopt
or implement any NAAQS. Thus, Executive Order 13175 does not apply to
this rule.
Although Executive Order 13175 does not apply to this rule, EPA
contacted tribal environmental professionals during the development of
the March 2008 rule. The EPA staff participated in the regularly
scheduled Tribal Air call sponsored by the National Tribal Air
Association during the spring of 2007 as the proposal was under
development. EPA specifically solicits additional comment on this
proposed rule from Tribal officials.
[[Page 3040]]
G. Executive Order 13045: Protection of Children From Environmental
Health and Safety Risks
Executive Order 13045, ``Protection of Children from Environmental
Health Risks and Safety Risks'' (62 FR 19885, April 23, 1997) applies
to any rule that: (1) Is determined to be ``economically significant''
as defined under Executive Order 12866, and (2) concerns an
environmental health or safety risk that EPA has reason to believe may
have a disproportionate effect on children. If the regulatory action
meets both criteria, the Agency must evaluate the environmental health
or safety effects of the planned rule on children, and explain why the
planned regulation is preferable to other potentially effective and
reasonably feasible alternatives considered by the Agency.
This proposed rule is subject to Executive Order 13045 because it
is an economically significant regulatory action as defined by
Executive Order 12866, and we believe that the environmental health
risk addressed by this action may have a disproportionate effect on
children. The proposed rule will establish uniform national ambient air
quality standards for O3; these standards are designed to
protect public health with an adequate margin of safety, as required by
CAA section 109. However, the protection offered by these standards may
be especially important for children because children, especially
children with asthma, along with other sensitive population subgroups
such as all people with lung disease and people active outdoors, are
potentially susceptible to health effects resulting from O3
exposure. Because children are considered a potentially susceptible
population, we have carefully evaluated the environmental health
effects of exposure to O3 pollution among children.
Discussions of the results of the evaluation of the scientific
evidence, policy considerations, and the exposure and risk assessments
pertaining to children are contained in sections II.B and II.C of this
preamble. A listing of the documents that contain the evaluation of
scientific evidence, policy considerations, and exposure and risk
assessments that pertain to children is found in the section on
Children's Environmental Health in the Supplementary Information
section of this preamble, and a copy of all documents have been placed
in the public docket for this action. The public is invited to submit
comments or identify peer-reviewed studies and data that assess effects
of early life exposure to O3.
H. Executive Order 13211: Actions That Significantly Affect Energy
Supply, Distribution or Use
This proposed rule is not a ``significant energy action'' as
defined in Executive Order 13211, ``Actions Concerning Regulations That
Significantly Affect Energy Supply, Distribution, or Use'' (66 FR 28355
(May 22, 2001)) because in the Agency's judgment it is not likely to
have a significant adverse effect on the supply, distribution, or use
of energy. The purpose of this rule is to establish revised NAAQS for
O3. The rule does not prescribe specific pollution control
strategies by which these ambient standards will be met. Such
strategies will be developed by States on a case-by-case basis, and EPA
cannot predict whether the control options selected by States will
include regulations on energy suppliers, distributors, or users. Thus,
EPA concludes that this rule is not likely to have any adverse energy
effects and does not constitute a significant energy action as defined
in Executive Order 13211.
I. National Technology Transfer and Advancement Act
Section 12(d) of the National Technology Transfer and Advancement
Act of 1995 (NTTAA), Public Law 104-113, section 12(d) (15 U.S.C. 272
note) directs EPA to use voluntary consensus standards in its
regulatory activities unless to do so would be inconsistent with
applicable law or otherwise impractical. Voluntary consensus standards
are technical standards (e.g., materials specifications, test methods,
sampling procedures, and business practices) that are developed or
adopted by voluntary consensus standards bodies. The NTTAA directs EPA
to provide Congress, through OMB, explanations when the Agency decides
not to use available and applicable voluntary consensus standards.
This proposed rulemaking does not involve technical standards.
