[Federal Register: March 27, 2008 (Volume 73, Number 60)]
[Rules and Regulations]
[Page 16435-16514]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr27mr08-8]
[[Page 16435]]
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Part II
Environmental Protection Agency
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40 CFR Parts 50 and 58
National Ambient Air Quality Standards for Ozone; Final Rule
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Parts 50 and 58
[EPA-HQ-OAR-2005-0172; FRL-8544-3]
RIN 2060-AN24
National Ambient Air Quality Standards for Ozone
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: Based on its review of the air quality criteria for ozone
(O3) and related photochemical oxidants and national ambient
air quality standards (NAAQS) for O3, EPA is making
revisions to the primary and secondary NAAQS for O3 to
provide requisite protection of public health and welfare,
respectively. With regard to the primary standard for O3,
EPA is revising the level of the 8-hour standard to 0.075 parts per
million (ppm), expressed to three decimal places. With regard to the
secondary standard for O3, EPA is revising the current 8-
hour standard by making it identical to the revised primary standard.
EPA is also making 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.
DATES: This final rule is effective on May 27, 2008.
ADDRESSES: EPA has established a docket for this action under Docket ID
No. EPA-HQ-OAR-2005-0172. All documents in the docket are listed on the
www.regulations.gov Web site. Although listed in the index, some
information is not publicly available, e.g., confidential business
information or other information whose disclosure is restricted by
statute. Certain other material, such as copyrighted material, is not
placed on the Internet and will be publicly available only in hard copy
form. Publicly available docket materials are available either
electronically through 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. This Docket Facility
is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding
legal holidays. The Docket telephone number is 202-566-1742. The
telephone number for the Public Reading Room is 202-566-1744.
FOR FURTHER INFORMATION CONTACT: Dr. David J. McKee, 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: 919-541-5288; fax: 919-
541-0237; e-mail: mckee.dave@epa.gov.
SUPPLEMENTARY INFORMATION:
Table of Contents
The following topics are discussed in this preamble:
I. Background
A. Summary of Revisions to the O3 NAAQS
B. Legislative Requirements
C. Review of Air Quality Criteria and Standards for
O3
D. Summary of Proposed Revisions to the O3 NAAQS
E. Organization and Approach to Final Decision on O3
NAAQS
II. Rationale for Final Decision on the Primary O3
Standard
A. Introduction
1. Overview
2. Overview of Health Effects
3. Overview of Human Exposure and Health Risk Assessments
B. Need for Revision of the Current Primary O3
Standard
1. Introduction
2. Comments on the Need for Revision
3. Conclusions Regarding the Need for Revision
C. Conclusions on the Elements of the Primary O3
Standard
1. Indicator
2. Averaging Time
3. Form
4. Level
D. Final Decision on the Primary O3 Standard
III. Communication of Public Health Information
IV. Rationale for Final Decision on the Secondary O3
Standard
A. Introduction
1. Overview
2. Overview of Vegetation Effects Evidence
3. Overview of Biologically Relevant Exposure Indices
4. Overview of Vegetation Exposure and Risk Assessments
B. Need for Revision of the Current Secondary O3
Standard
1. Introduction
2. Comments on the Need for Revision
3. Conclusions Regarding the Need for Revision
C. Conclusions on the Secondary O3 Standard
1. Staff Paper Evaluation
2. CASAC Views
3. Administrator's Proposed Conclusions
4. Comments on the Secondary Standard Options
5. Administrator's Final Conclusions
D. Final Decision on the Secondary O3 Standard
V. Creation of Appendix P--Interpretation of the NAAQS for
O3
A. General
B. Data Completeness
C. Data Reporting and Handling and Rounding Conventions
VI. Ambient Monitoring Related to Revised O3 Standards
VII. Implementation and Related Control Requirements
A. Future Implementation Steps
1. Designations
2. State Implementation Plans
3. Trans-boundary Emissions
4. Monitoring Requirements
B. Related Control Requirements
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 & 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
K. Congressional Review Act
References
I. Background
A. Summary of Revisions to the O3 NAAQS
Based on its review of the air quality criteria for O3
and related photochemical oxidants and national ambient air quality
standards (NAAQS) for O3, EPA is making revisions to the
primary and secondary NAAQS for O3 to provide protection of
public health and welfare, respectively, that is appropriate under
section 109, and is making corresponding revisions in data handling
conventions for O3.
With regard to the primary standard for O3, EPA is
revising the level of the 8-hour standard to a level of 0.075 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 nonaccidental and cardiorespiratory mortality. EPA is
specifying the level of the primary standard to the nearest thousandth
ppm.
With regard to the secondary standard for O3, EPA is
revising the standard by making it identical to the revised primary
standard.
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B. 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'' emissions of
which ``in his judgment, cause or contribute to air pollution which may
reasonably be anticipated to endanger public health or welfare,'' whose
``presence * * * in the ambient air results from numerous or diverse
mobile or stationary sources,'' and for which the Administrator plans
to issue air quality criteria, and to issue air quality criteria for
those that are listed. Air quality criteria are to ``accurately reflect
the latest scientific knowledge useful in indicating the kind and
extent of identifiable effects on public health or welfare which may be
expected from the presence of [a] pollutant in ambient air, in varying
quantities * * *.'' Section 109 (42 U.S.C. 7409) directs the
Administrator to propose and promulgate ``primary'' and ``secondary''
NAAQS for pollutants listed under section 108. 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
[the] 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, manmade 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 provide 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 provide 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.
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. 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 that must be addressed.
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. Further the Supreme Court ruled that ``[t]he text of
Sec. 109(b), interpreted in its statutory and historical context and
with appreciation for its importance to the CAA as a whole,
unambiguously bars cost considerations from the NAAQS-setting process *
* *'' Id. at 472.\3\
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\3\ In considering whether the CAA allowed for economic
considerations to play a role in the promulgation of the NAAQS, the
Supreme Court rejected arguments that because many more factors than
air pollution might affect public health, EPA should consider
compliance costs that produce health losses in setting the NAAQS.
531 U.S. at 466. Thus, EPA may not take into account possible public
health impacts from the economic cost of implementation. Id.
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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 in
accordance with section 108 and [109(b)].'' 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 under section 108 and
[section 109(b)].'' This independent review function is performed by
the Clean Air Scientific Advisory Committee (CASAC) of EPA's Science
Advisory Board.
C. Review of Air Quality Criteria and Standards for O3
Ground-level O3 is formed from biogenic and
anthropogenic precursor emissions. Naturally occurring O3 in
the troposphere can result from biogenic organic precursors reacting
with naturally occurring nitrogen oxides (NOX) and by
stratospheric O3 intrusion into the troposphere.
Anthropogenic precursors of O3, specifically NOX
and volatile organic compounds (VOC), originate from a wide variety of
stationary and mobile sources. Ambient O3 concentrations
produced by these emissions are directly affected by temperature, solar
radiation, wind speed and other meteorological factors.
The last review of the O3 NAAQS was completed on July
18, 1997, based on the 1996 O3 Air Quality Criteria Document
(EPA, 1996a) and 1996 O3 Staff Paper (EPA, 1996b). EPA
revised the primary and secondary O3 standards on the basis
of the then latest scientific evidence linking exposures to ambient
O3 to adverse health and welfare effects at levels allowed
by the 1-hour average standards (62 FR 38856). The O3
standards were revised by replacing the existing primary 1-hour average
standard with an 8-hour average O3 standard set at a level
of 0.08 ppm, which is equivalent to 0.084 ppm using the standard
rounding conventions. The form of the primary standard was changed to
the annual fourth-highest daily maximum 8-hour average concentration,
averaged over 3 years. The secondary O3 standard was changed
by making it identical in all respects to the revised primary standard.
EPA initiated this current review in September 2000 with a call for
information (65 FR 57810) for the development of a revised Air Quality
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Criteria Document for O3 and Other Photochemical Oxidants
(henceforth the ``Criteria Document''). A project work plan (EPA, 2002)
for the preparation of the Criteria Document was released in November
2002 for CASAC O3 Panel \4\ (henceforth, ``CASAC Panel'')
and public review. 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 Panel and public review on January
31, 2005; a CASAC Panel 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 Panel and public review on August 31,
2005, and was discussed along with a first draft Staff Paper (EPA,
2005c) at a CASAC Panel meeting held on December 6-8, 2005. In a
February 16, 2006 letter to the Administrator, the CASAC Panel offered
final comments on all chapters of the Criteria Document (Henderson,
2006a), and the final Criteria Document (EPA, 2006a) was released on
March 21, 2006. In a June 8, 2006 letter (Henderson, 2006b) to the
Administrator, the CASAC Panel offered additional advice to the Agency
concerning chapter 8 of the final Criteria Document (Integrative
Synthesis) to help inform the second draft Staff Paper.
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\4\ The CASAC O3 Review Panel includes the seven
members of the chartered CASAC, supplemented by fifteen subject-
matter experts appointed by the Administrator to provide additional
scientific expertise relevant to this review of the O3
NAAQS.
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A second draft Staff Paper (EPA, 2006b) was released on July 17,
2006 and reviewed by the CASAC Panel on August 24 and 25, 2006. In an
October 24, 2006 letter to the Administrator, CASAC Panel provided
advice and recommendations to the Agency concerning the second draft
Staff Paper (Henderson, 2006c). A final Staff Paper (EPA, 2007a) was
released on January 31, 2007. Around the time of the release of the
final Staff Paper in January 2007, EPA discovered a small error in the
exposure model that when corrected resulted in slight increases in the
human exposure estimates. 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
final rule reflect the corrected estimates, and thus are slightly
different than the exposure and risk estimates cited in the January 31,
2007 Staff Paper.\5\ In a March 26, 2007 letter (Henderson, 2007), the
CASAC Panel offered additional advice to the Administrator with regard
to recommendations and revisions to the primary and secondary
O3 NAAQS.
