[Federal Register Volume 76, Number 29 (Friday, February 11, 2011)]
[Proposed Rules]
[Pages 8158-8220]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2011-2404]
[[Page 8157]]
Vol. 76
Friday,
No. 29
February 11, 2011
Part VI
Environmental Protection Agency
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40 CFR Parts 50, 53 and 58
National Ambient Air Quality Standards for Carbon Monoxide; Proposed
Rule
Federal Register / Vol. 76, No. 29 / Friday, February 11, 2011 /
Proposed Rules
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Parts 50, 53 and 58
[EPA-HQ-OAR-2008-0015; FRL-9261-4; 2060-AI43]
National Ambient Air Quality Standards for Carbon Monoxide
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
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SUMMARY: Based on its review of the air quality criteria and the
national ambient air quality standards (NAAQS) for carbon monoxide
(CO), EPA is proposing to retain the current standards. EPA is also
proposing changes to the ambient air monitoring requirements for CO
including those related to network design.
DATES: Comments must be received on or before April 12, 2011.
Public Hearings: If, by February 18, 2011, EPA receives a request
from a member of the public to speak at a public hearing concerning the
proposed regulation, we will hold a public hearing on February 28, 2011
in Arlington, Virginia.
ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2008-0015 by one of the following methods:
http://www.regulations.gov: Follow the on-line
instructions for submitting comments.
E-mail: [email protected].
Fax: 202-566-9744.
Mail: Docket No. EPA-HQ-OAR-2008-0015, Environmental
Protection Agency, Mail code 6102T, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460. Please include a total of two copies.
Hand Delivery: Docket No. EPA-HQ-OAR-2008-0015,
Environmental Protection Agency, EPA West, Room 3334, 1301 Constitution
Ave., NW., Washington, DC. Such deliveries are only accepted during the
Docket's normal hours of operation, and special arrangements should be
made for deliveries of boxed information.
Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2008-0015. EPA's policy is that all comments received will be included
in the public docket without change and may be made available online at
http://www.regulations.gov, including any personal information
provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through http://www.regulations.gov or e-mail. The http://www.regulations.gov Web site
is an ``anonymous access'' system, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment. If you send an e-mail comment directly to EPA without
going through www.regulations.gov your e-mail address will be
automatically captured and included as part of the comment that is
placed in the public docket and made available on the Internet. If you
submit an electronic comment, EPA recommends that you include your name
and other contact information in the body of your comment and with any
disk or CD-ROM you submit. If EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, EPA
may not be able to consider your comment. Electronic files should avoid
the use of special characters, any form of encryption, and be free of
any defects or viruses. For additional information about EPA's public
docket visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm.
Public Hearing. If a public hearing is held, it will be held at the
U.S. Environmental Protection Agency Conference Center, First Floor
Conference Center South, One Potomac Yard, 2777 S. Crystal Drive,
Arlington, VA 22202. All visitors will need to go through security and
present a valid photo identification, such as a driver's license. To
request a public hearing or information pertaining to a public hearing,
contact Ms. Jan King, Health and Environmental Impacts Division, Office
of Air Quality Planning and Standards (C504-02), Environmental
Protection Agency, Research Triangle Park, North Carolina 27711;
telephone number (919) 541- 5665; fax number (919) 541-2664; e-mail
address: [email protected]. See the SUPPLEMENTARY INFORMATION for
further information about a possible public hearing.
Docket: All documents in the docket are listed in the http://www.regulations.gov index. Although listed in the index, some
information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in http://www.regulations.gov or in hard copy at the Air and Radiation
Docket and Information Center, EPA/DC, EPA West, Room 3334, 1301
Constitution Ave., NW., Washington, DC. The Public Reading Room is open
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal
holidays. The telephone number for the Public Reading Room is (202)
566-1744 and the telephone number for the Air and Radiation Docket and
Information Center is (202) 566-1742.
FOR FURTHER INFORMATION CONTACT: Dr. Deirdre Murphy, 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: 919-541-0729; fax: 919-
541-0237; e-mail: [email protected]. For further information
specifically with regard to section IV of this notice, contact Mr.
Nealson Watkins, Air Quality Analysis Division, Office of Air Quality
Planning and Standards, U.S. Environmental Protection Agency, Mail code
C304-06, Research Triangle Park, NC 27711; telephone: 919-541-5522;
fax: 919-541-1903; e-mail: [email protected]. To request a public
hearing or information pertaining to a public hearing, contact Ms. Jan
King, Health and Environmental Impacts Division, Office of Air Quality
Planning and Standards (C504-02), Environmental Protection Agency,
Research Triangle Park, North Carolina 27711; telephone number (919)
541- 5665; fax number (919) 541-2664; e-mail address: [email protected].
SUPPLEMENTARY INFORMATION:
General Information
What should I consider as I prepare my comments for EPA?
1. Submitting CBI. Do not submit this information to EPA through
http://www.regulations.gov or e-mail. Clearly mark the part or all of
the information that you claim to be CBI. For CBI information in a disk
or CD ROM that you mail to EPA, mark the outside of the disk or CD ROM
as CBI and then identify electronically within the disk or CD ROM the
specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2.
2. Tips for Preparing Your Comments. When submitting comments,
remember to:
[[Page 8159]]
Identify the rulemaking by docket number and other
identifying information (subject heading, Federal Register date and
page number).
Follow directions--the agency may ask you to respond to
specific questions or organize comments by referencing a Code of
Federal Regulations (CFR) part or section number.
Explain why you agree or disagree, suggest alternatives,
and substitute language for your requested changes.
Describe any assumptions and provide any technical
information and/or data that you used.
Provide specific examples to illustrate your concerns, and
suggest alternatives.
Explain your views as clearly as possible, avoiding the
use of profanity or personal threats.
Make sure to submit your comments by the comment period
deadline identified.
Availability of Related Information
A number of the documents that are relevant to this rulemaking are
available through EPA's Office of Air Quality Planning and Standards
(OAQPS) Technology Transfer Network (TTN) Web site at http://www.epa.gov/ttn/naaqs/standards/co/s_co_index.html. These documents
include the Plan for Review of the National Ambient Air Quality
Standards for Carbon Monoxide (Integrated Review Plan or IRP, USEPA,
2008), available at http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_pd.html, the Integrated Science Assessment for Carbon Monoxide
(USEPA, 2010a), available at http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_isa.html, the Quantitative Risk and Exposure Assessment for
Carbon Monoxide--Amended (USEPA, 2010b), available at http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_rea.html, and the Policy
Assessment for the Review of the Carbon Monoxide National Ambient Air
Quality Standards (USEPA, 2010c), available at http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_pa.html. These and other related
documents are also available for inspection and copying in the EPA
docket identified above.
How can I find information about a possible public hearing?
To request a public hearing or information pertaining to a public
hearing on this document, contact Ms. Jan King, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards (C504-02), Environmental Protection Agency, Research Triangle
Park, North Carolina 27711; telephone number (919) 541- 5665; fax
number (919) 541-2664; e-mail address: [email protected]. If a request
for a public hearing is received by February 18, 2011, information
about the hearing will be posted prior to the hearing on EPA's Web site
for carbon monoxide regulatory actions at http://www.epa.gov/airquality/urbanair/co/.
Table of Contents
The following topics are discussed in this preamble:
I. Background
A. Legislative Requirements
B. Related Carbon Monoxide Control Programs
C. Review of the Air Quality Criteria and Standards for Carbon
Monoxide
II. Rationale for Proposed Decisions on the Primary Standards
A. Air Quality Information
1. Anthropogenic Sources and Emissions of Carbon Monoxide
2. Ambient Concentrations
B. Health Effects Information
1. Carboxyhemoglobin as Biomarker and Mechanism of Toxicity
2. Nature of Effects
3. At-Risk Populations
4. Potential Impacts on Public Health
C. Human Exposure and Dose Assessment
1. Summary of Design Aspects
2. Key Limitations and Uncertainties
D. Conclusions on Adequacy of the Current Standards
1. Approach
2. Evidence-Based and Exposure/Dose-Based Considerations in the
Policy Assessment
3. CASAC Advice
4. Administrator's Proposed Conclusions Concerning Adequacy
E. Summary of Proposed Decisions on Primary Standards
III. Consideration of a Secondary Standard
A. Background and Considerations in Previous Reviews
B. Evidence-Based Considerations in the Policy Assessment
C. CASAC Advice
D. Administrator's Proposed Conclusions Concerning a Secondary
Standard
IV. Proposed Amendments to Ambient Monitoring Requirements
A. Monitoring Methods
1. Proposed Changes to Part 50, Appendix C
2. Proposed Changes to Part 53
3. Implications for Air Monitoring Networks
B. Network Design
1. Background
2. On-Road Mobile Sources
3. Near-Road Environment
4. Urban Downtown Areas and Urban Street Canyons
5. Meteorological and Topographical Influences
6. Proposed Changes
7. Microscale Carbon Monoxide Monitor Siting Criteria
V. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
B. Paperwork Reduction Act
C. Regulatory Flexibility Act
D. Unfunded Mandates Reform Act
E. Executive Order 13132: Federalism
F. Executive Order 13175: Consultation and Coordination with
Indian Tribal Governments
G. Executive Order 13045: Protection of Children from
Environmental Health and Safety Risks
H. Executive Order 13211: Actions that Significantly Affect
Energy Supply, Distribution or Use
I. National Technology Transfer and Advancement Act
J. Executive Order 12898: Federal Actions to Address
Environmental Justice in Minority Populations and Low-Income
Populations References
I. Background
A. Legislative Requirements
Two sections of the Clean Air Act (CAA) govern the establishment
and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the
Administrator to identify and list ``air pollutant[s]'' that in her
``judgment, cause or contribute to air pollution which may reasonably
be anticipated to endanger public health or welfare'' and satisfy two
other criteria, including ``whose presence * * * in the ambient air
results from numerous or diverse mobile or stationary sources'' and to
issue air quality criteria for those that are listed. Air quality
criteria are intended to ``accurately reflect the latest scientific
knowledge useful in indicating the kind and extent of all identifiable
effects on public health or welfare which may be expected from the
presence of [a] pollutant in the ambient air * * * .''
Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants for
which air quality criteria are issued. Section 109(b)(1) defines a
primary standard as one ``the attainment and maintenance of which in
the judgment of the Administrator, based on such criteria and allowing
an adequate margin of safety, are requisite to protect the public
health.'' \1\ A secondary standard, as defined in section 109(b)(2),
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on such criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects
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associated with the presence of such air pollutant in the ambient
air.'' \2\
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\1\ The legislative history of section 109 indicates that a
primary standard is to be set at ``the maximum permissible ambient
air level * * * which will protect the health of any [sensitive]
group of the population,'' and that for this purpose ``reference
should be made to a representative sample of persons comprising the
sensitive group rather than to a single person in such a group'' [S.
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970)].
\2\ Welfare effects as defined in section 302(h) (42 U.S.C.
7602(h)) include, but are not limited to, ``effects on soils, water,
crops, vegetation, man-made materials, animals, wildlife, weather,
visibility, and climate, damage to and deterioration of property,
and hazards to transportation, as well as effects on economic values
and on personal comfort and well-being.''
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The requirement that primary standards include an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (DC
Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176, 1186 (DC Cir. 1981), cert. denied,
455 U.S. 1034 (1982). Both kinds of uncertainties are components of the
risk associated with pollution at levels below those at which human
health effects can be said to occur with reasonable scientific
certainty. Thus, in selecting primary standards that include an
adequate margin of safety, the Administrator is seeking not only to
prevent pollution levels that have been demonstrated to be harmful but
also to prevent lower pollution levels that may pose an unacceptable
risk of harm, even if the risk is not precisely identified as to nature
or degree. The CAA does not require the Administrator to establish a
primary NAAQS at a zero-risk level or at background concentration
levels, see Lead Industries Association v. EPA, 647 F.2d at 1156 n. 51,
but rather at a level that reduces risk sufficiently so as to protect
public health with an adequate margin of safety.
In addressing the requirement for an adequate margin of safety, EPA
considers such factors as the nature and severity of the health effects
involved, the size of the population(s) at risk, and the kind and
degree of the uncertainties that must be addressed. The selection of
any particular approach to providing an adequate margin of safety is a
policy choice left specifically to the Administrator's judgment. Lead
Industries Association v. EPA, 647 F.2d at 1161-62; Whitman v. American
Trucking Associations, 531 U.S. 457, 495 (2001).
In setting standards that are ``requisite'' to protect public
health and welfare, as provided in section 109(b), EPA's task is to
establish standards that are neither more nor less stringent than
necessary for these purposes. Whitman v. American Trucking
Associations, 531 U.S. 457, 473. In establishing ``requisite'' primary
and secondary standards, EPA may not consider the costs of implementing
the standards. Id. at 471.
Section 109(d)(1) of the CAA requires that ``[n]ot later than
December 31, 1980, and at 5-year intervals thereafter, the
Administrator shall complete a thorough review of the criteria
published under section 108 and the national ambient air quality
standards * * * and shall make such revisions in such criteria and
standards and promulgate such new standards as may be appropriate * *
*'' Section 109(d)(2) requires that an independent scientific review
committee ``shall complete a review of the criteria * * * and the
national primary and secondary ambient air quality standards * * * and
shall recommend to the Administrator any new * * * standards and
revisions of existing criteria and standards as may be appropriate. * *
*'' This independent review function is performed by the Clean Air
Scientific Advisory Committee (CASAC).
B. Related Carbon Monoxide Control Programs
States are primarily responsible for ensuring attainment and
maintenance of ambient air quality standards once EPA has established
them. Under section 110 of the Act, and related provisions, States are
to submit, for EPA approval, State implementation plans (SIPs) that
provide for the attainment and maintenance of such standards through
control programs directed to sources of the pollutants involved. The
States, in conjunction with EPA, also administer the prevention of
significant deterioration program. See CAA sections 160-169. In
addition, Federal programs provide for nationwide reductions in
emissions of these and other air pollutants through the Federal motor
vehicle and motor vehicle fuel control program under title II of the
Act, (CAA sections 202-250) which involves controls for emissions from
moving sources and controls for the fuels used by these sources; new
source performance standards under section 111; and title IV of the Act
(CAA sections 402-416), which specifically provides for major
reductions in CO emissions.
C. Review of the Air Quality Criteria and Standards for Carbon Monoxide
EPA initially established NAAQS for CO on April 30, 1971. The
primary standards were established to protect against the occurrence of
carboxyhemoglobin levels in human blood associated with health effects
of concern. The standards were set at 9 parts per million (ppm), as an
8-hour average and 35 ppm, as a 1-hour average, neither to be exceeded
more than once per year (36 FR 8186). In the 1971 decision, the
Administrator judged that attainment of these standards would provide
the requisite protection of public health with an adequate margin of
safety and would also provide requisite protection against known and
anticipated adverse effects on public welfare, and accordingly set the
secondary (welfare-based) standards identical to the primary (health-
based) standards.
In 1985, EPA concluded its first periodic review of the criteria
and standards for CO (50 FR 37484). In that review, EPA updated the
scientific criteria upon which the initial CO standards were based
through the publication of the 1979 Air Quality Criteria Document for
Carbon Monoxide (AQCD; USEPA, 1979a) and prepared a Staff Paper (USEPA,
1979b), which, along with the 1979 AQCD, served as the basis for the
development of the notice of proposed rulemaking which was published on
August 18, 1980 (45 FR 55066). Delays due to uncertainties regarding
the scientific basis for the final decision resulted in EPA's
announcing a second public comment period (47 FR 26407). Following
substantial reexamination of the scientific data, EPA prepared an
Addendum to the 1979 AQCD (USEPA, 1984a) and an updated Staff Paper
(USEPA, 1984b). Following review by CASAC (Lippmann, 1984), EPA
announced its decision not to revise the existing primary standard and
to revoke the secondary standard for CO on September 13, 1985, due to a
lack of evidence of effects on public welfare at ambient concentrations
(50 FR 37484).
On August 1, 1994, EPA concluded its second periodic review of the
criteria and standards for CO by deciding that revisions to the CO
NAAQS were not warranted at that time (59 FR 38906). This decision
reflected EPA's review of relevant scientific information assembled
since the last review, as contained in the 1991 AQCD (USEPA, 1991) and
the 1992 Staff Paper (USEPA, 1992). Thus, the primary standards were
retained at 9 ppm with an 8-hour averaging time, and 35 ppm with a 1-
hour averaging time, neither to be exceeded more than once per year (59
FR 38906).
EPA initiated the next periodic review in 1997 and the final 2000
AQCD (U.S. EPA, 2000) was released in August 2000. After release of the
AQCD, Congress requested that the National Research Council (NRC)
review the
[[Page 8161]]
impact of meteorology and topography on ambient CO concentrations in
high altitude and extreme cold regions of the U.S. The NRC convened the
Committee on Carbon Monoxide Episodes in Meteorological and
Topographical Problem Areas, which focused on Fairbanks, Alaska as a
case-study.
A final report, ``Managing Carbon Monoxide Pollution in
Meteorological and Topographical Problem Areas,'' was published in 2003
(NRC, 2003) and offered a wide range of recommendations regarding
management of CO air pollution, cold start emissions standards,
oxygenated fuels, and CO monitoring. Following completion of the NRC
report, EPA did not conduct rulemaking to complete the review.
On September 13, 2007, EPA issued a call for information from the
public (72 FR 52369) requesting the submission of recent scientific
information on specified topics. A workshop was held on January 28-29,
2008 (73 FR 2490) to discuss policy-relevant scientific and technical
information to inform EPA's planning for the CO NAAQS review. Following
the workshop, a draft Integrated Review Plan (IRP) (USEPA, 2008a) was
made available in March 2008 for public comment and was discussed by
the CASAC via a publicly accessible teleconference consultation on
April 8, 2008 (73 FR 12998; Henderson, 2008). EPA made the final IRP
available in August 2008 (USEPA, 2008b).
In preparing the Integrated Science Assessment for Carbon Monoxide
(ISA or Integrated Science Assessment), EPA held an authors'
teleconference in November 2008 with invited scientific experts to
discuss preliminary draft materials prepared as part of the ongoing
development of the CO ISA and its supplementary annexes. The first
draft ISA (USEPA, 2009a) was made available for public review on March
12, 2009 (74 FR 10734) and reviewed by CASAC at a meeting held on May
12-13, 2009 (74 FR 15265). A second draft ISA (USEPA, 2009b) was
released for CASAC and public review on September 23, 2009 (74 FR
48536), and it was reviewed by CASAC at a meeting held on November 16-
17, 2009 (74 FR 54042). The final ISA was released in January 2010
(USEPA, 2010a).
In May 2009, OAQPS released a draft planning document, the draft
Scope and Methods Plan (USEPA, 2009c), for consultation with CASAC and
public review at the CASAC meeting held on May 12-13, 2009. Taking into
consideration comments on the draft Plan from CASAC (Brain, 2009) and
the public, OAQPS staff developed and released for CASAC review and
public comment a first draft Risk and Exposure Assessment (REA) (USEPA,
2009d), which was reviewed at the CASAC meeting held on November 16-17,
2009. Subsequent to that meeting and taking into consideration comments
from CASAC (Brain and Samet, 2010a) and public comments on the first
draft REA, a second draft REA (USEPA, 2010d) was released for CASAC
review and public comment in February 2010, and reviewed at a CASAC
meeting held on March 22-23, 2010. Drawing from information in the
final CO ISA and the second draft REA, EPA released a draft Policy
Assessment (PA) (USEPA, 2010e) in early March, 2010 for CASAC review
and public comment at the same meeting. Taking into consideration
comments on the second draft REA and the draft PA from CASAC (Brain and
Samet, 2010b, 2010c) and the public, staff completed the quantitative
assessments which are presented in the final REA (USEPA, 2010b). Staff
additionally took into consideration those comments and the final REA
analyses in completing the final Policy Assessment (USEPA, 2010c) which
was released in October, 2010.
The schedule for completion of this review is governed by a court
order resolving a lawsuit filed in March 2003 by a group of plaintiffs
who alleged that EPA had failed to perform its mandatory duty, under
section 109(d)(1), to complete a review of the CO NAAQS within the
period provided by statute. The court order that governs this review,
entered by the court on November 14, 2008 and amended on August 30,
2010, provides that EPA will sign, for publication, notices of proposed
and final rulemaking concerning its review of the CO NAAQS no later
than January 28, 2011 and August 12, 2011, respectively.
This action presents the Administrator's proposed decisions on the
current CO standards. Throughout this preamble a number of conclusions,
findings, and determinations proposed by the Administrator are noted.
Although they identify the reasoning that supports this proposal, they
are not intended to be final or conclusive in nature. The EPA invites
general, specific, and technical comments on all issues involved with
this proposal, including all such proposed judgments, conclusions,
findings, and determinations.
II. Rationale for Proposed Decisions on the Primary Standards
This section presents the rationale for the Administrator's
proposed decision to retain the existing CO primary standards.\3\ As
discussed more fully below, this rationale is based on a thorough
review, in the Integrated Science Assessment, of the latest scientific
information, published through mid-2009, on human health effects
associated with the presence of CO in the ambient air. This proposal
also takes into account: (1) Staff assessments of the most policy-
relevant information in the ISA and staff analyses of air quality,
human exposure and health risks presented in the REA and the Policy
Assessment, upon which staff conclusions regarding appropriate
considerations in this review are based; (2) CASAC advice and
recommendations, as reflected in discussions of drafts of the ISA, REA
and PA at public meetings, in separate written comments, and in CASAC's
letters to the Administrator; and (3) public comments received during
the development of these documents, either in connection with CASAC
meetings or separately.
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\3\ As explained below in section IV.A, EPA is proposing to
repromulgate the Federal reference method for CO, as set forth in
Appendix C of 40 CFR part 50. Consistent with EPA's proposed
decision to retain the standards, the recodification clarifies and
updates the text of the FRM, but does not make substantive changes
to it.
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In presenting the rationale and its foundations, this section
begins with a summary of current air quality information in section
II.A. Section II.B summarizes the body of evidence supporting this
rationale, including key health endpoints associated with exposure to
ambient CO. This rationale also draws upon the results of the
quantitative exposure and risk assessments, discussed below in section
II.C. Evidence- and exposure/dose-based considerations that form the
basis for the Administrator's proposed decisions on the adequacy of the
current standard are discussed in section II.D.2.a and II.D.2.b,
respectively. CASAC advice is summarized in section II.D.3. The
Administrator's proposed conclusions are presented in section II.D.4.
A. Air Quality Information
This section provides a general overview of the current air quality
conditions to provide context for this consideration of the current
standards for carbon monoxide. A more comprehensive discussion of air
quality information is provided in the ISA (ISA, sections 3.2 and 3.4)
and summarized in the Policy Assessment, and a more detailed discussion
of aspects particularly relevant to the exposure assessment is provided
in the REA (REA, chapter 3).
[[Page 8162]]
1. Anthropogenic Sources and Emissions of Carbon Monoxide
Carbon monoxide in ambient air is formed primarily by the
incomplete combustion of carbon-containing fuels and by photochemical
reactions in the atmosphere. As a result of the combustion conditions,
CO emissions from large fossil-fueled power plants are typically very
low because optimized fuel consumption conditions make boiler
combustion highly efficient. In contrast, internal combustion engines
used in many mobile sources have widely varying operating conditions.
Therefore, higher and more varying CO formation results from the
operation of these mobile sources (ISA, section 3.2). As with previous
reviews of the CO NAAQS, mobile sources continue to be a significant
source sector for CO in ambient air, as indicated by national emissions
estimates from on-road vehicles, which accounted for approximately half
of the total CO emissions by individual source sectors in 2002 (ISA,
Figure 3-1).\4\ National-scale anthropogenic CO emissions have
decreased by approximately 45% between 1990 and 2005, with nearly all
of this national-scale reduction coming from reductions in on-road
vehicle emissions (ISA, Figure 3-2; PA, Figure 1-1; 2005 NEI \5\). The
role of mobile source emissions is evident in the spatial and temporal
patterns of ambient CO concentrations, which are heavily influenced by
the patterns associated with mobile source emissions (ISA, chapter 3).
In some metropolitan areas of the U.S., due to their greater motor
vehicle density relative to rural areas, on-road mobile source
contribution to all ambient CO emissions was estimated to be as high as
approximately 75%, based on the 2002 National Emissions Inventory (ISA,
p. 3-2). However, the mobile source contribution can vary widely in
specific areas. As an example, 2002 NEI estimates of on-road mobile
source emissions in urban Denver County, Colorado are about 74% of
total CO emissions and emissions from all mobile sources (on-road and
non-road combined) are estimated to contribute about 98% (ISA, section
3.2.1). In contrast, 2002 NEI estimates of on-road CO emissions were
just 20% of the total for rural Garfield County, Colorado\6\ (ISA,
chapter 3, Figure 3-6).
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\4\ EPA compiles CO emissions estimates for the U.S. in the
National Emissions Inventory (NEI). Estimates come from various
sources and different data sources use different data collection
methods, most of which are based on engineering calculations and
estimates rather than measurements. Although these estimates are
generated using well-established approaches, uncertainties are
inherent in the emission factors and models used to represent
sources for which emissions have not been directly measured.
Uncertainties vary by source category, season and region (ISA,
section 3.2.1). At the time of the ISA development, the 2002 NEI was
providing the most recent publicly available CO emissions estimates
for the U.S. that meet EPA's data quality assurance objectives. Such
estimates are now available from the 2005 NEI.
\5\ The emissions trends information in this statement is drawn
from recently available 2005 National Emissions Inventory estimates
(http://www.epa.gov/ttn/chief/net/2005inventory.html, Tier
Summaries) and 1990 and other estimates, available at http://www.epa.gov/ttn/chief/net/critsummary.html Figure 3-2 from the ISA
provides estimates through 2002.
\6\ The 2002 National Emissions Inventory estimate for on-road
emissions in Garfield County is 20,000 tons, and the total emissions
from all sources is estimated to be 98,831 (99K) tons. Thus, in this
example the on-road vehicles accounts for 20.2% of the total
emissions (ISA, section 3, figure 3-6). In contrast, the 2002 Denver
County on-road emissions account for 74% of the total for the county
which is estimated at approximately 180,000 tons.
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2. Ambient Concentrations
As described in section II.A.1 above, mobile source emissions are
major contributors to CO emissions in urban areas, with corresponding
influence on ambient CO concentrations and associated concentration
gradients, with highest ambient concentrations occurring on or nearest
roadways, particularly highly travelled roadways, and lowest
concentrations in more distant locations (ISA, section 3.5.1.3; REA,
section 3.1.3). For example, as described in the ISA CO concentrations
measured within 20 meters of an interstate highway can range from 2 to
10 times greater than CO concentrations measured as far as 300 meters
from a major road, possibly influenced by wind direction and on-road
vehicle density (ISA, section 3.5.1.3, Figures 3-29 and 3-30; Zhu et
al., 2002; Baldauf et al., 2008a,b). Additionally, the role of motor
vehicles in influencing ambient concentrations contributes to the
occurrence of diurnal variation in concentrations reflecting rush hour
patterns (ISA, 3.5.2.2; REA, p. 3-8). The influence of motor vehicle
emissions on ambient concentrations contributes to the important role
of in-vehicle microenvironments in influencing short-term ambient CO
exposures, as described in more detail in the REA and summarized in
sections II.C.1 and II.D.2 below.
In 2009, approximately 350 ambient monitoring stations across the
U.S. reported continuous hourly averages of CO concentrations to EPA's
Air Quality System.\7\ For the most recent period for which air quality
status relative to the CO NAAQS has been analyzed (2009), all areas of
the U.S. meet both CO NAAQS.\8\ As of September 27, 2010, there are no
areas designated as nonattainment for the CO NAAQS (75 FR 59090). Since
2005, one area (Jefferson County, Alabama) has failed to meet the 8-
hour standard during some periods. Large CO emissions sources in this
area are associated with an integrated iron and steel facility. As
described in section 1.3.3 of the Policy Assessment, 2009
concentrations of CO at most currently operating monitors are well
below the current standards, with just a few locations having
concentrations near the controlling 8-hour standard of 9 ppm as a
second maximum 8-hour average.\9\ Of the counties with monitoring sites
in 2009, sites in 3 counties reported second maximum 8-hour average
concentrations at or above 6.4 ppm (PA, Figure 1-2).
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\7\ http://www.epa.gov/ttn/airs/airsaqs/.
\8\ The air quality status in areas monitored relative to the CO
NAAQS is provided at http://www.epa.gov/air/airtrends/values.html.
\9\ As the form of the CO 8-hour standard is not-to-be-exceeded
more than once per year, the second highest 8-hour average in a year
is the design value for this standard. Based on the current rounding
convention, the standard is met if the CO concentrations over a year
result in a design value at or below 9.4 ppm. Additional information
is available at http://www.epa.gov/airtrends/values.html.
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The current levels of ambient CO across the U.S. reflect the steady
declines in ambient concentrations that have occurred over the past
several years. Both the second highest 1-hour and 8-hour concentrations
have significantly declined since the last review. At the set of sites
across the U.S. that have been continuously monitored since 1990 the
average second highest 8-hour and 1-hour concentrations have declined
by nearly 70% (PA, section 1.3.3).
B. Health Effects Information
1. Carboxyhemoglobin as Biomarker and Mechanism of Toxicity
As discussed in the Integrated Science Assessment, in this review,
as in the past (e.g., USEPA, 2000; USEPA, 1991), the best characterized
mechanism of action of CO is tissue hypoxia caused by binding of CO to
hemoglobin to form carboxyhemoglobin (COHb). Accordingly, COHb level in
blood continues to be well recognized as an important internal dose
metric and the one most commonly used in evaluating CO exposure and the
potential for health effects (ISA, p. 2-4, sections 4.1, 4.2, 5.1.1;
1991 AQCD, 2000 AQCD, 2010 ISA).
Increasing levels of COHb with subsequent decrease in oxygen
availability for organs and tissues are of
[[Page 8163]]
concern in people with pre-existing heart disease who have compromised
compensatory mechanisms (e.g., lack of capacity to increase blood flow
in response to increased CO). The integrative review of health effects
of CO indicates that ``the clearest evidence indicates that individuals
with [coronary artery disease] are most susceptible to an increase in
CO-induced health effects'' (ISA, section 5.7.8) and the evidence
continues to support levels of COHb in the blood as the most useful
indicator of CO exposure that is related to the health effects of CO of
major concern.
Carboxyhemoglobin occurs in the blood due to endogenous CO
production from biochemical reactions associated with normal breakdown
of heme proteins, as well as in response to inhaled (exogenous) CO
exposures (ISA, section 4.5). The production of endogenous CO and
levels of endogenous COHb vary with several physiological
characteristics (e.g., slower COHb elimination with increasing age), as
well as some disease states, which can lead to higher endogenous levels
in some individuals (ISA, section 4.5). The amount of COHb formed in
response to exogenous CO is dependent on the CO concentration and
duration of exposure, exercise (which increases the amount of air
removed and replaced per unit of time for gas exchange), the pulmonary
diffusing capacity for CO, ambient pressure, health status, and the
specific metabolism of the exposed individual (ISA, chapter 4; 2000
AQCD, chapter 5). The formation of COHb is a reversible process, but
the high affinity of CO for hemoglobin, which affects the elimination
half-time for COHb, can lead to increased COHb levels in some
circumstances.