Therefore, EPA is not considering the use of any voluntary consensus
standards.
J. Executive Order 12898: Federal Actions To Address Environmental
Justice in Minority Populations and Low-Income Populations
Executive Order 12898 (59 FR 7629 (Feb. 16, 1994)) establishes
federal executive policy on environmental justice. Its main provision
directs federal agencies, to the greatest extent practicable and
permitted by law, to make environmental justice part of their mission
by identifying and addressing, as appropriate, disproportionately high
and adverse human health or environmental effects of their programs,
policies, and activities on minority populations and low-income
populations in the United States.
EPA has determined that this proposed rule will not have
disproportionately high and adverse human health or environmental
effects on minority or low-income populations because it increases the
level of environmental protection for all affected populations without
having any disproportionately high and adverse human health or
environmental effects on any population, including any minority or low-
income population. The proposed rule will establish uniform national
standards for O3 air pollution.
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particles and sulfur dioxides on preterm delivery: a community-based
cohort study. Arch. Environ. Health 50: 407-415.
Young, T. F.; Sanzone, S., eds. (2002) A framework for assessing and
reporting on ecological condition: an SAB report. Washington, DC:
U.S. Environmental Protection Agency, Science Advisory Board; report
no. EPA-SAB-EPEC-02-009. Available online at: http://
yosemite.epa.gov/sab/sabproduct.nsf/
C3F89E598D843B58852570CA0075717E/$File/epec02009a.pdf.
Zeger, S. L.; Thomas, D.; Dominici, F.; Samet, J. M.; Schwartz, J.;
Dockery, D.; Cohen, A. (2000) Exposure measurement error in time-
series studies of air pollution: concepts and consequences. Environ.
Health Perspect. 108: 419-426.
Zhang, L.-Y.; Levitt, R. C.; Kleeberger, S. R. (1995) Differential
susceptibility to ozone-induced airways hyperreactivity in inbred
strains of mice. Exp. Lung Res. 21: 503-518.
Zidek, J. V.; White, R.; Le, N. D.; Sun, W.; Burnett, R. T. (1998)
Imputing unmeasured explanatory variables in environmental
epidemiology with application to health impact analysis of air
pollution. Environ. Ecol. Stat. 5: 99-115.
List of Subjects in 40 CFR Parts 50 and 58
Environmental protection, Air pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.
Dated: January 6, 2010.
Lisa P. Jackson,
Administrator.
For the reasons set forth in the preamble, parts 50 and 58 of
chapter 1 of title 40 of the code of Federal regulations are proposed
to be amended as follows:
PART 50--NATIONAL PRIMARY AND SECONDARY AMBIENT AIR QUALITY
STANDARDS
1. The authority citation for part 50 continues to read as follows:
Authority: 42 U.S.C. 7401 et seq.
2. Section 50.15 is revised to read as follows:
Sec. 50.15 National primary and secondary ambient air quality
standards for ozone.
(a) The level of the national 8-hour primary ambient air quality
standard for O3 is (0.060-0.070) parts per million (ppm),
daily maximum 8-hour average, measured by a reference method based on
Appendix D to this part and designated in accordance with part 53 of
this chapter or an equivalent method designated in accordance with part
53 of this chapter.
(b) The 8-hour primary O3 ambient air quality standard
is met at an ambient air quality monitoring site when the average of
the annual fourth-highest daily maximum 8-hour average O3
concentration is less than or equal to (0.060-0.070) ppm, as determined
in accordance with appendix P to this part.
(c) The level of the national secondary ambient air quality
standard for O3 is a cumulative index value of (7-15) ppm-
hours, measured by a reference method based on Appendix D to this part
and designated in accordance with part 53 of this chapter or an
equivalent method designated in accordance with part 53 of this
chapter.