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\5\ EPA made available corrected versions of the final Staff
Paper (EPA, 2007b, henceforth, ``Staff Paper'') and the human
exposure and health risk assessment technical support documents on
July 31, 2007 on the EPA Web site http://www.epa.gov/ttn/naaqs.
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The schedule for completion of this review has been governed by a
consent decree resolving a lawsuit filed in March 2003 by a group of
plaintiffs representing national environmental and public health
organizations, alleging that EPA had failed to complete the current
review within the period provided by statute.\6\ The modified consent
decree that currently governs this review provides that EPA sign for
publication notices of proposed and final rulemaking concerning its
review of the O3 NAAQS no later than June 20, 2007 and March
12, 2008, respectively. The proposed decision (henceforth ``proposal'')
was signed on June 20, 2007 and published in the Federal Register on
July 11, 2007.
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\6\ American Lung Association v. Whitman (No. 1:03CV00778,
D.D.C. 2003).
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A large number of comments were received from various commenters on
the proposed revisions to the O3 NAAQS. Significant issues
raised in the public comments are discussed throughout the preamble of
this final action. A comprehensive summary of all significant comments,
along with EPA's responses (henceforth ``Response to Comments''), can
be found in the docket for this rulemaking.
Various commenters have referred to and discussed a number of new
scientific studies on the health effects of O3 that had been
published recently and therefore were not included in the Criteria
Document (EPA, 2006a, henceforth ``Criteria Document).\7\ EPA has
provisionally considered any significant ``new'' studies, including
those submitted during the public comment period. The purpose of this
effort was to ensure that the Administrator was fully aware of the
``new'' science before making a final decision on whether to revise the
current O3 NAAQS. EPA provisionally considered these studies
to place their results in the context of the findings of the Criteria
Document.
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\7\ For ease of reference, these studies will be referred to as
``new'' studies or ``new'' science, using quotation marks around the
word new. Referring to studies that were published too recently to
have been included in the 2004 Criteria Document as ``new'' studies
is intended to clearly differentiate such studies from those that
have been published since the last review and are included in the
2004 Criteria Document (these studies are sometimes referred to as
new (without quotation marks) or more recent studies, to indicate
that they were not included in the 1996 Criteria Document and thus
are newly available in this review.
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As in prior NAAQS reviews, EPA is basing its decision in this
review on studies and related information included in the Criteria
Document and Staff Paper, which have undergone CASAC and public review.
The studies assessed in the Criteria Document, and the integration of
the scientific evidence presented in that document, have undergone
extensive critical review by EPA, CASAC, and the public during the
development of the Criteria Document. The rigor of that review makes
these studies, and their integrative assessment, the most reliable
source of scientific information on which to base decisions on the
NAAQS, decisions that all parties recognize as of great import. NAAQS
decisions can have profound impacts on public health and welfare, and
NAAQS decisions should be based on studies that have been rigorously
assessed in an integrative manner not only by EPA but also by the
statutorily mandated independent advisory committee, as well as the
public review that accompanies this process. As described above, EPA's
provisional consideration of these studies did not and could not
provide that kind of in-depth critical review.
This decision is consistent with EPA's practice in prior NAAQS
reviews. Since the 1970 amendments, the EPA has taken the view that
NAAQS decisions are to be based on scientific studies and related
information that have been assessed as a part of the pertinent air
quality criteria, and has consistently followed this approach. See 71
FR 61144, 61148 (October 17, 2006) (final decision on review of PM
NAAQS) for a detailed discussion of this issue and EPA's past practice.
As discussed in EPA's 1993 decision not to revise the NAAQS for
O3 ``new'' studies may sometimes be of such significance
that it is appropriate to delay a decision on revision of a NAAQS and
to supplement the pertinent air quality criteria so the studies can be
taken into account (58 FR at 13013-13014, March 9, 1993). In the
present case, EPA's provisional consideration of ``new'' studies
concludes that, taken in context, the ``new'' information and findings
do not materially change any of the broad scientific conclusions
regarding the health effects of O3 exposure made in the
Criteria Document. For this reason, reopening the air quality criteria
review would not be warranted even if there were time to do so under
the court order
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governing the schedule for this rulemaking. Accordingly, EPA is basing
the final decisions in this review on the studies and related
information included in the O3 air quality criteria that
have undergone CASAC and public review. EPA will consider the newly
published studies for purposes of decision making in the next periodic
review of the O3 NAAQS, which will provide the opportunity
to fully assess them through a more rigorous review process involving
EPA, CASAC, and the public. Further discussion of these ``new'' studies
can be found in the Response to Comments document.
This action presents the Administrator's final decisions on the
review of the current primary and secondary O3 standards.
Throughout this preamble a number of conclusions, findings, and
determinations made by the Administrator are noted. They identify the
reasoning that supports this final decision and are intended to be
final and conclusive.
D. Summary of Proposed Revisions to the O3 NAAQS
For reasons discussed in the proposal, the Administrator proposed
to revise the current primary and secondary O3 standards.
With regard to the primary O3 standard, the Administrator
proposed to revise the level of the 8-hour O3 standard to a
level within the range of 0.070 ppm to 0.075 ppm, based on a 3-year
average of the fourth-highest maximum 8-hour average concentration.
Related revisions for O3 data handling conventions and for
the reference method for monitoring O3 were also proposed.
These revisions were proposed 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 nonaccidental and
cardiorespiratory mortality. EPA also proposed to specify the level of
the primary standard to the nearest thousandth ppm. EPA solicited
comment on alternative levels down to 0.060 ppm and up to and including
retaining the current 8-hour standard of 0.08 ppm (effectively 0.084
ppm using current data rounding conventions).
With regard to the secondary standard for O3, EPA
proposed to revise the current 8-hour standard with one of two options
to provide increased protection against O3-related adverse
impacts on vegetation and forested ecosystems. One option was to
replace the current standard with a cumulative, seasonal standard
expressed as an index of the annual 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 21 ppm-
hours. The other option was to make the secondary standard identical to
the proposed primary 8-hour standard. EPA solicited comment on
specifying a cumulative, seasonal standard in terms of a 3-year average
of the annual sums of weighted hourly concentrations; on the range of
alternative 8-hour standard levels for which comment was being
solicited for the primary standard, including retaining the current
secondary standard, which is identical to the current primary standard;
and on an alternative approach to setting a cumulative, seasonal
secondary standard.
E. Organization and Approach to Final O3 NAAQS Decisions
This action presents the Administrator's final decisions regarding
the need to revise the current primary and secondary O3
standards. Revisions to the primary standard for O3 are
addressed below in section II, and a discussion on communication of
public health information regarding revisions to the primary
O3 standard is presented in section III. The secondary
O3 standard is addressed below in section IV. Related data
completeness and data handling and rounding conventions are addressed
in section V, and federal reference methods for monitoring
O3 are addressed below in section VI. Future implementation
steps and related control requirements are discussed in section VII. A
discussion of statutory and executive order reviews is provided in
section VIII.
Today's final decisions are based on a thorough review in the
Criteria Document of scientific information on known and potential
human health and welfare effects associated with exposure to
O3 at levels typically found in the ambient air. These final
decisions also take into account: (1) Staff assessments in the Staff
Paper of the most policy-relevant information in the Criteria Document
as well as quantitative exposure and risk assessments based on that
information; (2) CASAC Panel advice and recommendations, as reflected
in its letters to the Administrator, its discussions of drafts of the
Criteria Document and Staff Paper at public meetings, and separate
written comments prepared by individual members of the CASAC Panel; (3)
public comments received during the development of these documents,
either in connection with CASAC Panel meetings or separately; and (4)
extensive public comments received on the proposed rulemaking.
II. Rationale for Final Decisions on the Primary O3 Standard
A. Introduction
1. Overview
This section presents the Administrator's final decisions regarding
the need to revise the current primary O3 NAAQS, and the
appropriate revision to the level of the 8-hour standard. As discussed
more fully below, the rationale for the final decision on appropriate
revisions to the primary O3 NAAQS includes consideration of:
(1) Evidence of health effects related to short-term exposures to
O3; (2) insights gained from quantitative exposure and
health risk assessments; (3) public and CASAC Panel comments received
during the development and review of the Criteria Document, Staff
Paper, exposure and risk assessments and on the proposal notice.
In developing this rationale, EPA has drawn upon an integrative
synthesis of the entire body of evidence \8\ relevant to examining
associations between exposure to ambient O3 and a broad
range of health endpoints (EPA, 2006a, Chapter 8), focusing on those
health endpoints for which the Criteria Document concluded that the
associations are causal or likely to be causal. This body of evidence
includes hundreds of studies conducted in many countries around the
world. In its assessment of the evidence judged to be most relevant to
decisions on elements of the primary O3 standards, EPA has
placed greater weight on U.S. and Canadian studies, since studies
conducted in other countries may well reflect different demographic and
air pollution characteristics.
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\8\ The word ``evidence'' is used in this notice to refer to
studies that provide information relevant to an area of inquiry,
which can include studies that report positive or negative results
or that provide interpretative information.
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As discussed below, a significant amount of new research has been
conducted since the last review, with important new information coming
from epidemiological, toxicological, controlled human exposure, and
dosimetric studies. Moreover, the newly available research studies
evaluated in the Criteria Document have undergone intensive scrutiny
through multiple layers of peer review, with extended
[[Page 16440]]
opportunities for review and comment by CASAC Panel and the public. As
with virtually any policy-relevant scientific research, there is
uncertainty in the characterization of health effects attributable to
exposure to ambient O3, most generally with regard to
whether observed health effects and associations are causal or likely
causal in nature and, if so, the certainty of causal associations at
various exposure levels. While important uncertainties remain, the
review of the health effects information has been extensive and
deliberate. In the judgment of the Administrator, this intensive
evaluation of the scientific evidence provides an adequate basis for
regulatory decision making at this time. This review also provides
important input to EPA's research plan for improving our future
understanding of the relationships between exposures to ambient
O3 and health effects.