As discussed in the REA, exposure to CO in ambient air can occur
outdoors as well as through infiltration of ambient air into indoor
locations (REA, section 2.3). Additionally, indoor sources such as gas
stoves and tobacco smoke can, where present, be important contributors
to total CO exposure and can result in much greater CO exposures and
associated COHb levels than those associated with ambient sources (ISA,
section 3.6.5.2).\10\ For example, indoor source-related exposures,
such as faulty furnaces or other combustion appliances, have been
estimated in the past to lead to COHb levels on the order of twice as
high as those short-term exposures to ambient CO considered more likely
to be encountered by the general public (2000 AQCD, p. 7-4). Further,
some assessments performed for previous reviews have included modeling
simulations both without and with indoor sources (gas stoves and
tobacco smoke) to provide context for the assessment of ambient CO
exposure and dose (e.g., U.S. EPA, 1992; Johnson et al., 2000), and
these assessments have found that nonambient sources have a
substantially greater impact on the highest total exposures experienced
by the simulated population than do ambient sources (Johnson et al.,
2000; REA, sections 1.2 and 6.3).\11\. However, the focus of this REA,
conducted to inform the current review of the CO NAAQS, is on sources
of ambient CO. While recognizing this information regarding the
potential for indoor sources, where present, to play a role in CO
exposures and COHb levels, the exposure modeling in the current review
(described in section II.C below) did not include indoor CO sources in
order to focus on the impact of ambient CO sources on population COHb
levels.
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\10\ A significant source of nonambient CO long recognized as
contributing to elevated COHb levels is tobacco smoking (e.g., ISA,
Figure 4-12). Further, baseline COHb levels in active smokers have
been estimated to range from 3 to 8% for one- to two-pack-per-day
smokers. As a result of their higher baseline COHb levels, smokers
may exhale more CO into the air than they inhale from the ambient
environment when not smoking. Tobacco smoking can also contribute to
increased CO exposures and associated COHb levels in nonsmokers
(2000 AQCD, p. 7-4).
\11\ As has been recognized in previous CO NAAQS reviews, such
sources cannot be effectively mitigated by setting more stringent
ambient air quality standards (59 FR 38914).
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Apart from the impaired oxygen delivery to tissues related to COHb
formation, the evidence also indicates alternative mechanisms of CO-
induced effects independent of limited oxygen availability (2000 AQCD,
section 5.9; ISA, section 5.1.3). These mechanisms are primarily
associated with CO's ability to bind heme-containing proteins other
than hemoglobin and myoglobin, and involve a wide range of molecular
targets and CO concentrations, as described in the 2000 AQCD (USEPA,
2000, section 5.6) and in the ISA (ISA, section 5.1.3). Older
toxicological studies demonstrated that exposure to high concentrations
of CO resulted in altered functions of heme proteins other than
myoglobin and hemoglobin, potentially interfering with basic cell and
molecular processes and leading to dysfunction and/or disease. More
recent toxicological in vitro and in vivo studies have provided
evidence of alteration of nitric oxide signaling, inhibition of
cytochrome C oxidase, heme loss from protein, disruption of iron
homeostasis and alteration of cellular reduction-oxidation status (ISA,
section 5.1.3.2). The ISA notes that these mechanisms may be
interrelated. The evidence for these alternative mechanisms and the
role they may play in CO-induced health effects at concentrations
relevant to the current NAAQS is not clear.
As noted in the ISA, ``CO may be responsible for a continuum of
effects from cell signaling to adaptive responses to cellular injury,
depending on intracellular concentrations of CO, heme proteins and
molecules which modulate CO binding to heme proteins'' (ISA, section
5.1.3.3). However, as noted in the Policy Assessment, new research
based on this evidence for pathways other than those related to
impaired oxygen delivery to tissues is needed to further understand
these pathways and their linkage to CO-induced effects in susceptible
populations. Thus, the evidence indicates that COHb continues to be the
most useful and well-supported indicator of CO exposures and the best
biomarker to characterize the potential for health effects associated
with exposures to ambient CO at this time (PA, section 2.2.1).
2. Nature of Effects
As observed in the Policy Assessment, the long-standing body of
evidence that has established many aspects of the biological effects of
CO continues to contribute to our understanding of the health effects
of ambient CO (PA, section 2.2.1). Binding to heme proteins and the
alteration of their function is the common mechanism underlying
biological responses to CO. Upon inhalation, CO diffuses through the
respiratory zone (alveoli) to the blood where it binds to hemoglobin,
forming COHb. Accordingly, inhaled CO elicits various health effects
through binding to, and associated alteration of the function of, a
number of heme-containing molecules, mainly hemoglobin (see e.g., ISA,
section 4.1). The best characterized health effect associated with CO
levels of concern is hypoxia (reduced oxygen availability) induced by
increased COHb levels in blood and decreased oxygen availability to
critical tissues and organs, specifically the heart (ISA, section
5.1.2). Consistent with this, medical conditions that affect the
biological mechanisms to compensate for this effect (e.g., vasodilation
and increased coronary blood flow with increased oxygen delivery to the
myocardium) can contribute to a reduced amount of oxygen available to
key body tissues, potentially affecting organ system
[[Page 8164]]
function and limiting exercise capacity (2000 AQCD, section 7.1).\12\
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\12\ For example, people with peripheral vascular diseases and
heart disease patients often have markedly reduced circulatory
capacity and reduced ability to compensate for increased circulatory
demands during exercise and other stress (2000 AQCD, p. 7-7).
---------------------------------------------------------------------------
The body of health effects evidence for CO has grown considerably
since the review completed in 1994 with the addition of numerous
epidemiological and toxicological studies (ISA; 2000 AQCD). This
evidence provides additional detail and support to our prior
understanding of CO effects and population susceptibility. Most
notably, the current evidence includes much expanded epidemiological
evidence that is consistent with previous conclusions regarding
cardiovascular disease-related susceptibility (ISA, section 5.7; 2000
AQCD, section 7.7). In this review, the clearest evidence for ambient
CO-related effects is available for cardiovascular effects. Using an
established framework to characterize the evidence as to likelihood of
causal relationships between exposure to ambient CO and specific health
effects (ISA, chapter 1) the ISA states that ``Given the consistent and
coherent evidence from epidemiologic and human clinical studies, along
with biological plausibility provided by CO's role in limiting oxygen
availability, it is concluded that a causal relationship is likely to
exist between relevant \13\ short-term CO exposures and cardiovascular
morbidity'' (ISA, p. 2-6, section 2.5.1). Additionally, as mentioned
above, the ISA judges the evidence to be suggestive of causal
relationships between relevant short- and long-term CO exposures and
CNS effects, birth outcomes and developmental effects following long-
term exposure, respiratory morbidity following short-term exposure, and
mortality following short-term exposure (ISA, section 2.5, Table 2-1).
---------------------------------------------------------------------------
\13\ Relevant CO exposures are defined in the ISA as ``generally
within one or two orders of magnitude of ambient CO concentrations''
(ISA, section 2.5).
---------------------------------------------------------------------------
Similar to the previous review, results from controlled human
exposure studies of individuals with coronary artery disease (CAD) \14\
(Adams et al., 1988; Allred et al., 1989a, 1989b, 1991; Anderson et
al., 1973; Kleinman et al., 1989, 1998; Sheps et al., 1987 \15\) are
the ``most compelling evidence of CO-induced effects on the
cardiovascular system'' (ISA, section 5.2). Additionally, the use of an
internal dose metric, COHb, adds to the strength of the findings in
these controlled exposure studies. As a group, these studies
demonstrate the role of short-term CO exposures in increasing the
susceptibility of people with CAD to incidents of exercise-associated
myocardial ischemia. Toxicological studies described in the current
review provide evidence of CO effects on the cardiovascular system,
including electrocardiographic effects of 1-hour exposures to 35 ppm CO
in a rat strain developed as an animal model of cardiac susceptibility
(ISA, section 5.2.5.3).
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\14\ Coronary artery disease (CAD), often also called coronary
heart disease or ischemic heart disease is a category of
cardiovascular disease associated with narrowed heart arteries.
Individuals with this disease may have myocardial ischemia, which
occurs when the heart muscle receives insufficient oxygen delivered
by the blood. Exercise-induced angina pectoris (chest pain) occurs
in many of them. Among all patients with diagnosed CAD, the
predominant type of ischemia, as identified by ST segment
depression, is asymptomatic (i.e., silent). Patients who experience
angina typically have additional ischemic episodes that are
asymptomatic (2000 AQCD, section 7.7.2.1). In addition to such
chronic conditions, CAD can lead to sudden episodes, such as
myocardial infarction (ISA, p. 5-24).
\15\ Statistical analyses of the data from Sheps et al., (1987)
by Bissette et al (1986) indicate a significant decrease in time to
onset of angina at 4.1% COHb if subjects that did not experience
exercise-induced angina during air exposure are also included in the
analyses.
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Among the controlled human exposure studies, the ISA places
principal emphasis on the study of CAD patients by Allred et al.
(1989a, 1989b, 1991) \16\ (which was also considered in the previous
review) for the following reasons: (1) Dose-response relationships were
observed; (2) effects were observed at the lowest COHb levels tested
(mean of 2-2.4% COHb \17\ following experimental CO exposure), with no
evidence of a threshold; (3) objective measures of myocardial ischemia
(ST-segment depression) \18\ were assessed, as well as the subjective
measure of decreased time to induction of angina; (4) measurements were
taken both by CO-oximetry (CO-Ox) and by gas chromatography (GC), which
provides a more accurate measurement of COHb blood levels \19\; (5) a
large number of study subjects were used; (6) a strict protocol for
selection of study subjects was employed to include only CAD patients
with reproducible exercise-induced angina; and (7) the study was
conducted at multiple laboratories around the U.S. This study evaluated
changes in time to exercise-induced onset of markers of myocardial
ischemia resulting from two short (approximately 1-hour) CO exposures
targeted to result in mean study subject COHb levels of 2% and 4%,
respectively (ISA, section 5.2.4). In this study, subjects (n=63) on
three separate occasions underwent an initial graded exercise treadmill
test, followed by 50 to 70-minute exposures under resting conditions to
room air CO concentrations or CO concentrations targeted for each
subject to achieve blood COHb levels of 2% and 4%. The exposures were
to average CO concentrations of 0.7 ppm (room air concentration range
0-2 ppm), 117 ppm (range 42-202 ppm) and 253 ppm (range 143-357 ppm).
After the 50- to 70-minute exposures, subjects underwent a second
graded exercise treadmill test, and the percent change in time to onset
of angina and time to ST endpoint between the first and second exercise
tests was determined. For the two CO exposures, the average post-
exposure COHb concentrations were reported as 2.4% and 4.7%, and the
subsequent post-exercise average COHb concentrations were reported as
2.0% and 3.9%.\20\
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\16\ Other controlled human exposure studies of CAD patients
(listed in Table 2-2 of the PA, and discussed in more detail in the
1991 and 2000 AQCDs) similarly provide evidence of reduced time to
exercise-induced angina associated with elevated COHb resulting from
controlled short-duration exposure to increased concentrations of
CO.
\17\ These levels and other COHb levels described for this study
below are based on GC analysis unless otherwise specified. Matched
measurements available for CO-oximetry (CO-Ox) and gas
chromatography (GC) in this study indicate CO-Ox measurements of
2.65% (post-exercise mean) and 3.21% (post-exposure mean)
corresponding to the GC measurement levels of 2.00% (post-exercise
mean) to 2.38% (post-exposure mean) for the lower exposure level
assessed in this study (Allred et al., 1991).
\18\ The ST-segment is a portion of the electrocardiogram,
depression of which is an indication of insufficient oxygen supply
to the heart muscle tissue (myocardial ischemia). Myocardial
ischemia can result in chest pain (angina pectoris) or such
characteristic changes in ECGs or both. In individuals with coronary
artery disease, it tends to occur at specific levels of exercise.
The duration of exercise required to demonstrate chest pain and/or a
1-mm change in the ST segment of the ECG were key measurements in
the multicenter study by Allred et al (1989a, 1989b, 1991).
\19\ As stated in the ISA, the gas chromatographic technique for
measuring COHb levels ``is known to be more accurate than
spectrophotometric measurements, particularly for samples containing
COHb concentrations < 5%'' (ISA, p. 5-41). CO-oximetry is a
spectrophotometric method commonly used to rapidly provide
approximate concentrations of COHb during controlled exposures (ISA,
p. 5-41). At the low concentrations of COHb (<5%) more relevant to
ambient CO exposures, co-oximeters are reported to overestimate COHb
levels compared to GC measurements, while at higher concentrations,
this method is reported to produce underestimates (ISA, p.4-18).
\20\ While the COHb blood level for each subject during the
exercise tests was intermediate between the post-exposure and
subsequent post-exercise measurements (e.g., mean 2.4-2.0% and 4.7-
3.9%), the study authors noted that the measurements at the end of
the exercise test represented the COHb concentrations at the
approximate time of onset of myocardial ischemia as indicated by
angina and ST segment changes. The corresponding ranges of CO-Ox
measurements for the two exposures were 2.7-3.2% and 4.7-5.6%. In
this document, we refer to the GC-measured mean of 2.0% or 2.0-2.4%
for the COHb levels resulting from the lower experimental CO
exposure.
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[[Page 8165]]
Across all subjects, the mean time to angina onset for control
(``room'' air) exposures was approximately 8.5 minutes, and the mean
time to ST endpoint was approximately 9.5 minutes (Allred et al.,
1989b). Relative to room-air exposure that resulted in a mean COHb
level of 0.6% (post-exercise), exposure to CO resulting in post-
exercise mean COHb concentrations of 2.0% and 3.9% were observed to
decrease the exercise time required to induce ST-segment depression by
5.1% (p=0.01) and 12.1% (p<0.001), respectively. These changes were
well correlated with the onset of exercise-induced angina, the time to
which was shortened by 4.2% (p=0.027) and 7.1% (p=0.002), respectively,
for the two experimental CO exposures (Allred et al., 1989a, 1989b,
1991).\21\ As at the time of the last review, while ST-segment
depression is recognized as an indicator of myocardial ischemia, the
exact physiological significance of the observed changes among those
with CAD is unclear (ISA, p. 5-48).
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\21\ Another indicator measured in the study was the combination
of heart rate and systolic blood pressure which provides a clinical
index of the work of the heart and myocardial oxygen consumption,
since heart rate and blood pressure are major determinants of
myocardial oxygen consumption (Allred et al., 1991). A decrease in
oxygen to the myocardium would be expected to be paralleled by
ischemia at lower heart rate and systolic blood pressure. This heart
rate-systolic blood pressure indicator at the time to ST-endpoint
was decreased by 4.4% at the 3.9% COHb dose level and by a
nonstatistically-significant, smaller amount at the 2.0% COHb dose
level.
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No controlled human exposure studies have been specifically
designed to evaluate the effect of controlled short-term exposures to
CO resulting in COHb levels lower than a study mean of 2% (ISA, section
5.2.6). However, an important finding of the multi-laboratory study was
the dose-response relationship observed between COHb and the markers of
myocardial ischemia, with effects observed at the lowest increases in
COHb tested, without evidence of a measurable threshold effect. As
reported by the authors, the results comparing ``the effects of
increasing COHb from baseline levels (0.6%) to 2 and 3.9% COHb showed
that each produced further changes in objective ECG measures of
ischemia'' implying that ``small increments in COHb could adversely
affect myocardial function and produce ischemia'' (Allred et al.,
1989b, 1991).
The epidemiological evidence has expanded considerably since the
last review including numerous additional studies that are coherent
with the evidence on markers of myocardial ischemia from controlled
human exposure studies of CAD patients (ISA, section 2.7). The most
recent set of epidemiological studies in the U.S. have evaluated the
associations between ambient concentrations of multiple pollutants
(i.e. fine particles or PM2.5, nitrogen dioxide, sulfur
dioxide, ozone, and CO) at fixed-site ambient monitors and increases in
emergency department visits and hospital admissions for specific
cardiovascular health outcomes including ischemic heart disease (IHD),
myocardial infarction (MI), congestive heart failure (CHF), and
cardiovascular diseases (CVD) as a whole (Bell et al., 2009; Koken et
al., 2003; Linn et al., 2000; Mann et al., 2002; Metzger et al., 2004;
Symons et al., 2006; Tolbert et al., 2007; Wellenius et al., 2005).
Findings of positive associations for these outcomes with metrics of
ambient CO concentrations are coherent with the evidence from
controlled human exposure studies of myocardial ischemia-related
effects resulting from elevated CO exposures (ISA, section 2.5.1; ISA,
Figure 2-1). In these studies, the ambient CO concentration averaging
time for which health outcomes were analyzed varied from 1 hour to 24
hours, with the air quality metrics based on either a selected central-
site monitor for the area or an average for multiple monitors in the
area of interest. The study areas for which positive associations of
these metrics were reported with IHD, MI and CVD outcomes include: the
Atlanta, Georgia metropolitan statistical area; the greater Los
Angeles, California area; and a group of 126 urban counties. Together
the individual study periods spanned the years from 1988 through 2005.
The risk estimates from these studies indicate statistically
significant positive associations were observed with ambient CO
concentrations based on air quality for the day of hospital admission
or based on the average of the selected ambient CO concentration metric
across that day and 2 or 3 days previous (ISA, Figures 5-2 and 5-5).
Many of the studies for these outcomes include same day or next day lag
periods, which, as noted in the ISA ``are consistent with the proposed
mechanism and biological plausibility of these CVD outcomes'' (ISA, p.
5-40).\22\
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\22\ Of the studies for which risk estimates are based on multi-
day averages (the Atlanta studies and the California study by Mann
et al., 2002), the California study by Mann et al., (2002) also
observed a significant positive association with same day CO
concentration.
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Additionally, there are U.S. studies reporting associations with
hospital admissions for CHF, a condition that affects an individual's
ability to compensate for reduced oxygen availability. These include
one in southern California which reported a significant association for
ambient CO with hospital admissions for CHF (Linn et al., 2000), as
well as studies in Allegheny County (Pittsburgh) for 1987-1999 study
period (Wellenius et al., 2005), and Denver for the months of July-
August during 1993-1997 (Koken et al., 2003; ISA, pp. 5-31 to 5-33).
Risk estimates for all three of these studies are based on the 24-hour
CO concentration, with the California and Allegheny County studies'
association with same-day air quality, while the association shown for
the Denver study was with ambient CO concentration three days prior to
health outcome (PA, Table 2-1).
As noted by the ISA, ``[s]tudies of hospital admissions and ED
visits for IHD provide the strongest [epidemiological] evidence of
ambient CO being associated with adverse CVD outcomes'' (ISA, p. 5-40,
section 5.2.3). With regard to studies for other measures of
cardiovascular morbidity, the ISA notes that ``[t]hough not as
consistent as the IHD effects, the effects for all CVD hospital
admissions (which include IHD admissions) and CHF hospital admissions
also provide evidence for an association of cardiovascular outcomes and
ambient CO concentrations'' (ISA, section 5.2.3). While noting the
difficulty in determining the extent to which CO is independently
associated with CVD outcomes in this group of studies as compared to CO
as a marker for the effects of another traffic-related pollutant or mix
of pollutants, the ISA concludes that the epidemiological evidence,
particularly when considering the copollutant analyses, provides
support to the clinical evidence for a direct effect of short-term
ambient CO exposure on CVD morbidity (ISA, pp. 5-40 to 5-41).
As discussed in detail in the ISA, additional epidemiological
studies have evaluated associations of ambient CO with other
cardiovascular effects since the last review. For example, preliminary
evidence of a link between exposure to CO and alteration of blood
markers of coagulation and inflammation in individuals with CAD or CVD
has been provided by a few well conducted and informative studies (ISA,
Table 5-6; Delfino et al., 2008; Liao et al., 2005). As noted by the
ISA, however, further studies are warranted to investigate the role of
these markers in prothrombotic events and their possible contribution
to the pathophysiology of CO-induced aggravation of ischemic heart
disease
[[Page 8166]]
(ISA, section 5.2.1.8). Other epidemiological studies (including field
and panel studies) also provide some evidence of a link between CO
exposure and heart rate and heart rate variability (ISA, section
5.2.1.1). With regard to the two of three studies reporting a positive
association with heart rate, the ISA concluded that ``further research
is warranted'' to corroborate the results, while the larger number of
studies for heart rate variability parameters is characterized as
having mixed associations (ISA, p. 5-15). Additionally, of the two
studies of electrocardiogram changes indicative of ischemic events
(ISA, section 5.2.1.2), one found no association and, in the other
study, the association with CO did not remain statistically significant
in multipollutant models, unlike the association with black carbon in
that study (ISA, p. 5-16). A limited number of epidemiological studies
(Bell et al., 2009; Linn et al., 2000) have investigated hospital
admissions for stroke (including both hemorrhagic and ischemic forms)
and generally report small or no associations with ambient CO
concentrations (ISA, section 5.2.1.9, Table 5-8 and Figure 5-3).
At the time of the last review, there was evidence for effects
other than cardiovascular morbidity, including neurological,
respiratory and developmental effects. Evidence for these effects
includes the following.
With regard to neurological effects, acute exposures to CO
have long been known to induce CNS effects such as those observed with
CO poisoning, although limited and equivocal evidence available at the
time of the last review included indications of some neurobehavioral
effects to result from CO exposures resulting in a range of 5-20% COHb
(2000 AQCD, section 6.3.2). No additional clinical or epidemiological
studies are now available that investigated such effects of CO at
ambient levels (ISA, section 5.3).
With regard to potential effects of CO on birth outcomes
and developmental effects, the potential vulnerability of the fetus and
very young infant to CO was recognized during the 1994 review and in
the 2000 AQCD. The CO-specific evidence available, however, included
limited epidemiological analyses focused primarily on very high CO
exposures associated with maternal smoking, and animal studies
involving very high CO exposures (USEPA, 1992; 2000 AQCD). The 2000
AQCD concluded that typical ambient CO levels were unlikely to cause
increased fetal risk (2000 AQCD, p. 6-44). The current review includes
additional epidemiological and animal toxicological studies. The
currently available evidence includes limited but suggestive
epidemiologic evidence for a CO-induced effect on preterm-birth, birth
defects, decrease in birth weight, other measures of fetal growth, and
infant mortality (ISA, section 5.4.3). The available animal
toxicological studies provide some support and coherence for these
birth and developmental outcomes at higher than ambient exposures,\23\
although a clear understanding of the mechanisms underlying potential
reproductive and developmental effects is still lacking (ISA, section
2.5.3).
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\23\ The lowest exposures eliciting an effect in the animal
studies were exposures of 22 hours per day over about 14 prenatal
days at a concentration of 12 ppm (ISA, Table 5-17).
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With regard to respiratory effects, the 2000 AQCD
concluded it unlikely that CO has direct effects on lung tissue, except
at extremely high concentrations (2000 AQCD, p. 6-45). There is
currently limited, suggestive evidence of an association between short-
term exposure to CO and respiratory-related outcomes. Only preliminary
evidence is available, however, regarding a mechanism that could
provide plausibility for CO-induced effects (ISA, section 5.5.5.1).
Thus, while there is some additional evidence on neurological,
respiratory and developmental effects, it remains limited.
In summary, rather than altering conclusions from the previous
review, the current evidence provides continued support and some
additional strength to the previous conclusions regarding the health
effects associated with exposure to CO and continues to indicate
cardiovascular effects, particularly effects related to the role of CO
in limiting oxygen availability, as those of greatest concern at low
exposures.
3. At-Risk Populations
In identifying population groups or life stages at greatest risk
for health risk from a specific pollutant, the terms susceptibility,
vulnerability, sensitivity, and at-risk are commonly employed. The
definition for these terms sometimes varies, but in most instances
``susceptibility'' refers to biological or intrinsic factors (e.g.,
lifestage, gender) while ``vulnerability'' refers to nonbiological or
extrinsic factors (e.g., visiting a high-altitude location, medication
use). Additionally, in some cases, the terms ``at-risk'' and sensitive
have been used to encompass both of these concepts. At times, however,
factors of ``susceptibility'' and ``vulnerability'' are intertwined and
are difficult to distinguish. In the ISA for this review, the term
susceptibility has been used broadly to recognize populations that have
a greater likelihood of experiencing effects related to ambient CO
exposure, such that use of the term susceptible populations in the ISA
is defined as follows (ISA, section 5.7, p. 5-115):
Populations that have a greater likelihood of experiencing
health effects related to exposure to an air pollutant (e.g., CO)
due to a variety of factors including, but not limited to: genetic
or developmental factors, race, gender, lifestage, lifestyle (e.g.,
smoking status and nutrition) or preexisting disease, as well as
population-level factors that can increase an individual's exposure
to an air pollutant (e.g., CO) such as socioeconomic status [SES],
which encompasses reduced access to health care, low educational
attainment, residential location, and other factors.
Thus, susceptible populations are at greater risk of CO effects and
are also referred to as at-risk in the corresponding discussion in the
REA and Policy Assessment and the summary below.
The current evidence, while much expanded in a number of ways,
continues to support the conclusions from the previous review regarding
susceptible populations for exposure to ambient CO. In the AQCD for the
review completed in 1994 and in the 2000 AQCD, the evidence best
supported the identification of patients with CAD as a population at
increased risk from low levels of CO (USEPA, 1992; 2000 AQCD). Other
groups were also recognized as potentially susceptible in the 2000 AQCD
based on consideration of the clinical evidence and theoretical work,
as well as laboratory animal research (2000 AQCD, p. 7-6). These
include fetuses and young infants; pregnant women; the elderly,
especially those with compromised cardiovascular function; people with
conditions affecting oxygen absorption, blood flow, oxygen carrying
capacity or transport; people using drugs with central nervous system
depressant properties or exposed to chemical substances that increase
endogenous formation of CO; and people who have not adapted to high
altitude and are exposed to a combination of high altitude and CO. For
these potentially susceptible groups, little empirical evidence was
available by which to specify health effects associated with ambient or
near-ambient CO exposures (2000 AQCD, p. 7-6).
As summarized in the Policy Assessment, based on the evidence from
controlled human exposure studies also considered in the last review,
and the
[[Page 8167]]
now much-expanded epidemiological evidence base which is coherent with
the evidence from these studies, the population with pre-existing
cardiovascular disease associated with limitation in oxygen
availability continues to be the best characterized population at risk
of adverse CO-induced effects, with CAD recognized as ``the most
important susceptibility characteristic for increased risk due to CO
exposure'' (ISA, section 2.6.1). An important factor determining the
increased susceptibility of this population is their inability to
compensate for the reduction in oxygen levels due to an already
compromised cardiovascular system. Individuals with a healthy
cardiovascular system (i.e., with healthy coronary arteries) have
operative physiologic compensatory mechanisms (e.g., increased blood
flow and oxygen extraction) for CO-induced hypoxia and are unlikely to
be at increased risk of CO-induced effects (ISA, p. 2-10).\24\ In
addition, the high oxygen consumption of the heart, together with the
inability to compensate for the hypoxic effects of CO, make the cardiac
muscle of a person suffering with CAD a critical target for the hypoxic
effects of CO.
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\24\ The other well-studied individuals at the time of the last
review were healthy male adults that experienced decreased exercise
duration at similar COHb levels during short term maximal exercise.
This population was of lesser concern since it represented a smaller
sensitive group, and potentially limited to individuals that would
engage in vigorous exercise such as competing athletes (1991 AQCD,
section 10.3.2).
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In the Integrated Science Assessment for the current review,
recognition of susceptibility of the population with pre-existing
cardiovascular disease, such as CAD, is supported by the expanded
epidemiological database, which includes a number of studies reporting
significant increases in hospital admissions for IHD, angina and MI in
relation to CO exposures (ISA, section 2.7). Further support is
provided by epidemiologic studies (Mann et al., 2002; and Peel et al.,
2007) of increased hospital admissions and emergency department visits
for IHD among individuals with secondary diagnoses for other
cardiovascular outcomes including arrhythmia and congestive heart
failure (ISA, section 5.7), and toxicological studies reporting altered
cardiac outcomes in animal models of cardiovascular disease (ISA,
section 5.2.1.9).
Cardiovascular disease comprises many types of medical disorders,
including heart disease, cerebrovascular disease (e.g., stroke),
hypertension (high blood pressure), and peripheral vascular diseases.
Heart disease, in turn, comprises several types of disorders, including
ischemic heart disease (CHD or CAD, myocardial infarction, angina),
congestive heart failure, and disturbances in cardiac rhythm (2000
AQCD, section 7.7.2.1). Types of cardiovascular disease other than
those discussed above may also contribute to increased susceptibility
to the adverse effects of low levels of CO (ISA, section 5.7.1.1). For
example, some evidence with regard to other types of cardiovascular
disease such as congestive heart failure, arrhythmia, and non-specific
cardiovascular disease, although more limited for peripheral vascular
and cerebrovascular disease, indicates that ``the continuous nature of
the progression of CAD and its close relationship with other forms of
cardiovascular disease suggest that a larger population than just those
individuals with a prior diagnosis of CAD may be susceptible to health
effects from CO exposure'' (ISA, p. 5-117).
Although there were little experimental data available at the time
of the last review to adequately characterize specific health effects
of CO at ambient levels for other potentially at-risk populations,
several other populations were identified as being potentially more at
risk of CO-induced effects due to a number of factors. These factors
include pre-existing diseases that could inherently decrease oxygen
availability to tissues, lifestage vulnerabilities (e.g., fetuses,
young infants or newborns, the elderly), gender, lifestyle, medications
or alterations in the physical environment (e.g., increased altitude).
This is consistent with the ISA conclusions in the current review which
recognize other populations that may be potentially susceptible to the
effects of CO as including: Those with other pre-existing diseases that
may have already limited oxygen availability or increased COHb
production or levels, such as people with obstructive lung diseases,
diabetes and anemia; older adults; fetuses during critical phases of
development and young infants or newborns; those who spend a
substantial time on or near heavily traveled roadways; visitors to
high-altitude locations; and people ingesting medications and other
substances that enhance endogenous or metabolic CO formation (ISA,
section 2.6.1). In recognizing the potential susceptibility of these
populations, the Policy Assessment also noted the lack of information
on specific COHb levels that may be associated with health effects in
these other groups and the nature of those effects, as well as a way to
relate the specific evidence available for the CAD population to these
other populations (PA, section 2.2.1).