(d) The secondary O3 ambient air quality standard is a
seasonal standard expressed as a sum of weighted hourly concentrations,
cumulated over the 12 hour daylight period from 8 a.m. to 8 p.m. local
standard time, during the consecutive 3-month period within the
O3 monitoring season with the maximum index value. The
secondary O3 standard is met at an ambient air quality
monitoring site when the annual maximum consecutive 3-month cumulative
index value (W126) is less than or equal to (7-15) ppm-hours, as
determined in accordance with appendix P to this part.
3. Section 50.14 is amended by adding entries for primary and
secondary ozone standards to the end of Table 1 in paragraph (c)(2)(vi)
to read as follows:
Sec. 50.14 Treatment of air quality monitoring data influenced by
exceptional events.
* * * * *
(c) * * *
(2) * * *
(vi) * * *
Table 1--Schedule for Exceptional Event Flagging and Documentation Submission for Data To Be Used in
Designations Decisions for New NAAQS
----------------------------------------------------------------------------------------------------------------
Air quality
NAAQS pollutant/ standard/(level)/ data collected Event flagging & initial Detailed documentation
promulgation date for calendar description deadline submission deadline
year
----------------------------------------------------------------------------------------------------------------
* * * * * * *
Primary Ozone/8-Hr...................... 2007-2009 November 1, 2010 \b\...... November 1, 2010.\b\
Standard (Level TBD)/promulgated by 2010 60 Days after the end of 60 Days after the end of
August 31, 2010. the calendar quarter in the calendar quarter in
which the event occurred which the event occurred
or March 1, 2011, or March 1, 2011,
whichever date occurs whichever date occurs
first.\b\ first.\b\
Secondary Ozone/(Level TBD) Alternative 2008 July 1, 2011 \b\.......... July 1, 2011.\a\
2-year Schedule--to be Promulgated by
August 31, 2010.
2009-2010 July 1, 2011 \b\.......... July 1, 2011.\b\
2011 60 Days after the end of 60 Days after the end of
the calendar quarter in the calendar quarter in
which the event occurred which the event occurred
or March 1, 2012, or March 1, 2012,
whichever occurs whichever occurs
first.\b\ first.\b\
Secondary Ozone/(Level TBD)--Alternative 2007-2009 November 1, 2010 \b\...... November 1, 2010.\b\
Accelerated Schedule--to be promulgated
by August 31, 2010.
2010 60 Days after the end of 60 Days after the end of
the calendar quarter in the calendar quarter in
which the event occurred which the event occurred
or March 1, 2011, or March 1, 2011,
whichever date occurs whichever date occurs
first.\b\ first.\b\
[[Page 3049]]
* * * * * * *
----------------------------------------------------------------------------------------------------------------
\a\ These dates are unchanged from those published in the original rulemaking.
\b\ Indicates change from general schedule in 40 CFR 50.14.
Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final
initial designations for new NAAQS. The general schedule applies for all other purposes, most notably, for
data used by EPA for redesignations to attainment.
4. Appendix P to part 50 is revised to read as follows:
Appendix P to Part 50--Interpretation of the Primary and Secondary
National Ambient Air Quality Standards for Ozone
1. General
(a) This appendix explains the data handling conventions and
computations necessary for determining whether the 8-hour primary
and secondary national ambient air quality standards for ozone
specified in Sec. 50.15 are met at an ambient ozone air quality
monitoring site. Ozone is measured in the ambient air by a reference
method based on Appendix D of this part, as applicable, and
designated in accordance with part 53 of this chapter, or by an
equivalent method designated in accordance with part 53 of this
chapter. Data reporting, data handling, and computation procedures
to be used in making comparisons between reported ozone
concentrations and the levels of the ozone standards are specified
in the following sections.
(b) Whether to exclude, retain, or make adjustments to the data
affected by exceptional events, including stratospheric ozone
intrusion and other natural events, is determined by the
requirements under Sec. Sec. 50.1, 50.14 and 51.930.
(c) The terms used in this appendix are defined as follows:
8-hour average is the rolling average of eight hourly ozone
concentrations as explained in section 3 of this appendix.