The health effects information and quantitative exposure and health
risk assessment were summarized in sections II.A and II.B of the
proposal (72 FR at 37824-37862) and are only briefly outlined below in
sections II.A.2 and II.A.3. Subsequent sections of this preamble
provide a more complete discussion of the Administrator's rationale, in
light of key issues raised in public comments, for concluding that the
current standard is not requisite to protect public health with an
adequate margin of safety, and it is appropriate to revise the current
primary O3 standards to provide additional public health
protection (section II.B), as well as a more complete discussion of the
Administrator's rationale for retaining or revising the specific
elements of the primary O3 standards (section II.C), namely
the indicator (section II.C.1); averaging time (section II.C.2); form
(section II.C.3); and level (section II.C.4). A summary of the final
decisions on revisions to the primary O3 standards is
presented in section II.D.
2. Overview of Health Effects
This section outlines the information presented in Section II.A of
the proposal on known or potential effects on public health which may
be expected from the presence of O3 in ambient air. The
decision in the last 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 visits for respiratory causes. The Criteria Document
prepared for this review emphasizes a 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 emphasizes 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 at and below 0.080 ppm, which was the
lowest exposure level that had been examined in the last review.
(2) Numerous recent controlled human-exposure studies have examined
indicators of O3-induced inflammatory response in both the
upper respiratory tract (URT) and lower respiratory tract (LRT), while
other studies have examined changes in host defense capability
following O3 exposure of healthy young adults and increased
airway responsiveness to allergens in subjects with allergic asthma and
allergic rhinitis exposed to O3.
(3) New evidence from controlled human exposure studies showing
that asthmatics have greater respiratory-related physiological
responses than healthy subjects and new evidence from epidemiological
studies showing associations between O3 exposure and lung
function and respiratory symptom responses; these findings differ from
the presumption in the last review that people with asthma had
generally the same magnitude of respiratory responses to O3
as those experienced by healthy individuals.
(4) Animal toxicology studies provide new information regarding
potential mechanisms of action, increased susceptibility to respiratory
infection, and biological plausibility of acute effects as well as
chronic, irreversible respiratory damage observed in animals.
(5) Numerous epidemiological studies published during the past
decade offer added evidence of associations between acute ambient
O3 exposures and lung function decrements and respiratory
symptoms in physically active healthy subjects and asthmatic subjects,
as well as new evidence regarding additional health endpoints,
including relationships between ambient O3 concentrations
and school absenteeism and between ambient O3 and cardiac-
related physiological endpoints.
(6) Several additional studies have been published over the last
decade examining the temporal associations between acute O3
exposures and both emergency department visits for respiratory diseases
and respiratory-related hospital admissions.
(7) A large number of newly available epidemiological studies have
examined the effects of acute exposure to PM and O3 on
premature mortality, notably including large multi-city studies that
provide much more robust information than was available in the last
review, as well as recent meta-analyses that have evaluated potential
sources of heterogeneity in O3-mortality associations.
Section II.A of the proposal provides a detailed summary of key
information contained in the Criteria Document (chapters 4-8) and in
the Staff Paper (chapter 3), on the known and potential effects of
O3 exposure and information on the effects of O3
exposure in combination with other pollutants that are routinely
present in the ambient air (72 FR 37824-37851). The information there
summarizes:
(1) New information available on potential mechanisms for morbidity
and mortality effects associated with exposure to O3,
including potential mechanisms or pathways related to direct effects on
the respiratory system, systemic effects that are secondary to effects
in the respiratory system (e.g., cardiovascular effects);
(2) The nature of effects that have been associated directly with
exposure to O3 or indirectly with the presence of
O3 in ambient air, including premature mortality,
aggravation of respiratory and cardiovascular disease (as indicated by
increased hospital admissions and emergency department visits), changes
in lung function and increased respiratory symptoms, as well as new
evidence for more subtle indicators of cardiovascular health;
(3) An integrative interpretation of the health effects evidence,
focusing on the biological plausibility and coherence of the evidence
and key issues raised in interpreting epidemiological studies, along
with supporting evidence from experimental (e.g., dosimetric and
toxicological) studies as well as the limitations of the evidence; and
(4) Considerations in characterizing the public health impact of
O3, including the identification of sensitive and vulnerable
subpopulations that are potentially at risk to such effects, including
active people, people with pre-existing lung and heart diseases,
children and older adults, and people with increased responsiveness to
O3.
[[Page 16441]]
3. Overview of Human Exposure and Health Risk Assessments
To put judgments about health effects that are adverse for
individuals into a broader public health context, EPA developed and
applied models to estimate human exposures and health risks. This
broader public health context included consideration of the size of
particular population groups at risk for various effects, the
likelihood that exposures of concern would 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 in more detail in section II.B of the proposal, 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 since the last review in both the
exposure and health risk models. The CASAC Panel 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).
In modeling exposures and health risks associated with just meeting
the current and alternative O3 standards, EPA simulated air
quality just meeting these standards based on O3 air quality
patterns in several recent years and on how the shape of the
O3 air quality distributions has changed over time based on
historical trends in monitored O3 air quality data. As
discussed in the proposal notice and in the Staff Paper (section
4.5.8), recent O3 air quality distributions were
statistically adjusted to simulate just meeting the current and
selected alternative standards. Specifically, the exposure and risk
assessment included estimates for a recent year of air quality and for
air quality adjusted to simulate just meeting the current and
alternative standards based on O3 season data from a recent
three-year period (2002-2004). The O3 season in each area
included the period of the year for which routine hourly O3
monitoring data are available. Typically this period spans from March
or April through September or October, although in some areas it
includes 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. (see Staff Paper, Figure
2-16), with the mean of the distribution of annual 4th highest daily
maximum 8-hour O3 levels for urban monitors nationwide being
in the upper third among the years 1990 through 2004. In contrast, on a
national basis, 2004 was the lowest year on record with respect to the
mean of the distribution of annual 4th highest daily maximum 8-hour
O3 levels for this same 15 year period. The 4th highest
daily maximum 8-hour levels observed in most, but not all of the 12
urban areas included in the exposure and risk assessment, were
relatively low in 2004 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. As a result of the variability in air quality, the
exposure and risk estimates associated with just meeting the current or
any alternative standard also will vary depending on the year chosen
for the analysis. Thus, exposure and risk estimates based on 2002 air
quality generally show relatively higher numbers of children affected
and the estimates based on 2004 air quality generally show relatively
fewer numbers of children affected.
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.\9\ Instead these simulations
represent a projection of the kind of air quality levels that would be
likely to occur in areas just attaining various alternative standards,
when historical patterns of air quality, reflecting averages over many
areas, are applied in the urban areas examined.
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\9\ For informational purposes only, modeling that projects how
areas might attain alternative standards in a future year as a
result of Federal, State, local, and Tribal efforts is presented in
the final Regulatory Impact Analysis being prepared in connection
with this decision.
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a. Exposure Analyses
As discussed in section II.B.1 of the proposal, EPA conducted human
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 current
8-hour O3 standard is not met. The emphasis on children
reflected the finding of the last review that children are an important
at-risk group. 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. This exposure
assessment is more fully described and presented in the Staff Paper and
in a technical support document, Ozone Population Exposure Analysis for
Selected Urban Areas (EPA, 2007c; henceforth ``Exposure Analysis
TSD''). As noted in the proposal, the scope and methodology for this
exposure assessment were developed over the last few years with
considerable input from the CASAC Panel and the public.
As discussed in the proposal notice and in greater detail in the
Staff Paper (chapter 4) and Exposure Analysis TSD, EPA recognized that
there are many sources of variability and uncertainty inherent in the
input to this assessment and that there was uncertainty in the
resulting O3 exposure estimates. 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 Staff Paper (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. These are
the relevant exposures since O3-related effects observed in
clinical 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
Staff Paper (section 4.6) and in a technical memorandum describing the
exposure modeling uncertainty analysis (Langstaff, 2007).
The exposure assessment, which provided estimates of the number of
people exposed to different levels of
[[Page 16442]]
ambient O3 while at elevated exertion \10\, served two
purposes. First, the entire range of modeled personal exposures to
ambient O3 was 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 specified benchmark levels while at
elevated exertion provided some perspective on the public health
impacts of health effects that we cannot currently evaluate in
quantitative risk assessments but 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. In the proposal, we
referred to exposures at and above these benchmark levels while at
elevated exertion as ``exposures of concern.''
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\10\ As discussed in section II.A of the proposal, O3
health responses observed in controlled human exposure studies are
associated with exposures while subjects are engaged in moderate or
greater exertion on average over the exposure period (hereafter
referred to as ``elevated exertion'') and, therefore, these are the
exposures of interest.
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Based on the observation from the exposure analyses conducted in
the prior review that children represented the population subgroup with
the greatest exposure to ambient O3, EPA chose to model 8-
hour exposures at elevated exertion for all school age children, and
separately for asthmatic school age children, as well as for the
general population in the current exposure assessment. While outdoor
workers and other adults who engage in moderate or greater exertion for
prolonged periods while outdoors during the day in areas experiencing
elevated O3 concentrations also are at risk for
O3-related health effects, EPA did not focus on developing
quantitative exposure estimates for these population subgroups due to
the lack of information about the number of individuals who regularly
work or exercise outdoors. Thus, as presented in the proposal and in
the Staff Paper the exposure estimates are most useful for making
relative comparisons of estimated exposures in school age children
across alternative air quality scenarios. This assessment does not
provide information on exposures for adult subgroups within the general
population associated with the air quality scenarios.
EPA noted in the proposal key observations that were important to
consider in comparing exposure estimates associated with just meeting
the current NAAQS and alternative standards considered. These included:
(1) As shown in Table 6-1 of the Staff Paper, the patterns of
exposures in terms of percentages of the population exceeding given
exposure levels were very similar for the general population and for
asthmatic and all school age (5-18) children, although children were
about twice as likely as the general population to be exposed at any
given level.