The current evidence continues to support the identification of
people with cardiovascular disease as having susceptibility to CO-
induced health effects (ISA, 2-12), with those having CAD as the
population with the best characterized susceptibility to CO-induced
health effects (ISA, sections 5.7.1.1 and 5.7.8).\25\ An important
susceptibility consideration for this population is the inability to
compensate for CO-induced hypoxia since individuals with CAD have an
already compromised cardiovascular system. Included in this susceptible
population are those with angina pectoris (cardiac chest pain), those
who have experienced a heart attack, and those with silent ischemia or
undiagnosed IHD (AHA, 2003). People with other cardiovascular diseases,
particularly heart diseases, are also at risk of CO-induced health
effects. We also recognize other populations potentially susceptible to
CO-induced effects, most particularly those with other pre-existing
diseases that cause limited oxygen availability, increased COHb levels,
or increased endogenous CO production, such as people with obstructive
lung diseases, diabetes and anemia; however, information characterizing
susceptibility for this population is limited.
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\25\ As recognized in the ISA, ``Although the weight of evidence
varies depending on the factor being evaluated, the clearest
evidence indicates that individuals with CAD are most susceptible to
an increase in CO-induced health effects'' (ISA, p. 2-12).
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4. Potential Impacts on Public Health
In light of the evidence described above with regard to factors
contributing to greater susceptibility to health effects of ambient CO,
this section, drawing from the Integrated Science Assessment and
discussion in the Policy Assessment, discusses the health significance
of the effects occurring with the lowest relevant (short-term)
exposures to ambient CO and the size of the at-risk populations in the
U.S. These considerations are important elements in the
characterization of potential public health impacts associated with
exposure to ambient CO.
We first consider the effects identified by the evidence at the
lowest studied short-term exposures. As discussed in section II.B.2
above, the study by Allred et al., (1989a, 1989b, 1991) indicates that
increases in blood COHb in response to 1-hour CO exposures
[[Page 8168]]
produce evidence of myocardial ischemia in CAD patients with
reproducible exercise-induced angina. At a study group average COHb
level of 2-2.4%, the statistically significant reduction in the time to
exercise-induced markers of myocardial ischemia in CAD patients was 4-
5% on average (approximately 30 seconds), with larger reductions
observed at the higher studied COHb level. In discussing public health
implications of the observed responses, the study authors noted that
the responses observed at the studied COHb levels were similar to those
considered clinically significant when evaluating medications to treat
angina from coronary artery disease (Allred et al., 1989a, 1991). The
independent review panel for the study further noted that frequent
encounters in ``everyday life'' with increased COHb levels on the order
of those tested in the study might be expected to limit activity and
affect quality of life (Allred et al., 1989b, pp. 38, 92-94; 1991 AQCD,
p. 10-35).
In the review completed in 1994, the body of evidence that
demonstrated cardiovascular effects in CAD patients exposed to CO was
given primary consideration, with the Administrator judging that
``cardiovascular effects, as measured by decreased time to onset of
angina pain and by decreased time to onset of significant ST-segment
depression, are the health effects of greatest concern, which clearly
have been associated with CO exposures at levels observed in the
ambient air'' (59 FR 38913). Additionally, as discussed in section
II.B.2 above, a dose-response relationship has been documented for COHb
resulting from brief, elevated CO exposures in persons with pre-
existing CAD, with no evidence of threshold (59 FR 38910; ISA, section
5.2.4; Allred et al., 1989a, 1989b, 1991).
In the 1994 review decision (as discussed in section II.D.1.a
below), less significance was ascribed to the effects at the lower COHb
level assessed in the Allred et al., study (1989a, 1989b, 1991), which
were described to be of less certain clinical importance, than effects
reported from short-term CO exposure studies that assessed higher COHb
levels (59 FR 38913-38914). In the current review of the evidence, the
ISA describes the physiological significance of the changes at the
lowest tested dose level (e.g., 2% COHb from Allred et al., 1989b) as
unclear, additionally noting that variability in severity of disease
among individuals with CAD is likely to influence the critical level of
COHb which leads to adverse cardiovascular effects (ISA, p. 2-6).
In considering potential public health impacts of CO in ambient
air, we also consider the size of the at-risk populations. The
population with CAD is well recognized as susceptible to increased risk
of CO-induced health effects (ISA, sections 5.7.1.1 and 5.7.8). The
2007 estimate from the National Health Interview Survey (NHIS)
performed by the U.S. Centers for Disease Control of the size of the
U.S. population with coronary heart disease, angina pectoris (cardiac
chest pain) or who have experienced a heart attack (ISA, Table 5-26) is
13.7 million people (ISA, pp. 5-117). Further, there are estimated to
be three to four million additional people with silent ischemia or
undiagnosed IHD (AHA, 2003). In combination, this represents a large
population that is more susceptible to ambient CO exposure when
compared to the general population (ISA, section 5.7).
In addition to the population with diagnosed and undiagnosed CAD,
the ISA notes the size of the larger population of people with all
types of heart disease (HD), which may also be at increased risk of CO-
induced health effects (ISA, section 2.6.1). Within this broader group,
implications of CO exposures are more significant for those persons for
whom their disease state affects their ability to compensate for the
hypoxia-related effects of CO (ISA, section 4.4.4). The NHIS estimates
for 2007 indicate there is a total of approximately 25 million people
with heart disease of any type (ISA, Table 5-26).
Other populations potentially susceptible to the effects of CO
include people with chronic obstructive pulmonary disease, diabetes and
anemia, as well as older adults and fetuses during critical phases of
development (as discussed in section II.B.3 above). In considering
potential impacts on such populations, we recognize that the evidence
is limited or lacking with regard to effects of CO at ambient levels,
and associated exposures and COHb levels, while providing no indication
of susceptibility to ambient CO greater than that of CHD and HD
populations.
C. Human Exposure and Dose Assessment
Our consideration of the scientific evidence in the current review,
as at the time of the last review (summarized in section II.D.1 below),
is informed by results from a quantitative analysis of estimated
population exposure and resultant COHb levels. This analysis provides
estimates of the percentages of simulated at-risk populations expected
to experience daily maximum COHb levels at or above a range of
benchmark levels under varying air quality scenarios (e.g., just
meeting the current or alternative standards). The benchmark COHb
levels were identified based on consideration of the evidence discussed
in section II.B above. The following subsections summarize the design
and methods of the quantitative assessment (section II.C.1) and the
important uncertainties associated with these analyses (section
II.C.2). The results of the analyses, as they relate to considerations
of the adequacy of the current standards, are discussed in section
II.D.2 below.
1. Summary of Design Aspects
In this section, we provide a summary of key aspects of the
assessment conducted for this review, including the study areas and air
quality scenarios investigated, modeling tools used, at-risk
populations simulated, and COHb benchmark levels of interest. The
assessment is described in detail in the REA and summarized in the PA
(section 2.2.2).
The assessment estimated CO exposure and associated COHb levels in
simulated at-risk populations in two urban study areas in Denver and
Los Angeles, in which current ambient CO concentrations are below the
current standards. We selected these areas because: (1) Areas of both
cities have been included in prior CO NAAQS exposure assessments and
thus serve as an important connection with past assessments; (2)
historically, they have generally had the highest ambient CO
concentrations among urban areas in the U.S.; and (3) Denver is at high
altitude and represents an important risk scenario due to the potential
increased susceptibility to CO exposure associated with high altitudes.
In addition, of 10 urban areas across the continental U.S. selected for
detailed air quality analysis in the ISA and having ambient monitors
meeting a 75% completeness criterion, the two study area locations were
ranked first (Los Angeles) and second (Denver) regarding the percentage
of elderly population within 5, 10, and 15 km of monitor locations, and
ranked first (Los Angeles) and fifth (Denver) regarding number of 1-
and 8-hour daily maximum CO concentration measurements (ISA, section
3.5.1.1).
Estimates were developed for exposures to ambient CO associated
with current ``as is'' conditions (2006 air quality) and also for
higher ambient CO concentrations associated with air quality conditions
simulated to just
[[Page 8169]]
meet the current 8-hour standard,\26\ as well as for air quality
conditions simulated to just meet several alternative standards.
Although we consider it unlikely that air concentrations in many urban
areas across the U.S. that are currently well below the current
standards would increase to just meet the 8-hour standard, we recognize
the potential for CO concentrations in some areas currently below the
standard to increase to just meet the standard. We additionally
recognize that this simulation can provide useful information in
evaluating the current standard. Accordingly, we simulated conditions
of increased CO concentrations that just meet the current 8-hour
standard in the two study areas. In so doing, we recognize the
uncertainty associated with simulating this hypothetical profile of
higher CO concentrations that just meet the current 8-hour standard. We
note, however, that an analysis of the ratios of 1-hour to 8-hour
design value metrics based on 2009 ambient CO concentrations in U.S.
locations indicates that the relationships between design values for
the two study areas under the air quality conditions simulated to just
meet the current 8-hour standard fall well within the 2009 national
distribution of such ratios (Policy Assessment, section 2.2.2).\27\
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\26\ As noted elsewhere, the 8-hour standard is the controlling
standard for ambient CO concentrations.
\27\ More specifically, the ratio of the 1-hour design value to
the 8-hour design value for the Los Angeles study area corresponds
to approximately the 25th percentile of U.S. counties in 2009 and
the ratio for the Denver study area corresponds to approximately the
75th percentile of U.S. counties in 2009. Under ``as is'' conditions
the ratios for these two study areas correspond to approximately the
40th percentile of the 2009 national distribution (Policy
Assessment, section 2.2.2).
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The exposure and dose modeling for the assessment, presented in
detail in the REA, relied on version 4.3 of EPA's Air Pollutant
Exposure model (APEX4.3), which estimates human exposure using a
stochastic, event-based microenvironmental approach (REA, chapter 4).
This model has a history of application, evaluation, and progressive
model development in estimating human exposure and dose for several
NAAQS reviews, including CO, ozone (O3), nitrogen dioxide
(NO2), and sulfur dioxide (SO2). As described in
section II.D.1 below, the review of the CO standards completed in 1994
relied on population exposure and dose estimates generated from the
probabilistic NAAQS exposure model (pNEM), a model that, among other
differences from the current modeling approach with APEX4.3, employed a
cohort-based approach (Johnson et al., 1992; U.S. EPA,
1992).28 29 Each of the model developments since the use of
pNEM in that review have been designed to allow APEX to better
represent human behavior, human physiology, and microenvironmental
concentrations and to more accurately estimate variability in CO
exposures and COHb levels (REA, chapter 4).\30\
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\28\ When using the cohort approach, each cohort is assumed to
contain persons with identical exposures during the specified
exposure period. Thus, variability in exposure will be attributed to
differences in how the cohorts are defined, not necessarily
reflecting differences in how individuals might be exposed in a
population. In the assessment for the review completed in 1994, a
total of 420 cohorts were used to estimate population exposure based
on selected demographic information (11 groups using age, gender,
work status), residential location, work location, and presence of
indoor gas stoves (Johnson, et al., 1992; USEPA, 1992).
\29\ The use of pNEM in the prior review also (1) relied on a
limited set of activity pattern data (approximately 3,600 person-
days), (2) used four broadly defined categories to estimate
breathing rates, and (3) implemented a geodesic distance range
methodology to approximate workplace commutes (Johnson et al., 1992;
U.S. EPA, 1992). Each of these approaches used by pNEM, while
appropriate given the data available at that time, would tend to
limit the ability to accurately model expected variability in the
population exposure and dose distributions.
\30\ APEX4.3 includes new algorithms to (1) simulate
longitudinal activity sequences and exposure profiles for
individuals, (2) estimate activity-specific minute-by-minute oxygen
consumption and breathing rates, (3) address spatial variability in
home and work-tract ambient concentrations for commuters, and (4)
estimate event-based microenvironmental concentrations (PA, section
2.2.2).
---------------------------------------------------------------------------
As used in the current assessment, APEX probabilistically generates
a sample of hypothetical individuals from an actual population database
and simulates each individual's movements through time and space (e.g.,
indoors at home, inside vehicles) to estimate his or her exposure to
ambient CO (REA, chapter 4). The individual's movements are simulated
based on data available from recent activity pattern surveys (CHAD \31\
now has about 34,000 person-days of data) and the most recent U.S.
census data on population demographics and home-to-workplace commutes.
Based on exposure concentrations, minute-by-minute activity levels, and
physiological characteristics of the simulated individuals (see REA,
chapters 4 and 5), APEX estimates the level of COHb in the blood for
each individual at the end of each hour based on a nonlinear solution
to the Coburn-Forster-Kane equation (REA, section 4.4.7). These results
across each simulated individual were then summarized in the REA and
discussed in the Policy Assessment in terms of the percent of the
simulated at-risk populations expected to experience one or more
occurrences of daily maximum end-of-hour COHb levels of interest.
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\31\ CHAD is EPA's Comprehensive Human Activity Database which
provides input data for APEX model simulations (REA, sections 4.3
and 4.4).
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As discussed in section II.B above, people with cardiovascular
disease are the population of primary focus in this review, and more
specifically, as described in the ISA, coronary artery disease, also
known as coronary heart disease, is the ``most important susceptibility
characteristic for increased risk due to CO exposure'' (ISA, p. 2-11).
Controlled human exposure studies have provided quantitative COHb dose-
response information for this specific population with regard to
effects on markers of myocardial ischemia. Accordingly, based on the
current evidence with regard to quantitative information of COHb levels
and association with specific health effects, the at-risk populations
simulated in the quantitative assessment were (1) adults with CHD (also
known as ischemic heart disease [IHD] or CAD), both diagnosed and
undiagnosed, and (2) adults with any heart diseases, including
undiagnosed ischemia.\32\ Evidence characterizing the nature of
specific health effects of CO in other populations is limited and does
not include specific COHb levels related to health effects in those
groups. As a result, the quantitative assessment does not develop
separate quantitative dose estimates for populations other than those
with CHD or HD.
---------------------------------------------------------------------------
\32\ As described in section 1.2 above, this is the same
population group that was the focus of the CO NAAQS exposure/dose
assessments conducted previously (e.g., USEPA, 1992; Johnson et al.,
2000).
---------------------------------------------------------------------------
In representing the two at-risk populations and their activity
patterns, individuals were simulated based on age and gender
distributions for CHD and HD populations. These distributions were
developed by augmenting the prevalence estimates provided by the
National Health Interview Survey for adults with CAD and adults with
heart diseases of any type (HD) with estimates of undiagnosed ischemia
(as described in section 5.5.1 of the REA). The undiagnosed ischemia
estimates were developed based on two assumptions: (1) There are 3.5
million persons in U.S. with undiagnosed IHD (AHA, 2003) and (2)
persons with undiagnosed IHD are distributed within the population in
the same manner as persons with diagnosed IHD (REA, section 5.5.1).
APEX simulations performed for this review focused on exposures to
ambient
[[Page 8170]]
CO occurring in eight microenvironments,\33\ absent any contribution to
microenvironment concentrations from indoor (nonambient) CO sources. As
noted in section II.B.1 above, however, where present, indoor sources,
including gas stoves, attached garages and tobacco smoke, can also be
important contributors to total CO exposure (ISA, sections 3.6.1 and
3.6.5). Previous assessments, that have included modeling simulations
both with and without certain indoor sources, indicated that the impact
of such sources can be substantial with regard to the portion of the
at-risk population experiencing higher exposures and COHb levels
(Johnson et al., 2000). While we are limited with regard to information
regarding CO emissions from indoor sources today and how they may
differ from the time of the 2000 assessment, we note that ambient
contributions have notably declined, and indoor source contributions
from some sources may also have declined. Thus, as indicated in the
Policy Assessment, we have no firm basis to conclude a different role
for indoor sources today with regard to contribution to population CO
exposure and COHb levels.
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\33\ The 8 microenvironments modeled in the REA comprised a
range of indoor and outdoor locations including residences as well
as motor vehicle-related locations such as inside vehicles, and
public parking and fueling facilities, where the highest exposures
were estimated (REA, sections 5.9 and 6.1).
---------------------------------------------------------------------------
The REA developed COHb estimates for the simulated at-risk
populations with attention to both COHb in absolute terms and in terms
of the contribution to absolute levels associated with ambient CO
exposures. Absolute COHb refers to the REA estimates of COHb levels
resulting from endogenously produced CO and exposure to ambient CO (in
the absence of any nonambient sources). The additional REA estimates of
ambient CO exposure contribution to COHb levels were calculated by
subtracting COHb estimates obtained in the absence of CO exposure--
i.e., that due to endogenous CO production alone (see REA, Appendix
B.6)--from the corresponding end-of-hour absolute COHb estimates for
each simulated individual. Thus, the REA reports estimates of the
maximum end-of-hour ambient contributions across the simulated year, in
addition to the maximum absolute end-of hour COHb levels.
As discussed in the Policy Assessment (section 2.2.2), the absence
of indoor (nonambient) sources in the REA simulations is expected to
result in simulated individuals with somewhat higher estimates of the
contribution of short-duration increases in ambient CO exposure to COHb
levels (ambient contribution) than would be expected for individuals in
situations where the presence of nonambient sources contributes to
higher baseline COHb levels (i.e., COHb prior to a short-duration
exposure event). The amount by which the ambient contribution estimates
might differ is influenced by the magnitude of nonambient-source
exposures and associated baseline COHb levels. One reason for this is
that in the presence of indoor sources, baseline COHb levels will be
higher for a given population group than COHb levels for that group
arising solely from endogenous CO in the absence of any exposure, which
is the ``baseline'' for the REA estimates of ambient contribution to
COHb (REA, appendix B.6).\34\ As CO uptake depends in part on the
amount of CO already present in the blood (and the blood-air CO
concentration gradient), in general, a higher baseline COHb, with all
other variables unchanged, will lead to relatively lesser uptake of CO
from short-duration exposures (ISA, section 4.3; AQCD, section 5.2).
Additionally, as is indicated by the REA estimates, the attainment of a
particular dose level is driven largely by short-term (and often high
concentration) exposure events. This is because of the relatively rapid
uptake of CO into a person's blood, as demonstrated by the pattern in
the REA time-series of ambient concentrations, microenvironmental
exposures, and COHb levels (REA, Appendix B, Figure B-2). For example
the time lag for response of an individual's COHb levels to variable
ambient CO (and hence exposure) concentrations may be only a few hours
(e.g., REA, Figure B-2).
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\34\ As they result only from endogenous CO formation, the REA
``baseline'' COHb levels would also be expected to be, and generally
are, lower than the initial, pre-exposure, COHb levels of subjects
in the controlled exposure studies. REA estimates of endogenously
formed COHb averaged about 0.3% across the simulated populations,
with slightly higher levels in the higher altitude Denver study area
(REA, pp. B-21 to B-22). Levels in the Denver study population
ranged from 0.1 to 1.1% COHb, with an average of 0.31%, while levels
for Los Angeles ranged from 0.1 to 0.7% with an average of 0.27%
COHb. Initial, pre-exposure COHb levels in the subjects of the
Allred et al. study (1989b), which reflect the subjects pre-study
exposure history as well as endogenous CO formation, ranged from 0.2
to 1.1%, averaging about 0.6% COHb.
---------------------------------------------------------------------------
In considering the REA dose estimates in the Policy Assessment, as
described in section II.D.2 below, staff considered estimates of the
portion of the simulated at-risk populations estimated to experience
daily maximum end-of-hour absolute COHb levels above identified
benchmark levels (at least once and on multiple occasions), as well as
estimates of the percentage of population person-days (the only metric
available from the modeling for the 1994 review), and also population
estimates of daily maximum ambient contribution to end-of-hour COHb
levels. In identifying COHb benchmark levels of interest, primary
attention was given to the multi-laboratory study in which COHb was
analyzed by the more accurate GC method (Allred et al., 1989a, 1989b,
1991) discussed in section II.B.2 above. The REA identified a series of
benchmark levels for considering estimates of absolute COHb: 1.5%,
2.0%, 2.5% and 3% COHb (REA, section 2.6). This range includes the
range of COHb levels identified as levels of concern in the review
completed in 1994 (2.0 to 2.9%) and the level given particular focus
(2.1%) at that time, as described in section 2.1.1 above (USEPA, 1992;
59 FR 48914). Selection of this range of benchmark levels is based on
consideration of the evidence from controlled human exposure studies of
subjects with CAD (discussed in section 2.2.1 above), with the lower
end of the range extending below the lowest mean COHb level resulting
from controlled exposure to CO in the clinical evidence (e.g., 2.0%
post-exercise in Allred et al., 1989b). The extension of this range
reflects a number of considerations, including: (1) Comments from the
CASAC CO panel on the draft Scope and Methods Plan (Brain, 2009); (2)
consideration of the uncertainties regarding the actual COHb levels
experienced in the controlled human exposure studies; (3) that these
studies did not include individuals with most severe cardiovascular
disease;\35\ (4) the lack of studies that have evaluated effects of
experimentally controlled short-term CO exposures resulting in mean
COHb levels below 2.0-2.4%; and (5) the lack of evidence of a threshold
at the increased COHb levels evaluated. We note that CASAC comments on
the first draft REA recommended the addition of a benchmark at 1.0%
COHb and results are presented for this COHb level in the REA. Given
that this level overlaps with the upper part of the range of endogenous
levels in healthy individuals as characterized in the ISA (ISA, p. 2-
6), and is within the upper
[[Page 8171]]
part of the range of baseline COHb levels in the study by Allred et al
(1989b, Appendix B), however, we considered that it may not be
appropriate to place weight on it as a benchmark level and accordingly
have not focused on interpreting absolute COHb estimates at and below
this level in the discussion below. Additionally we note the REA
estimates indicating that, in the absence of CO exposure, approximately
0.5% to 2% of the simulated at-risk populations in the two study areas
were estimated to experience a single daily maximum end-of-hour COHb
level, arising solely from endogenous CO production, at or above 1%
(REA, Appendix B, Figure B-3).
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\35\ Although the CAD patients evaluated in the controlled human
exposure study by Allred et al. (1989a, 1989b, 1991) are not
necessarily representative of the most sensitive population, the
level of disease in these individuals ranged from moderate to
severe, with the majority either having a history of myocardial
infarction or having >=70% occlusion of one or more of the coronary
arteries (ISA, p. 5-43).
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The Policy Assessment also considered the evidence from controlled
human exposure studies in interpreting the REA estimates of maximum
ambient exposure contributions to end-of-hour COHb levels (described in
sections 4.4.7 and 5.10.3 of the REA). As discussed above, the study by
Allred et al (1989a, 1989b, 1991) observed reduced time to exercise-
induced angina and ST-segment change in groups of subjects with pre-
existing CAD for which controlled CO exposures increased their COHb
levels by on average 1.4-1.8% and 3.2-4.0% COHb from initial COHb
levels of on average 0.6% COHb (ISA, section 5.2.4; Allred et al.,
1989a, 1989b, 1991). The study reported a dose-response relationship in
terms of time reduction per 1% increase in COHb concentration based on
analysis of the full data set across both exposure groups. For purposes
of the discussion in this document, we have presented the percentage of
the simulated at-risk populations estimated to experience maximum
ambient contribution to end-of-hour COHb levels above and below a range
of levels extending from 1.4 to 2.0%. As noted above, the Policy
Assessment recognized distinctions between the REA ``baseline''
(arising from prior ambient exposure and endogenous CO production) and
the pre-exposure COHb levels in the controlled human exposure study
(arising from ambient and nonambient exposure history, as well as from
endogenous CO production), and also noted the impact of ``baseline''
COHb levels on COHb levels occurring in response to short ambient CO
exposure events such as those simulated in the REA as discussed above.
2. Key Limitations and Uncertainties
Numerous improvements have been made over the last decade that have
reduced the uncertainties associated with the models used to estimate
COHb levels resulting from ambient CO exposures under different air
quality conditions, including those associated with just meeting the
current CO NAAQS (REA, section 4.3). This progression in exposure model
development has led to the model currently used by the Agency
(APEX4.3), which has an enhanced capacity to estimate population CO
exposures and more accurately predicts COHb levels in persons exposed
to CO. Our application of APEX4.3 in this review, using updated data
and new algorithms to estimate exposures and doses experienced by
individuals, better represents the variability in population exposure
and COHb dose levels than the model version used in previous CO
assessments.\36\ However, while APEX 4.3 is greatly improved when
compared with previously used exposure models, its application is still
limited with regard to data to inform our understanding of spatial
relationships in ambient CO concentrations and within microenvironments
of particular interest. Further information regarding model
improvements and remaining exposure modeling uncertainties are
summarized in section 2.2.2 of the Policy Assessment and described in
detail in chapter 7 of the REA.
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\36\ APEX4.3 provides estimates for percent of population
projected to experience a single or multiple occurrences of a daily
maximum COHb level above the various benchmark levels, as well as
percent of person-days.
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The uncertainties associated with the quantitative estimates of
exposure and dose were considered using a generally qualitative
approach intended to identify and compare the relative impact that
important sources of uncertainty may have on the estimated potential
health effect endpoints (i.e., estimates of the maximum end-of-hour
COHb levels in the simulated at-risk population). The approach used was
developed using World Health Organization (WHO) guidelines on
conducting a qualitative uncertainty characterization (WHO, 2008) and
was also applied in the most recent NO2 (USEPA, 2008c) and
SO2 NAAQS reviews (USEPA, 2009e). A qualitative approach was
employed given the extremely limited data available to inform
probabilistic uncertainty analyses. The qualitative approach used
varies from that of WHO (2008) in that a greater focus of the
characterization performed was placed on evaluating the direction and
the magnitude of the uncertainty; that is, qualitatively rating how the
source of uncertainty, in the presence of alternative information, may
affect the estimated exposures and health risk results. Additionally,
consistent with the WHO (2008) guidance, the REA discusses the
uncertainty in the knowledge base (e.g., the accuracy of the data used,
acknowledgement of data gaps) and decisions made where possible (e.g.,
selection of particular model forms), though qualitative ratings were
assigned only to uncertainty regarding the knowledge base.
Sixteen separate sources of uncertainty associated with four main
components of the assessment were identified. By comparing judgments
made regarding the magnitude and direction of influence that the
identified sources have on estimated exposure concentrations and dose
levels and the existing uncertainties in the knowledge base, seven
sources of uncertainty (i.e., the spatial and temporal representation
of ambient monitoring data, historical data used in representing
alternative air quality scenarios, activity pattern database,
longitudinal profile algorithm, microenvironmental algorithm and input
data, and physiological factors) were identified as the most important
areas of uncertainty in this assessment (PA, section 2.2.2). Taking
into consideration improvements in the model algorithms and data since
the last review, and having identified and characterized these
uncertainties here, the Policy Assessment concludes that the estimates
associated with the current analysis, at a minimum, better reflect the
full distribution of exposures and dose as compared to results from the
1992 analysis. As noted in the Policy Assessment, however, potentially
greater uncertainty remains in our characterization of the upper and
lower percentiles of the distribution of population exposures and COHb
dose levels relative to that of other portions of the respective
distribution. When considering the overall quality of the current
exposure modeling approach, the algorithms, and input data used,
alongside the identified limitations and uncertainties, the REA and
Policy Assessment conclude that the quantitative assessment provides
reasonable estimates of CO exposure and COHb dose for the simulated
population the assessment is intended to represent (i.e., the
population residing within the urban core of each study area).
The Policy Assessment additionally notes the impact on the REA dose
estimates for ambient CO contribution to COHb of the lack of nonambient
sources in the model simulations. This aspect of the assessment design
may contribute to higher estimates of the contribution of short-
duration ambient CO exposures to total COHb than would
[[Page 8172]]
result from simulations that include the range of commonly encountered
CO sources beyond just those contributing to ambient air CO
concentrations. Although the specific quantitative impact of this on
estimates of population percentages discussed in this document is
unknown, consideration of COHb estimates from the 2000 assessment
indicates a potential for the inclusion of nonambient sources to
appreciably affect absolute COHb (REA, section 6.3) and accordingly
implies the potential, where present, for an impact on overall ambient
contribution to a person's COHb level.
D. Conclusions on Adequacy of the Current Standards
The initial issue to be addressed in the current review of the
primary CO standards is whether, in view of the advances in scientific
knowledge and additional information now available, the existing
standards should be retained or revised. In evaluating whether it is
appropriate to retain or revise the current standards, the
Administrator builds upon the last review and reflects the broader body
of evidence and information now available. The Administrator has taken
into account both evidence-based and quantitative exposure- and risk-
based considerations in developing conclusions on the adequacy of the
current primary CO standards. Evidence-based considerations include the
assessment of evidence from controlled human exposure, toxicological
and epidemiological studies evaluating short- or long-term exposures to
CO, with supporting evidence related to dosimetry and potential mode of
action, as well as the integration of evidence across each of these
disciplines, and with a focus on policy-relevant considerations as
discussed in the PA. The exposure/dose-based considerations draw from
the results of the quantitative analyses presented in the REA and
summarized in section II.C above, and consideration of those results in
the PA. More specifically, estimates of the magnitude of ambient CO-
related exposures and associated COHb levels associated with just
meeting the current primary CO NAAQS have been considered. Together the
evidence-based and risk-based considerations have informed the
Administrator's proposed conclusions related to the adequacy of the
current CO standards in light of the currently available scientific
evidence.
1. Approach
In considering the evidence and quantitative exposure and dose
estimates with regard to judgments on the adequacy afforded by the
current standards, we note that the final decision is largely a public
health policy judgment. A final decision must draw upon scientific
information and analyses about health effects and risks, as well as
judgments about how to consider the range and magnitude of
uncertainties that are inherent in the scientific evidence and
analyses. Our approach to informing these judgments, discussed more
fully below, is based on the recognition that the available health
effects evidence generally reflects a continuum, consisting of ambient
levels at which scientists generally agree that health effects are
likely to occur, through lower levels at which the likelihood and
magnitude of the response become increasingly uncertain. This approach
is consistent with the requirements of the NAAQS provisions of the Act
and with how EPA and the courts have historically interpreted the Act.
These provisions require the Administrator to establish primary
standards that, in the Administrator's judgment, are requisite to
protect public health with an adequate margin of safety. In so doing,
the Administrator seeks to establish standards that are neither more
nor less stringent than necessary for this purpose. The Act does not
require that primary standards be set at a zero-risk level, but rather
at a level that avoids unacceptable risks to public health, including
the health of sensitive groups.\37\
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\37\ The sensitive population groups identified in a NAAQS
review may (or may not) be comprised of low income or minority
groups. Where low income/minority groups are among the sensitive
groups, the rulemaking decision will be based on providing
protection for these and other sensitive population groups. To the
extent that low income/minority groups are not among the sensitive
groups, a decision based on providing protection of the sensitive
groups would be expected to provide protection for the low income/
minority groups (as well as any other less sensitive population
groups).
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The following subsections include background information on the
approach used in the previous review of the CO standards (section
II.D.1.a) and also a description of the approach for the current review
(section II.D.1.b).
a. Previous Reviews
The current primary standards for CO are set at 9 parts per million
(ppm) as an 8-hour average and 35 ppm as a 1-hour average, neither to
be exceeded more than once per year. These standards were initially set
in 1971 to protect against the occurrence of carboxyhemoglobin (COHb)
levels that may be associated with effects of concern (36 FR 8186).