Annual fourth-highest daily maximum refers to the fourth-highest
value measured at a monitoring site during a particular year.
Annual Cumulative W126 Index is the maximum sum over three
consecutive calendar months of the monthly W126 index in a year, as
explained in section 4 of this appendix.
Daily maximum 8-hour average concentration refers to the maximum
calculated 8-hour average for a particular day as explained in
section 3 of this appendix.
Daily W126 Index is the sum of the sigmoidally weighted hourly
ozone concentrations during the 12-hour daylight period, 8 a.m. to
7:59 p.m. local standard time (LST).
Design values are the metrics (i.e., statistics) that are
compared to the primary and secondary NAAQS levels to determine
compliance, calculated as shown in sections 3 and 4 of this
appendix.
Monthly W126 Index is the sum of the daily W126 index over one
calendar month during the required ozone monitoring season, adjusted
for incomplete data if appropriate, as explained in section 4 of
this appendix.
Required ozone monitoring season refers to the span of time
within a calendar year when individual States are required to
measure ambient ozone concentrations as listed in part 58 Appendix D
to this chapter.
Year refers to calendar year.
2. Requirements for Data Used for Comparisons With the Ozone NAAQS
(a) All valid FRM/FEM ozone data submitted to EPA's Air Quality
System (AQS), or otherwise available to EPA, meeting the
requirements of part 58 of this chapter including appendices A, C,
and E shall be used in design value calculations.
(b) When two or more ozone monitors are operated at a site, the
state may in advance designate one of them as the primary monitor.
If the state has not made this designation, the Administrator will
make the designation, either in advance or retrospectively. Design
values will be developed using only the data from the primary
monitor, if this results in a valid design value. If data from the
primary monitor do not allow the development of a valid design
value, data solely from the other monitor(s) will be used in turn to
develop a valid design value, if this results in a valid design
value. If there are three or more monitors, the order for such
comparison of the other monitors will be determined by the
Administrator. The Administrator may combine data from different
monitors in different years for the purpose of developing a valid
primary or secondary standard design value, if a valid design value
cannot be developed solely with the data from a single monitor.
However, data from two or more monitors in the same year at the same
site will not be combined in an attempt to meet data completeness
requirements, except if one monitor has physically replaced another
instrument permanently, in which case the two instruments will be
considered to be the same monitor, or if the state has switched the
designation of the primary monitor from one instrument to another
during the year.
(c) Hourly average concentrations shall be reported in parts per
million (ppm) to the third decimal place, with additional digits to
the right of the third decimal place truncated. The start of each
hour shall be identified in local standard time (LST).
3. Comparison to the Primary Standard for Ozone
(a) Computing 8-Hour Averages
Running 8-hour averages shall be computed from the hourly ozone
concentration data for each hour of the year and shall be stored in
the first, or start, hour of the 8-hour period. In the event that
only 6 or 7 hourly averages are available, the valid 8-hour average
shall be computed on the basis of the hours available, using 6 or 7
as the divisor. In the event that only 1, 2, 3, 4, or 5 hourly
averages are available, the 8-hour average shall be computed on the
basis of substituting for all the hours without hourly averages a
low hourly average value selected as follows, using 8 as the
divisor. For days within the required ozone monitoring season, the
substitution value shall be the lowest hourly average ozone
concentration observed during the same hour (local standard time) of
any day in the required ozone monitoring season of that year, or
one-half of the method detection limit of the ozone instrument,
whichever is higher. However, if the number of same-hour
concentration values available for the required ozone monitoring
season for the year, from which the lowest observed hourly
concentration would be identified for purposes of this substitution,
is less than 50% of the number of days during the required ozone
monitoring season, one-half the method detection limit of the ozone
instrument shall be used in the substitution. For days outside the
required ozone monitoring season, the substitution value shall be
one-half the method detection limit of the ozone instrument. An 8-
hour period with no available hourly averages does not have a valid
8-hour average. The computed 8-hour average ozone concentrations are
not rounded or truncated.