(2) As shown in Table 1 in the proposal (72 FR 37855), the number
and percentage of asthmatic and all school age children aggregated
across the 12 urban areas estimated to experience 1 or more exposures
of concern declined from simulations of just meeting the current
standard to simulations of alternative 8-hour standards by varying
amounts, depending on the benchmark level, the population subgroup
considered, and the air quality year chosen.\11\
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\11\ While the proposal notice stated in the text that
``approximately 2 to 4 percent of all and asthmatic children'' were
estimated to experience exposures of concern at and above the 0.070
ppm benchmark level for standards in the range of 0.070 to 0.075 ppm
(72 FR 37879), the correct range is about 1 to 5 perecent consistent
with the estimates provided in Table 1 of the proposal (72 FR
37855).
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(3) Substantial year-to-year variability in exposure estimates was
observed over the three-year modeling period.
(4) There was substantial variability observed across the 12 urban
areas in the percent of the population subgroups estimated to
experience exposures at and above specified benchmark levels while at
elevated exertion.
(5) Of particular note, there is high inter-individual variability
in responsiveness such that only a subset of individuals who were
exposed at and above a given benchmark level while at elevated exertion
would actually be expected to experience any such potential adverse
health effects.
(6) In considering these observations, it was 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.
b. Quantitative Health Risk Assessment
As discussed in section II.B.2 of the proposal, the approach used
to develop quantitative risk estimates associated with exposures to
O3 builds upon the risk assessment conducted during the last
review.\12\ The expanded and updated assessment conducted in this
review 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 short-term ambient O3 levels; (2) risk reductions and
remaining risks associated with just meeting the current 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. The health risk assessment
was discussed in the Staff Paper (chapter 5) and presented more fully
in a technical support document, Ozone Health Risk Assessment for
Selected Urban Areas (Abt Associates, 2007a). As noted in the proposal,
the scope and methodology for this risk assessment was developed over
several years with considerable input from the CASAC Panel and the
public.
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\12\ 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).
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EPA recognized that there were many sources of uncertainty and
variability inherent in the inputs to these assessments and that there
was a high degree of uncertainty in the resulting O3 risk
estimates. Such uncertainties generally relate to a lack of clear
understanding of a number of important factors, including, for example,
the shape of exposure-response and concentration-response functions,
particularly when, as here, effect thresholds can neither be discerned
nor determined not to exist; issues related to selection of appropriate
statistical models for the analysis of the epidemiologic data; the role
of potentially confounding and modifying factors in the concentration-
response relationships; and issues related to simulating how
O3 air quality distributions will likely change in any given
area upon attaining a particular standard, since strategies to reduce
emissions are not yet fully defined. While some of these uncertainties
were addressed quantitatively in the form of estimated confidence
ranges around central risk estimates, other uncertainties and the
variability in key inputs were not reflected in these confidence
ranges, but rather were partially characterized through separate
sensitivity analyses or discussed qualitatively.
Key observations and insights from the O3 risk
assessment, together with important caveats and limitations, were
discussed in section II.B of the proposal. In general, estimated risk
reductions associated with going from current O3 levels to
just meeting the current and
[[Page 16443]]
alternative 8-hour standards show patterns of increasing estimated risk
reductions associated with just meeting the lower alternative 8-hour
standards considered. Furthermore, the estimated percentage reductions
in risk were strongly influenced by the baseline air quality year used
in the analysis (see Staff Paper, Figures 6-1 through 6-6)
Key observations important in comparing estimated health risks
associated with attainment of the current NAAQS and alternative
standards included:
(1) As discussed in the 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 the current and
potential alternative 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 the current and selected
potential alternative standards. This variability is likely due to
differences in air quality distributions, differences in estimated
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 (PRB) concentrations,\13\ as discussed in the 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.\14\ With respect to O3-related non-accidental
mortality, while notable differences (i.e., greater than 50 percent)
were observed in some areas, particularly for more stringent standards,
the overall pattern of estimated reductions, expressed in terms of
percentage reduction relative to the current standard, was
significantly less impacted.
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\13\ PRB O3 concentrations used in the O3
risk assessment were defined in chapter 2 of the Staff Paper (EPA,
2007, pp. 2-48, 2-54) 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. Based on runs of the GEOS-CHEM model (a global
tropospheric O3 model) applied for the 2001 warm season
(i.e., April to September), monthly background daily diurnal
profiles for each of the 12 urban areas for each month of the
O3 season were simulated using meteorology for the year
2001. Based on these model runs, the Criteria Document states that
current estimates of PRB O3 concentrations are generally
in the range of 0.015 to 0.035 ppm in the afternoon, and they are
generally lower under conditions conducive to high O3
episodes. They are highest during spring due to contributions from
hemispheric pollution and stratospheric intrusions. The Criteria
Document states that the GEOS-CHEM model applied for the 2001 warm
season reports PRB O3 concentrations for afternoon
surface air over the United States that are likely 10 ppbv too high
in the southeast in summer, and accurate within 5 ppbv in other
regions and seasons.
\14\ Sensitivity analyses examining the impact of alternative
assumptions about PRB were only conducted for lung function
decrements and non-accidental mortality.
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(5) 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 in the proposal, 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. EPA recognizes that these credible
intervals do not reflect all of the uncertainties noted above.
B. Need for Revision of the Current Primary O3 Standard
1. Introduction
The initial issue to be addressed in this review of the primary
O3 standard is whether, in view of the advances in
scientific knowledge reflected in the Criteria Document and Staff
Paper, the current standard should be revised. As discussed in section
II.C of the proposal, in evaluating whether it was appropriate to
propose to retain or revise the current standard, the Administrator
built upon the last review and reflected the broader body of evidence
and information now available. In the proposal, EPA presented
information, judgments, and conclusions from the last review, which
revised the level, averaging time, and form of the standard, from the
Staff Paper's evaluation of the adequacy of the current primary
standard, including both evidence- and exposure/risk-based
considerations, as well as from the CASAC Panel's advice and
recommendations. The Staff Paper evaluation, CASAC Panel's views, and
the Administrator's proposed conclusions on the adequacy of the current
primary standard are presented below.
a. Staff Paper Evaluation
The Staff Paper considered the evidence presented in the Criteria
Document as a basis for evaluating the adequacy of the current
O3 standard, recognizing that important uncertainties
remain. The extensive body of human clinical, toxicological, and
epidemiological evidence, highlighted above in section II.A.2 and
discussed in section II.A of the proposal, serves as the basis for
judgments about O3-related health effects, including
judgments about causal relationships with a range of respiratory
morbidity effects, including lung function decrements, increased
respiratory symptoms, airway inflammation, increased airway
responsiveness, and respiratory-related hospitalizations and emergency
department visits in the warm season, and about the evidence being
highly suggestive that O3 directly or indirectly contributes
to non-accidental and cardiorespiratory-related mortality.
[[Page 16444]]
These judgments take into account important uncertainties that
remain in interpreting this evidence. For example, with regard to the
utility of time-series epidemiological studies to inform judgments
about a NAAQS for an individual pollutant, such as O3,
within a mix of highly correlated pollutants, such as the mix of
oxidants produced in photochemical reactions in the atmosphere, the
Staff Paper noted that there are limitations especially at ambient
O3 concentrations below levels at which O3-
related effects have been observed in controlled human exposure
studies. The Staff Paper also recognized that 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
variability in susceptibility to O3-related effects in
populations.
While noting these limitations in the interpretation of the
findings from the epidemiological studies, the Staff Paper concluded
that if a population threshold level does exist, it would likely be
well below the level of the current O3 standard and possibly
within the range of background levels. This conclusion is supported by
several epidemiological studies that have explored the question of
potential thresholds either by using a statistical curve-fitting
approach to evaluate whether linear or non-linear models fit the data
better using, or by analyzing, sub-sets of the data where days over or
under a specific cutpoint (e.g., 0.080 ppm or even lower O3
levels) were excluded and then evaluating the association for
statistical significance. In addition to consideration of the
epidemiological studies, findings from controlled human exposure
studies indicate that prolonged exposures produced statistically
significant group mean FEV1 decrements and symptoms in
healthy adult subjects at levels down to at least 0.060 ppm, with a
small percentage of subjects experiencing notable effects (e.g., >10
percent FEV1 decrement, pain on deep inspiration).
Controlled human exposure studies evaluated in the last review also
found significant responses in indicators of lung inflammation and cell
injury at 0.080 ppm in healthy adult subjects. The effects in these
controlled human exposure studies were observed in healthy young adult
subjects, and it is likely that more serious responses, and responses
at lower levels, would occur in people with asthma and other
respiratory diseases. These physiological effects can lead to
aggravation of asthma and increased susceptibility to respiratory
infection. The observations provide support for the conclusion in the
Staff Paper that the associations observed in the epidemiological
studies, particularly for respiratory-related effects such as increased
medication use, increased school and work absences, increased visits to
doctors' offices and emergency departments, and increased hospital
admissions, extend down to O3 levels well below the current
standard (i.e., 0.084 ppm) (p. 6-7).
The newly available information reinforces the judgments in the
Staff Paper from the last review about the likelihood of causal
relationships between O3 exposures and respiratory effects
and broadens the evidence of O3-related associations to
include additional respiratory-related endpoints, newly identified
cardiovascular-related health endpoints, and mortality. Newly available
evidence also led the Staff Paper to conclude that people with asthma
are likely to experience more serious effects than people who do not
have asthma. The Staff Paper also concluded that substantial progress
has been made since the last review in advancing the understanding of
potential mechanisms by which ambient O3, alone and in
combination with other pollutants, is causally linked to a range of
respiratory-related health endpoints, and may be causally linked to a
range of cardiovascular-related health endpoints. Thus, the Staff Paper
found strong support in the evidence available since the last review,
for consideration of an O3 standard that is at least as
protective as the current standard and finds no support for
consideration of an O3 standard that is less protective than
the current standard. This conclusion is consistent with the advice and
recommendations of the CASAC Panel and with the views expressed by all
interested parties who provided comments on drafts of the Staff Paper.