Reviews of these standards in the 1980s and early 1990s identified
additional evidence regarding ambient CO, CO exposures, COHb levels,
and associated health effects (USEPA, 1984a, 1984b; USEPA, 1991; USEPA,
1992; McClellan, 1991, 1992). Assessment of the evidence in those
reviews, completed in 1985 and 1994, led the EPA to retain the existing
primary standards without revision (50 FR 37484, 59 FR 38906).
The 1994 decision to retain the primary standards without revision
was based on the evidence published through 1990 and reviewed in the
1991 AQCD (USEPA, 1991), the 1992 Staff Paper assessment of the policy-
relevant information contained in the AQCD and the quantitative
exposure assessment (USEPA, 1992), and the advice and recommendations
of CASAC (McClellan 1991, 1992). At that time, as at the time of the
first NAAQS review (50 FR 37484), COHb levels in blood were recognized
as providing the most useful estimate of exogenous CO exposures and
serving as the best biomarker of CO toxicity for ambient-level
exposures to CO (59 FR 38909). Consequently, COHb levels were used as
the indicator of health effects in the identification of health effect
levels of concern for CO (59 FR 38909).
In reviewing the standards in 1994 the Administrator first
recognized the need to determine the COHb levels of concern ``taking
into account a large and diverse health effects database.'' The more
uncertain and less quantifiable evidence was taken into account to
identify the lower end of this range to provide an adequate margin of
safety for effects of clear concern. To consider ambient CO
concentrations likely to result in COHb levels of concern, a model
solution to the Coburn-Forster-Kane (CFK) differential equation was
employed in the analysis of CO exposures expected to occur under air
quality scenarios related to just meeting the current 8-hour CO NAAQS,
the controlling standard (USEPA, 1992).\38\ Key considerations in this
approach are described below.
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\38\ Air quality analyses of CO levels in the U.S. consistently
demonstrate that meeting the 8-hour standard results in 1-hour
maximum concentrations well below the corresponding 1-hour standard.
---------------------------------------------------------------------------
The assessment of the science that was presented in the 1991 AQCD
(USEPA, 1991) indicated that CO is associated with effects in the
cardiovascular system, central nervous system (CNS), and the developing
fetus. Additionally, factors recognized as having the potential to
alter the effects
[[Page 8173]]
of CO included exposures to other pollutants, some drugs and some
environmental factors, such as altitude. Cardiovascular effects of CO,
as measured by decreased time to onset of angina and to onset of
significant electrocardiogram (ECG) ST-segment depression were judged
by the Administrator to be ``the health effects of greater concern,
which clearly had been associated with CO exposures at levels observed
in ambient air'' (59 FR 38913).
Based on the consistent findings of response in patients with
coronary artery disease across the controlled human exposure evidence
(Adams et al., 1988; Allred et al., 1989a, 1989b, 1991; Anderson et
al., 1973; Kleinman et al., 1989, 1998; Sheps et al., 1987 \39\) and
discussions of adverse health consequences in the 1991 AQCD and the
1992 Staff Paper,\40\ at the CASAC meetings and in the July 1991 CASAC
letter, the Administrator concluded that ``CO exposures resulting in
COHb levels of 2.9-3.0 percent (CO-Ox) or higher in persons with heart
disease have the potential to increase the risk of decreased time to
onset of angina pain and ST-segment depression'' (59 FR 38913). While
EPA and CASAC recognized the existence of a range of views among health
professionals on the clinical significance of these responses, CASAC
noted that the dominant view was that they should be considered
``adverse or harbinger of adverse effect'' (McClellan, 1991) and EPA
recognized that it was ``important that standards be set to
appropriately reduce the risk of ambient exposures which produce COHb
levels that could induce such potentially adverse effects'' (59 FR
38913).
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\39\ See footnote 15 above.
\40\ Based on consideration of the key studies, including those
two that investigated more than a single target COHb level,
discussions in the 1991 AQCD and with CASAC, the 1992 Staff Paper
recommended that ``2.9-3.0% COHb (CO-Ox), representing an increase
above initial COHb of 1.5 to 2.2% COHb, be considered a level of
potential adversity for individuals at risk'' (59 FR 38911; USEPA,
1992; USEPA, 1991, pp. 1-11 to 1-12; Allred et al., 1989a, 1989b,
1991; Anderson et al., 1973).
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In further considering additional results from the controlled human
exposure evidence, such as the results from Allred et al. (1989a,
1989b) at 2.0% COHb (using GC measurement) induced by short
(approximately 1-hour) CO exposure, as well as other aspects of the
available evidence and uncertainties regarding modeling estimates of
COHb formation and human exposure to COHb levels in the population
associated with attainment of a given CO NAAQS, the Administrator
recognized the need to extend the range of COHb levels for
consideration in evaluating whether the current CO standards provide an
adequate margin of safety to those falling between 2.0 to 2.9% COHb (59
FR 38913). Factors considered in recognizing this margin of safety
included the following (59 FR 38913).
Uncertainty regarding the clinical importance of
cardiovascular effects associated with exposures to CO that resulted in
COHb levels of 2 to 3 percent. Although recognizing the possibility
that there is no threshold for these effects even at lower COHb levels,
the clinical importance of cardiovascular effects associated with short
(approximately 1-hour) exposures to CO resulting in COHb levels as low
as 2.0% COHb by GC (Allred et al., 1989a,b) was described as ``less
certain'' than effects noted for exposures contributing to higher COHb
(CO-Ox) levels (59 FR 38913).
Findings of short-term reduction in maximal work capacity
measured in trained athletes exposed to CO at levels resulting in COHb
levels of 2.3 to 7 percent.
The potential that the most sensitive individuals have not
been studied, the limited information regarding the effects of ambient
CO in the developing fetus, and concern about visitors to high
altitudes, individuals with anemia or respiratory disease, or the
elderly.
Potential for short term peak CO exposures to be
responsible for impairments (impairment of visual perception,
sensorimotor performance, vigilance or other CNS effects) which could
be a matter of concern for complex activities such as driving a car,
although these effects had not been demonstrated to be caused by CO
concentrations in ambient air.
Concern based on limited evidence for individuals exposed
to CO concurrently with drugs (e.g., alcohol), during heat stress, or
co-exposure to other pollutants.
Uncertainties, described as ``large,'' that remained
regarding modeling COHb formation and estimating human exposure to CO
which could lead to overestimation of COHb levels in the population
associated with attainment of a given CO NAAQS.
Uncertainty associated with COHb measurements made using
CO-Ox which may not reflect COHb levels in angina patients studied,
thereby creating uncertainty in establishing a lowest effects level for
CO.
Based on these considerations of the evidence, the Administrator
identified a range of COHb levels for considering margin of safety,
extending from 2.9% COHb (representing an increase of 1.5% above
baseline when using CO-Ox measurements) at the upper end down to 2% at
the lower end (59 FR 38913), and also concluded that ``evaluation of
the adequacy of the current standard should focus on reducing the
number of individuals with cardiovascular disease from being exposed to
CO levels in the ambient air that would result in COHb levels of 2.1
percent'' (59 FR 38914). She additionally concluded that standards that
``protect against COHb levels at the lower end of the range should
provide an adequate margin of safety against effects of uncertain
occurrence, as well as those of clear concern that have been associated
with COHb levels in the upper-end of the range'' (59 FR 38914).
To estimate CO exposures and resulting COHb levels that might be
expected under air quality conditions that just met the current
standards, an analysis of exposure and associated internal dose in
terms of COHb levels in the population of interest in the city of
Denver, Colorado was performed (59 FR 38906; USEPA, 1992). That
analysis indicated that if the 9 ppm 8-hour standard were just met, the
proportion of the nonsmoking population with cardiovascular disease
experiencing a daily maximum 8-hour exposure at or above 9 ppm for 8
hours decreased by an order of magnitude or more as compared to the
proportion under then-existing CO levels, down to less than 0.1 percent
of the total person-days in that population. Further, upon meeting the
8-hour standard, EPA estimated that less than 0.1% of the nonsmoking
cardiovascular-disease population would experience a COHb level greater
than or equal to 2.1% and a smaller percentage of the at-risk
population was estimated to exceed higher COHb levels (59 FR
38914).\41\ Based on these estimates, the Administrator concluded that
``relatively few people of the cardiovascular sensitive population
group analyzed will experience COHb levels >= 2.1 percent when exposed
to CO levels in absence of indoor sources when the current standards
are attained.'' The analysis also took into account that certain indoor
sources (e.g., passive smoking, gas stove usage) contributed to total
CO exposure and EPA recognized that such sources may be of concern for
such high risk groups
[[Page 8174]]
as individuals with cardiovascular disease, pregnant women, and their
unborn children but concluded that ``the contribution of indoor sources
cannot be effectively mitigated by ambient air quality standards'' (59
FR 38914).
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\41\ In the 1992 assessment, the person-days (number of persons
multiplied by the number of days per year exposed) and person-hours
(number of persons multiplied by the number of hours per year
exposed) were the reported exposure metrics. Upon meeting the 8-hour
standard, it was estimated that less than 0.1% of the total person-
days simulated for the nonsmoking cardiovascular-disease population
were associated with a maximum COHb level greater than or equal to
2.1% (USEPA, 1992; Johnson et al., 1992).
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Based on consideration of the evidence and the quantitative results
of the exposure assessment, the Administrator concluded that revisions
of the current primary standards for CO were not appropriate at that
time (59 FR 38914). The Administrator additionally concluded that both
averaging times for the primary standards, 1 hour and 8 hours, be
retained. The 1-hour and 8-hour averaging times were first chosen when
EPA promulgated the primary NAAQS for CO in 1971. The selection of the
8-hour averaging time was based on the following: (a) Most individuals'
COHb levels appeared to approach equilibrium after 8 hours of exposure,
(b) the 8-hour time period corresponded to the blocks of time when
people were often exposed in a particular location or activity (e.g.,
working or sleeping), and (c) judgment that this provided a good
indicator for tracking continuous exposures during any 24-hour period.
The 1-hour averaging time was selected as better representing a time
period of interest to short-term CO exposure and providing protection
from effects which might be encountered from very short duration peak
exposures in the urban environment (59 FR 38914).
b. Current Review
To evaluate whether it is appropriate to consider retaining the
current primary CO standards, or whether consideration of revisions is
appropriate, we adopted an approach in this review that builds upon the
general approach used in the last review and reflects the broader body
of evidence and information now available. As summarized above, the
Administrator's decisions in the previous review were based on an
integration of information on health effects associated with exposure
to ambient CO; expert judgment on the adversity of such effects on
individuals; and a public health policy judgment as to what standard is
requisite to protect public health with an adequate margin of safety,
which were informed by air quality and related analyses, quantitative
exposure and risk assessments when possible, and qualitative assessment
of impacts that could not be quantified. Similarly, in this review, as
described in the Policy Assessment, we draw on the current evidence and
quantitative assessments of exposure pertaining to the public health
risk of ambient CO. In considering the scientific and technical
information, here as in the Policy Assessment, we consider both the
information available at the time of the last review and information
newly available since the last review, including the current ISA and
the 2000 AQCD (USEPA, 2010a; USEPA, 2000), as well as current and
preceding quantitative exposure/dose assessments (USEPA 2010b; Johnson
et al., 2000; USEPA 1992).
As described earlier, at this time as at the time of the last
review, the best characterized health effect associated with CO levels
of concern is hypoxia (reduced oxygen availability) induced by
increased COHb levels in blood (ISA, section 5.1.2). Accordingly, CO
exposure is of particular concern for those with impaired
cardiovascular systems, and the most compelling evidence of
cardiovascular effects is that from a series of controlled human
exposure studies among exercising individuals with CAD (ISA, sections
5.2.4 and 5.2.6). Additionally available in this review are a number of
epidemiological studies that investigated the association of
cardiovascular disease-related health outcomes with concentrations of
CO at ambient monitors. To inform our review of the ambient standards,
we performed a quantitative exposure and dose modeling analysis that
estimated COHb levels associated with different air quality conditions
in simulated at-risk populations in two U.S. cities, as described in
detail in the REA and summarized in the Policy Assessment (PA, section
2.2.2). Thus, in developing conclusions with regard to the CO NAAQS,
EPA has taken into account both evidence-based and exposure/dose-based
considerations.
The approach to reaching a decision on the adequacy of the current
primary standards is framed by consideration of the following series of
key policy-relevant questions.
Does the currently available scientific evidence- and
exposure/dose/risk-based information, as reflected in the ISA and REA,
support or call into question the adequacy of the protection afforded
by the current CO standards?
Does the current evidence alter our conclusions from the
previous review regarding the health effects associated with exposure
to CO?
Does the current evidence continue to support a focus on
COHb levels as the most useful indicator of CO exposures and the best
biomarker to characterize potential for health effects associated with
exposures to ambient CO? Or does the current evidence provide support
for a focus on alternate dose indicators to characterize potential for
health effects?
Does the current evidence alter our understanding of
populations that are particularly susceptible to CO exposures? Is there
new evidence that suggest additional susceptible populations that
should be given increased focus in this review?
Does the current evidence alter our conclusions from the
previous review regarding the levels of CO in ambient air associated
with health effects?
To what extent have important uncertainties identified in
the last review been reduced and/or have new uncertainties emerged?
The following sections describe the assessment of these issues in
the Policy Assessment, the advice received from CASAC, as well as the
comments received from various parties, and then presents the
Administrator's proposed conclusions regarding the adequacy of the
current primary standards.
2. Evidence-Based and Exposure/Dose-Based Considerations in the Policy
Assessment
The Policy Assessment (chapter 2) considers the evidence presented
in the Integrated Science Assessment, and preceding AQCDs, as discussed
above in section II.B as a basis for evaluating the adequacy of the
current CO standards, recognizing that important uncertainties remain.
The Policy Assessment concludes that the combined consideration of the
body of evidence and the results from the quantitative exposure and
dose assessment provide support for standards at least as protective as
the current suite of standards to provide appropriate public health
protection for susceptible populations, including most particularly
individuals with cardiovascular disease, against effects of CO in
exacerbating conditions of reduced oxygen availability to the heart
(PA, section 2.4). More specifically, the Policy Assessment concludes
that the combined consideration of the evidence and quantitative
estimates from the REA may be viewed as providing support for either
retaining or revising the current suite of standards (PA, p. 2-59).
CASAC stated agreement with this conclusion, while additionally
expressing a ``preference'' for revisions to a lower standard. Members
of the public who provided comments on the draft Policy Assessment
supported retaining the current standard without revision. The specific
considerations on which the Policy Assessment conclusions are based are
described in the subsections below.
[[Page 8175]]
a. Evidence-Based Considerations
In considering the evidence available for the current review of the
CO NAAQS, the Policy Assessment discussed whether or not, or the extent
to which, the current evidence alters conclusions reached in the
previous review regarding levels of CO in ambient air associated with
health effects and associated judgments on adequacy of the current
standards. With this discussion, the Policy Assessment also considered
the extent to which important uncertainties identified in the last
review have been reduced or new uncertainties have emerged.
As an initial matter, the Policy Assessment recognized that at the
time of the last review, EPA's conclusions regarding the adequacy of
the existing CO standards were drawn from the combined consideration of
the evidence of COHb levels for which cardiovascular effects of concern
had been reported and the results of an exposure and dose modeling
assessment (59 FR 38906). As described in more detail above, the key
effects judged to be associated with CO exposures resulting from
concentrations observed in ambient air were cardiovascular effects, as
measured by decreased time to onset of exercise-induced angina and to
onset of ECG ST-segment depression (59 FR 38913). As at the time of the
last review, the Policy Assessment noted that the evidence available in
this review includes multiple studies that document decreases in time
to onset of exercise-induced angina (a symptom of myocardial ischemia)
in multiple studies at post-exposure COHb levels ranging from 2.9 to
5.9% (CO-Ox), which represent incremental increases of approximately
1.4-4.4% COHb from baseline (CO-Ox) (PA, Table 2-2; Adams et al., 1988;
Allred et al., 1989a, 1989b, 1991; Anderson et al., 1973; Kleinman et
al., 1989, 1998 \42\; Sheps et al., 1987 \43\). The study results from
Allred et al. (1989a, 1989b, 1991) also provide evidence for these
effects in terms of COHb measurements using gas
chromatography.44 45 Evidence also available at the time of
the last review of effects in other clinical study groups includes
effects in subjects with cardiac arrhythmias and effects on exercise
duration and maximal aerobic capacity in healthy adults. Among the
studies of myocardial ischemia indicators in patients with CAD, none
provide evidence of a measurable threshold at the lowest experimental
CO exposures and associated COHb levels assessed (e.g., mean of 2.0-
2.4% COHb, GC) which resulted in average increases in COHb of about
1.5% over pre-exposure baseline (Anderson et al., 1973; Kleinman et
al., 1989; Allred et al. 1989a, 1989b, 1991).\46\ Allred et al. (1989a,
1989b, 1991) further reported a dose-response relationship between the
increased COHb levels and the response of the assessed indicators of
myocardial ischemia (Allred et al., 1989a, 1989b, 1991). While this
evidence informs our conclusions regarding COHb levels associated with
health effects, the CO exposure concentrations employed in the studies
to achieve these COHb levels were substantially above ambient
concentrations. Thus, an exposure and dose assessment was performed to
consider the COHb levels that might be attained as a result of
exposures to ambient CO allowed under the current NAAQS, as described
in section II.C above.
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\42\ One new study of this type is available since the 1994
review. This study, which focused on a target COHb level of 3.9%
COHb (CO-Ox) and is discussed in the 2000 AQCD is generally
consistent with the previously available studies (2000 AQCD, section
6.2.2; Kleinman et al., 1998).
\43\ See footnote 15 above.
\44\ Gas chromatography is generally recognized to be the more
accurate method for COHb levels below 5% (ISA, section 5.2.4).
\45\ In the lower CO exposure group, the post-exposure mean COHb
was 3.21% by CO-Ox and 2.38% by GC, while the post-exercise mean
COHb was 2.65% by CO-Ox and 2.00% by GC (Allred et al., 1989a,
1989b, 1991).
\46\ The studies by Anderson et al. (1973) and Kleinman et al.
(1989) did not use GC to measure COHb levels, and reported reduced
exercise duration due to increased chest pain at CO exposures
resulting in 2.8-3.0% COHb (CO-Ox). The COHb levels assessed in
these two studies represented increase in average COHb levels over
baseline of 1.4% and 1.6% COHb.
---------------------------------------------------------------------------
Since the time of the last review, there have been no new
controlled human exposure studies specifically designed to evaluate the
effects of CO exposure in susceptible populations at study mean COHb
levels at or below 2% COHb. Thus, similar to the last review, the
multilaboratory study by Allred et al. (1989a, 1989b, 1991) continues
to be the study that has evaluated cardiovascular effects of concern
(i.e., reduced time to exercise-induced myocardial ischemia as
indicated by ECG ST-segment changes and angina) at the lowest tested
COHb levels (ISA, section 2.7). This study is also of particular
importance in this review because it is considered the most rigorous
and well designed study, presenting the most sensitive analysis methods
(GC used in addition to CO-Ox) to quantify COHb blood levels. Key
findings from that study with regard to levels of CO associated with
health effects, as discussed in section II.B.2 above, include the
following:
Short (50-70 minute) exposure to increased CO
concentrations that resulted in increases in COHb to mean levels of
2.0% and 3.9% (post-exercise) from mean a baseline level of 0.6%
significantly reduced exercise time required to induce markers of
myocardial ischemia in CAD patients. For the more objective marker of
ST-segment change, the lower exposure reduced the time to onset by 5.1%
(approximately one half minute) and the higher exposure reduced the
time to onset by 12.1%.\47\
---------------------------------------------------------------------------
\47\ Across all subjects, the mean time to angina onset for
baseline or control (``clean'' air) exposures was approximately 8.5
minutes, and the mean time to ST endpoint was approximately 9.5
minutes, with the ``time to onset'' reductions of the two exposure
levels being approximately one half and one minute, respectively for
ST-segment change, and slightly less and slightly more than one half
minute, respectively, for angina (Allred et al., 1989b).
---------------------------------------------------------------------------
The associated dose-response relationship between
incremental changes in COHb and change in time to myocardial ischemia
in CAD patients indicates a 1.9% and 3.9% reduction in time to onset of
exercise-induced angina and ST-segment change, respectively, per 1%
increase in COHb concentration from average baseline COHb of 0.6%
without evidence of a measurable threshold.
As described in section II.B.2 above, a number of epidemiological
studies of health outcome associations with ambient CO have been
conducted since the last review. These include studies that have
reported associations with different ambient CO metrics (e.g., 1-hour
and 8-hour averages, often as central-site estimates) derived from CO
measurements at fixed-site ambient monitors in selected urban areas of
the U.S. and cardiovascular endpoints other than stroke, particularly
hospitalizations and emergency department visits for specific
cardiovascular health outcomes including IHD, CHF and CVD (Bell et al.,
2009; Koken et al., 2003; Linn et al., 2000; Mann et al., 2002; Metzger
et al., 2004; Symons et al., 2006; Tolbert et al., 2007; Wellenius et
al., 2005). In general, these studies, many of which were designed to
evaluate the effects of a variety of air pollutants, including CO,
report positive associations, a number of which are statistically
significant (ISA, sections 5.2.3 and 5.2.1.9). The long-standing body
of evidence for CO summarized above, including the well-characterized
role of CO in limiting oxygen availability, lends biological
plausibility to the ischemia-related health outcomes reported in the
epidemiological studies, providing coherence between these studies and
the clinical evidence of short-term exposure to CO and health effects.
Thus, although there is no new evidence
[[Page 8176]]
regarding the effects of short-term controlled CO exposures that result
in lower COHb levels, the evidence is much expanded with regard to
epidemiological \48\ analyses of ambient monitor concentrations, which
observed associations between specific and overall cardiovascular-
related outcomes and ambient CO measurements.
---------------------------------------------------------------------------
\48\ Few epidemiological studies that had investigated the
relationship between CO exposure and ischemic heart disease were
available at the time of the last completed review (1991 AQCD,
section 10.3.3).
---------------------------------------------------------------------------
The Policy Assessment considered the combined evidence base for CO
cardiovascular effects in the context of a conceptual model of the
pathway from CO exposures to the occurrence of these effects (as
described in section 2.2.1 of the PA). In this context, the Policy
Assessment noted differences between the controlled human exposure and
epidemiological studies, described above, with regard to the elements
along this pathway that have been investigated in those studies. The
controlled human exposure studies document relationships between
directly measured controlled short-term CO exposures and specific
levels of an internal dose metric, COHb, which elicited specific
myocardial ischemia-related responses in CAD patients. These studies
inform our interpretation of the associations we observed in the
epidemiological studies. The epidemiological studies reported
associations between CO levels measured at fixed-site monitors and
emergency department visits and/or hospital admissions for IHD and
other cardiovascular disease-related outcomes that are plausibly
related to the effects on physiological indicators of myocardial
ischemia (e.g., ST-segment changes) demonstrated in the controlled
human exposure studies, providing coherence between the two sets of
findings (ISA, p. 5-48). With regard to extending our understanding of
effects occurring below levels of CO evaluated in the controlled human
exposure studies, however, the epidemiological evidence for CO is
somewhat limited. The epidemiological evidence lacks measurements of
COHb or personal exposure concentrations that would facilitate
integration with the controlled human exposure study data. Furthermore,
the epidemiological evidence base for IHD outcomes or CVD outcomes as a
whole includes a number of studies involving conditions in which the
current standard was not met. Though these studies are informative to
consideration of the relationship of health effects to the full range
of ambient CO concentrations, the Policy Assessment indicated that they
are less useful to informing our conclusions regarding adequacy of the
current standards.
As discussed in the Policy Assessment, the smaller set of
epidemiological studies, under conditions where the current standards
were met, is considered to better inform our assessment of the adequacy
of the standards or conditions of lower ambient concentrations. Among
the few studies conducted during conditions in which the current
standards were always met, however, the studies reporting statistical
significance for IHD or all CVD outcomes are limited to a single study
area (i.e. Atlanta). When the analyses reporting significance for
association with CHF outcomes are also considered, a second study area
is identified (Allegheny County, PA) in which the current standard is
met throughout the study period. The analyses for both areas involve
the use of central site monitor locations or area-wide average
concentrations, which given the significant concentration gradients of
CO in urban areas (ISA, section 3.6.8.2), complicates our ability to
draw conclusions from them regarding ambient CO concentrations of
concern. Therefore, the Policy Assessment primarily focused
consideration of the epidemiological studies on the extent to which
this evidence is consistent with and generally supportive of
conclusions drawn from the combined consideration of the controlled
human exposure evidence with estimates from the exposure and dose
assessment, as discussed below. The Policy Assessment indicated that,
as in the previous review, the integration of the controlled human
exposure evidence with the exposure and dose estimates will be most
important to informing conclusions regarding ambient CO concentrations
of public health concern.
With regard to areas of uncertainty, the Policy Assessment
recognized that some important uncertainties have been reduced since
the time of the last review, some still remain and others, associated
with newly available evidence, have been identified. This range of
uncertainties identified at the time of the last review (59 FR 38913,
USEPA, 1992), as well as any newly identified uncertainties were
considered in the Policy Assessment as discussed below (PA, section
2.2.1).
The CO-induced effects considered of concern at the time of the
last review were reduced time to exercise-induced angina and ST-segment
depression in patients suffering from coronary artery disease as a
result of increases in COHb associated with short CO exposures. These
effects had been well documented in multiple studies, and it was
recognized that the majority of cardiologists at the time believed that
recurrent exercise-induced angina was associated with substantial risk
of precipitating myocardial infarction, fatal arrhythmia, or slight but
cumulative myocardial damage (USEPA, 1992, p. 22; 59 FR 38911; Basan,
1990; 1991 AQCD). As at the time of the last review, although ST-
segment depression is a recognized indicator of myocardial ischemia,
the exact physiological significance of the observed changes among
individuals with CAD is unclear (ISA, p. 5-48).
In interpreting the study results at the time of the last review,
EPA recognized uncertainty in the COHb measurements made using CO-Ox
and associated uncertainty in establishing a lowest effects level for
CO (USEPA, 1992, p. 31). A then-recent multicenter study (Allred et
al., 1989a, 1989b, 1991) was of great importance at that time for
reasons identified above. Similarly, the Science and Policy Assessments
place primary emphasis on the findings from this study in the current
review of the evidence related to cardiovascular effects associated
with CO exposure, recognizing the superior quality of the study, both
in terms of the rigorous study design as well as the sensitivity of the
analytical methods used in determining COHb concentrations (ISA,
section 2.7). No additional controlled human exposure studies are
available that evaluate responses to lower COHb levels in the
cardiovascular-disease population, and uncertainties still remain in
determining specific and quantitative relationships between the CO-
induced effects in these studies and the increased risk of specific
health outcomes. Further, with regard to then-unidentified effects at
lower COHb levels, no studies have identified other effects on the CAD
population or on other populations at lower exposures (ISA, sections
5.2.2).
The last review recognized uncertainty with regard to the potential
for short-term CO exposures to contribute to CNS effects which might
affect an individual's performance of complex activities such as
driving a car or to contribute to other effects of concern. It was
concluded, however, that the focus of the review on cardiovascular
effects associated with COHb levels below 5% also provided adequate
protection against potential
[[Page 8177]]
adverse neurobehavioral effects.\49\ No new controlled human exposure
studies have evaluated CNS or behavioral effects of exposure to CO
(ISA, section 5.3.1). However, given the drastic reduction in CO
ambient concentrations, the Policy Assessment concludes that occurrence
of these effects in response to ambient CO would be expected to be rare
within the current population. Thus, the Policy Assessment concludes
that uncertainty with regard to the potential for such effects to be
associated with current ambient CO exposures is reduced (PA, p. 2-35).
---------------------------------------------------------------------------
\49\ The evidence available at the time of the last review was
based on a series of studies conducted from the mid 1960's through
the early 1990's, with inconsistent findings of neurological effects
at exposures to CO resulting in COHb levels ranging from 5-20% (1991
AQCD).
---------------------------------------------------------------------------
Since the 1994 review, the epidemiologic and toxicological evidence
of effects on birth and developmental outcomes has expanded, although
the available evidence is still considered limited with regard to
effects on preterm birth, birth defects, decreases in birth weight,
measures of fetal growth, and infant mortality (ISA, section 5.4).
Further, while animal toxicological studies provide support and
coherence for those effects, the understanding of the mechanisms
underlying reproductive and developmental effects is still lacking
(ISA, section 5.4.1). Thus, the Policy Assessment recognizes that
although the evidence continues to ``suggest[s] that critical
developmental phases may be characterized by enhanced sensitivity to CO
exposure'' (ISA, p. 2-11), evidence is lacking for adverse
developmental or reproductive effects at CO exposure concentrations
near those associated with current levels of ambient CO (PA, pp. 2-35
to 2-36).
As described above, the much-expanded epidemiologic database in the
current review includes studies that show associations between ambient
CO concentrations and increases in emergency room visits and
hospitalizations for disease events plausibly linked to the effects
observed in the controlled human exposure studies of CAD patients (ISA,
section 2.5.1), providing support for the ISA's conclusion regarding
coronary artery disease as the most important susceptibility
characteristic for increased health risk due to CO exposure (ISA, p. 2-
10). However, the Policy Assessment recognizes aspects of this
epidemiological evidence that complicate quantitative interpretation of
it with regard to ambient concentrations that might be eliciting the
reported health outcomes. As an initial matter, the Policy Assessment
notes the substantially fewer studies conducted in areas meeting the
current CO standards than is the case for NO2 and PM (USEPA,
2008d, 2009f). Further, the Policy Assessment recognizes complicating
aspects of the evidence that relate to conclusions regarding CO as the
pollutant eliciting the effect reported in the epidemiological studies
and to our understanding of the ambient CO and nonambient
concentrations to which study subjects demonstrating these outcomes are
exposed.
With regard to these complications, the Policy Assessment first
considers the extent to which the use of two-pollutant regression
models, a commonly used statistical method (ISA, section 1.6.3), inform
conclusions regarding CO as the pollutant eliciting the effects in
these studies (PA, pp. 2-36 to 2-37). Although CO associations, in some
studies, are slightly attenuated in models that adjusted for other
combustion-related pollutants (e.g., PM2.5 or
NO2), they generally remain robust (ISA, Figures 5-6 and 5-
7).\50\ In considering these two-pollutant model results, however, the
Policy Assessment recognizes the potential for there to be
etiologically relevant pollutants that are correlated with CO yet
absent from the analysis. Similarly, CASAC commented that ``the problem
of co-pollutants serving as potential confounders is particularly
problematic for CO''. They stated that ``consideration needs to be
given to the possibility that in some situations CO may be a surrogate
for exposure to a mix of pollutants generated by fossil fuel
combustion'' and ``a better understanding of the possible role of co-
pollutants is relevant to * * * the interpretation of epidemiologic
studies on the health effects of CO'' (Brain and Samet, 2010d). This
issue is particularly important in the case of CO in light of
uncertainty associated with CO-related effects at low ambient
concentrations (discussed below) and in light of the sizeable portion
of ambient CO measurements that are at or below monitor detection
limits. Consequently, the extent to which multi-pollutant regression
models effectively disentangle and quantitatively interpret a CO-
specific effect distinct from that of other pollutants remains an area
of uncertainty.