(b) Daily Maximum 8-Hour Average Concentrations
There are 24 8-hour periods in each calendar day. Some of these
may not have valid 8-hour averages, under section 3(a). The daily
maximum 8-hour concentration for a given calendar day is the highest
of the valid 8-hour average concentrations computed for that day.
This process is repeated, yielding a daily maximum 8-hour average
ozone concentration for each day with ambient ozone monitoring data,
including days outside the required ozone monitoring season if data
are available. The daily maximum 8-hour concentrations from two
consecutive days may have some hourly concentrations in common.
Generally, overlapping daily maximum 8-hour averages are not likely,
[[Page 3050]]
except in those non-urban monitoring locations with less pronounced
diurnal variation in hourly concentrations. In these cases, the
maximum 8-hour average concentration from each day is used, even if
the two averages have some hours in common.
(c) Primary Standard Design Value
The primary standard design value is the annual fourth-highest
daily maximum 8-hour ozone concentration considering all days with
monitoring data including any days outside the required ozone
monitoring season, expressed in parts per million, averaged over
three years. The 3-year average shall be computed using the three
most recent, consecutive years of monitoring data that can yield a
valid design value. For a design value to be valid for comparison to
the standard, the monitoring data set on which it is based must meet
the data completeness requirements described in section 3(d). The
computed 3-year average of the annual fourth-highest daily maximum
8-hour average ozone concentrations shall be rounded to three
decimal places. Values equal to or greater than 0.xxx5 ppm shall
round up.
(d) Data Completeness Requirements for a Valid Design Value
(i) A design value greater than the standard is valid if in each
of the three years there are at least four days with a daily maximum
8-hour average concentration. Under sections 3(a) and 3(b), there
will be a daily maximum 8-hour average concentration on any day with
at least one hourly concentration. One or more of these four days
may be outside the required ozone monitoring season.
(ii) A design value less than or equal to the standard is valid
if for at least 75% of the days in the required ozone monitoring
season in each of the three years there are at least 18 8-hour
averages in the day that are based on at least 6 measured hourly
average concentrations.
(iii) When computing whether the minimum data completeness
requirement in section 3(d)(ii) has been met for the purpose of
showing that a design value equal to or less than the standard is
valid, meteorological or ambient data may be sufficient to
demonstrate that ozone levels on days with missing data would not
have affected the design value. At the request of the state, the
Regional Administrator may consider demonstrations that
meteorological conditions on one or more days in the required ozone
monitoring season which do not have at least 18 8-hour averages in
the day that are based on at least 6 measured hourly average
concentrations could not have caused a daily maximum 8-hour
concentration high enough to have been one of the four highest daily
maximum 8-hour concentrations for the year. At the request of the
state, days so demonstrated may be counted towards the 75%
requirement for the purpose of validating the design value, subject
to the approval of the Regional Administrator.
(vi) Years that do not meet the completeness criteria stated in
3(d)(ii) may nevertheless be used to calculate a design value that
will be deemed valid with the approval of, or at the initiative of,
the Administrator, who may consider factors such as monitoring site
closures/moves, monitoring diligence, the consistency and levels of
the valid concentration measurements that are available, and nearby
concentrations in determining whether to use such data.
(e) Comparison With the Primary Ozone Standard
(i) The primary ozone ambient air quality standard is met at an
ambient air quality monitoring site when the design value is less
than or equal to [0.075] ppm.
(ii) Comparison with the primary ozone standard is demonstrated
by examples 1 and 2 as follows:
Example 1. Ambient monitoring site attaining the primary ozone
standard.