While the CASAC Panel and some commenters on drafts of the Staff Paper
supported revising the current standard to provide increased public
health protection and other such commenters supported retaining the
current standard, no one who provided comments on drafts of the Staff
Paper supported a standard that would be less protective than the
current standard.
i. Evidence-Based Considerations
In looking more specifically at the controlled human exposure and
epidemiological evidence, the Staff Paper first noted that controlled
human exposure studies provide the clearest and most compelling
evidence for an array of human health effects that are directly
attributable to acute exposures to O3 per se. Evidence from
such human studies, together with animal toxicological studies, help to
provide biological plausibility for health effects observed in
epidemiological studies. In considering the available evidence, the
Staff Paper focused on studies that examined health effects that have
been demonstrated to be caused by exposure to O3, or for
which the Criteria Document judges associations with O3 to
be causal or likely causal, or for which the evidence is highly
suggestive that O3 contributes to the reported effects.
In considering the epidemiological evidence as a basis for reaching
conclusions about the adequacy of the current standard, the Staff Paper
focused on studies reporting effects in the warm season, for which the
effect estimates are more consistently positive and statistically
significant than those from all-year studies. The Staff Paper
considered the extent to which such studies provide evidence of
associations that extend down to ambient O3 concentrations
below the level of the current standard, which would thereby call into
question the adequacy of the current standard. In so doing, the Staff
Paper noted that if a population threshold level does exist for an
effect observed in such studies, it would likely be at a level well
below the level of the current standard. The Staff Paper also attempted
to characterize whether the area in which a study was conducted likely
would or would not have met the current standard during the time of the
study, although it recognizes that the confidence that would
appropriately be placed on the associations observed in any given
study, or on the extent to which the association would likely extend
down to relatively low O3 concentrations, is not dependent
on this distinction. Further, the Staff Paper considered studies that
examined subsets of data that include only days with ambient
O3 concentrations below the level of the current
O3 standard, or below even lower O3
concentrations, and continue to report statistically significant
associations. The Staff Paper judged that such studies are directly
relevant to considering the adequacy of the current standard,
particularly in light of reported responses to O3 at
[[Page 16445]]
levels below the current standard found in controlled human exposure
studies.
The Staff Paper evaluation of such studies is discussed below and
in section II.C.2.a of the proposal, focusing in turn on studies of (1)
lung function, respiratory symptoms and other respiratory-related
physiological effects, (2) respiratory hospital admissions and
emergency department visits, and (3) mortality.
(1) Lung function, respiratory symptoms and other respiratory-
related physiological effects. Health effects for which the Criteria
Document continued to find clear evidence of causal associations with
short-term O3 exposures include lung function decrements,
respiratory symptoms, pulmonary inflammation, and increased airway
responsiveness. In the last review, these O3-induced effects
were demonstrated with statistical significance down to the lowest
level tested in controlled human exposure studies at that time (i.e.,
0.080 ppm). Two new studies are notable in that they are the only
controlled human exposure studies that examined respiratory effects,
including lung function decrements and respiratory symptoms, in healthy
adults at lower exposure levels than had previously been examined.
EPA's reanalysis of the data from the most recent study shows small
group mean decrements in lung function responses to be statistically
significant at the 0.060 ppm exposure level, while the author's
analysis did not yield statistically significant lung function
responses but did yield some statistically significant respiratory
symptom responses toward the end of the exposure period. These studies
report a small percentage of subjects experiencing lung function
decrements (>= 10 percent) at the 0.060 ppm exposure level. These
studies provide very limited evidence of O3-related lung
function decrements and respiratory symptoms at this lower exposure
level.
The Staff Paper noted that evidence from controlled human exposures
studies indicates that people with moderate-to-severe asthma have
somewhat larger decreases in lung function in response to O3
relative to healthy individuals. In addition, lung function responses
in people with asthma appear to be affected by baseline lung function
(i.e., magnitude of responses increases with increasing disease
severity). This newer information expands our understanding of the
physiological basis for increased sensitivity in people with asthma and
other airway diseases, recognizing that people with asthma present a
different response profile for cellular, molecular, and biochemical
responses than people who do not have asthma. New evidence indicates
that some people with asthma have increased occurrence and duration of
nonspecific airway responsiveness, which is an increased
bronchoconstrictive response to airway irritants. Controlled human
exposure studies also indicate that some people with allergic asthma
and rhinitis have increased airway responsiveness to allergens
following O3 exposure. Exposures to O3
exacerbated lung function decrements in people with pre-existing
allergic airway disease, with and without asthma. 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.
The Staff Paper also concluded that newly available human exposure
studies suggest that some people with asthma also have increased
inflammatory responses, relative to non-asthmatic subjects, and that
this inflammation may take longer to resolve. 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
qualitatively informs the Staff Paper's evaluation of the adequacy of
the current O3 standard in that it 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 Staff Paper noted that in addition to the experimental evidence
of lung function decrements, respiratory symptoms, and other
respiratory effects in healthy and asthmatic populations discussed
above, epidemiological studies have reported associations of lung
function decrements and respiratory symptoms in several locations. Two
large U.S. panel studies which together followed over 1,000 asthmatic
children on a daily basis (Mortimer et al., 2002, the National
Cooperative Inner-City Asthma Study, or NCICAS; and Gent et al., 2003),
as well as several smaller U.S. and international studies, have
reported robust associations between ambient O3
concentrations and measures of lung function, daily respiratory
symptoms (e.g., chest tightness, wheeze, shortness of breath), and
increased asthma medication use in children with moderate to severe
asthma. Mortimer et al. (2002) found that of the pollutants measured
(including O3, NO2, SO2 and
PM10), O3 was the only one that had a
statistically significant effect on lung function. (Mortimer et al.
2002) also found associations between NO2, SO2
and PM10 and respiratory symptoms that were stronger than
those between O3 and respiratory symptoms. Gent et al.
(2003) found that in co-pollutant models, O3 but not PM2.5
significantly predicted increased risk of respiratory symptoms and
rescue medication use among children using asthma maintenance
medication. Overall, the multi-city NCICAS (Mortimer et al., 2002),
(Gent et al. 2003), and several other single-city studies indicate a
robust positive association between ambient O3
concentrations and increased respiratory symptoms and increased
medication use in asthmatic children.
In considering the large number of single-city epidemiological
studies reporting lung function or respiratory symptoms effects in
healthy or asthmatic populations, the Staff Paper noted that most such
studies that reported positive and often statistically significant
associations in the warm season were conducted in areas that likely
would not have met the current standard. In considering the large
multi-city NCICAS (Mortimer et al., 2002), the Staff Paper noted that
the 98th percentile 8-hour daily maximum O3 concentrations
at the monitor reporting the highest O3 concentrations in
each of the study areas ranged from 0.084 ppm to > 0.10 ppm. However,
the authors indicate that less than 5 percent of the days in the eight
urban areas had 8-hour daily O3 concentrations exceeding
0.080 ppm. Moreover, the authors observed that when days with 8-hour
average O3 levels greater than 0.080 ppm were excluded,
similar effect estimates were seen compared to estimates that included
all of the days. There are also a few other studies in which the
relevant air quality statistics provide some indication that lung
function and respiratory symptom effects may be occurring in areas that
likely would have met the current standard (EPA, 2007b, p. 6-12).
(2) Respiratory hospital admissions and emergency department
visits. At the time of the last review, many time-series studies
indicated positive associations between ambient O3 and
increased respiratory hospital admissions and emergency room visits,
providing strong evidence for a relationship between O3
exposure and increased exacerbations of
[[Page 16446]]
preexisting lung disease extending below the level of the then current
1-hour O3 standard (EPA 2007b, section 3.3.1.1.6). Analyses
of data from studies conducted in the northeastern U.S. indicated that
O3 air pollution was consistently and strongly associated
with summertime respiratory hospital admissions.
Since the last review, new epidemiological studies have evaluated
the association between short-term exposures to O3 and
unscheduled hospital admissions for respiratory causes. Large multi-
city studies, as well as many studies from individual cities, have
reported positive and often statistically significant O3
associations with total respiratory hospitalizations as well as asthma-
and chronic obstructive pulmonary disease (COPD)-related
hospitalizations, especially in studies analyzing the O3
effect during the summer or warm season. Analyses using multipollutant
regression models generally indicate that copollutants do not confound
the association between O3 and respiratory hospitalizations
and that the O3 effect estimates were robust to PM
adjustment in all-year and warm-season only data. The Criteria Document
concluded that the evidence supports a causal relationship between
acute O3 exposures and increased respiratory-related
hospitalizations during the warm season.
In looking specifically at U.S. and Canadian respiratory
hospitalization studies that reported positive and often statistically
significant associations (and that either did not use GAM or were
reanalyzed to address GAM-related problems), the Staff Paper noted that
many such studies were conducted in areas that likely would not have
met the current O3 standard, with many providing only all-
year effect estimates, and with some reporting a statistically
significant association in the warm season. Of the studies that provide
some indication that O3-related respiratory hospitalizations
may be occurring in areas that likely would have met the current
standard, the Staff Paper noted that some are all-year studies, whereas
others reported statistically significant warm-season associations.
Emergency department visits for respiratory causes have been the
focus of a number of new studies that have examined visits related to
asthma, COPD, bronchitis, pneumonia, and other upper and lower
respiratory infections, such as influenza, with asthma visits typically
dominating the daily incidence counts. Among studies with adequate
controls for seasonal patterns, many reported at least one significant
positive association involving O3. However, inconsistencies
were observed which were at least partially attributable to differences
in model specifications and analysis approach among various studies. 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. Almost all of the studies that reported
statistically significant effect estimates were conducted in areas that
likely would not have met the current standard. The Criteria Document
concluded that analyses stratified by season generally supported a
positive association between O3 concentrations and emergency
department visits for asthma in the warm season. These studies provide
evidence of effects in areas that likely would not have met the current
standard and evidence of associations that likely extend down to
relatively low ambient O3 concentrations.