---------------------------------------------------------------------------
\50\ In interpreting the epidemiological evidence for
cardiovascular morbidity the ISA notes that it ``is difficult to
determine from this group of studies the extent to which CO is
independently associated with CVD outcomes or if CO is a marker for
the effects of another traffic-related pollutant or mix of
pollutants. On-road vehicle exhaust emissions are a nearly
ubiquitous source of combustion pollutant mixtures that include CO
and can be an important contributor to CO in near-road locations.
Although this complicates the efforts to disentangle specific CO-
related health effects, the evidence indicates that CO associations
generally remain robust in copollutant models and supports a direct
effect of short-term ambient CO exposure on CVD morbidity.'' (ISA,
pp. 5-40 to 5-41).
---------------------------------------------------------------------------
In considering ambient concentrations that may be triggering health
outcomes analyzed in the epidemiological studies, the Policy Assessment
recognizes the uncertainty introduced by exposure error. Exposure error
can occur when a surrogate is used for the actual ambient exposure
experienced by the study population (e.g., ISA, section 3.6.8). There
are two aspects to the epidemiological studies in the specific case of
CO, as contrasted with the cases of other pollutants such as
NO2 and PM, that may contribute to exposure error in the CO
studies. The first relates to the low concentrations of CO considered
in the epidemiological studies and monitor detection limits. The second
relates to the use in the epidemiological studies of area-wide or
central-site monitor CO concentrations in light of information about
the gradient in CO concentrations with distance from source locations
such as highly-trafficked roadways (ISA, section 3.5.1.3).
As discussed in the Policy Assessment, uncertainty in the
assessment of exposure to ambient CO concentrations is related to the
prevalence of ambient CO monitor concentrations at or below detection
limits, which is a greater concern for the more recently available
epidemiological studies in which the study areas have much reduced
ambient CO concentrations compared with those in the past (PA, pp. 2-37
to 2-38). For example, the ISA notes that roughly one third of the 1-
hour ambient CO measurements reported to AQS for 2005-2007 were below
the method limit of detection for the monitors analyzed (ISA, p. 3-34).
A similarly notable proportion of measurements occur below the monitor
detection limit for epidemiological study areas meeting the current
standards (e.g., Atlanta, Allegheny County) (PA, Appendix B). This
complicates our interpretation of specific ambient CO concentrations
associated with health effects (ISA, p. 3-91; Brain and Samet, 2010d).
In contrast to CO, other combustion-related criteria pollutants such as
PM2.5 and NO2 generally occur above levels of
detection, providing us with greater confidence in quantitative
interpretations of epidemiological studies for those pollutants.
There are also differences in the spatial variability associated
with PM2.5 and NO2 concentrations as compared to
CO concentrations that add complexity
[[Page 8178]]
to the estimation of CO exposures in epidemiological studies. In
general, PM2.5 concentrations tend to be more spatially
homogenous across an urban area than CO concentrations. CO
concentrations in urban areas are largely driven by mobile sources,
while urban PM2.5 concentrations substantially reflect
contributions from mobile and a variety of stationary sources. The
greater spatial homogeneity in PM2.5 concentrations is due
in part to the transport and dispersion of small particles from the
multiple sources (USEPA, 2009f, sections 3.5.1.2 and 3.9.1.3), as well
as to contributions from secondarily formed components ``produced by
the oxidation of precursor gases (e.g., sulfur dioxide and nitrogen
oxides) and reactions of acidic products with NH3 and
organic compounds'' (USEPA, 2009f, p. 3-185), which likely contribute
to spatial homogeneity. Similarly, ``because NO2 in the
ambient air is due largely to the atmospheric oxidation of NO emitted
from combustion sources (ISA, section 2.2.1), elevated NO2
concentrations can extend farther away from roadways than the primary
pollutants also emitted by on-road mobile sources'' (40 FR 6479,
February 9, 2010). In contrast to PM2.5 and NO2,
CO is not formed through common atmospheric oxidation processes, which
may contribute to the steeper CO gradient observed near roadways.
Therefore, the misclassification of exposure arising from the
utilization of central site monitors to measure PM2.5 and
NO2 exposures is likely to be smaller than is the case for
CO exposures.
An additional complication to a comparison of our consideration of
the CO epidemiological evidence to that for other criteria pollutants
is that, in contrast to the situation for all other criteria
pollutants, the epidemiological studies for CO use a different
exposure/dose metric from that which is the focus of the broader health
evidence base, and additional information that might be used to bridge
this gap is lacking. In the case of CO, the epidemiological studies use
air concentration as the exposure/dose metric, while the broader health
effects evidence for CO demonstrates and focuses on an internal
biomarker of CO exposure (COHb) which has been considered a critical
key to CO toxicity. In the case of the only other criteria pollutant
for which the health evidence relies on an internal dose metric--lead--
the epidemiological studies also use that metric.\51\ For other
criteria pollutants, including PM and NO2, air
concentrations are used as the exposure/dose metric in both the
epidemiological studies and the other types of health evidence. Thus,
there is no comparable aspect in the PM or NO2 evidence
base. The strong evidence describing the role of COHb in CO toxicity is
important to consider in interpreting the CO epidemiological studies
and contributes to the biological plausibility of the ischemia-related
health outcomes that have been associated with ambient CO
concentrations. Yet, we do not have information on the COHb levels of
epidemiological study subjects that we can evaluate in the context of
the COHb levels eliciting health effects in the controlled human
exposure studies. Further, we lack additional information on the CO
exposures of the epidemiological study subjects to both ambient and
nonambient sources of CO that might be used to estimate their COHb
levels and bridge the gap between the two study types.
---------------------------------------------------------------------------
\51\ In the case of lead (Pb), in contrast to that of CO, the
epidemiological evidence is focused on associations of Pb-related
health effects with measurements of Pb in blood, providing a direct
linkage between the pollutant, via the internal biomarker of dose,
and the health effects. Thus, for Pb, as compared to the case for
CO, we have less uncertainty in our interpretations of the
epidemiological studies with regard to the pollutant responsible for
the health effects observed.
---------------------------------------------------------------------------
Additionally the ISA recognizes that the changes in COHb that would
likely be associated with exposure to the low ambient CO concentrations
assessed in some of the epidemiological studies would be smaller than
changes associated with ``substantially reduced {oxygen{time} delivery
to tissues,'' that might plausibly lead to the outcomes observed in
those studies, with additional investigation needed to determine
whether there may be another mechanism of action for CO that
contributes to the observed outcomes at low ambient concentrations
(ISA, p. 5-48). Thus, there are uncertainties associated with the
epidemiological evidence that ``complicate the quantitative
interpretation of the epidemiologic findings, particularly regarding
the biological plausibility of health effects occurring at COHb levels
resulting from exposures to the ambient CO concentrations'' assessed in
these studies (ISA, p. 2-17).
In summary, the Policy Assessment concludes that some important
uncertainties from the last review have been reduced, including those
associated with concerns for ambient levels of CO to pose
neurobehavioral risks as current concentrations of ambient CO are well
below those that might be expected to result in COHb levels as high as
those associated with these effects. Additionally, our exposure and
dose models have improved giving us increased confidence in their
estimates. A variety of uncertainties still remain including the
adverse nature and significance of the small changes in time to ST-
segment depression identified at the lowest COHb levels investigated,
and the magnitude of associated risk of specific health outcomes, as
well as the potential for as-yet-unidentified health effects at COHb
levels below 2%. Additionally, although the evidence base is somewhat
expanded with regard to the potential for CO effects on the developing
fetus, uncertainties remain in our understanding of the potential
influence of low, ambient CO exposures on conditions existing in the
fetus and newborn infant and on maternal-fetal relationships. We
additionally recognize that the expanded body of epidemiological
evidence includes its own set of uncertainties which complicates its
interpretation, particularly with regard to ambient concentrations that
may be eliciting health outcomes.
b. Exposure/Dose-Based Considerations
In considering the evidence from controlled human exposure studies
to address the question regarding ambient CO concentrations associated
with health effects, we have developed estimates of COHb associated
with different air quality conditions using quantitative exposure and
dose modeling, as was done at the time of the last review. The current
estimates are presented in the REA and discussed with regard to policy-
relevant considerations in this review in the Policy Assessment (PA,
section 2.2.2). Since the last review, there have been numerous
improvements to the exposure and COHb models that we use to estimate
exposure and dose for the current review. The results of modeling using
these improved tools in the current review and associated conclusions
in the Policy Assessment are described below with regard to the
expectation for COHb levels of concern to occur in the at-risk
population under air quality conditions associated with the current CO
standards.
In considering the results from the REA, the Policy Assessment
considered several questions including those concerning the magnitude
of COHb levels estimated in the simulated at-risk populations in
response to ambient CO exposure, as well as the extent to which such
estimates may be judged to be important from a public health
perspective.
In addressing the questions concerning the magnitude of at-risk
population COHb levels estimated to
[[Page 8179]]
occur in areas simulated to just meet the current, controlling, 8-hour
standard and what portion of the at-risk population is estimated to
experience maximum COHb levels above levels of potential health
concern, the Policy Assessment first noted the context for the
population COHb estimates provided by the REA simulations of exposure
to ambient CO (REA, section 6.2). As in the last review, the Policy
Assessment recognized that indoor sources of CO can be important
determinants of population exposures to CO and to population
distributions of daily maximum COHb levels, and that for some portions
of the population, these sources may dominate CO exposures and related
maximum COHb levels. The Policy Assessment additionally took note of
the conclusions drawn in the previous review that the contribution of
indoor sources to individual exposures and associated COHb levels
cannot be effectively mitigated by ambient air quality standards (e.g.,
59 FR 38914) and so focused on COHb levels resulting from ambient CO
exposures. In so doing, however, the Policy Assessment also recognized
as noted in section II.C above, that simulations focused solely on
exposures associated with ambient CO may overestimate the response of
COHb levels to short-duration ambient exposures (the ambient
contribution) as pre-exposure baseline COHb levels will necessarily not
reflect the contribution of both nonambient and ambient sources.
Additionally, these simulations may underestimate COHb levels that
would occur in situations with appreciable nonambient exposure.
As recognized in the Policy Assessment and described in detail in
the REA, estimates for exposure concentrations indicated that highest
ambient CO exposures occurred in in-vehicle microenvironments, with
next highest exposures in microenvironments where running vehicles
congregate such as parking areas and fueling stations, (REA, section
6.1).
In considering the REA estimates for current or ``as is'' air
quality conditions and conditions simulated to just meet the current 8-
hour standard, the Policy Assessment particularly focused on the extent
to which the current standards provide protection to the simulated at-
risk population from COHb levels of potential concern, by comparing the
estimated levels in the population to the benchmarks described above.
As described above, the REA presents two sets of COHb estimates: the
first set of absolute estimates reflect the impact of ambient CO
exposures in the absence of exposure to nonambient CO, but in the
presence of endogenous CO production, while the second set are
estimates of the portion of absolute COHb estimated to occur in
response to the simulated ambient CO exposures, i.e., after subtraction
of COHb resulting from endogenous CO production (REA, sections 4.4.7
and 5.10.3). In describing the REA results, the Policy Assessment draws
from exposure and dose estimates for both the HD and CHD populations
(REA, section 6.2), recognizing that, in terms of percentages of
persons exposed and experiencing daily maximum end-of-hour COHb at or
above specific levels, the results are similar for the two simulated
at-risk populations (HD and CHD). We note that, in terms of absolute
numbers of persons, the results differ due to differences in the size
of the two populations.
The Policy Assessment first considered the absolute COHb results
with regard to the percentage of simulated populations experiencing at
least one day with an end-of hour COHb level above selected benchmarks
(Table 1 includes these results for the HD populations). Another
dimension of the analysis, presented in Table 2 (for the CHD
populations),\52\ is the percentage of simulated populations
experiencing multiple days in the simulated year with an end-of-hour
COHb level above the same benchmarks. These two dimensions of the dose
estimates are combined in the metric, person-days, which is presented
in Tables 6-15, 6-16, 6-18 and 6-19 of the REA. The metric, person-
days, was the focus of exposure/dose considerations in the last review
for which a previous version of the exposure/dose model was used (59 FR
38914; USEPA, 1992).\53\ The person-days metric, which summarizes
occurrences across the number of persons in the at-risk population
multiplied by the number of days in the year, is a common cumulative
measure of population exposure/dose that simultaneously takes into
account both the number of people affected and the numbers of times
each is affected.
---------------------------------------------------------------------------
\52\ As described in the REA, the analyses providing results for
Table 2 were only performed for the CHD populations, and so are not
available for the larger HD population, although as mentioned above
the results in terms of percentage are expected to be similar.
\53\ As described in section II.C. above, pNEM, the model used
in the last review, employed a cohort-based approach from which
person-days were the exposure and dose metrics (USEPA, 1992; Johnson
et al., 1992).
---------------------------------------------------------------------------
As expected, given that current ambient concentrations in the two
study areas are well below the CO standards, the absolute COHb
estimates under current air quality conditions are appreciably lower
than the corresponding estimates for conditions of higher ambient CO
concentrations in which the current 8-hour standard is just met (Table
1). Under ``as is'' (2006) conditions in the two study areas, no person
in the simulated at-risk populations is estimated to experience any
days in the year with end-of-hour COHb concentrations at or above 3%
COHb, and less than 0.1% of the simulated at-risk populations are
estimated to experience at least one end-of-hour COHb concentration at
or above 2% (Table 1).
Under conditions with higher ambient CO concentrations simulated to
just meet the current 8-hour standard, the portion of the simulated at-
risk populations estimated to experience daily maximum end-of-hour COHb
levels at or above benchmarks is greater in both study areas, with
somewhat higher percentages for the Denver study area population (Table
1). In both study areas, nonetheless, less than 1% of the simulated at-
risk populations is estimated to experience a single day with a maximum
end-of hour COHb level at or above 3% (Table 1) and no person is
estimated to experience more than one such day in a year (Table 2).
Further, less than 0.1% of either simulated population in either study
area is estimated to experience a single day with maximum end-of-hour
COHb at or above 4%. A difference between the study areas is more
evident for lower benchmarks, with less than 5% of the simulated at-
risk population in the Denver study area and less than 1% of the
corresponding population in the Los Angeles study area estimated to
experience any days with a maximum end-of-hour COHb level at or above
2% (Table 1). Appreciably smaller percentages of the simulated at-risk
population were estimated to experience more than one day with such
levels (Table 2). For example, less than 1.5% of the population is
estimated to experience more than one day in a year with a maximum COHb
level at or above 2.0%, and less than 0.1% are estimated to experience
six or more such days in a year. Additionally, consistent with the
findings of the assessment performed for the review completed in 1994,
less than 0.1% of person-days for the simulated at-risk populations
were estimated to have end-of-hour COHb levels at or above 2% COHb
(REA, Tables 6-18 and 6-19).
[[Page 8180]]
Table 1--Portion of Simulated HD Populations With at Least One Daily Maximum End-of-Hour COHb Level (Absolute) at or Above Indicated Levels Under Air
Quality Conditions Simulated to Just Meet the Current Standard and ``as is'' Conditions
--------------------------------------------------------------------------------------------------------------------------------------------------------
Percentage (%) of simulated HD population \A\
---------------------------------------------------------------------------------------------------
Just meeting current 8-hour standard (8-hr DV = ``As is'' (2006) conditions
Daily maximum end-of-hour COHb (absolute) 9.4 ppm) -------------------------------------------------
-------------------------------------------------- Los Angeles (8-hr DV = Denver (8-hr DV = 3.1
Los Angeles (1-hr DV = Denver (1-hr DV = 16.2 5.6 ppm) (1-hr DV = 8.2 ppm) (1-hr DV = 4.6
11.8 ppm) ppm) ppm) ppm)
--------------------------------------------------------------------------------------------------------------------------------------------------------
>= 4.0%............................................. 0 \B\ < 0.1 0 0
>= 3.0%............................................. \B\ < 0.1 0.3
>= 2.5%............................................. \B\ < 0.1 0.9
>= 2.0%............................................. 0.6 4.5 \B\ < 0.1 \B\ < 0.1
>= 1.5%............................................. 5.0 24.5 1.6 1.2
--------------------------------------------------------------------------------------------------------------------------------------------------------
\A\ Drawn from Tables 6-15 through 6-19 of the REA.
\B\ <0.1 is used to represent nonzero estimates below 0.1%.
Abbreviations: hr = hour, DV = Design Value.
Table 2--Portion of Simulated CHD Population With Multiple Days of Maximum End-of-Hour COHb Levels (Absolute) at or Above the Indicated Levels Under Air
Quality Conditions Simulated To Just Meet the Current Standard and ``as is'' Conditions
--------------------------------------------------------------------------------------------------------------------------------------------------------
Percentage (%) of simulated CHD population \A\
-----------------------------------------------------------------------------------------------------------
Just meeting current 8-hour standard (8-hr DV = 9.4 ``As is'' (2006) conditions
ppm) -----------------------------------------------------
------------------------------------------------------ Los Angeles (8-hr DV = Denver (8-hr DV = 3.1
Maximum end-of-hour COHb level (absolute) Los Angeles (1-hr DV = Denver (1-hr DV = 16.2 5.6 ppm) (1-hr DV = 8.2 ppm) (1-hr DV = 4.6 ppm)
11.8 ppm) ppm) ppm) --------------------------
---------------------------------------------------------------------------------
>= 2 >= 4 >= 6 >= 2 >= 4 >= 6 >= 2 >= 4 >= 6 >= 2 >= 4 >= 6
days days days days days days days days days days days days
--------------------------------------------------------------------------------------------------------------------------------------------------------
>= 3.0%..................................... 0 0 0 0 0 0 0 0 0 0 0 0
>= 2.5%..................................... \B\ < 0 0 \B\ < 0 0 0 0 0 0 0 0
0.1 0.1
>= 2.0%..................................... 0.2 \B\ < \B\ < 1.4 0.2 \B\ < 0 0 0 \B\ < \B\ < \B\ <
0.1 0.1 0.1 0.1 0.1 0.1
>= 1.5%..................................... 2.2 0.7 0.5 11.2 5.0 3.3 0.5 0.2 0.1 0.7 0.5 0.4
--------------------------------------------------------------------------------------------------------------------------------------------------------
\A\ These estimates are drawn mainly from Figures 6-5 and 6-6 of the REA and represent the percentage of persons experiencing greater than or equal to
2, 4, or 6 days with a maximum end-of-hour COHb (absolute) at or above the selected level.
\B\ <0.1 is used to represent nonzero estimates below 0.1%.
As described above, the REA also presented estimates of the portion
of the absolute COHb levels occurring in response to the simulated
ambient CO exposures (i.e., that not derived from endogenous CO
production). The REA refers to these estimates as the ambient CO
contribution to (absolute) COHb. As observed with the absolute COHb
estimates under conditions just meeting the standard, the results for
the Denver study area included larger percentages of the population
above specific COHb ambient contribution levels than those for the Los
Angeles study area, reflecting the study area difference in 1-hour peak
concentrations. Although estimates of population percentages for
multiple occurrences are not available for the ambient contribution
estimates, it is expected that similar to those for absolute COHb, they
would be appreciably lower than those shown here for at least one
occurrence. Additionally, as mentioned above, somewhat lower ambient
contribution estimates might be expected if other (nonambient) CO
sources were present in the simulations.
In considering the estimates of population occurrences of daily
maximum COHb levels for REA simulations under conditions just meeting
the current 8-hour standard (presented in Tables 1 and 2 above), the
Policy Assessment notes that an important contributing factor to the
higher percentages estimated for the Denver study area population is
the occurrence of higher 1-hour peak ambient CO concentrations and
consequent higher CO exposures than occur in the corresponding Los
Angeles study area simulation (REA, section 6.1.2, Tables 6-7 and 6-
10). The difference in the peak 1-hour ambient concentrations is
illustrated by the higher 1-hour design value for Denver as compared to
Los Angeles (16.2 ppm versus 11.8 ppm), as noted in Tables 1 and 2.
This difference, particularly at the upper percentiles of the air
quality distribution, is likely driving the higher population
percentages estimated to experience higher 1-hour and 8-hour exposures
in the Denver study area as compared to Los Angeles (REA, Tables 6-7
and 6-10).\54\ The situation is largely reversed under ``as is''
conditions, where the Los Angeles study area has generally higher 1-
hour and 8-hour ambient CO concentrations as illustrated by the design
values for as is conditions in Tables 1 and 2 above (as well as Tables
3-1 to 3-6, 5-14 and 5-16 of the REA), and Los Angeles also has higher
percentages of people estimated to be exposed to the higher exposure
concentrations (REA, Tables 6-1 and 6-4). Thus, the Policy Assessment
recognizes the impact on daily maximum COHb levels of 1-hour
[[Page 8181]]
ambient concentrations separate from the impact of 8-hour average
concentrations, and takes note of this in considering the REA results
with regard to the adequacy of the 1-hour standard. The Policy
Assessment concludes that, taken together, the REA results indicate
occurrences of COHb levels above the benchmarks considered here that
are associated with 1-hour ambient concentrations that are not
controlled by the current suite of standards (PA, section 2.2.2).
---------------------------------------------------------------------------
\54\ Other factors that contribute less to differences in COHb
estimates between the two study areas include altitude, which
slightly enhances endogenous CO and COHb formation and can enhance
COHb formation induced by CO exposure under resting conditions (ISA,
p. 4-19), and design aspects of the study areas with regard to
spatial variation in monitor CO concentrations and population
density near these monitors (REA, section 7.2.2.1).
---------------------------------------------------------------------------
In considering the public health implications of the quantitative
dose estimates, the Policy Assessment considered the daily maximum end-
of-hour levels estimated in the REA for conditions just meeting the
current suite of standards in light of the effects identified by the
evidence at the COHb benchmark levels considered. For example, as a
result of ambient CO exposures occurring under air quality conditions
adjusted to just meet the current 8-hour standard, the REA estimates
that 0.6 percent of the Los Angeles and 4.5 percent of the Denver study
at-risk populations may experience an occurrence of a daily maximum
end-of-hour COHb level at or above 2% COHb, the low end of the range of
average COHb levels experienced by the lower controlled exposure group
in the study by Allred et al. (1989a, 1989b, 1991), while 0.2 and 1.4
percent, respectively, of the simulated at-risk populations are
estimated to experience more than one such occurrence. Additionally,
less than 0.1 percent of the simulated populations in either study area
are estimated to experience a COHb level similar to the higher
controlled exposure group (4% COHb). As discussed in II.B.4 above, the
Policy Assessment recognized the magnitude of the ``time to onset''
reductions observed in the study by Allred et al. (1989a, 1989b, 1991),
the similarity of the study responses to responses considered
clinically significant when evaluating medications to treat angina from
coronary artery disease, and conclusions reached by the independent
review panel for the study regarding the expectation that frequent
encounters in ``everyday life'' with increased COHb levels on the order
of those tested in the study might limit activity and affect quality of
life (Allred et al., 1989b, pp. 38, 92-94; 1991 AQCD, p. 10-35), as
well as considerations in the review completed in 1994 and assessment
of the study findings in the current ISA.
In considering public health implications of the REA estimates, the
Policy Assessment also considered the size of the at-risk populations
simulated as described in section II.B.4 above, recognizing that the
U.S. population with coronary heart disease, angina pectoris (cardiac
chest pain) or who have experienced a heart attack in combination with
those with silent or undiagnosed ischemia comprises a large population
represented by the REA analyses and for which the COHb benchmarks
described above (based on studies of CAD patients) are relevant, that
is, more susceptible to ambient CO exposure when compared to the
general population (ISA, section 5.7). The Policy Assessment also
recognized that the REA also simulated ambient CO exposures for the
larger HD population, which may also be at increased risk of CO-induced
health effects (ISA, section 2.6.1), while noting that within this
broader group, implications of CO exposures are more significant for
those persons for whom their disease state affects their ability to
compensate for the hypoxia-related effects of CO (ISA, section 4.4.4).
In summary, the Policy Assessment, while noting the substantial
size of the population of individuals with CHD or other heart diseases
in the U.S., recognized that the REA results for conditions just
meeting the current standards indicate a very small portion of this
population that might be expected to experience more than one
occurrence of COHb above 2%, with less than 0.1% of this population
expected to experience such a level on as many as six days in a year or
a single occurrence as high as 4%, and 0% of the population expected to
experience more than one occurrence above 4% COHb. In light of the
implications of the health evidence discussed in section II.B.4 and
summarized above, the Policy Assessment concluded that the public
health significance of these REA results and conclusions regarding the
extent to which they are important from a public health perspective
depends in part on public health policy judgments about the public
health significance of effects at the COHb benchmark levels considered
and judgments about the level of public health protection with an
adequate margin of safety.
c. Summary
With regard to the different elements of the current standards, the
Policy Assessment concludes that it is appropriate to continue to use
measurements of CO in accordance with Federal reference methods as the
indicator to address effects associated with exposure to ambient CO,
and that it is appropriate to continue to retain standards with
averaging times of 1 and 8 hours. With regard to form and level for
these standards, the Policy Assessment concludes that the information
available in this review supports consideration of either retaining the
current suite of standards or revising one or both standards.
The Policy Assessment concludes that the extent to which the
current standards are judged to be adequate depends on a variety of
factors inclusive of science policy judgments and public health policy
judgments. These factors include public health policy judgments
concerning the appropriate COHb benchmark levels on which to place
weight, as well as judgments on the public health significance of the
effects that have been observed at the lowest levels evaluated,
particularly with regard to relatively rare occurrences. The factors
relevant to judging the adequacy of the standards also include
consideration of the uncertainty associated with interpretation of the
epidemiological evidence as providing information on ambient CO as
distinct from information on the mixture of pollutants associated with
traffic, and, given this uncertainty, the weight to place on
interpretations of ambient CO concentrations for the few
epidemiological studies available for air quality conditions that did
not exceed the current standards. And, lastly these factors include the
interpretation of, and decisions as to the weight to place on, the
results of the exposure assessment for the two areas studied relative
to each other and to results from past assessments, recognizing the
implementation of an improved modeling approach and new input data, as
well as distinctions between the REA simulations and resulting COHb
estimates and the response of COHb levels to experimental CO exposure
as recorded in the controlled human exposure studies.
The Policy Assessment conclusions with regard to the adequacy of
the current standards are drawn from both the evidence and from the
exposure and dose assessment, taking into consideration related
information, limitations and uncertainties recognized above. The
combined consideration of the body of evidence and the quantitative
exposure and dose estimates are concluded to provide support for a
suite of standards at least as protective as the current suite.
Further, the Policy Assessment recognizes that conclusions regarding
the adequacy of the current standards depend in part on public health
policy judgments identified above and judgments about the level of
public health protection with an adequate margin of safety.
[[Page 8182]]
The Policy Assessment additionally notes the influence that hourly
ambient CO concentrations well below the current 1-hour standard may
have on ambient CO exposures and resultant COHb levels under conditions
just meeting the 8-hour standard, as indicated by the REA results. The
REA results are concluded to indicate the potential for the current
controlling 8-hour standard to allow the occurrence of 1-hour ambient
concentrations that contribute to population estimates of daily maximum
COHb levels, that depending on public health judgments in the areas
identified above, may be considered to call into question the adequacy
of the 1-hour standard and support consideration of revisions of that
standard in order to reduce the likelihood of such occurrences in areas
just meeting the 8-hour standard. Thus, the Policy Assessment concludes
that the combined consideration of the evidence and quantitative
estimates may be viewed as providing support for either retaining or
revising the current suite of standards.
The Policy Assessment conclusion that it is appropriate to consider
retaining the current suite of standards without revision is based on
consideration of the health effects evidence in combination with the
results of the REA (PA, sections 2.2.1, 2.2.2, 2.3.2 and 2.3.3) and
what may be considered reasonable judgments on the public health
implications of the COHb levels estimated to occur under the current
standard, the public health significance of the CO effects being
considered, the weight to be given to findings in the epidemiological
studies in locations where the current standards are met, and advice
from CASAC. Such a conclusion takes into account the long-standing body
of evidence that supports our understanding of the role of COHb in
eliciting effects in susceptible populations, most specifically the
evidence for those with cardiovascular disease, and gives particular
weight to findings of controlled exposure studies of CAD patients in
which sensitive indicators of myocardial ischemia were associated with
COHb levels resulting from short-duration, high-concentration CO
exposures. This conclusion also takes into account uncertainties
associated with the differing circumstances of ambient air CO exposures
from the CO exposures in the controlled human exposure studies, as well
as the unclear public health significance of the size of effects at the
lowest studied exposures. As in the last review, this conclusion gives
more weight to the significance of the effects observed in these
studies at somewhat higher COHb levels. Additionally, this conclusion
takes into account judgments in interpreting the public health
implications of the REA estimates of COHb associated with ambient
exposures based on the application of our current exposure modeling
tools, and the size of the at-risk populations estimated to be
protected from experiencing daily maximum COHb levels of potential
concern by the current standard. Further, this conclusion considers the
uncertainties in quantitative interpretations associated with the
epidemiological studies to be too great for reliance on information
from the few studies where the current standards were met as a basis
for selection of alternative standards.
In addition to considering retaining the current suite of standards
without revision, the Policy Assessment also concludes that it is
reasonable to consider revising the 1-hour standard downward to provide
protection from infrequent short-duration peak ambient concentrations
that may not be adequately provided by the current standards. While the
quantitative analyses for this review focused predominantly on the
controlling, 8-hour standard, the analyses have indicated the
influential role of elevated 1-hour concentrations in contributing to
daily maximum COHb levels over benchmark levels. In addition to the REA
results, the Policy Assessment notes the health effects evidence from
1-hour controlled exposures, which indicates the effects in susceptible
groups from such short duration exposures. The Policy Assessment
interpreted the evidence and REA estimates to indicate support for
consideration of a range of 1-hour standard levels which would address
the potential for the current 8-hour standard, as the controlling
standard, to ``average away'' high short-duration exposures that may
contribute to exposures of concern. Consequently, in considering
alternative standard levels, the Policy Assessment focuses on the 1-
hour standard as providing the most direct approach for controlling the
likelihood of such occurrences.
With regard to a revision of the 1-hour standard, the Policy
Assessment identified a range of 1-hour standard levels from 15 to 5
ppm as being an appropriate range for consideration. These levels are
in terms of a 99th percentile daily maximum form, averaged over three
years, which the Policy Assessment considers to provide increased
regulatory stability over the current form. The Policy Assessment
additionally takes note of CASAC's preference for a revision to the
standards to provide greater protection and observes that the range of
1-hour standard levels discussed is also the range that the CASAC CO
Panel suggested was appropriate for consideration.