--------------------------------------------------------------------------------------------------------------------------------------------------------
Percent valid
days (within 1st Highest 2nd Highest 3rd Highest 4th Highest 5th Highest
Year the required daily max 8- daily max 8- daily max 8- daily max 8- daily max 8-
monitoring hour conc. hour conc. hour conc. hour conc. hour conc.
season) (ppm) (ppm) (ppm) (ppm) (ppm)
--------------------------------------------------------------------------------------------------------------------------------------------------------
2006.................................................... 80 0.092500 0.090375 0.085125 0.078375 0.078125
2007.................................................... 96 0.084750 0.083500 0.075375 0.071875 0.070625
2008.................................................... 98 0.080875 0.079750 0.077625 0.075500 0.060375
-----------------------------------------------------------------------------------------------
Average............................................. .............. .............. .............. .............. 0.075250 ..............
-----------------------------------------------------------------------------------------------
Rounded............................................. .............. .............. .............. .............. 0.075 ..............
--------------------------------------------------------------------------------------------------------------------------------------------------------
As shown in Example 1, this monitoring site meets the primary
ozone standard because the 3-year average of the annual fourth-
highest daily maximum 8-hour average ozone concentrations (i.e.,
0.075256 ppm, rounded to 0.075 ppm) is less than or equal to [0.075]
ppm. The data completeness requirement is also met because no single
year has less than 75% data completeness. In Example 1, the
individual 8-hour averages and the 3-year average are shown with six
decimal digits. In actual calculations, all digits supported by the
calculator or calculation software must be retained.
Example 2. Ambient monitoring site failing to meet the primary
ozone standard.
--------------------------------------------------------------------------------------------------------------------------------------------------------
Percent valid
days (within 1st Highest 2nd Highest 3rd Highest 4th Highest 5th Highest
the required daily max 8- daily max 8- daily max 8- daily max 8- daily max 8-
Year monitoring hour conc. hour conc. hour conc. hour conc. hour conc.
season) (ppm) (ppm) (ppm) (ppm) (ppm)
(percent)
--------------------------------------------------------------------------------------------------------------------------------------------------------
2006.................................................... 96 0.105125 0.103500 0.101125 0.078625 0.072375
2007.................................................... 74 0.104250 0.103625 0.093000 0.080250 0.069500
2008.................................................... 98 0.103125 0.101875 0.101750 0.075375 0.074625
-----------------------------------------------------------------------------------------------
Average............................................. .............. .............. .............. .............. 0.078083 ..............
-----------------------------------------------------------------------------------------------
Rounded............................................. .............. .............. .............. .............. 0.078 ..............
--------------------------------------------------------------------------------------------------------------------------------------------------------
As shown in Example 2, the data capture in 2007 is less than
75%. The primary ozone standard is not met for this monitoring site
because the 3-year average of the fourth-highest daily maximum 8-
hour average ozone concentrations (i.e., 0.078083 ppm, rounded to
0.078 ppm) is greater than [0.075] ppm and is therefore valid
despite this incompleteness. In Example 2, the individual 8-hour
averages and the 3-year average are shown with six decimal digits.
In actual calculations, all digits supported by the
[[Page 3051]]
calculator or calculation software must be retained.
4. Secondary Ambient Air Quality Standard for Ozone
(a) Computing the daily W126 index value.
The secondary ozone ambient air quality standard is a seasonal
standard expressed as a sum of weighted hourly concentrations,
cumulated over the 12 hour daylight period from 8 a.m. to 8 p.m.
local standard time, during the consecutive 3-month period within
the ozone monitoring season with the maximum index value. The first
step in determining whether the standard is met at a monitoring site
is to compute the daily W126 index value for each day by applying
the sigmoidal weighting function in Equation 1 to each reported
measurement of hourly average concentration.
[GRAPHIC] [TIFF OMITTED] TP19JA10.001
Where:
Ci = hourly O3 at hour i, and
[GRAPHIC] [TIFF OMITTED] TP19JA10.002
The computed value of the sigmoidally weighted hourly
concentration is not rounded or truncated. The daily W126 index is
formed by summing the twelve computed hourly values, retaining all
decimal places. An illustration of computing a daily W126 index
value is below:
Example 3. Daily W126 index value calculation for an ambient
ozone monitoring site.