(3) Mortality. The 1996 Criteria Document concluded that an
association between daily mortality and O3 concentrations
for areas with high O3 levels (e.g., Los Angeles) was
suggested. However, due to inconsistencies in the results from the very
limited number of studies available at that time, there was
insufficient evidence to determine whether the observed association was
likely causal, and thus the possibility that O3 exposure may
be associated with mortality was not relied upon in the 1997 decision
on the O3 primary standard.
Since the last review, the body of evidence with regard to
O3-related health effects has been expanded by animal,
controlled human exposure, and epidemiological studies and now
identifies biologically plausible mechanisms by which O3 may
affect the cardiovascular system. In addition, there is stronger
information linking O3 to serious morbidity outcomes, such
as hospitalization, that are associated with increased mortality. Thus,
there is now a coherent body of evidence that describes a range of
health outcomes from lung function decrements to hospitalization and
premature mortality.
Newly available large multi-city studies and related analyses (Bell
et al., 2004; Huang et al., 2005; and Schwartz, 2005) designed
specifically to examine the effect of O3 and other
pollutants on mortality have provided much more robust and credible
information. Together these studies have reported significant
associations between O3 and mortality that were robust to
adjustment for PM and different adjustment methods for temperature and
suggest that the effect of O3 on mortality may be immediate
but may also persist for several days. Further analysis of one of these
multi-city studies (Bell et al., 2006) examined the shape of the
concentration-response function for the O3-mortality
relationship in 98 U.S. urban communities for the period 1987 to 2000
specifically to evaluate whether a threshold level exists. Results from
various analytic methods all indicated that any threshold, if it
exists, would likely occur at very low concentrations, far below the
level of the current O3 NAAQS and nearing background levels.
New data are also available from several single-city studies
conducted worldwide, as well as from several meta-analyses that have
combined information from multiple studies. Three recent meta-analyses
evaluated potential sources of heterogeneity in O3-mortality
associations. All three analyses reported common findings, including
effect estimates that were statistically significant and larger in warm
season analyses. Reanalysis of results using default GAM criteria did
not change the effect estimates, and there was no strong evidence of
confounding by PM.
Overall, the Criteria Document (p. 8-78) found that the results
from U.S. multi-city time-series studies, along with the meta-analyses,
provide relatively strong evidence for associations between short-term
O3 exposure and all-cause mortality even after adjustment
for the influence of season and PM. The results of these analyses of
studies considered in this review indicate that copollutants generally
do not appear to substantially confound the association between
O3 and mortality. In addition, several single-city studies
observed positive associations of ambient O3 concentrations
with total nonaccidental and cardiorespiratory mortality.
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; effect estimates for respiratory
mortality are less consistent in size, possibly due to reduced
statistical power in this subcategory of mortality. For cardiovascular
mortality, the Criteria Document (p. 7-106) suggested that effect
estimates are consistently positive and more likely to be larger and
statistically significant in warm season analyses. The Criteria
Document (p. 8-78) concluded that these findings are highly suggestive
that short-term O3 exposure directly or indirectly
contributes to nonaccidental and cardiorespiratory-related mortality,
but
[[Page 16447]]
additional research is needed to more fully establish underlying
mechanisms by which such effects occur.\15\
---------------------------------------------------------------------------
\15\ 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)
---------------------------------------------------------------------------
ii. Exposure- and Risk-Based Considerations
In evaluating the adequacy of the current standard, the Staff Paper
also considered estimated quantitative exposures and health risks, and
important uncertainties and limitations in those estimates, which are
highlighted above in section II.A.3 and discussed in section II.B of
the proposal. These estimates are derived from an EPA assessment of
exposures and health risks associated with recent air quality levels
and with air quality simulated to just meet the current standard to
help inform judgments about whether or not the current standard
provides adequate protection of public health.
The Staff Paper (and the CASAC Panel) 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
Staff Paper did not have sufficient information to evaluate all
relevant at-risk groups (e.g., outdoor workers, children under age 5)
or all O3-related health outcomes (e.g., increased
medication use, school absences, and emergency department visits that
are part of a broader pyramid of effects), and the scope of the 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, due to
the limited geographic scope of the exposure and risk assessments, EPA
recognizes that national-scale public health impacts of ambient
O3 exposures would be much larger than the quantitative
exposure and risk estimates associated with recent air quality or air
quality that just meets the current or alternative standards in the 12
urban areas analyzed. On the other hand, inter-individual variability
in responsiveness means that only a subset of individuals in each group
estimated to experience exposures at and above a given benchmark level
while at elevated exertion would actually be expected to experience
such adverse health effects.
The Staff Paper estimated exposures and risks for the three most
recent years (2002-2004) for which data were available at the time of
the analyses. As discussed above in section II.A.3.a, within this 3-
year period, 2002 was a year with relatively higher O3
levels in most, but not all, areas and simulation of just meeting the
current standard based on 2002 air quality data provides a generally
higher-end estimate of exposures and risks, while 2004 was a year with
relatively lower O3 levels in most, but not all, areas and
simulation of just meeting the current standard using 2004 air quality
data provides a generally lower-end estimate of exposures and risks.
The Staff Paper consideration of such exposure and risk analyses is
discussed below and in section II.C.2.b of the proposal, focusing on
both the exposure analyses and the human health risk assessment.
(1) Exposure analyses. EPA's exposure analysis estimated personal
exposures to ambient O3 levels at and above specific
benchmark levels while at elevated exertion to provide some perspective
on the potential public health impacts of respiratory symptoms and
respiratory-related physiological effects that cannot currently be
evaluated in quantitative risk assessments but 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. As noted
above in section II.A.3, the Staff Paper referred to exposures at and
above these benchmark levels as ``exposures of concern.'' The Staff
Paper noted that potential public health impacts likely occur across a
range of O3 exposure levels, such that there is no one
exposure level that addresses all relevant public health impacts.
Therefore, with the concurrence of the CASAC Panel, the Staff Paper
estimated exposures of concern not only at 0.080 ppm O3, a
level at which there are demonstrated effects, but also at 0.070 and
0.060 ppm O3. The Staff Paper recognized that there will be
varying degrees of concern about exposures at each of these levels,
based in part on the population subgroups 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 O3 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 Staff Paper focused on exposures at or above
benchmark levels of 0.070 and 0.060 ppm O3 while at elevated
exertion for purposes of evaluating the adequacy of the current
standard.
Exposure estimates were presented in the Staff Paper and in section
II.B (Table 1) of the proposal for the number and percent of all school
age children and asthmatic school age 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. The percent of population exposed at any
given level is very similar for all and asthmatic school age children.
Substantial year-to-year variability in exposure estimates is observed,
ranging to over an order of magnitude at the current standard level, in
estimates of the number of children and the number of occurrences of
exposures at both of these benchmark levels while at elevated exertion.
The Staff Paper stated that it is appropriate to consider not just the
average estimates across all years, but also to consider public health
impacts in years with relatively higher O3 levels. The Staff
Paper also noted 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 where these estimates are higher than
the average upon meeting the current standard.
About 50 percent of asthmatic of all school age children,
representing nearly 1.3 million asthmatic children and about 8.5
million school age children in the 12 urban areas examined, are
estimated to experience exposures at or above the 0.070 ppm benchmark
level while at elevated exertion (i.e., these individuals are estimated
to experience 8-hour O3 exposures at or above 0.070 ppm
while engaged in moderate or greater exertion 1 or more times during
the O3 season) associated with 2002 O3 air
quality levels. In contrast, about 17 percent of asthmatic and all
school age children are estimated to experience exposures at or above
the 0.070 ppm benchmark level while at elevated exertion associated
with 2004 O3 air quality levels. Just meeting the current
standard results in an aggregate estimate of about 20 percent of
asthmatic or 18 percent of all school age children likely to experience
exposures at or above the
[[Page 16448]]
0.070 ppm benchmark level while at elevated exertion using the 2002
simulation. The exposure estimates for this benchmark level range up to
about 40 percent of asthmatic or all school age children in the single
city with the highest estimate among the cities analyzed. Just meeting
the current standard based on the 2004 simulation, results in an
aggregate estimate of about 1 percent of asthmatic or all school age
children experiencing exposures exceeding the 0.070 ppm benchmark level
while at elevated exertion.
At the benchmark level of 0.060 ppm, about 70 percent of all or
asthmatic school age children are estimated to experience exposures at
or above this benchmark level while at elevated exertion for the
aggregate of the 12 urban areas associated with 2002 O3
levels. Just meeting the current standard would result in an aggregate
estimate of about 45 percent of asthmatic or all school age children
likely to experience exposures at or above the 0.060 ppm benchmark
level while at elevated exertion using the 2002 simulation. The
exposure estimates for this benchmark level range up to nearly 70
percent of all or asthmatic school age children in the single city with
the highest estimate among the cities analyzed associated with just
meeting the current standard using the 2002 simulation. The Staff Paper
indicated an aggregate estimate of about 10 percent of asthmatic or all
school age children would experience exposures at or above the 0.060
ppm benchmark level while at elevated exertion associated with just
meeting the current standard using the 2004 simulation.
(2) Risk assessment. The health risk assessment estimated risks for
several important health endpoints, including: (1) Lung function
decrements (i.e., >= 15 percent and >= 20 percent reductions in
FEV1) in all school age children for 12 urban areas; (2)
lung function decrements (i.e., >= 10 percent and >= 20 percent
reductions in FEV1) in asthmatic school age children for 5
urban areas (a subset of the 12 urban areas); (3) respiratory symptoms
(i.e., chest tightness, shortness of breath, wheeze) in moderate to
severe asthmatic children for the Boston area; (4) respiratory-related
hospital admissions for 3 urban areas; and (5) nonaccidental and
cardiorespiratory mortality for 12 urban areas for three recent years
(2002 to 2004) and for just meeting the current standard using a 2002
simulation and a 2004 simulation.