The Policy Assessment indicates that the upper part of the range of
1-hour standard levels for consideration (11-15 ppm) was identified
based on the objective of providing generally equivalent protection,
nationally, to that provided by current 8-hour standard and potentially
providing increased protection in some areas, such as those with
relatively higher 1-hour peaks that are allowed by the current 8-hour
standard. This part of the range is estimated to generally correspond
to 1-hour CO levels occurring under conditions just meeting the current
8-hour standard based on current relationships between 1-hour and 8-
hour average concentrations at current U.S. monitoring locations (PA,
Appendix C). The Policy Assessment states that selection of a 1-hour
standard within this upper part of the range would be expected to allow
for a somewhat similar pattern of ambient CO concentrations as the
current, controlling 8-hour standard, although with explicit and
independent control against shorter-duration peak concentrations which
may contribute to daily maximum COHb levels in those exposed.
Consideration of 1-hour standard levels in this part of the range would
take into account the factors recognized with regard to the option of
retaining the current standards. But it would give greater weight to
the importance of limiting 1-hour concentrations that are not
controlled by the current 8-hour standard but that may contribute to
exceedances of relevant COHb benchmark levels.
The Policy Assessment also concluded that, based on the evidence
and REA estimates and alternative judgments regarding appropriate
population targets for maximum COHb levels induced by ambient CO
exposures, it may be appropriate to consider standard levels that
provide additional protection than that afforded by the current
standards against the occurrence of short-duration peak ambient CO
exposures and associated COHb levels. With this policy objective in
mind, the Policy Assessment also described a rationale for
consideration of 1-hour standard levels of 9-10 ppm, which comprise the
middle part of the range of 1-hour standard levels suggested for
consideration (PA, section 2.3.5). Additionally, the Policy
[[Page 8183]]
Assessment identified 1-hour standard levels of 5-8 ppm, in the lower
part of the range for consideration in light of alternative judgments
with regard to the evidence and REA, including the weight to place on
public health significance of smaller changes in COHb and the small
number of epidemiological studies in areas meeting the current
standards (PA, section 2.3.5).
In considering the relative strength of the evidence supporting
each of the 3 parts of the range, the Policy Assessment concludes that
the upper part of the range is most strongly supported, both with
regard to judgments concerning adversity and quantitative
interpretation of the epidemiological studies with regard to ambient
concentrations that may elicit effects. For the lower parts of the
range, the Policy Assessment concludes that support provided by the
available information is more limited, especially for the lowest part
of the range.
In conjunction with consideration of a revised 1-hour standard, the
Policy Assessment, also concludes it is appropriate to consider
retaining a standard with an 8-hour averaging time, recognizing that,
as when it was established, the 8-hour standard continues to provide
protection from multiple-hour ambient CO exposures which may contribute
to elevated COHb levels and associated effects. In conjunction with
consideration of a revised 1-hour standard, the Policy Assessment
additionally describes revision to the 8-hour standard form that may be
appropriate to consider to potentially provide greater regulatory
stability, with adjustment to level to provide generally equivalent
protection as the current 8-hour standard or as a revised 1-hour
standard level (PA, section 2.3.5). The range of 8-hour levels
identified in the Policy Assessment is inclusive of the range of levels
included in the example policy option suggested by CASAC.
3. CASAC Advice
In our consideration of the adequacy of the current standards, in
addition to the evidence- and exposure/dose-based information discussed
above, we have also considered the advice and recommendations of CASAC,
based on their review of the ISA, the REA, and the draft Policy
Assessment, as well as comments from the public on drafts of these
documents.\55\ In these reviews, CASAC has provided an array of advice,
both with regard to interpreting the scientific evidence and
quantitative exposure/dose assessment, as well as with regard to
consideration of the adequacy of the current standards (Brain and
Samet, 2009, 2010a, 2010b, 2010c, 2010d).
---------------------------------------------------------------------------
\55\ All written comments submitted to the Agency thus far in
this review are available in the docket for this rulemaking, as are
transcripts of the public meetings held in conjunction with CASAC's
review of the draft PA, of drafts of the REA, and of drafts of the
ISA.
---------------------------------------------------------------------------
In their review of the draft ISA, CASAC noted various limitations
and uncertainties associated with the evidence, particularly from the
epidemiological studies, as noted in section II.D.2.1 above. For
example, they recognized limitations in representation of population
exposure to ambient CO. Further they noted that ``[t]he problem of co-
pollutants serving as potential confounders is particularly problematic
for CO'' and that CO may be serving as a surrogate for a mixture of
pollutants generated by fossil fuel combustion (Brain and Samet, 2010d)
as well as noting uncertainty regarding the possibility for confounding
effects of indoor sources of CO (Brain and Samet, 2010c).
In their comments on the draft PA, the CASAC CO Panel stated
overall agreement with staff's conclusion that the body of evidence and
the quantitative exposure and risk assessment provide support for
retaining or revising the current 8-hour standard. They additionally,
however, expressed a ``preference'' for a lower standard and stated
that ``[i]f the epidemiological evidence is given additional weight,
the conclusion could be drawn that health effects are occurring at
levels below the current standard, which would support the tightening
of the current standard.'' Taking this into account, the Panel further
advised that ``revisions that result in lowering the standard should be
considered'' (Brain and Samet, 2010c).
As noted in section I.C. above, the final Policy Assessment was
completed with consideration of CASAC comments on the draft document,
as well as their comments on the second draft REA, and also public
comments. Among the revisions made in completing the final Policy
Assessment were those based on additional consideration of the
epidemiological studies in light of CASAC comments. Discussion of these
studies and the complications with regard to their quantitative
interpretation is described in section II.D.2.a above, in addition to
other evidence-based considerations described in the final Policy
Assessment, and is considered in the Administrator's proposed
conclusions below.
The few public comments received on this review to date that have
addressed adequacy of the current standards conveyed the view that the
current standards are adequate. In support of this view, these
commenters disagreed with the REA estimates of in-vehicle exposure
concentrations and argued that little weight should be given to the
epidemiological studies.
4. Administrator's Proposed Conclusions Concerning Adequacy
Based on the large body of evidence concerning the public health
impacts of exposure to ambient CO available in this review, the
Administrator proposes that the current primary standards provide the
requisite protection of public health with an adequate margin of safety
and should be retained.
In considering the adequacy of the current standards, the
Administrator has carefully considered the available evidence and
conclusions contained in the Integrated Science Assessment; the
information, exposure/dose assessment, rationale and conclusions
presented in the Policy Assessment; the advice and recommendations from
CASAC; and public comments to date. In the discussion below, the
Administrator considers first the long-standing evidence base
concerning effects associated with exposure to CO, including the
controlled human exposure studies, and the health significance of
responses observed at the 2% COHb level induced by 1-hour CO exposure,
as compared to higher COHb levels. As at the time of the review
completed in 1994, the Administrator also takes note of the results for
the modeling of exposures to ambient CO under conditions simulated to
just meet the current, controlling, 8-hour standard in two study areas,
as described in the REA and Policy Assessment, and the public health
significance of those results. She also considers the newly available
and much-expanded epidemiological evidence, including the complexity
associated with quantitative interpretation of these studies,
particularly the few studies available in areas where the current
standards are met. Further, the Administrator considers the advice of
CASAC, including both their overall agreement with the Policy
Assessment conclusion that the current evidence and quantitative
exposure and dose estimates provide support for retaining the current
standard, as well as their view that in light of the epidemiological
studies, revisions to lower the standards should be considered and
their preference for a lower standard.
[[Page 8184]]
As an initial matter, the Administrator takes note of the Policy
Assessment's consideration of the long-standing body of evidence for
CO, augmented in some aspects since the last review, as summarized in
the current Integrated Science Assessment. This long-standing evidence
base has established the following key aspects of CO toxicity that are
relevant to this review as they were to the review completed in 1994.
The common mechanism of CO health effects involves binding of CO to
reduced iron in heme proteins and the alteration of their function.
Hypoxia (reduced oxygen availability) induced by increased COHb blood
levels plays a key role in eliciting CO-related health effects.
Accordingly, COHb is commonly used as the bioindicator and dose metric
for evaluating CO exposure and the potential for health effects.
Further, people with cardiovascular disease are a key population at
risk from short-term ambient CO exposures.
With regard to the evidence of health effects associated with
ambient CO exposures relevant to this review, the Administrator first
recognizes the Integrated Science Assessment's conclusion that a causal
relationship is likely to exist between relevant short-term exposures
to CO and cardiovascular morbidity. Further, as at the time of the
review completed in 1994, the Administrator takes particular note of
the evidence from controlled human exposure studies that demonstrates a
reduction in time to onset of exercise-induced markers of myocardial
ischemia in response to increased COHb resulting from short-term CO
exposures, and recognizes the greater significance accorded both to
larger reductions in time to myocardial ischemia, and to more frequent
occurrences of myocardial ischemia. The Administrator also recognizes
the uncertain health significance associated with the smaller responses
to the lowest COHb level assessed in the study given primary
consideration in this review (Allred et al., 1989a, 1989b, 1991) and
with single occurrences of such responses. In the study by Allred et
al. (1989a, 1989b, 1991), a 4-5% reduction in time (approximately 30
seconds) to the onset of exercise-induced markers of myocardial
ischemia was associated with the 2% COHb level induced by 1-hour CO
exposure. In considering the significance of the magnitude of the time
decrement to onset of myocardial ischemia observed at the 2% COHb level
induced by short-term CO exposure, as well as the potential for
myocardial ischemia to lead to more adverse outcomes, the EPA generally
places less weight on the health significance associated with
infrequent or rare occurrences of COHb levels at or just above 2% as
compared to that associated with repeated occurrences and occurrences
of appreciably higher COHb levels in response to short-term CO
exposures. For example, at the 4% COHb level, the study by Allred et
al., (1989a, 1989b, 1991) observed a 7-12% reduction in time to the
onset of exercise-induced markers of myocardial ischemia. The
Administrator places more weight on this greater reduction in time to
onset of exercise-induced markers compared to the reduction in time to
onset at 2% COHb. The Administrator also notes that at the time of the
1994 review, an intermediate level of approximately 3% COHb was
identified as a level at which adverse effects had been demonstrated in
persons with angina. Now, as at the time of the 1994 review, the
Administrator primarily considers the 2% COHb level, resulting from 1-
hour CO exposure, with regard to providing a margin of safety against
effects of concern that have been associated with higher COHb levels,
such as 3-4% COHb.
As at the time of the last review, the Administrator additionally
considers the exposure and dose modeling results, taking note of key
limitations and uncertainties associated with the exposure and dose
assessment summarized in section II.C.2. above, and in light of
judgments above regarding the health significance of findings from the
controlled human exposure studies, placing less weight on the health
significance of infrequent or rare occurrences of COHb levels at or
just above 2% and more weight to the significance of repeated such
occurrences, as well as occurrences of higher COHb levels. Under air
quality conditions just meeting the current, controlling, 8-hour
standard, the assessment estimates that, as was the case for the
assessment conducted for the 1994 review, daily maximum COHb levels
were below 2% COHb for more than 99.9% of person-days in the study
areas evaluated. Further, under these conditions, greater than 99.9% of
the at-risk populations in the study areas evaluated would not be
expected to experience daily maximum COHb levels at or above 4% COHb,
and more than 95% and 98.6% of those populations would be expected to
avoid single or multiple occurrences, respectively, at or just above 2%
COHb.
The Administrator additionally takes note of the now much-expanded
evidence base of epidemiological studies, including the multiple
studies that observe positive associations between cardiovascular
outcomes and short-term ambient CO concentrations across a range of CO
concentrations, including conditions above as well as below the current
NAAQS. She notes particularly the Integrated Science Assessment finding
that these studies are logically coherent with the larger, long-
standing health effects evidence base for CO and the conclusions drawn
from it regarding cardiovascular disease-related susceptibility. In
further considering the epidemiological evidence base with regard to
the extent to which it provides support for conclusions regarding
adequacy of the current standards, the Administrator takes note of
CASAC's conclusions that ``[i]f the epidemiological evidence is given
additional weight, the conclusion could be drawn that health effects
are occurring at levels below the current standard, which would support
the tightening of the current standard'' (Brain and Samet, 2010c).
Additionally, the Administrator places weight on the final Policy
Assessment consideration of aspects that complicate quantitative
interpretation of the epidemiological studies with regard to ambient
concentrations that might be eliciting the reported health outcomes.
For purposes of evaluating the adequacy of the current standards,
there are multiple complicating features of the epidemiological
evidence base, as described in more detail in the final Policy
Assessment and in section II.D.2.a, above. First, while a number of
studies observed positive associations of cardiovascular disease-
related outcomes with short-term CO concentrations, very few of these
studies were conducted in areas that met the current standards
throughout the period of study. In addition, CASAC, in their advice
regarding interpretation of the currently available evidence commented
that ``[t]he problem of co-pollutants serving as potential confounders
is particularly problematic for CO'' and that given the currently low
ambient CO levels, there is a possibility that CO is acting as a
surrogate for a mix of pollutants generated by fossil fuel combustion.
CASAC further stated that ``[a] better understanding of the possible
role of co-pollutants is relevant to regulation'' (Brain and Samet,
2010d). As described in the Policy Assessment, there are also
uncertainties related to representation of ambient CO exposures given
the steep concentration gradient near roadways, as well as the
prevalence of measurements below the method detection limit across the
database. CASAC additionally indicated the need to consider the
potential for
[[Page 8185]]
confounding effects of indoor sources of CO. As discussed in section
II.D.2.a above, the interpretation of epidemiological studies for CO is
further complicated because, in contrast to the situation for all other
criteria pollutants, the epidemiological studies for CO use an
exposure/dose metric (air concentration) that differs from the metric
commonly used in the other key CO health studies (COHb).
Although CASAC expressed a preference for a lower standard, CASAC
also indicated that the current evidence provides support for retaining
the current suite of standards. CASAC's recommendations appear to
recognize that their preference for a lower standard was contingent on
a judgment as to the weight to be placed on the epidemiological
evidence. For the reasons explained above, after full consideration of
CASAC's advice and the epidemiological evidence, as well as its
associated uncertainties and limitations, the Administrator judges
those uncertainties and limitations to be too great for the
epidemiological evidence to provide a basis for revising the current
standards.
In considering the adequacy of the level of protection provided by
the current standards, the Administrator notes the findings of the
exposure and dose assessment in light of considerations discussed above
regarding the weight given to different COHb levels and their frequency
of occurrence. The exposure and dose assessment results indicate that
only a very small percentage of the at-risk population is estimated to
experience a single occurrence in a year of daily maximum COHb at or
above 3.0% COHb under conditions just meeting the current 8-hour
standard in the two study areas evaluated, and no multiple occurrences
are estimated. The Administrator also notes the results indicating that
only a small percentage of the at-risk populations are estimated to
experience a single occurrence of 2% COHb in a year under conditions
just meeting the standard, and still fewer estimated to experience
multiple such occurrences. Taken together, the Administrator considers
the current standard to provide a very high degree of protection for
the COHb levels and associated health effects of concern, as indicated
by the extremely low estimates of occurrences, and provides slightly
less but a still high degree of protection for the effects associated
with lower COHb levels, the physiological significance of which is less
clear. Additionally, the Administrator proposes to conclude that
consideration of the epidemiological studies does not lead her to
identify a need for any greater protection. Thus, the Administrator
proposes to conclude that the current suite of standards provides an
adequate margin of safety against adverse effects associated with
short-term ambient CO exposures. For these and all of the reasons
discussed above, and recognizing the CASAC conclusion that, overall,
the current evidence and REA results provide support for retaining the
current standard, the Administrator proposes to conclude that the
current suite of primary CO standards are requisite to protect public
health with an adequate margin of safety from effects of ambient CO.
The Administrator also solicits comment on whether it would be
appropriate to revise the current primary standards. The Administrator
takes note that, while CASAC indicated their view that the evidence and
exposure and dose estimates provide support for retaining the current
NAAQS, they also indicated their preference for a lower standard. For
example, the CASAC CO Panel stated that giving additional weight to the
epidemiological evidence would support a tightening of the current
standard. The Administrator also takes note of the Policy Assessment
conclusions, summarized in section II.D.2.c above. Thus, in light of
views expressed by CASAC, as well as the Policy Assessment conclusions,
the Administrator additionally solicits comment on the appropriateness
of potential revisions to the form and level of the standards. Any
comments on such revisions should include an explanation of the basis
for the commenters' views.
E. Summary of Proposed Decisions on Primary Standards
For the reasons discussed above, and taking into account
information and assessments presented in the Integrated Science
Assessment and Policy Assessment, the advice and recommendations of
CASAC, and the public comments to date, the Administrator proposes to
retain the existing suite of primary CO standards. Additionally, the
Administrator solicits comment on the appropriateness of revisions to
the form and level of the standards.
III. Consideration of a Secondary Standard
This section focuses on the key policy-relevant issues related to
the review of public welfare-related effects of CO. Under section
109(b) of the Clean Air Act, a secondary standard is to be established
at a level ``requisite to protect the public welfare from any known or
anticipated adverse effects associated with the presence of the
pollutant in ambient air.'' Section 302(h) of the Act defines effects
on welfare in part as ``effects on soils, water, crops, vegetation,
man-made materials, animals, weather, visibility, and climate.'' We
first summarize the history of EPA's consideration of secondary
standards for CO in section III.A. In section III.B, we then discuss
the evidence currently available for welfare effects to inform
decisions in this review as to whether, and if so how, to establish
secondary standards for CO based on public welfare considerations as
presented in the Policy Assessment. Advice from CASAC is summarized in
section III.C. Lastly, the Administrator's proposed conclusions are
presented in section III.D.
A. Background and Considerations in Previous Reviews
With the establishment of the first NAAQS for CO in 1971, secondary
standards were set identical to the primary standards. CO was not shown
to produce detrimental effects on certain higher plants at levels below
100 ppm. The only significant welfare effect identified for CO levels
possibly approaching those in ambient air was inhibition of nitrogen
fixation by microorganisms in the root nodules of legumes associated
with CO levels of 100 ppm for one month (U.S. DHEW, 1970). In the first
review of the CO NAAQS, which was completed in 1985, the threshold
level for plant effects was recognized to occur well above ambient CO
levels, such that vegetation damage as a result of CO in ambient air
was concluded to be very unlikely (50 FR 37494). As a result, EPA
concluded that the evidence did not support maintaining a secondary
standard for CO, as welfare-related effects had not been documented to
occur at ambient concentrations (50 FR 37494). Based on that
conclusion, EPA revoked the secondary standard. In the most recent
review of CO, which was completed in 1994, EPA again concluded there
was insufficient evidence of welfare effects occurring at or near
ambient levels to support setting a secondary NAAQS (59 FR 38906). That
review did not consider climate-related effects.
B. Evidence-Based Considerations in the Policy Assessment
To evaluate whether establishment of a secondary standard for CO is
appropriate, we adopted an approach in this review that builds upon the
general approach used in the last review and reflects the broader body
of evidence
[[Page 8186]]
and information now available. Considerations of the evidence available
in this review in the Policy Assessment were organized around the
following overarching question: Does the currently available scientific
information provide support for considering the establishment of a
secondary standard for CO?
In considering this overarching question, the Policy Assessment
first noted that the extensive literature search performed for the
current review did not identify any evidence of ecological effects of
CO unrelated to climate-related effects, at or near ambient levels
(ISA, section 1.3 and p. 1-3). However, ambient CO has been associated
with welfare effects related to climate (ISA, section 3.3). Climate-
related effects of CO were considered for the first time in the 2000
AQCD. The greater focus on climate in the current ISA relative to the
2000 AQCD reflects comments from CASAC and increased attention to the
role of CO in climate forcing (Brain and Samet, 2009; ISA, section
3.3). Based on the current evidence, the ISA concludes that ``a causal
relationship exists between current atmospheric concentrations of CO
and effects on climate'' (ISA, section 2.2). Accordingly, the following
discussion focuses on climate-related effects of CO in addressing the
question posed above.
As concluded in the Policy Assessment, recently available
information does not alter the current well-established understanding
of the role of urban and regional CO in continental and global-scale
chemistry, as outlined in the 2000 AQCD (PA, section 3.2). As
recognized in the ISA, CO is a weak direct contributor to greenhouse
warming. The most significant effects on climate result indirectly from
CO chemistry, related to the role of CO as the major atmospheric sink
for hydroxyl radicals. Increased concentrations of CO can lead to
increased concentrations of other gases whose loss processes also
involve hydroxyl radical chemistry. Some of these gases, such as
methane and ozone (O3), contribute to the greenhouse effect
directly while others deplete stratospheric O3 (ISA, section
3.3 and p. 3-11).
Advances in modeling and measurement have improved our
understanding of the relative contribution of CO to climate forcing
(PA, section 3.2). CO contributes to climate forcing through both
direct radiative forcing (RF) of CO, estimated at 0.024 watts per
square meter (W/m\2\) by Sinha and Toumi (1996), and indirect effects
of CO on climate through methane, O3 and carbon dioxide
(Forster et al. 2007). The Intergovernmental Panel on Climate Change
estimated the combined RF for these indirect effects of CO to be ~0.2
W/m\2\ over the period 1750-2005 (Forster et al., 2007), with more than
one-half of the forcing attributed to O3 formation (ISA,
section 3.3 and p. 3-13).
As discussed in the Policy Assessment, CO is classified as a short-
lived climate forcing agent, prompting CO emission reductions to be
considered as a possible strategy to mitigate effects of global warming
(PA, section 3.2). However, in considering the information presented in
the ISA, the Policy Assessment notes that it is highly problematic to
evaluate the indirect effects of CO on climate due to the spatial and
temporal variation in emissions and concentrations of CO and due to the
localized chemical interdependencies involving CO, methane, and
O3 (ISA section 3.3 and p. 3-12). Most climate model
simulations are based on global-scale scenarios and have a high degree
of uncertainty associated with short-lived climate forcers such as CO
(ISA, section 3.3 and p. 3-16). These models may fail to consider the
local variations in climate forcing due to emissions sources and local
meteorological patterns (ISA, section 3.3 and p. 3-16). It is possible
to compute individual contributions to RF of CO from separate emissions
sectors, although uncertainty in these estimates has not been
quantified (ISA, section 3.3, p. 3-13 and Figure 3-7).
Uncertainties in the estimates of the indirect RF from CO are noted
in the Policy Assessment to be related to uncertainties in the chemical
interdependencies of CO and trace gases, as described above. Large
regional variations in CO concentrations also contribute to the
uncertainties in the RF from CO and other trace gases (ISA section 3.3
and p. 3-12). Although measurement of and techniques for assessing
climate forcing are improving, estimates of RF still have approximately
50% uncertainty (ISA, section 3.3, and p. 3-13).
In summary, the Policy Assessment drew the following conclusions
based on the considerations identified above. As an initial matter,
with respect to non-climate welfare effects, including ecological
effects and impacts to vegetation, the Policy Assessment concluded that
there is no currently available scientific information that supports a
CO secondary standard (PA, section 3.4). Secondly, with respect to
climate-related effects, the Policy Assessment recognized the evidence
of climate forcing effects associated with CO (ISA, sections 2.2 and
3.3), while also noting that the available information provides no
basis for estimating how localized changes in the temporal and spatial
patterns of ambient CO likely to occur across the U.S. with (or
without) a secondary standard would affect local, regional, or
nationwide changes in climate. Moreover, more than half of the indirect
forcing effect of CO is attributable to O3 formation, and
welfare-related effects of O3 are more appropriately
considered in the context of the review of the O3 NAAQS,
rather than in this CO NAAQS review (PA, section 3.4). For these
reasons, the Policy Assessment concluded that there is insufficient
information at this time to support the consideration of a secondary
standard based on CO effects on climate processes (PA, section 3.4).
C. CASAC Advice
In consideration of a secondary standard, in addition to the
evidence discussed above, EPA has also considered the advice and
recommendations of CASAC, based on their review of the ISA, and the
draft Policy Assessment.\56\
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\56\ Thus far in this review, no public comments have been
received regarding the secondary standard.
---------------------------------------------------------------------------
In their comments on the draft Policy Assessment, CASAC took note
of the substantial evidence that CO has adverse effects on climate and
recommended that staff summarize information that is currently lacking
and would assist in consideration of a secondary standard in the future
(ISA, sections 3.2 and 3.3; Brain and Samet, 2010c).\57\ CASAC noted
without objection or disagreement the staff's conclusions that there is
insufficient information to support consideration of a secondary
standard at this time (Brain and Samet, 2010c).
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\57\ This recommendation is addressed in section 3.5 of the
Policy Assessment.
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D. Administrator's Proposed Conclusions Concerning a Secondary Standard
The proposed conclusions presented here are based on the assessment
and integrative synthesis of the scientific evidence presented in the
ISA, building on the evidence described in the 2000 AQCD, as well as
staff consideration of this evidence in the Policy Assessment and CASAC
advice. In considering whether the currently available scientific
information supports setting a secondary standard for CO, EPA takes
note of the Policy Assessment consideration of the body of available
evidence (briefly summarized above in
[[Page 8187]]
section III.B). First, EPA concludes that the currently available
scientific information with respect to non-climate welfare effects,
including ecological effects and impacts to vegetation, does not
support a CO secondary standard. Secondly, with respect to climate-
related effects, the EPA takes note of staff considerations in the
Policy Assessment and concurs with staff conclusions that this
information is insufficient at this time to provide support for a CO
secondary standard. Thus, in considering the evidence, staff
considerations in the Policy Assessment summarized here, as well as the
views of CASAC, summarized above, the Administrator proposes to
conclude that no secondary standards should be set at this time
because, as in the past reviews, having no standard is requisite to
protect public welfare from any known or anticipated adverse effects
from ambient CO exposures.
IV. Proposed Amendments to Ambient Monitoring Requirements
The EPA is proposing changes to the ambient air monitoring network
design requirements to support the NAAQS for CO discussed above in
section II. Because the availability of ambient CO monitoring data is
an essential element of the NAAQS implementation framework, EPA is
proposing to revise the requirements for the ambient CO monitoring
network to include a minimum set of monitors to provide data for
comparison to the NAAQS (i.e., for determining whether areas are
attaining the standards) in locations near roads where CO emissions
associated with mobile source related activity lead to increased
ambient concentrations. Under such requirements, State, local, and
Tribal monitoring agencies (``monitoring agencies'') collect ambient CO
monitoring data in accordance with the monitoring requirements
contained in 40 CFR parts 50, 53, and 58 for comparison to the NAAQS
and to meet other objectives.
A. Monitoring Methods
Ambient air monitoring data are used for various purposes,
including determining compliance with the NAAQS. The use of reference
methods provides uniform, reproducible measurements of pollutant
concentrations in ambient air. Equivalent methods allow for the
introduction of new or alternative technologies for the same purpose,
provided these methods produce measurements directly comparable to the
reference methods. EPA has established procedures for determining and
designating reference and equivalent methods, known as Federal
Reference Methods (FRMs) and Federal Equivalent Methods (FEMs), at 40
CFR part 53.
Ambient air monitoring data for CO must be obtained using an FRM or
an FEM, as defined in 40 CFR parts 50 and 53, for such data to be
comparable to the NAAQS for CO. All CO monitoring methods in use
currently by State and local monitoring agencies are EPA-designated FRM
analyzers (USEPA, 2010f). No FEM analyzer, i.e. one using an
alternative measurement principle, has yet been designated by EPA for
CO. These continuous FRM analyzers have been used in monitoring
networks for many years (USEPA, 2010f) and provide CO monitoring data
adequate for determining CO NAAQS compliance. The current list of all
approved FRMs capable of providing ambient CO data for this purpose may
be found on the EPA Web site, http://www.epa.gov/ttn/amtic/files/ambient/criteria/reference-equivalent-methods-list.pdf. Although both
the existing CO FRM in 40 CFR part 50 and the FRM and FEM designation
requirements in part 53 remain adequate to support the CO NAAQS, EPA is
nevertheless proposing editorial revisions to the CO FRM and both
technical and editorial revisions to part 53, as discussed below.
1. Proposed Changes to Part 50, Appendix C
Reference methods for criteria pollutants are described in several
appendices to 40 CFR part 50; the CO FRM is set forth in appendix C of
part 50. A nondispersive infrared photometry (NDIR) measurement
principle is formally prescribed as the basis for the CO FRM. Appendix
C describes the technical nature of the NDIR measurement principle
stipulated for FRM CO analyzers as well as two acceptable calibration
procedures for CO FRM analyzers. It further requires that an FRM
analyzer must meet specific performance, performance testing, and other
requirements set forth in 40 CFR part 53.
From time to time, as pollutant measurement technology advances,
EPA assesses the FRMs in the 40 CFR part 50 FRM appendices to determine
if they are still adequate or if improved or more suitable measurement
technology has become available to better meet current FRM needs as
well as potential future FRM requirements. The CO FRM was originally
promulgated on April 30, 1971 (36 FR 8186), in conjunction with EPA's
establishment (originally as 42 CFR part 410) of the first NAAQS for
six pollutants (including CO) as now set forth in 40 CFR part 50. The
method was amended in 1982 and 1983 (47 FR 54922; 48 FR 17355) to
incorporate minor updates, but no substantive changes in the
fundamental NDIR measurement technique have been made since its
original promulgation. (Those updates included clarification that the
FRM NDIR measurement principle encompassed the specific ``gas filter
correlation'' measurement technique now used by many commercial FRM
analyzers.).
In connection with the current review of the NAAQS for CO, EPA is
proposing to again update the existing CO FRM--with no substantive
changes--as explained in further detail below. This action is based on
the scientific view that the CO FRM, as originally established and
updated in the 1980's, is still fully adequate for FRM purposes and is
fulfilling that role well. Further, the FRM is also well suited for use
in routine CO monitoring, and several high quality FRM analyzer models
have been available for many years and continue to be offered and
supported by multiple analyzer manufacturers. Finally, EPA has
determined that no new ambient CO measurement technique has become
available that is superior to the NDIR technique specified for the
current FRM.
While EPA believes that the current CO FRM is adequate, we also
believe that the existing CO FRM should be improved by implementing
updates to clarify the language of some provisions, to make the format
match more closely the format of more recently promulgated automated
FRMs, and to better reflect the design and improved performance of
current, commercially available CO FRM analyzers. EPA found that no
substantive changes were needed to the basic NDIR FRM measurement
principle; therefore, the proposed updates are of a very minor,
editorial nature. However, these proposed changes are numerous enough
so that EPA is proposing to re-promulgate the entire CO FRM in appendix
C of 40 CFR part 50, replacing the existing FRM language with revised
language.
2. Proposed Changes to Part 53
In close association with the proposed editorial revision to the CO
FRM described above, EPA is also proposing to update the performance
requirements for FRM CO analyzers currently contained in 40 CFR part
53. These requirements were established in the 1970's, based primarily
on the NDIR CO measurement technology available at that time. While the
fundamental NDIR measurement principle, as implemented in commercial
FRM analyzers, has changed little over several decades,
[[Page 8188]]
FRM analyzer performance has improved markedly. Contemporary advances
in digital electronics, sensor technology, and manufacturing
capabilities have permitted today's NDIR analyzers to exhibit
substantially improved measurement performance, reliability, and
operational convenience at modest cost. This improved instrument
performance is not reflected in the current performance requirements
for CO FRM analyzers specified in 40 CFR part 53, indicating a need for
an update to reflect that improved performance. The updated part 53
performance requirements would also apply to candidate FEM CO
analyzers, if any new, alternative CO measurement technology should be
developed.