------------------------------------------------------------------------
Weighted
Start of hour Concentration concentration
(ppm) (ppm)
------------------------------------------------------------------------
8:00 a.m.......................... 0.045 0.002781
9:00 a.m.......................... 0.060 0.018218
10:00 a.m......................... 0.075 0.055701
11:00 a.m......................... 0.080 0.067537
12:00 p.m......................... 0.079 0.065327
1:00 p.m.......................... 0.082 0.071715
2:00 p.m.......................... 0.085 0.077394
3:00 p.m.......................... 0.088 0.082448
4:00 p.m.......................... 0.083 0.073683
5:00 p.m.......................... 0.081 0.069667
6:00 p.m.......................... 0.065 0.029260
7:00 p.m.......................... 0.056 0.011676
-------------------------------------
Sum=Daily W126 index value.... ................. * 0.625406
------------------------------------------------------------------------
* ppm-hours.
In Example 3, the individual weighted concentrations and their
sum are shown with six decimal digits. In actual calculations, all
digits supported by the calculator or calculation software must be
retained. There are no data completeness requirements for the daily
index. If fewer than 12 hourly values are available, only the
available hours are weighted and summed. However, there are data
completeness requirements for the monthly W126 index values and a
required adjustment for incomplete data, as describe in the next
section.
(b) Computing the Monthly W126 Index
As described in section 4(a), the daily index value is computed
at each monitoring site for each calendar day in each month during
the required ozone monitoring season with no rounding or truncation.
The monthly W126 index is the sum of the daily index values over one
calendar month. At an individual monitoring site, a monthly W126
index is valid if hourly average ozone concentrations are available
for at least 75% of the possible daylight hours in the month. For
months with more than 75% but less than 100% data completeness, the
monthly W126 value shall be adjusted for incomplete data by
multiplying the unadjusted monthly W126 index value by the ratio of
the number of possible reporting hours to the number of hours with
reported ambient hourly concentrations using Equation 2 in this
appendix:
[GRAPHIC] [TIFF OMITTED] TP19JA10.003
where
M.I. = the adjusted monthly W126 index,
D.I. = daily W126 index (i.e., the daily sum of the sigmoidally
weighted daylight hourly concentrations),
n = the number of days in the calendar month,
v = the number of daylight reporting hours (8 a.m.-7:59 p.m. LST) in
the month with reported valid hourly ozone concentrations.
The resulting adjusted value of the monthly W126 index shall not
be rounded or truncated.
(c) Secondary Standard Design Value
The secondary standard design value is the 3-year average of the
annual maximum consecutive 3-month sum of adjusted monthly W126
index values expressed in ppm-hours. Specifically, the annual W126
index value is computed on a calendar year basis using the three
highest, consecutive adjusted monthly W126 index values. The 3-year
average shall be computed using the most recent, consecutive three
calendar years of monitoring data meeting the data completeness
requirements described in section 4(c). The computed 3-year average
of the annual maximum consecutive 3-month sum of adjusted monthly
W126 index values in ppm-hours shall be rounded to a whole number
with decimal values equal to or greater than 0.500 rounding up.
(c) Data Completeness Requirement
(i) The annual W126 index is valid for purposes of calculating a
3-year design value if each full calendar month in the required
ozone monitoring season has at least 75% data completeness for
daylight hours.
(ii) If one or more months during the ozone monitoring seasons
of three successive years has less than 75% data completeness, the
three years shall nevertheless be used in the computation of a valid
design value for the site if substituting the lowest hourly ozone
concentration observed during daylight hours in the required ozone
monitoring season of each year, or one-half of the method detection
limit of the ozone instrument, whichever is higher, for enough of
the missing hourly concentrations within each incomplete month to
make the month 75% complete, and then adjusting for the remaining
missing data using Equation 2, above results in a design value
greater than the level of the standard.