With regard to estimates of moderate lung function decrements,
meeting the current standard substantially reduces the estimated number
of school age children experiencing one or more occurrences of
FEV1 decrements >= 15 percent for the 12 urban areas, going
from about 1.3 million children (7 percent of children) under 2002 air
quality to about 610,000 (3 percent of children) based on the 2002
simulation, and from about 620,000 children (3 percent of children) to
about 230,000 (1 percent of children) using the 2004 simulation. In
asthmatic children, the estimated number of children experiencing one
or more occurrences of FEV1 decrements >= 10 percent for the
5 urban areas goes from about 250,000 children (16 percent of asthmatic
children) under 2002 air quality to about 130,000 (8 percent of
asthmatic children) using the 2002 simulation, and from about 160,000
(10 percent of asthmatic children) to about 70,000 (4 percent of
asthmatic children) using the 2004 simulation. Thus, even when the
current standard is met, about 4 to 8 percent of asthmatic school age
children are estimated to experience one or more occurrences of
moderate lung function decrements, resulting in about 1 million
occurrences (using the 2002 simulation) and nearly 700,000 occurrences
(using the 2004 simulation) in just 5 urban areas. Moreover, the
estimated number of occurrences of moderate or greater lung function
decrements per child is on average approximately 6 to 7 in all children
and 8 to 10 in asthmatic children in an O3 season, even when
the current standard is met, depending on the year used to simulate
meeting the current standard. In the 1997 review of the O3
standard a general consensus view of the adversity of such moderate
responses emerged as the frequency of occurrences increases, with the
judgment that repeated occurrences of moderate responses, even in
otherwise healthy individuals, may be considered adverse since they may
well set the stage for more serious illness.
With regard to estimates of large lung function decrements, the
Staff Paper noted that FEV1 decrements > 20 percent would
likely interfere with normal activities in many healthy individuals,
therefore single occurrences would be considered to be adverse. In
people with asthma, large lung function responses would likely
interfere with normal activities for most individuals and would also
increase the likelihood that these individuals would use additional
medication or seek medical treatment. Single occurrences would be
considered to be adverse to asthmatic individuals under the ATS
definition. They also would be cause for medical concern in some
individuals. While the current standard reduces the occurrences of
large lung function decrements in all children and asthmatic children
from about 60 to 70%, in a year with relatively higher O3
levels (2002), there are estimated to be about 500,000 occurrences in
all school children across the entire 12 urban areas, and about 40,000
occurrences in asthmatic children across just 5 urban areas. As noted
above, it is clear that even when the current standard is met over a
three-year period, O3 levels in each year can vary
considerably, as evidenced by relatively large differences between risk
estimates based on 2002 to 2004 air quality. The Staff Paper expressed
the view that it was appropriate to consider this yearly variation in
O3 levels allowed by the current standard in judging the
extent to which impacts on members of at-risk groups in a year with
relatively higher O3 levels remain of concern from a public
health perspective.
With regard to other O3-related health effects, the
estimated risks of respiratory symptom days in moderate to severe
asthmatic children, respiratory-related hospital admissions, and non-
accidental and cardiorespiratory mortality, respectively, are not
reduced to as great an extent by meeting the current standard as are
lung function decrements. For example, just meeting the current
standard reduces the estimated average incidence of chest tightness in
moderate to severe asthmatic children living in the Boston urban area
by 11 to 15%, based on 2002 and 2004 simulations, respectively,
resulting in an estimated incidence of about 23,000 to 31,000 per
100,000 children attributable to O3 exposure (Table 6-4).
Just meeting the current standard is estimated to reduce the incidence
of respiratory-related hospital admissions in the New York City urban
area by about 16 to 18%, based on 2002 and 2004 simulations,
respectively, resulting in an estimated incidence per 100,000
population of 4.6 to 6.4, respectively. Across the 12 urban areas, the
estimates of non-accidental mortality incidence per 100,000 relevant
population range from 0.4 to 2.6 (for 2002) and 0.5 to 1.5 (for 2004).
Meeting the current standard results in a reduction of the estimated
incidence per 100,000 population to a range of 0.3 to 2.4 based on the
2002 simulation and a range of 0.3 to 1.2 based on the 2004 simulation.
Estimates for cardiorespiratory mortality show similar patterns.
In considering the estimates of the proportion of population
affected and the number of occurrences of the health effects that are
included in the risk assessment, the Staff Paper noted that
[[Page 16449]]
these limited estimates are indicative of a much broader array of
potential O3-related health endpoints that we consider 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, emergency department visits)
and which primarily affect members of at-risk groups. While the Staff
Paper had sufficient information to estimate and consider the number of
symptom days in children with moderate to severe asthma, it recognized
that there are many other effects that may be associated with symptom
days, such as increased medication use, school and work absences, or
visits to doctors' offices, for which there was not sufficient
information to estimate risks but which are important to consider in
assessing the adequacy of the current standard. The same is true for
more serious, but less frequent effects. The Staff Paper estimated
hospital admissions, but there was not sufficient information to
estimate emergency department visits in a quantitative risk assessment.
Consideration of such unquantified risks in the Staff Paper reinforced
the Staff Paper conclusion that consideration should be given to
revising the standard so as to provide increased public health
protection, especially for at-risk groups such as people with asthma or
other lung diseases, as well as children and older adults, particularly
those active outdoors, and outdoor workers.
iii. Summary of Staff Paper Considerations
The Staff Paper concluded that the overall body of evidence clearly
calls into question the adequacy of the current standard in protecting
at-risk groups against an array of adverse health effects that range
from decreased lung function and respiratory symptoms to serious
indicators of respiratory morbidity including emergency department
visits and hospital admissions for respiratory causes, nonaccidental
mortality, and possibly cardiovascular effects. These at-risk groups
notably include asthmatic children and other people with lung disease,
as well as all children and older adults, especially those active
outdoors, and outdoor workers.\16\ The available information provides
strong support for consideration of an O3 standard that
would provide increased health protection for these at-risk groups. The
Staff Paper also concluded that risks projected to remain upon meeting
the current standard are indicative of risks to at-risk groups that can
be judged to be important from a public health perspective. This
information reinforced the Staff Paper conclusion that consideration
should be given to revising the level of the standard so as to provide
increased public health protection.
---------------------------------------------------------------------------
\16\ In defining at-risk groups this way we are including both
groups with greater inherent sensitivity and those more likely to be
exposed.
---------------------------------------------------------------------------
b. CASAC Views
The CASAC Panel unanimously concluded in a letter to the
Administrator that there is ``no scientific justification for
retaining'' the current primary O3 standard, and the current
standard ``needs to be substantially reduced to protect human health,
particularly in sensitive subpopulations'' (Henderson, 2006c, pp. 1-2).
In its rationale for this conclusion, the CASAC Panel concluded that
``new evidence supports and builds-upon key, health-related conclusions
drawn in the 1997 O3 NAAQS review'' (id., p. 3). The Panel
noted that several new single-city studies and large multi-city studies
have provided more evidence for adverse health effects at
concentrations lower than the current standard, and that these
epidemiological studies are backed-up by evidence from controlled human
exposure studies. The Panel specifically noted evidence from the recent
Adams (2006) study that reported statistically significant decrements
in the lung function of healthy, moderately exercising adults at a
0.080 ppm exposure level, and importantly, also reported adverse lung
function effects in some healthy individuals at 0.060 ppm. The CASAC
Panel concluded that these results indicate that the current standard
``is not sufficiently health-protective with an adequate margin of
safety,'' noting that while similar studies in sensitive groups such as
asthmatics have yet to be conducted, ``people with asthma, and
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 volunteers (Mortimer et al.,
2002)'' (Henderson, 2006c, p. 4).
The CASAC Panel also highlighted a number of O3-related
adverse health effects that are associated with exposure to ambient
O3, below the level of the current standard based on a broad
range of epidemiological studies (Henderson, 2006c). These adverse
health effects include increases in school absenteeism, respiratory
hospital emergency department visits among asthmatics and patients with
other respiratory diseases, hospitalizations for respiratory illnesses,
symptoms associated with adverse health effects (including chest
tightness and medication usage), and premature mortality
(nonaccidental, cardiorespiratory deaths) reported at exposure levels
well below the current standard. ``The CASAC considers each of these
findings to be an important indicator of adverse health effects''
(Henderson, 2006c).
The CASAC Panel expressed the view that more emphasis should be
placed on the subjects in controlled human exposure studies with FEV1
decrements greater than 10 percent, which can be clinically
significant, rather than on the relatively small average decrements.
The Panel also emphasized significant O3-related
inflammatory responses and markers of injury to the epithelial lining
of the lung that are independent of spirometric responses. Further, the
Panel expressed the view that the Staff Paper did not place enough
emphasis on serious morbidity (e.g., hospital admissions) and mortality
observed in epidemiological studies. On the basis of the large amount
of recent data evaluating adverse health effects at levels at and below
the current O3 standard, it was the unanimous opinion of the
CASAC Panel that the current primary O3 standard is not
adequate to protect human health, that the relevant scientific data do
not support consideration of retaining the current standard, and that
the current standard needs to be substantially reduced to be protective
of human health, particularly in sensitive subpopulations (Henderson,
2006c, pp. 4-5).