As noted previously, the performance of FRM analyzers designated
under the presently specified performance requirements of Part 53 is
fully adequate for current monitoring needs. A review of analyzer
manufacturers' specifications has determined that all existing CO
analyzer models currently in use in the monitoring network already meet
the proposed new requirements (for the standard measurement range).
Upgrading the analyzer performance requirements to be more consistent
with the typical performance capability available in contemporary FRM
analyzers would ensure that newly designated FRM analyzers will have
this improved measurement performance. Therefore, EPA believes that the
Part 53 requirements should be updated to be at least commensurate with
this typical level of CO analyzer performance. In addition, this
modernization also provides for optional, new performance requirements
applicable to lower, more sensitive measurement ranges that would
support improved monitoring data quality in areas of low CO
concentrations. Accordingly, EPA is proposing to amend the performance
requirements applicable to CO FRMs (and any new FEMs) set forth in
subpart B of 40 CFR part 53, as described in the following discussion.
Subpart B of 40 CFR part 53 prescribes explicit test procedures to
be used for testing specified performance aspects of candidate FRM and
FEM analyzers, along with the minimum performance requirements that
such analyzers must meet to qualify for FRM or FEM designation. These
performance requirements are specified in Table B-1 of subpart B.
Although Table B-1 covers candidate methods for SO2,
O3, CO, and NO2, the updates to Table B-1 that
EPA is now proposing would be applicable only to candidate methods for
CO.
Some updated performance requirements are being proposed for
candidate CO analyzers that operate on the specified ``standard''
measurement range (0 to 50 ppm). This measurement range would remain
unchanged from the existing requirements as it appropriately addresses
the monitoring data needed for assessing attainment. However, based on
EPA's review of the performance of currently available CO FRM analyzers
(USEPA, 2010g), EPA is proposing revised performance requirements for
CO analyzers in Table B-1, as follows. The measurement noise limit
would be reduced from 0.5 to 0.2 ppm, and the lower detectable limit
would be reduced from 1 to 0.4 ppm. Zero drift would be reduced from
1.0 to 0.5 ppm, and span drift would be lowered from 2.5% to 2.0%. The
existing mid-span drift requirement, tested at 20% of the upper range
limit (URL), would be withdrawn. EPA has found that the mid-span drift
requirement is unnecessary for CO instruments because the upper level
span drift (tested at 80% of the URL) completely and much more
accurately defines analyzer span drift performance.
EPA proposes to change the lag time allowed from 10 to 2 minutes,
and the rise and fall times from 5 to 2 minutes. For precision, EPA
proposes to change the form of the precision limit specifications from
an absolute measure (ppm) to percent (of the URL) for CO analyzers and
to set the limit at 1 percent for both 20% and 80% of the URL. One
percent is equivalent to the existing limit value of 0.5 ppm for
precision for the standard (50 ppm) measurement range. This change in
units from ppm to percent will make the requirement responsive to
higher and lower measurement ranges (i.e., more demanding for lower
ranges).
The interference equivalent limit of 1 ppm for each interferent
would not be changed, but EPA proposes to withdraw the existing limit
requirement for the total of all interferents. EPA has found that the
total interferent limit is redundant with the individual interferent
limit for modern CO analyzers.
These proposed new performance requirements would apply only to
newly designated CO FRM or FEM analyzers. Essentially all existing FRM
analyzers in use today, as noted previously, are providing CO
monitoring data of adequate quality and fulfill the proposed
requirements. Thus, existing FRM analyzers would not be required to be
re-tested and re-designated under the proposed new requirements. All
currently designated FRM analyzers would retain their original FRM
designations.
EPA recognizes that some CO monitoring objectives (e.g., area-wide
monitoring away from major roads and rural area surveillance) require
analyzers with lower, more sensitive measurement ranges than the
standard range used for typical ambient monitoring. Part 53 (40 CFR
53.20(b)) allows an FRM or FEM designation to include lower ranges. To
make such lower-range measurements more meaningful, EPA is proposing a
separate set of performance requirements that would apply specifically
to lower ranges (i.e., those having a URL of less than 50 ppm) for CO
analyzers. The proposed additional, lower-range requirements are listed
in the proposed revised Table B-1. A candidate analyzer that meets the
Table B-1 requirements for the standard measurement range (0 to 50 ppm)
could optionally have one or more lower ranges included in its FRM or
FEM designation by further testing to show that it also meets these
proposed supplemental, lower-range requirements.
Although no substantive changes have been determined to be needed
to the test procedures and associated provisions of subpart B for CO,
the detailed language in many of the subpart B sections is in need of
significant updates, clarifications, refinement, and (in a few cases)
correction of minor typographical errors. EPA believes that these
provisions should be amended at this time in its on-going, pollutant-
by-pollutant effort to bring the entire content of subpart B fully up
to date.
The proposed changes to the subpart B text (apart from the changes
proposed for Table B-1 discussed above) are very minor and almost
entirely editorial in nature, with no changes to the substance of the
requirements. However, because these small changes are quite numerous,
EPA believes that it is expedient and advantageous to propose
replacement of the subpart B text, in its entirety, with the modified
text. As discussed previously, Table B-1, which sets forth the
pollutant-specific performance limits and was recently amended as
applicable primarily to SO2 analyzers, would be amended at
this time only as necessary and applicable to CO analyzers. EPA intends
to amend Table B-1 for the remaining pollutant methods (O3
and NO2) later, at such time as each of those pollutants--
along with its associated FRM in part 50--is addressed specifically.
[[Page 8189]]
3. Implications for Air Monitoring Networks
As noted previously, existing CO FRM analyzers (no CO FEMs are
presently available) are currently providing monitoring data that are
adequate for the current CO NAAQS. Although EPA is proposing to re-
promulgate the entire CO FRM, the changes are minor, with no
substantive changes being proposed. Thus, this action would have
little, if any, effect on existing air monitoring networks. Similarly,
EPA is proposing revisions to subpart B of part 53, which specifies the
testing and performance requirements for FRM and FEM analyzers. Again,
the changes are minor, with the exception of the CO analyzer
performance requirements in Table B-1, which EPA is proposing to make
more consistent with modern CO analyzers representative of monitors
used in the current CO monitoring network. These new requirements would
be used for designation of new CO FRM and FEM analyzers. Existing EPA-
designated FRMs would be unaffected by the proposed changes and would
continue to be designated. As most commercially available CO FRM
analyzers already meet the proposed new performance requirements, the
cost of new CO analyzers that would meet the proposed new performance
requirements would not be increased by the proposed new requirements.
Therefore, there would be no immediate impact on monitoring agencies or
on their CO monitoring networks due to the proposed amendments to the
CO FRM and the associated new performance requirements proposed for
subpart B.
In the longer term, the proposed new performance requirements would
ensure that CO network monitors, going forward, would maintain their
improved performance. Monitoring agencies would benefit by having
greater confidence in their CO monitoring data quality, particularly at
the lower ambient levels prevalent in most areas. Further, the
assurance of increased CO data quality in years to come will provide
better databases to support future reviews of the CO NAAQS.
B. Network Design
The objectives of an ambient monitoring network include the
collection and dissemination of air pollution data to the general
public in a timely manner, to determine compliance with ambient air
quality standards and the effectiveness of emissions control
strategies, and to provide support for air pollution research (40 CFR
part 58, appendix D). This section on CO network design provides
background on the monitoring network, information on the sources of CO,
information on factors affecting CO emissions, and provides rationale
for a proposed network design intended to support the implementation of
the CO NAAQS.
1. Background
EPA issued the first regulations for ambient air quality
surveillance, codified at 40 CFR part 58, for criteria pollutants
including CO in 1979 (44 FR 27558, May 10, 1979). These 1979
regulations established a monitoring network for CO (described in
detail in the CO Network Review and Background document [Watkins and
Thompson, 2010]) that required two CO monitors in urban areas with
500,000 or more people. The first of these two monitors was a ``peak''
concentration monitor, intended to be located in areas ``* * * around
major traffic arteries and near heavily traveled streets in downtown
areas.'' The second monitor was intended to represent a wider
geographic area, particularly at neighborhood scales ``where
concentration exposures are significant.'' The 2006 monitoring rule
(Revisions to Ambient Air Monitoring Regulations, 71 FR 61236 (October
17, 2006)) removed the minimum monitoring requirements for the ambient
CO monitoring network that were promulgated in 1979. However, the 2006
monitoring rule maintained a requirement that if there was ongoing CO
monitoring in an area, the area must have at least one monitor located
to measure maximum concentration of CO in that area. The 2006
monitoring rule also included a provision requiring the approval of the
EPA Regional Administrator before any existing CO ambient monitors
could be removed. Finally, the 2006 monitoring rule included a
requirement for CO monitors to be operated at all National Core (NCore)
multi-pollutant monitoring stations; with approximately 80 stations
projected to have been operational nationwide by January 1, 2011 to
support multi-pollutant monitoring objectives.
An analysis of the available CO monitoring network data in the Air
Quality System (AQS) database shows that the network was comprised of
approximately 345 monitors during 2009. Information stored in AQS for
these monitors describes the most frequently stated monitor objectives
for sites in the current CO network as assessment of concentrations for
general population exposure and maximum (highest) concentrations at the
neighborhood scale.\58\ Approximately 56 of the monitors operating in
2009 were at microscale sites, a majority of which were likely sites
representing ``peak'' concentrations which were required under the
monitoring regulations originally promulgated in 1979, intended to
characterize mobile source impacts in heavily traveled downtown streets
or near major arterial roads (Watkins and Thompson, 2010). The rest of
these sites were likely being operated to meet objectives including
NAAQS comparison, to support long-term trend determination, to meet
State Implementation Plan (SIP) and maintenance plan requirements, and
to support ongoing health studies.
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\58\ Spatial scales are defined in 40 CFR part 58 Appendix D,
Section 1.2, where the scales of representativeness of most interest
for the monitoring site types include:
1. Microscale--Defines the concentration in air volumes
associated with area dimensions ranging from several meters up to
about 100 meters.
2. Middle scale--Defines the concentration typical of areas up
to several city blocks in size, with dimensions ranging from about
100 meters to 0.5 kilometers.
3. Neighborhood scale--Defines concentrations within some
extended area of the city that has relatively uniform land use with
dimensions in the 0.5 to 4.0 kilometers range.
4. Urban scale--Defines concentrations within an area of city-
like dimensions, on the order of 4 to 50 kilometers. Within a city,
the geographic placement of sources may result in there being no
single site that can be said to represent air quality on an urban
scale. The neighborhood and urban scales have the potential to
overlap in applications that concern secondarily formed or
homogeneously distributed air pollutants.
5. Regional scale--Defines usually a rural area of reasonably
homogeneous geography without large sources, and extends from tens
to hundreds of kilometers.
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2. On-Road Mobile Sources
The REA for this review notes that ``motor vehicle emissions
continue to be important contributors to ambient CO concentrations''
(REA, section 2.2). Microenvironments influenced by on-road mobile
sources are important contributors to ambient CO exposures,
particularly in urban areas (REA, section 2.7), as indicated by
personal exposure studies that have generally shown that the highest
ambient CO exposure levels occur while people are in transit in motor
vehicles (ISA, section 2.3). Mobile sources are the primary
contributors to ambient CO emissions because CO is formed by incomplete
combustion of carbon-containing fossil fuels widely used in motor
vehicles (ISA, section 2.1; REA, section 3.3). Further, spark-ignition
engines (gasoline or light-duty engines) have higher CO emission rates
than diesel engines (heavy-duty engines) because they typically operate
closer to the stoichiometric air-to-fuel ratio, have
[[Page 8190]]
relatively short residence times at peak combustion temperatures, and
have very rapid cooling of cylinder exhaust gases (ISA, section 3.2.1).
Ambient CO concentrations have significantly declined over the past
20 years, reflecting reductions in on-road vehicle emissions, as
described in section II.A above. Overall, based on the 2002 National
Emissions Inventory (NEI), on-road mobile sources account for
approximately 52% of total CO emissions. Based on the more recent 2005
NEI, the contributions of on-road mobile sources has now risen to
approximately 60% of the total CO emissions inventory (not counting
wildfire emissions) (http://www.epa.gov/ttn/chief/eiinformation.html).
As described in section II.A above, in some metropolitan areas in the
U.S., as much as 75% of all CO emissions result from on-road vehicle
exhaust (ISA, section 2.1).
On-road vehicle CO emission rates vary depending on operating
conditions, such as cold-start conditions and operating speed. Under
cold start conditions, which only last for the first minutes of vehicle
operation, CO emissions are higher due to temporary ineffectiveness of
vehicle exhaust catalysts until they are heated to optimal operating
temperatures (ISA, section 3.2.1; Singer et al., 1999). Meanwhile, CO
emissions also vary based on vehicle operating speeds. Increased CO
emissions occur under conditions of high acceleration, rapid speed
fluctuations, and heavy vehicle loads (ISA, section 3.2.1). Studies
have found that CO emission rates for tested light-duty vehicles are
highest for accelerating vehicles, second highest for vehicles in
cruise, third highest for vehicles under deceleration, and fourth
highest (of four operating speed related categories) for vehicles at
idle (Frey et al., 2003). High acceleration and rapid speed
fluctuations (such as acceleration and deceleration occurring over a
short time period) can be associated with congested, stop-and-go
traffic conditions.
3. Near-Road Environment
Information in the ISA and other peer-reviewed literature suggest
that concentrations of mobile source pollutants, such as CO, typically
display peak concentrations on or immediately adjacent to roads,
typically producing a gradient in pollutant concentrations where
concentrations decrease with increasing distance from roads (ISA,
section 2.3; ISA, section 3.5.1.3; Baldauf et al., 2008; Clements et
al., 2009; Karner et al., 2010; Zhou and Levy, 2008; Zhu et al., 2002).
CO is emitted by on-road mobile sources, and is not secondarily formed
in the near-road environment like NO2 (which is both
primarily emitted and secondarily formed in the near-road environment).
As a result, the near-road gradient for CO can be quite steep, where
concentrations rapidly decay with increasing distance away from the
road when compared to other mobile source pollutants such as
NO2. Karner et al. (2010), synthesized findings from 41
near-road pollutant monitoring studies ranging from 1978 through June
2008 to advance the understanding of on-road mobile source pollutant
dispersion. They performed two regression analyses, one being a local
regression of background normalized concentrations on distance, and the
second being a local regression of edge [of road] normalized
concentrations on distance. These analyses found CO to have the highest
approximate edge-of-road peaks, as much as 21 times background
concentrations, of all pollutants analyzed, and also showed CO to have
one of the fastest decay rates with increasing distance from the road,
showing as much as a 90 percent drop in concentration 150 meters from
the edge of the road. A key reason in the difference in decay rate with
increasing distance from roads between CO and NO2 is due to
how the two pollutants are introduced into the near-road environment.
CO is a primary emission from motor vehicle fuel combustion, while
NO2 is both emitted as a primary emission and secondarily
formed in the near-road environment. The Integrated Science Assessment
for Oxides of Nitrogen--Health Criteria (NOX ISA; USEPA,
2008d) notes that the direct emission of NO2 from mobile
sources is estimated to be only a few percent of the total
NOX emissions for light duty gasoline vehicles, and from
less than 10 percent up to 70 percent of the total NOX
emission from heavy duty diesel vehicles, depending on the engine, the
use of emission control technologies such as catalyzed diesel
particulate filters (CDPFs), and mode of vehicle operation. Although
much of the NOX emissions are initially in the form of NO,
the rate of conversion of NO to NO2 is generally a rapid
process (i.e., on the order of a minute) (NOX ISA, section
2.2.2). Thus, more of the NO2 in the near-road environment
is a result of secondary formation than from primary emissions, while
CO is almost exclusively a result of direct emissions from tailpipes.
Overall, the literature suggests that CO concentrations generally
return to near-background levels within a few hundred meters from the
road (Karner et al., 2010; Zhou and Levy, 2007). The actual
concentrations of CO, and other mobile source pollutants such as
NOX and particulate matter, that occur in the near-road
environment, and the rate of decay of those pollutant concentrations
with increasing distance from the road, are dependent on a number of
variables including traffic volume, traffic fleet mix, roadway type,
roadway design, surrounding features, topography (or terrain), and
meteorology (Baldauf et al., 2009; Baldauf et al., 2008; Clements et
al., 2009; Hagler et al., 2010; Heist et al., 2009). EPA notes that
these factors were taken into account in the requirements for the near-
road NO2 monitoring network, promulgated in February 2010
(75 FR 6474), which required near-road NO2 sites to be
selected with consideration given to traffic volume (via use of Annual
Average Daily Traffic [AADT] counts), fleet mix, congestion patterns,
roadway design, terrain, and meteorology.
4. Urban Downtown Areas and Urban Street Canyons
As noted above in section IV.B.2, increased CO emissions occur
under operating conditions of high acceleration, rapid speed
fluctuations (such as acceleration and deceleration occurring over a
short time period), and increased vehicle loads (ISA, section 3.2.1).
High acceleration and rapid speed fluctuations can be associated with
congested traffic conditions, such as stop-and-go traffic, which can
occur on heavily trafficked roads such as highways, freeways, and along
major arterial roads, and also along roads with multiple intersections
in relatively close proximity to each other. Thus, elevated CO
concentrations, relative to surrounding background concentrations, can
occur not only along heavily trafficked roads but also may be found in
urban downtown areas, where a relatively higher number of roads exist
in an area (high density of roads per unit area) and a relatively
higher density of roadway intersections exist in an area (high roadway
intersection per unit area), which can lead to increased occurrences of
vehicles operating under modes of high acceleration and/or rapid speed
fluctuations. Even though streets in urban downtown areas may not
individually carry as much traffic as larger highways, freeways, or
major arterials, the impact of many relatively smaller streets in close
proximity carrying traffic experiencing periods of high acceleration
and/or rapid speed fluctuations, or congested traffic, may collectively
contribute to elevated CO concentrations in that downtown area.
[[Page 8191]]
In addition to traffic undergoing periods of high acceleration and/
or rapid speed fluctuations or experiencing general traffic congestion,
urban downtown areas often have a number of relatively tall buildings,
typically in close proximity to each other. Such configurations of tall
buildings in relatively close proximity often create urban features
called urban canyons or urban street canyons. Although the term urban
canyon, or urban street canyon, is not formally defined, it can
generally be described as an urban feature, resembling a natural canyon
\59\, where streets or roads exist within dense blocks of relatively
tall buildings. These urban features are of interest because, as noted
in the ISA, recent research by Kaur and Nieuwenhuijsen (2009), and
Carlaw et al. (2007), suggest CO concentrations are related to traffic
volume and fleet mix in the urban street canyon environment, which can
influence potential exposures. EPA has had monitoring requirements in
the past that characterized concentrations of CO in heavily trafficked
downtown streets, i.e. ``urban street canyons,'' (Watkins and Thompson,
2010), and notes such locations may have still have relevance going
forward.
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\59\ A natural canyon may be defined as a ``deep narrow valley
with steep sides'' (http://www.merriam-webster.com/dictionary/canyon).
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5. Meteorological and Topographical Influences
In 2003, the National Research Council (NRC) of the National
Academies published a document titled Managing Carbon Monoxide
Pollution in Meteorological and Topographical Problem Areas. This
report noted how drastically ambient CO concentrations had dropped
across the country from the 1970s through the early 2000s, and that
some of the remaining areas of the country that continued to have
relatively high concentrations tended to have meteorological and
topographical characteristics that exacerbate pollution. In particular,
meteorological impacts can concentrate pollutant build-up in an area
due to atmospheric inversions and cold temperatures. Atmospheric
inversions essentially prevent pollutant emissions in an area from
dispersing through vertical mixing. As explained by the NRC (NRC,
2003), the extent to which air mixes vertically depends on how the air
temperature changes with altitude. Warm air is less dense than cold air
and thus more buoyant, allowing surface air to mix upward as relatively
warmer air rises in the atmosphere. However, if the vertical
temperature profile is such that temperatures decrease more slowly than
normal, or increase with height, vertical mixing is inhibited.
Inversions can be caused by several different specific phenomena,
including surface based cooling (for example, due to snow on the
ground), due to high altitudes, and sometimes due to warm air advection
at higher altitudes.
The topographical impacts that can lead to pollutant build-up in an
area are typically due to physical terrain features that may aid in
trapping pollution in an area and/or contribute to meteorological
related inversions. An example of topographical impacts might be an
urban area within a valley, or surrounded on several sides by mountain
ranges. In such a case, pollutant dispersion is inhibited in the
horizontal, with terrain features effectively preventing mixing or
transport of pollution from a given area. Further, in some cases both
meteorological and topographical impacts can combine to exacerbate
pollutant build-up, such as in an area partially surrounded by high
terrain which is also subject to inversions.
Although there is available information on what can cause increased
potential for air pollutant build-up due to meteorological and
topographical impacts, there are no easily defined or applied criteria
that could be implemented nationally by which all such locations could
be identified. Identification of such locations would require a case-
by-case approach, where localized and detailed information on terrain
and meteorology would be needed, plus an understanding of the types and
amounts of emission sources in or around any particular area.
6. Proposed Changes
Although EPA is proposing to retain the current 8-hour and 1-hour
CO NAAQS, as discussed above in section II, the Agency is proposing to
revise the requirements for the ambient CO monitoring network to
include a minimum set of monitors to collect data for comparison to the
NAAQS in near-roadway locations where CO emissions associated with
mobile source related activity lead to increased ambient
concentrations. The current network of CO monitors, beyond those at
NCore sites, consists of monitors that were established to meet the
1979 monitoring rule requirements or which were placed by State and
local air monitoring agencies to meet their own needs or objectives.
These additional monitors in the current network are being operated
without being required under EPA monitoring network regulations and as
a result, they do not reflect a national monitoring network design. In
CASAC comments on the second draft REA, the CASAC panel, aware of the
current CO monitoring network configuration, commented on the need to
reconsider CO monitoring network designs, stating that `` * * * the
approach for siting [CO] monitors needs greater consideration. More
extensive coverage may be warranted for areas where concentrations may
be more elevated, such as near roadway locations'' (Brain and Samet,
2010b). Since there is a strong relationship between CO exposures and
mobile source activity, as described in the ISA and REA and summarized
in sections II.D.2 and IV.B.2 above, primarily in the near-road
environment, EPA believes that some CO monitors should be located near
on-road mobile source activity, where ambient concentrations are
expected to be more elevated, as noted by CASAC.
Accordingly, EPA is proposing to require locating ambient CO
monitors which would produce data for comparison to both the 8-hour and
1-hour NAAQS at a subset of near-road NO2 monitoring
stations, which are required under the Primary National Ambient Air
Quality Standards for Nitrogen Dioxide; Final Rule (75 FR 6474),
codified at 40 CFR part 58, appendix D. This requirement would support
the objective of characterizing ambient conditions at highly trafficked
near-road locations where elevated CO concentrations (relative to
surrounding background concentrations) are expected to occur.
The EPA is not proposing to require dedicated CO monitoring sites
to characterize area-wide concentrations representing neighborhood and
larger spatial scales. Based on a recent review of the current CO
monitoring network (Watkins and Thompson, 2010), EPA believes that the
required NCore sites and many of the existing monitoring sites in the
network provide data representative of neighborhood and larger spatial
scales. These monitors are useful in providing relative background
concentrations that, when compared to near-road CO monitors, could aid
in the quantification of the near-road gradient of CO in a given urban
area. Between the required NCore sites, and an expectation based on
experience that some number of non-required area-wide sites will
continue to operate in the future, we do not believe it is necessary to
propose a specific area-wide monitoring requirement in this rulemaking.
EPA believes that the proposed network design which places CO
monitors at a subset of near-road NO2
[[Page 8192]]
monitoring stations, as described in detail in the following sections,
will require a relatively modest amount of new resources by State and
local air agencies. Recalling that there were approximately 345 CO
monitors operating in 2009, which were largely discretionary monitors
not operated pursuant to Federal network design requirements, the
Agency believes that a large majority of State and local air agencies
could meet the proposed minimum monitoring requirements by relocating
an existing CO monitor to a near-road NO2 monitoring
station. In some of these cases, the EPA believes that the relocation
of a CO monitor from an existing stand-alone site to a multi-pollutant
near-road NO2 site may also result in additional operational
cost savings as, in some areas, the total number of ambient monitoring
sites for which operational support is needed could be reduced.
The EPA believes that the proposed requirement for placing CO
monitors at some of the forthcoming near-road NO2 monitoring
stations would provide an important benefit by facilitating the
implementation of a more targeted ambient CO monitoring network that
provides data for comparison to the NAAQS, and is considerably smaller
than the CO network currently in operation. EPA notes that under the
current regulation, the current CO network is subject to a potentially
significant reduction in size (as detailed in Watkins and Thompson,
2010) since non-required CO monitoring stations can be shut down upon
State request, an evaluation of historical data to evaluate
concentrations relative to the NAAQS (per 40 CFR 58.14), and EPA
Regional Administrator approval. The occurrence of such a reduction,
however, would lack the focus and direction needed to ensure retention
of a network with the surveillance aspects essential to supporting the
implementation of the CO NAAQS. In addition to ensuring that an
effective, modestly sized network shall operate in the future, other
benefits of the proposed approach of co-locating required CO monitors
at required near-road NO2 monitoring stations include:
ongoing comparison of data to the NAAQS (for assessing attainment),
providing data that can support health studies, providing data that can
be used in verification of modeling results, and supporting the
implementation of the Agency's multi-pollutant monitoring
objectives.\60\
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\60\ The EPA's strategy encouraging multi-pollutant monitoring
is presented most recently in the Ambient Air Monitoring Strategy
for State, Local, and Tribal Air Agencies document published
December 2008 (http://www.epa.gov/ttn/amtic/files/ambient/monitorstrat/AAMS%20for%20SLTs%20%20-%20FINAL%20Dec%202008.pdf).
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a. Monitoring for Carbon Monoxide at Required Near-Road Nitrogen
Dioxide Monitoring Stations
Traffic volume on urban area roads is much greater than in the more
rural areas of the country, as was noted in the preamble to the final
rule to the NO2 NAAQS (75 FR 6474). The U.S. Department of
Transportation Federal Highway Administration's Status of the Nation's
Highways, Bridges, and Transit: 2008 Conditions and Performance
document (http://www.fhwa.dot.gov/policy/2008cpr/es.htm#c2b) states
that ``while urban mileage constitutes only 25.8 percent of total
(U.S.) mileage, these roads carried 66.3 percent of the 3 trillion
vehicles miles travelled (VMT) in the United States in 2006.'' The
document also states that urban interstate highways made up only 0.8
percent of total (U.S.) mileage but carried 16.3 percent of total VMT.
The EPA notes that the 2007 American Housing Survey (http://www.census.gov/hhes/www/housing/ahs/ahs07/ahs07.html) estimates that
over 20 million housing units are within 300 feet (~91 meters) of a 4-
lane highway, airport, or railroad. Using the same survey, and
considering that the average number of residential occupants in a
housing unit is approximately 2.25, it is estimated that at least 45
million American citizens live near 4-lane highways, airports, or
railroads. Among these three transportation facilities, roads are the
most pervasive of the three, suggesting that a significant number of
people may live near major roads. Furthermore, the 2008 American Time
Use Survey (http://www.bls.gov/tus/) reported that the average U.S.
civilian spent over 70 minutes traveling per day, and as recognized in
section II.D.2.b, the exposure and dose assessment for this review
found in-vehicle microenvironments to be those with the highest ambient
CO exposures. Additionally, as described in the ISA, PA and the REA,
higher concentrations are reported at locations immediately near or on
roadways as compared to monitors somewhat removed from the roadways
(ISA, section 3.6; PA, section 2.2.1; REA, section 2.7). These
locations capture ambient concentrations that contribute to ambient
exposure concentrations occurring in vehicles. Accordingly, EPA
believes that air pollution monitors near major roads will provide
information pertaining to a significant component of ambient CO
exposure for a large portion of the population that would otherwise not
be available.
The EPA recognizes the information mentioned above regarding the
dominant role of mobile sources in the national CO emission inventory
(discussed in section IV.B.2 above), findings of the substantial near-
road concentration gradient, with elevated CO concentrations in the
near-road environment compared to relative background concentrations
(discussed in section IV.B.3 above), and the importance of on-road
mobile sources as contributors to ambient CO exposures particularly in
urban areas (REA, section 2.7). We also note that (as referenced above)
CASAC indicated that additional monitoring near roadways may be
warranted, and further stated ``the Panel found in some instances
current networks underestimated carbon monoxide levels near roadways.
Such underestimation is a critical issue * * *'' (Brain and Samet,
2010b). In light of this information, and the fact that we generally
expect the increased levels of ambient CO (and the greatest exposure to
ambient CO) to occur near-roadways, EPA has determined that it is
appropriate to propose requiring CO monitoring near heavily trafficked
roads in urban areas.
EPA additionally notes that near-road NO2 monitoring
sites will be placed near highly trafficked roads in urban areas, where
elevated CO concentrations due to on-road mobile sources are known to
occur, and that CASAC has recommended that EPA establish a near-road
monitoring network that would include sites with both NO2
and CO monitors (Russell and Samet, 2010). Accordingly, the EPA is
proposing to require CO monitors that will provide data for comparison
to the NAAQS to operate at a subset of required near-road
NO2 monitoring stations, which are required in 40 CFR part
58, appendix D. Specifically, the EPA is proposing that CO monitors be
required in any required near-road NO2 monitoring station in
a core based statistical area (CBSA) with a population of 1,000,000 or
more persons. Based on 2009 U.S. Census estimates (http://www.census.gov) and Federal Highway Administration data (http://www.fhwa.dot.gov/policyinformation/tables/02.cfm) applied to near-road
NO2 network design requirements (noted above), there would
be approximately 77 CO monitoring sites required within near-road
NO2 monitoring stations within 53 CBSAs (including San Juan,
PR).\61\
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\61\ The near-road NO2 monitoring stations, which are
proposed to house required CO monitors, shall be selected per
considerations spelled out in 40 CFR part 58, Appendix D, section
4.3.2(a)(1), which prescribes site selection by ranking all road
segments in a CBSA by AADT and then identifying a location or
locations adjacent to those highest ranked road segments,
considering fleet mix, roadway design, congestion patterns, terrain,
and meteorology.