(d) Comparisons With the Secondary Ozone Standard
(i) The secondary ambient ozone air quality standard is met at
an ambient air quality monitoring site when the design value is less
than or equal to [15] ppm-hours.
(ii) Comparison with the secondary ozone standard is
demonstrated by example 4 as follows:
Example 4. Ambient Monitoring Site Failing to Meet the
Secondary Ozone Standard
[[Page 3052]]
--------------------------------------------------------------------------------------------------------------------------------------------------------
April May June July August September October Overall
--------------------------------------------------------------------------------------------------------------------------------------------------------
2006
Adjusted monthly W126 index................................... 4.442 9.124 12.983 16.153 13.555 4.364 1.302 ..........
3-Month sum................................................... na na 26.549 38.260 42.691 34.072 19.221 ..........
2006 Maximum.................................................. ......... ......... ......... ......... 42.691 .......... ......... 42.691
--------------------------------------------------------------------------------------------------------------------------------------------------------
2007
Adjusted monthly W126 index................................... 3.114 7.214 8.214 8.111 7.455 7.331 5.115 ..........
3-Month sum................................................... na na 18.542 23.539 23.780 22.897 19.901 ..........
2007 Maximum.................................................. ......... ......... ......... ......... 23.780 .......... ......... 23.780
--------------------------------------------------------------------------------------------------------------------------------------------------------
2008
Adjusted monthly W126 index................................... 4.574 5.978 6.786 8.214 5.579 4.331 2.115 ..........
3-Month sum................................................... na na 17.338 20.978 20.579 18.124 12.025 ..........
2008 Maximum.................................................. ......... ......... ......... 20.978 ......... .......... ......... 20.978
3-Year average W126 index..................................... ......... ......... ......... ......... ......... .......... ......... 29.149666
-----------------------------------------------------------------------------------------
Rounded................................................... ......... ......... ......... ......... ......... .......... ......... 29
--------------------------------------------------------------------------------------------------------------------------------------------------------
As shown in example 4, the secondary ozone standard is not met
for this monitoring site because the 3-year average of the annual
W126 index value for this site is greater than [15] ppm-hours:
3-year average W126 index = (42.691 + 23.780 + 20.978)/3 =
29.149666, which rounds to 29 ppm-hours.
In Example 4, the adjusted monthly W126 index values and the 3-
month sums of the adjusted monthly W126 index values are shown with
three decimal digits. In actual calculations, all digits supported
by the calculator or calculation software must be retained.
PART 58--AMBIENT AIR QUALITY SURVEILLANCE
5. The authority citation for part 58 continues to read as follows:
Authority: 42 U.S.C. 7410 7403, 7410, 7601(a), 7611, and 7619.
6. Section 58.50 is amended by revising paragraph (c) and adding
paragraph (d) to read as follows:
Sec. 58.50 Index reporting.
* * * * *
(c) The population of a metropolitan statistical area for purposes
of index reporting is the latest available U.S. census population.
(d) For O3, reporting is required in metropolitan and
micropolitan statistical areas wherever monitoring is required under
Appendix D to Part 58--SLAMS Minimum O3 Monitoring
Requirements.
7. Appendix G of Part 58 is amended by revising section 3. to read
as follows:
Appendix G to Part 58--Uniform Air Quality Index (AQI) and Daily
Reporting
* * * * *
3. Must I Report the AQI?
You must report the AQI daily if yours is a metropolitan
statistical area (MSA) with a population over 350,000. For
O3, reporting is required in metropolitan and
micropolitan statistical areas wherever monitoring is required under
Appendix D to Part 58--SLAMS Minimum O3 Monitoring
Requirements.
* * * * *
[FR Doc. 2010-340 Filed 1-15-10; 8:45 am]
BILLING CODE 6560-50-P