Further, the CASAC letter noted that ``there is no longer
significant scientific uncertainty regarding the CASAC's conclusion
that the current 8-hour primary NAAQS must be lowered'' (Henderson,
2006c, p. 5). The Panel noted that a ``large body of data clearly
demonstrates adverse human health effects at the current level'' of the
standard, such that ``[R]etaining this standard would continue to put
large numbers of individuals at risk for respiratory effects and/or
significant impact on quality of life including asthma exacerbations,
emergency room visits, hospital admissions and mortality'' (Henderson,
2006c).
c. Administrator's Proposed Conclusions
At the time of proposal, in considering whether the current primary
standard should be revised, the Administrator carefully considered the
conclusions contained in the Criteria Document, the rationale and
recommendations contained in the Staff Paper, the advice and
recommendations
[[Page 16450]]
from CASAC, and public comments to date on this issue. In so doing, the
Administrator noted the following: (1) That evidence of a range of
respiratory-related morbidity effects seen in the last review has been
considerably strengthened, both through toxicological and controlled
human exposure studies as well as through many new panel and
epidemiological studies; (2) that new evidence from controlled human
exposure and epidemiological studies identifies people with asthma
(including children with asthma) as an important susceptible population
for which estimates of respiratory effects in the general population
likely underestimate the magnitude or importance of these effects; (3)
that new evidence about mechanisms of toxicity further contributes to
the biological plausibility of O3-induced respiratory
effects and is beginning to suggest mechanisms that may link
O3 exposure to cardiovascular effects; (4) that there is now
relatively strong evidence for associations between O3 and
total nonaccidental and cardiopulmonary mortality, even after
adjustment for the influence of season and PM; and (5) the limits of
the available evidence. Relative to the information that was available
to inform the Agency's 1997 decision to set the current standard, the
newly available evidence increased the Administrator's confidence that
respiratory morbidity effects such as lung function decrements and
respiratory symptoms are causally related to O3 exposures,
that indicators of respiratory morbidity such as emergency department
visits and hospital admissions are causally related to O3
exposures, and that the evidence is highly suggestive that
O3 exposures during the O3 season contribute to
premature mortality.
The Administrator judged that there is important new evidence
demonstrating that exposures to O3 at levels below the level
of the current standard are associated with a broad array of adverse
health effects, especially in at-risk populations that include people
with asthma or other lung diseases who are likely to experience more
serious effects from exposure to O3, children and older
adults with increased susceptibility, as well as those who are likely
to be vulnerable as a result of spending a lot of time outdoors engaged
in physical activity, especially active children and outdoor workers.
Examples of this important new evidence include demonstration of
O3-induced lung function effects and respiratory symptoms in
some healthy individuals down to the previously observed exposure level
of 0.080 ppm, as well as very limited new evidence at exposure levels
well below the level of the current standard. In addition, there is now
epidemiological evidence of statistically significant O3-
related associations with lung function and respiratory symptom
effects, respiratory-related emergency department visits and hospital
admissions, and increased mortality, in areas that likely would have
met the current standard. There are also many epidemiological studies
done in areas that likely would not have met the current standard but
which nonetheless report statistically significant associations that
generally extend down to ambient O3 concentrations that are
below the level of the current standard. Further, there are a few
studies that have examined subsets of data that include only days with
ambient O3 concentrations below the level of the current
standard, or below even much lower O3 concentrations, and
continue to report statistically significant associations with
respiratory morbidity outcomes and mortality. The Administrator
recognized that the evidence from controlled human exposure studies,
together with animal toxicological studies, provides considerable
support for the biological plausibility of the respiratory morbidity
associations observed in the epidemiological studies and for concluding
that the associations extend below the level of the current standard.
However, the Administrator recognized that in the body of
epidemiological evidence, many studies reported positive and
statistically significant associations, while others reported positive
results that were not statistically significant, and a few did not
report any positive O3-related associations. In addition,
the Administrator judged that evidence of a causal relationship between
adverse health outcomes and O3 exposures became increasingly
uncertain at lower levels of exposure.
Based on the strength of the currently available evidence of
adverse health effects, and on the extent to which the evidence
indicates that such effects likely result from exposures to ambient
O3 concentrations below the level of the current standard,
the Administrator judged that the current standard does not protect
public health with an adequate margin of safety and that the standard
should be revised to provide such protection, especially for at-risk
groups, against a broad array of adverse health effects.
In reaching this judgment, the Administrator had also considered
the results of both the exposure and risk assessments conducted for
this review, to provide some perspective on the extent to which at-risk
groups would likely experience ``exposures of concern'' \17\ and on the
potential magnitude of the risk of experiencing various adverse health
effects when recent air quality data (from 2002 to 2004) are used to
simulate meeting the current standard and alternative standards in a
number of urban areas in the U.S.\18\ In considering the results of the
health risk assessment, as discussed in the proposal notice (section
II.C.2), the Administrator noted that there were important
uncertainties and assumptions inherent in the risk assessment and that
this assessment was most appropriately used to simulate trends and
patterns that could be expected, as well as providing informed, but
still imprecise, estimates of the potential magnitude of risks.
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\17\ As discussed in section II.A.3 above, ``exposures of
concern'' are estimates of 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 with
varying degrees of certainty be inferred to occur in some
individuals. Estimates of exposures of concern provide some
perspective on the public health impacts of health effects that may
occur in some individuals at recent air quality levels but cannot be
evaluated in quantitative risk assessments, and the extent to which
such impacts might be reduced by meeting the current and alternative
standards.
\18\ As noted above in section II.A.3, recent O3 air
quality distributions have been statistically adjusted to simulate
just meeting the current and selected alternative standards. These
simulations do not represent predictions of when, whether, or how
areas might meet the specified standards.
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In considering the exposure assessment results at the time of
proposal, the Administrator considered analyses that define ``exposures
of concern'' by three benchmark exposure levels: 0.080, 0.070, and
0.060 ppm. Estimates of exposures in at-risk groups at and above these
benchmark levels while at elevated exertion, using O3 air
quality data in 2002 and 2004, provide some indication of the potential
magnitude of the incidence of health outcomes that cannot currently be
evaluated in a quantitative risk assessment, such as increased airway
responsiveness, increased pulmonary inflammation, increased cellular
permeability, and decreased pulmonary defense mechanisms. These
respiratory-related physiological effects have been demonstrated to
occur in healthy people at O3 exposures as low as 0.080 ppm,
the lowest level tested for these effects. These physiological effects
provide plausible mechanisms underlying observed associations with
aggravation of asthma, increased medication use, increased school and
work absences,
[[Page 16451]]
increased susceptibility to respiratory infection, increased visits to
doctors' offices and emergency departments, and increased admissions to
hospitals. In addition, these physiological effects, if repeated over
time, have the potential to lead to chronic effects such as chronic
bronchitis or long-term damage to the lungs that can lead to reduced
quality of life.
In considering these various benchmark levels for exposures of
concern at the time of proposal, the Administrator focused primarily on
estimated exposures at and above the 0.070 ppm benchmark level while at
elevated exertion as an important surrogate measure for potentially
more serious health effects in at-risk groups such as people with
asthma. This judgment was based on the strong evidence of effects in
healthy people at the 0.080 ppm exposure level and the new evidence
that people with asthma are likely to experience larger and more
serious effects than healthy people at the same level of exposure. In
the Administrator's view at the time of proposal, this evidence did not
support a focus on exposures at and above the benchmark level of 0.080
ppm O3, as it would not adequately account for the increased
risk of harm from exposure for members of at-risk groups, especially
people with asthma. The Administrator also judged that the evidence of
demonstrated effects is too limited to support a primary focus on
exposures down to the lowest benchmark level considered of 0.060 ppm.
The Administrator particularly noted that although the analysis of
``exposures of concern'' was conducted to estimate exposures at and
above three discrete benchmark levels (0.080, 0.070, and 0.060 ppm)
while at elevated exertion, the concept is appropriately viewed as a
continuum. In so doing, the Administrator sought to balance concern
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 exposure levels.
The Administrator observed that based on the aggregate exposure
estimates for the 2002 simulation (summarized in section II.B.1, Table
1, of the proposal) for the 12 U.S. urban areas included in the
exposure analysis, upon just meeting the current standard up to about
20 percent of asthmatic or all school age children are likely to
experience one or more exposures at and above the 0.070 ppm benchmark
level while at elevated exertion; the 2004 simulation yielded an
estimate of about 1 percent of such children. The Administrator noted
from this comparison that there is substantial year-to-year
variability, ranging up to an order of magnitude or more in estimates
of the number of people and the number of occurrences of exposures at
and above this benchmark level while at elevated exertion. Moreover,
within any given year, the exposure assessment indicates that there is
substantial city-to-city variability in the estimates of the children
exposed or the number of occurrences of exposure at and above this
benchmark level while at elevated exertion. For example, city-specific
estimates of the percent of asthmatic or all school age children likely
to experience exposures at and above the benchmark level of 0.070 ppm
while at elevated exertion ranges from about 1 percent up to about 40
percent across the 12 urban areas upon just meeting the current
standard based on the 2002 simulation; the 2004 simulation yielded
estimates that range from about 0 up to about 7 percent. The
Administrator judged that it was important to recognize the substantial
year-to-year and city-to-city variability in considering these
estimates.
With regard to the results of the risk assessment, the
Administrator focused on the risks estimated to remain upon just
meeting the current standard. Based on the aggregate risk estimates
(summarized in section II.B.2, Table 2, of the proposal), the
Administrator observed that upon just meeting the current standard
based on the 2002 simulation, approximately 8 percent of asthmatic
school age children across 5 urban areas (ranging up to about 11
percent in the city with the highest estimate among the cities
analyzed) would still be estimated to experience moderate or greater
lung function decrements one or more times within an O3
season. These estimated percentages would be approximately 3 percent of
all school age children across 12 urban areas (ranging up to over 5
percent in the city with the highest estimate among the cities
analyzed). The Administrator recognized that, as with the estimates of
exposures of concern, there is substantial year-to-year and city-to-
city variability in these risk estimates.
In addition to the percentage of asthmatic or all children
estimated to experience one or more occurrences of an effect, the
Administrator recognized that some individuals are estimated to have
multiple occurrences. For example, across all the cities in the
assessment, approximately 6 to 7 occurrences of moderate or greater
lung function decrements per child are estimated to occur in all
children and approximately 8 to 10 occurrences are estimated to occur
in asthmatic children in an O3 season, even upon just
meeting the current standard. In the last review, a general consensus
view of the adversity of such responses emerged as the frequency of
occurrences increases, with the judgment that repeated occurrences of
moderate responses, even in otherwise healthy individuals, may be
considered adverse since they may well set the stage for more ser