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[[Page 8193]]
In this proposal, EPA concludes that, given the strong relationship
between CO exposures and mobile source activity, placing CO monitors at
near-road NO2 monitoring sites (which will be near highly
trafficked roads in urban areas) is needed to fulfill the ambient CO
monitoring objectives identified in section IV.B above. While having
two monitors within CBSAs of 500,000 or more persons was the historical
monitoring requirement (discussed in detail in Watkins and Thompson,
2010), with declining ambient levels we believe there is less
likelihood for high CO concentrations in relatively smaller (in
population) CBSAs. Accordingly, we believe that proposing to require CO
monitoring only in near-road NO2 monitoring stations in
CBSAs of 1,000,000 or more persons is a reasonable approach that
results in a sufficient number of CO monitors near highly trafficked
roads in urban areas to provide data for supporting the NAAQS, for use
in health studies, for model validation, and to support multi-pollutant
monitoring objectives. The EPA solicits comment upon the proposed
requirement to require CO monitors to operate within a subset of
required near-road NO2 monitoring stations, specifically
those in CBSAs with 1,000,000 or more persons. The EPA solicits comment
on using alternative population thresholds within which CO monitors
might be required to operate in near-road NO2 monitoring
stations, e.g. CBSAs with 750,000 or 500,000 or more persons (which
would require approximately 92 and 126 monitors, respectively), in
light of the proposal to retain the existing CO NAAQS. Finally, the EPA
also solicits comment on the merits of having any minimum near-road
monitoring requirements for the CO monitoring network.
b. Regional Administrator Authority
The EPA is proposing to include a provision allowing the Regional
Administrators to have the discretion to require monitoring above the
minimum requirements as necessary to address situations where minimum
monitoring requirements are not sufficient to meet monitoring
objectives presented above in section IV.B.1. The EPA recognizes that
minimum monitoring requirements may not always result in a network
sufficient to fulfill one or more data needs or monitoring objectives
for a particular area. An example of when an EPA Regional Administrator
might require an additional monitor above the minimum requirements is
to address a situation where data or other information suggest that a
stationary CO source may be contributing to ground level concentrations
that are approaching or exceeding the NAAQS. A second example of where
an EPA Regional Administrator might require additional monitoring is in
otherwise unmonitored urban downtown areas or urban street canyons (as
discussed above in section IV.B.4), where data or other information
suggest CO concentrations may be approaching or exceeding the NAAQS. A
third example of where an EPA Regional Administrator might require
additional monitoring is in unmonitored areas that are subject to high
ground level CO concentrations particularly due to or enhanced by
topographical and meteorological impacts, as discussed in section
IV.B.5 above. In all cases, the Regional Administrator and the
responsible State or local air monitoring agency should work together
to design and/or maintain the most appropriate CO network to service
monitoring objectives and any particular variety of data needs for an
area.
c. Required Network Implementation
EPA proposes that state and, when appropriate, local air monitoring
agencies provide a plan for deploying required CO monitors by July 1,
2012. We also propose that the ambient CO monitoring network be
physically established no later than January 1, 2013. These dates
correspond with the implementation schedule of the required near-road
NO2 sites, which are the same locations at which CO monitors
have been proposed to be placed. EPA solicits comment on these proposed
implementation dates.
7. Microscale Carbon Monoxide Monitor Siting Criteria
Carbon monoxide monitors that are proposed to operate at near-road
NO2 sites would likely be classified as microscale-type
sites, per the general definition of microscale sites in 40 CFR part
58, appendix D, section 1.2. Such CO monitors would be paired with
NO2 monitors required to have inlet probe heights between 2
and 7 meters, and be placed within 50 meters of a target road segment.
However, when the original minimum monitoring requirements for CO were
introduced in the 1979 monitoring rule (44 FR 27571), the siting
criteria codified for microscale CO sites was specifically intended to
account for the installation of a near-road site in street canyon or
street corridor locations. The specific siting criteria for microscale
CO sites, currently located at 40 CFR part 58, appendix E, section 6.2,
and listed in Table E-4 of appendix E, state that ``the inlet probes
for microscale carbon monoxide monitors that are being used to measure
concentrations near roadways must be between 2.5 and 3.5 meters above
ground level.'' Likewise, criteria currently located at 40 CFR part 58,
appendix E, section 6.2, and listed in Table E-4 of appendix E state
that microscale CO monitors are to be between 2 and 10 meters from the
edge of the nearest traffic lane. These siting criteria, originally
developed in 1979, were for use primarily in the urban downtown and
urban street canyon environment. In that type of urban environment,
such specific and relatively tight siting criteria were, and still are,
appropriate since there is often little space within which ambient air
monitoring inlets can be accommodated due to the typical dense
configuration of buildings. However, outside of the urban downtown and
urban street canyon environment, such criteria may be less applicable,
considering site placement logistics and site safety for monitoring
near the major highways, freeways, interstates, and major arterials
that carry so much of today's urban traffic volume.
As noted above, the intent of existing microscale CO siting
criteria reflects the historical intent of monitoring in urban downtown
areas and urban street canyons. Since EPA is proposing that CO monitors
be required to operate at a subset of near-road NO2 sites to
characterize roadway pollutant concentrations the majority of which are
not anticipated to be in urban street canyons, EPA has revisited the
appropriateness of the existing microscale CO siting requirement,
particularly for near-road sites that exist outside of the downtown
urban areas and urban street canyons. EPA consulted on this issue with
the CASAC Ambient Air Monitoring and Methods Subcommittee (CASAC-AAMMS)
in September, 2010. Specifically, EPA requested feedback on whether it
would be appropriate to revise existing microscale CO siting criteria
to match those of near-road NO2 monitors and microscale
PM2.5 monitors. In their response to EPA, the CASAC-AAMMS
recommended ``that sampling criteria for CO and other monitors at sites
installed to monitor [at] near-road NO2 [sites] match those
for NO2.'' The CASAC-
[[Page 8194]]
AAMMS also noted that ``sampling configurations of existing microscale
CO monitors should be assessed in terms of their own sampling
objectives, and need not necessarily conform to those of near-road
NO2 monitors'' (Russell and Samet, 2010).
Based in part on the CASAC-AAMMS comments above, EPA believes that
it is appropriate to revise the existing siting criteria for microscale
CO monitors to encompass both the current criteria, which are still
appropriate when monitoring in the urban downtown and/or urban street
canyon environment, as well as the criteria for near-road
NO2 sites. Therefore, EPA is proposing that microscale CO
siting criteria for probe height and horizontal spacing be changed to
match those of near-road NO2 sites as prescribed in 40 CFR
part 58 appendix E, sections 2, 4(d), 6.4(a), and Table E-4.
Specifically, EPA proposes to allow microscale CO monitor inlet probes
to be between 2 and 7 meters above the ground; that CO monitor inlet
probes be placed so they have an unobstructed air flow, where no
obstacles exist at or above the height of the monitor probe, between
the monitor probe and the outside nearest edge of the traffic lanes of
the target road segment; and that the CO monitor inlet probe shall be
as near as practicable to the outside nearest edge of the traffic lanes
of the target road segment, but shall not be located at a distance
greater than 50 meters in the horizontal from the outside nearest edge
of the traffic lanes of the target road segment.
These proposed siting criteria encompass, or bracket, the current
allowable vertical and horizontal spacing criteria for microscale CO
sites, which will allow current microscale CO sites to continue to meet
siting criteria. EPA believes the proposed revision to the microscale
CO siting criteria presented above will allow States to meet siting
criteria while co-locating required microscale CO monitors with
required near-road NO2 monitors near heavily trafficked
roads outside of urban downtown areas and urban street canyons. EPA
solicits comment upon the revised CO siting requirements proposed
above. The Agency also solicits comment upon whether it should create
two distinct sets of siting criteria for microscale CO monitoring. One
set of siting criteria would be those proposed above, while the second
set would be the current siting criteria, but directed specifically to
apply to existing or new microscale CO monitoring sites located in
downtown urban areas and urban street canyons.
V. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
Under Executive Order 12866 (58 FR 51735, October 4, 1993), this
action is a ``significant regulatory action'' because it was deemed to
``raise novel legal or policy issues.'' Accordingly, EPA submitted this
action to the Office of Management and Budget (OMB) for review under
Executive Order 12866 and any changes made in response to OMB
recommendations have been documented in the docket for this action.
B. Paperwork Reduction Act
The information collection requirements in this final rule have
been submitted for approval to the Office of Management and Budget
(OMB) under the Paperwork Reduction Act, 44 U.S.C. 3501 et seq. The
information collection requirements are not enforceable until OMB
approves them. The Information Collection Request (ICR) document
prepared by EPA for these revisions to part 58 has been assigned EPA
ICR number 0940.23.
The information collected under 40 CFR part 53 (e.g., test results,
monitoring records, instruction manual, and other associated
information) is needed to determine whether a candidate method intended
for use in determining attainment of the National Ambient Air Quality
Standards (NAAQS) in 40 CFR part 50 will meet comparability
requirements for designation as a Federal reference method (FRM) or
Federal equivalent method (FEM). We do not expect the number of FRM or
FEM determinations to increase over the number that is currently used
to estimate burden associated with CO FRM/FEM determinations provided
in the current ICR for 40 CFR part 53 (EPA ICR numbers 0940.23). As
such, no change in the burden estimate for 40 CFR part 53 has been made
as part of this rulemaking.
The information collected and reported under 40 CFR part 58 is
needed to determine compliance with the NAAQS, to characterize air
quality and associated health impacts, to develop emissions control
strategies, and to measure progress for the air pollution program. The
amendments would revise the technical requirements for CO monitoring
sites, require the relocation or siting of ambient CO air monitors, and
the reporting of the collected ambient CO monitoring data to EPA's Air
Quality System (AQS). The annual average reporting burden for the
collection under 40 CFR part 58 (averaged over the first 3 years of
this ICR) for a network of 311 CO monitors is $7,235,483. Burden is
defined at 5 CFR 1320.3(b). State, local, and Tribal entities are
eligible for State assistance grants provided by the Federal government
under the CAA which can be used for monitors and related activities.
An agency may not conduct or sponsor, and a person is not required
to respond to, a collection of information unless it displays a
currently valid OMB control number. The OMB control numbers for EPA's
regulations in 40 CFR are listed in 40 CFR part 9.
To comment on the Agency's need for this information, the accuracy
of the provided burden estimates, and any suggested methods for
minimizing respondent burden, EPA has established a public docket for
this rule, which includes this ICR, under Docket ID number EPA-HQ-OAR-
2008-0015. Submit any comments related to the ICR to EPA and OMB. See
ADDRESSES section at the beginning of this notice for where to submit
comments to EPA. Send comments to OMB at the Office of Information and
Regulatory Affairs, Office of Management and Budget, 725 17th Street,
NW, Washington, DC 20503, Attention: Desk Office for EPA. Since OMB is
required to make a decision concerning the ICR between 30 and 60 days
after February 11, 2011, a comment to OMB is best assured of having its
full effect if OMB receives it March 14, 2011. The final rule will
respond to any OMB or public comments on the information collection
requirements contained in this proposal.
C. Regulatory Flexibility Act
The Regulatory Flexibility Act (RFA) generally requires an agency
to prepare a regulatory flexibility analysis of any rule subject to
notice and comment rulemaking requirements under the Administrative
Procedure Act or any other statute unless the agency certifies that the
rule will not have a significant economic impact on a substantial
number of small entities. Small entities include small businesses,
small organizations, and small governmental jurisdictions.
For purposes of assessing the impacts of today's proposed rule on
small entities, small entity is defined as: (1) A small business that
is a small industrial entity as defined by the Small Business
Administration's (SBA) regulations at 13 CFR 121.201; (2) a small
governmental jurisdiction that is a government of a city, county, town,
school district or special district with a population of less than
50,000; and (3) a small
[[Page 8195]]
organization that is any not-for-profit enterprise which is
independently owned and operated and is not dominant in its field.
After considering the economic impacts of this proposed rule on
small entities, I certify that this action will not have a significant
economic impact on a substantial number of small entities. This
proposed rule will not impose any requirements on small entities.
Rather, this rule proposes to retain existing national standards for
allowable concentrations of CO in ambient air as required by section
109 of the CAA. See also American Trucking Associations v. EPA. 175 F.
3d at 1044-45 (NAAQS do not have significant impacts upon small
entities because NAAQS themselves impose no regulations upon small
entities). Similarly, the proposed amendments to 40 CFR part 58 address
the requirements for States to collect information and report
compliance with the NAAQS and will not impose any requirements on small
entities. We continue to be interested in the potential impacts of the
proposed rule on small entities and welcome comments on issues related
to such impacts.
D. Unfunded Mandates Reform Act
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public
Law 104-4, establishes requirements for Federal agencies to assess the
effects of their regulatory actions on State, local, and Tribal
governments and the private sector. Unless otherwise prohibited by law,
under section 202 of the UMRA, EPA generally must prepare a written
statement, including a cost-benefit analysis, for proposed and final
rules with ``Federal mandates'' that may result in expenditures to
State, local, and Tribal governments, in the aggregate, or to the
private sector, of $100 million or more in any one year (adjusted for
inflation). Before promulgating an EPA rule for which a written
statement is required under section 202, section 205 of the UMRA
generally requires EPA to identify and consider a reasonable number of
regulatory alternatives and to adopt the least costly, most cost-
effective or least burdensome alternative that achieves the objectives
of the rule. The provisions of section 205 do not apply when they are
inconsistent with applicable law. Moreover, section 205 allows EPA to
adopt an alternative other than the least costly, most cost-effective
or least burdensome alternative if the Administrator publishes with the
final rule an explanation why that alternative was not adopted. Before
EPA establishes any regulatory requirements that may significantly or
uniquely affect small governments, including Tribal governments, it
must have developed under section 203 of the UMRA a small government
agency plan. The plan must provide for notifying potentially affected
small governments, enabling officials of affected small governments to
have meaningful and timely input in the development of EPA regulatory
proposals with significant Federal intergovernmental mandates, and
informing, educating, and advising small governments on compliance with
the regulatory requirements.
This action is not subject to the requirements of sections 202 and
205 of the UMRA. EPA has determined that this proposed rule does not
contain a Federal mandate that may result in expenditures of $100
million or more for State, local, and Tribal governments, in the
aggregate, or the private sector in any one year (adjusted for
inflation). This rule proposes to retain existing national ambient air
quality standards for carbon monoxide. The expected costs associated
with the monitoring requirements are described in EPA's ICR document,
but those costs are expected to be well less than $100 million
(adjusted for inflation) in the aggregate for any year. Furthermore, as
indicated previously, in setting a NAAQS, EPA cannot consider the
economic or technological feasibility of attaining ambient air quality
standards.
EPA has determined that this proposed rule contains no regulatory
requirements that might significantly or uniquely affect small
governments because it imposes no enforceable duty on any small
governments. Therefore, this rule is not subject to the requirements of
section 203 of the UMRA.
E. Executive Order 13132: Federalism
This action does not have federalism implications. It will not have
substantial direct effects on the States, on the relationship between
the national government and the States, or on the distribution of power
and responsibilities among the various levels of government, as
specified in Executive Order 13132. The rule does not alter the
relationship between the Federal government and the States regarding
the establishment and implementation of air quality improvement
programs as codified in the CAA. Under section 109 of the CAA, EPA is
mandated to establish and review NAAQS; however, CAA section 116
preserves the rights of States to establish more stringent requirements
if deemed necessary by a State. Furthermore, this proposed rule does
not impact CAA section 107 which establishes that the States have
primary responsibility for implementation of the NAAQS. Finally, as
noted in section D (above) on UMRA, this rule does not impose
significant costs on State, local, or Tribal governments or the private
sector. Thus, Executive Order 13132 does not apply to this rule.
However, as also noted in section D (above) on UMRA, EPA recognizes
that States will have a substantial interest in this rule, including
the proposed air quality surveillance requirements of 40 CFR part 58.
Therefore, in the spirit of Executive Order 13132, and consistent with
EPA policy to promote communications between EPA and State and local
governments, EPA specifically solicits comment on this proposed rule
from State and local officials.
F. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments
This action does not have Tribal implications, as specified in
Executive Order 13175 (65 FR 67249, November 9, 2000). It does not have
a substantial direct effect on one or more Indian Tribes, since Tribes
are not obligated to adopt or implement any NAAQS. Thus, Executive
Order 13175 does not apply to this rule.
G. Executive Order 13045: Protection of Children From Environmental
Health and Safety Risks
This action is not subject to EO 13045 (62 FR 19885, April 23,
1997) because it is not economically significant as defined in EO
12866, and because the Agency does not believe the environmental health
or safety risks addressed by this action present a disproportionate
risk to children. This action's health and risk assessments are
described in sections II.C and II.D.2.b.
The public is invited to submit comments or identify peer-reviewed
studies and data that assess effects of early life exposures to CO.
H. Executive Order 13211: Actions That Significantly Affect Energy
Supply, Distribution or Use
This action is not a ``significant energy action'' as defined in
Executive Order 13211, (66 FR 28355 (May 22, 2001)) because it is not
likely to have a significant adverse effect on the supply,
distribution, or use of energy. The rule concerns the review of the
NAAQS for CO. The rule does not prescribe specific pollution control
strategies by which these ambient standards will be met. Such
strategies are developed by States on a case-by-case basis, and EPA
cannot predict whether the control options selected by States will
include
[[Page 8196]]
regulations on energy suppliers, distributors, or users.
I. National Technology Transfer and Advancement Act
Section 12(d) of the National Technology Transfer and Advancement
Act of 1995 (NTTAA), Public Law 104- 113, section 12(d) (15 U.S.C. 272
note) directs EPA to use voluntary consensus standards in its
regulatory activities unless to do so would be inconsistent with
applicable law or otherwise impractical. Voluntary consensus standards
are technical standards (e.g., materials specifications, test methods,
sampling procedures, and business practices) that are developed or
adopted by voluntary consensus standards bodies. The NTTAA directs EPA
to provide Congress, through OMB, explanations when the Agency decides
not to use available and applicable voluntary consensus standards.
This proposed rulemaking involves technical standards with regard
to ambient monitoring of CO. We have not identified any potentially
applicable voluntary consensus standards that would adequately
characterize ambient CO concentrations for the purposes of determining
compliance with the CO NAAQS and none have been brought to our
attention.
EPA welcomes comments on this aspect of the proposed rule, and
specifically invites the public to identify potentially applicable
voluntary consensus standards and to explain why such standards should
be used in the regulation.
J. Executive Order 12898: Federal Actions To Address Environmental
Justice in Minority Populations and Low-Income Populations
Executive Order 12898 (59 FR 7629 (Feb. 16, 1994)) establishes
Federal executive policy on environmental justice. Its main provision
directs Federal agencies, to the greatest extent practicable and
permitted by law, to make environmental justice part of their mission
by identifying and addressing, as appropriate, disproportionately high
and adverse human health or environmental effects of their programs,
policies, and activities on minority populations and low-income
populations in the United States.
EPA has determined that this proposed rule will not have
disproportionately high and adverse human health or environmental
effects on minority or low-income populations because it does not
affect the level of protection provided to human health or the
environment. The action proposed in this notice is to retain without
revision the existing NAAQS for CO. Therefore this action will not
cause increases in source emissions or air concentrations.
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Research Triangle Park, NC. EPA-452/R-09-007. August 2009. Available
at http://www.epa.gov/ttn/naaqs/standards/so2/data/200908SO2REAFinalReport.pdf.
U.S. Environmental Protection Agency. (2009f) Integrated Science
Assessment for Particulate Matter (Final Report). National Center
for Environmental Assessment, Research Triangle Park, NC. EPA/600/R-
08/139F.
U.S. Environmental Protection Agency. (2010a) Integrated Science
Assessment for Carbon Monoxide. National Center for Environmental
Assessment, Research Triangle Park, NC. EPA/600/R-09/019F. Available
at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_isa.html
U.S. Environmental Protection Agency. (2010b) Quantitative Risk and
Exposure Assessment for Carbon Monoxide--Amended. Office of Air
Quality Planning and Standards, Research Triangle Park, NC. EPA-452/
R-10-009. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_rea.html
U.S. Environmental Protection Agency. (2010c) Policy Assessment for
the Review of the Carbon Monoxide National Ambient Air Quality
Standards. Office of Air Quality Planning and Standards, Research
Triangle Park, NC. EPA 452/R-10-007. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_pa.html
U.S. Environmental Protection Agency. (2010d) Risk and Exposure
Assessment to Support the Review of the Carbon Monoxide Primary
National Ambient Air Quality Standards, Second External Review
Draft, U.S Environmental Protection Agency, Research Triangle Park,
NC, report no. EPA-452/P-10-004. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_rea.html
U.S. Environmental Protection Agency. (2010e) Policy Assessment for
the Review of the Carbon Monoxide National Ambient Air Quality
Standards, External Review Draft. Office of Air Quality Planning and
Standards, Research Triangle Park, NC. EPA-452/P-10-005. Available
at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_pa.html
U.S. Environmental Protection Agency. (2010f) Analyzer Use in U.S.
Monitoring Networks. Spreadsheet of air monitoring method
utilization in U.S. monitoring networks by year. Office of Air
Quality Planning and Standards.
U.S. Environmental Protection Agency. (2010g) Modern CO Instrument
Performance Data. Spreadsheet of performance data for existing FRM
analyzers. Office of Research and Development.
Watkins N. and Thompson R. (2010) CO Monitoring Network Background
and Review. Memorandum to the Carbon Monoxide NAAQS Review Docket.
EPA-HQ-OAR-2008-0015.
Wellenius G.A.; Bateson T.F.; Mittleman M.A.; Schwartz J. (2005)
Particulate air pollution and the rate of hospitalization for
congestive heart failure among Medicare beneficiaries in Pittsburgh,
Pennsylvania. Am J Epidemiol 161:1030-1036.
WHO (2008). Harmonization Project Document No. 6. Part 1: Guidance
document on characterizing and communicating uncertainty in exposure
assessment. Available at: http://www.who.int/ipcs/methods/harmonization/areas/exposure/en/.
Zanobetti A. and Schwartz J. (2001) Are diabetics more susceptible
to the health effects of airborne particles? Am J Respir. Crit. Care
Med. 164:831-833.
Zhou, Y and Levy J.I. (2007) Factors influencing the spatial extent
of mobile source air pollution impacts: A meta-analysis. BMC Public
Health, 7:89.
Zhu Y.; Hinds W.C.; Kim S.; Shen S.; Sioutas C. (2002) Study of
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traffic. Atmos Environ, 36: 4323-4335.
List of Subjects
40 CFR Part 50
Environmental protection, Air pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.
40 CFR Part 53
Environmental protection, Administrative practice and procedure,
Air pollution control, Intergovernmental relations, Reporting and
recordkeeping requirements.
40 CFR Part 58
Environmental protection, Administrative practice and procedure,
Air pollution control, Intergovernmental relations, Reporting and
recordkeeping requirements.
Dated: January 28, 2011.
Lisa P. Jackson,
Administrator.
For the reasons stated in the preamble, title 40, chapter I of the
Code of Federal Regulations is proposed to be amended as follows:
PART 50--NATIONAL PRIMARY AND SECONDARY AMBIENT AIR QUALITY
STANDARDS
1. The authority citation for part 50 continues to read as follows:
Authority: 42 U.S.C. 7401, et seq.
2. Appendix C to Part 50 is revised to read as follows:
Appendix C to Part 50--Measurement Principle and Calibration Procedure
for the Measurement of Carbon Monoxide in the Atmosphere (Non-
Dispersive Infrared Photometry)
1.0 Applicability
1.1 This non-dispersive infrared photometry (NDIR) Federal
Reference Method (FRM) provides measurements of the concentration of
carbon monoxide (CO) in ambient air for determining compliance with the
primary and secondary National Ambient Air Quality Standards (NAAQS)
for CO as specified in Sec. 50.8 of this chapter. The method is
applicable to continuous sampling and measurement of ambient CO
concentrations suitable for determining 1-hour or longer average
measurements. The method may also provide measurements of shorter
averaging times, subject to specific analyzer performance limitations.
Additional CO
[[Page 8199]]
monitoring quality assurance procedures and guidance are provided in
part 58, appendix A, of this chapter and in reference 1 of this
appendix C.
2.0 Measurement Principle
2.1 Measurements of CO in ambient air are based on automated
measurement of the absorption of infrared radiation by CO in an ambient
air sample drawn into an analyzer employing non-wavelength-dispersive,
infrared photometry (NDIR method). Infrared energy from a source in the
photometer is passed through a cell containing the air sample to be
analyzed, and the quantitative absorption of energy by CO in the sample
cell is measured by a suitable detector. The photometer is sensitized
specifically to CO by employing CO gas in a filter cell in the optical
path, which, when compared to a differential optical path without a CO
filter cell, limits the measured absorption to one or more of the
characteristic wavelengths at which CO strongly absorbs. However, to
meet measurement performance requirements, various optical filters,
reference cells, rotating gas filter cells, dual-beam configurations,
moisture traps, or other means may also be used to further enhance
sensitivity and stability of the photometer and to minimize potential
measurement interference from water vapor, carbon dioxide
(CO2), or other species. Also, various schemes may be used
to provide a suitable zero reference for the photometer, and optional
automatic compensation may be provided for the actual pressure and
temperature of the air sample in the measurement cell. The measured
infrared absorption, converted to a digital reading or an electrical
output signal, indicates the measured CO concentration.
2.2 The measurement system is calibrated by referencing the
analyzer's CO measurements to CO concentration standards traceable to a
National Institute of Standards and Technology (NIST) primary standard
for CO, as described in the associated calibration procedure specified
in section 4 of this reference method.
2.3 An analyzer implementing this measurement principle will be
considered a reference method only if it has been designated as a
reference method in accordance with part 53 of this chapter.
2.4 Sampling considerations. The use of a particle filter in the
sample inlet line of a CO FRM analyzer is optional and left to the
discretion of the user unless such a filter is specified or recommended
by the analyzer manufacturer in the analyzer's associated operation or
instruction manual.
3.0 Interferences
3.1 The NDIR measurement principle is potentially susceptible to
interference from water vapor and CO2, which have some
infrared absorption at wavelengths in common with CO and normally exist
in the atmosphere. Various instrumental techniques can be used to
effectively minimize these interferences.
4.0 Calibration Procedures
4.1 Principle. Either of two methods may be selected for dynamic
multipoint calibration of FRM CO analyzers, using test gases of
accurately known CO concentrations obtained from one or more compressed
gas cylinders certified as CO transfer standards:
4.1.1 Dilution method: A single certified standard cylinder of CO
is quantitatively diluted as necessary with zero air to obtain the
various calibration concentration standards needed.
4.1.2 Multiple-cylinder method: Multiple, individually certified
standard cylinders of CO are used for each of the various calibration
concentration standards needed.
4.1.3 Additional information on calibration may be found in Section
12 of reference 1.
4.2 Apparatus. The major components and typical configurations of
the calibration systems for the two calibration methods are shown in
Figures 1 and 2. Either system may be made up using common laboratory
components, or it may be a commercially manufactured system. In either
case, the principal components are as follows:
4.2.1 CO standard gas flow control and measurement devices (or a
combined device) capable of regulating and maintaining the standard gas
flow rate constant to within 2 percent and measuring the
gas flow rate accurate to within 2 percent, properly
calibrated to a NIST-traceable standard.
4.2.2 For the dilution method (Figure 1), dilution air flow control
and measurement devices (or a combined device) capable of regulating
and maintaining the air flow rate constant to within 2
percent and measuring the air flow rate accurate to within
2 percent, properly calibrated to a NIST-traceable standard.
4.2.3 Standard gas pressure regulator(s) for the standard CO
cylinder(s), suitable for use with a high-pressure CO gas cylinder and
having a non-reactive diaphragm and internal parts and a suitable
delivery pressure.
4.2.4 Mixing chamber for the dilution method, of an inert material
and of proper design to provide thorough mixing of CO standard gas and
diluent air streams.
4.2.5 Output sampling manifold, constructed of an inert material
and of sufficient diameter to ensure an insignificant pressure drop at
the analyzer connection. The system must have a vent designed to ensure
nearly atmospheric pressure at the analyzer connection port and to
prevent ambient air from entering the manifold.
4.3 Reagents.
4.3.1 CO gas concentration transfer standard(s) of CO in air,
containing an appropriate concentration of CO suitable for the selected
operating range of the analyzer under calibration and traceable to a
NIST standard reference material (SRM). If the CO analyzer has
significant sensitivity to CO2, the CO standard(s) should
also contain 350 to 400 ppm CO2 to replicate the typical
CO2 concentration in ambient air. However, if the zero air
dilution ratio used for the dilution method is not less than 100:1 and
the zero air contains ambient levels of CO2, then the CO
standard may be contained in nitrogen and need not contain
CO2.
4.3.2 For the dilution method, clean zero air, free of contaminants
that could cause a detectable response on or a change in sensitivity of
the CO analyzer. The zero air should contain < 0.1 ppm CO.
4.4 Procedure Using the Dilution Method.
4.4.1 Assemble or obtain a suitable dynamic dilution calibration
system such as the one shown schematically in Figure 1. Generally, all
calibration gases including zero air must be introduced into the sample
inlet of the analyzer. However, if the analyzer has special, approved
zero and span inlets and automatic valves to specifically allow
introduction of calibration standards at near atmospheric pressure,
such inlets may be used for calibration in lieu of the sample inlet.
For specific operating instructions, refer to the manufacturer's
manual.
4.4.2 Ensure that there are no leaks in the calibration system and
that all flowmeters are properly and accurately calibrated, under the
conditions of use, if appropriate, against a reliable volume or flow
rate standard such as a soap-bubble meter or wet-test meter traceable
to a NIST standard. All volumetric flow rates should be corrected to
the same temperature and pressure such as 298.15 K (25 [deg]C) and 760
mm Hg (101 kPa), using a correction formula such as the following:
[[Page 8200]]
[GRAPHIC] [TIFF OMITTED] TP11FE11.154
Where:
Fc = corrected flow rate (L/min at 25 [deg]C and 760 mm Hg),
Fm = measured flow rate (at temperature Tm and pressure Pm),
Pm = measured pressure in mm Hg (absolute), and
Tm = measured temperature in degrees Celsius.
4.4.3 Select the operating range of the CO analyzer to be
calibrated.
4.4.4 Connect the inlet of the CO analyzer to the output-sampling
manifold of the calibration system.
4.4.5 Adjust the calibration system to deliver zero air to the
output manifold. The total air flow must exceed the total demand of the
analyzer(s) connected to the output manifold to ensure that no ambient
air is pulled into the manifold vent. Allow the analyzer to sample zero
air until a stable response is obtained. After the response has
stabilized, adjust the analyzer zero reading.
4.4.6 Adjust the zero air flow rate and the CO gas flow rate from
the standard CO cylinder to provide a diluted CO concentration of
approximately 80 percent of the measurement upper range limit (URL) of
the operating range of the analyzer. The total air flow rate must
exceed the total demand of the analyzer(s) connected to the output
manifold to ensure that no ambient air is pulled into the manifold
vent. The exact CO concentration is calculated from:
[GRAPHIC] [TIFF OMITTED] TP11FE11.155
Where:
[CO]OUT = diluted CO concentration at the output manifold (ppm),
[CO]STD = concentration of the undiluted CO standard (ppm),
FCO = flow rate of the CO standard (L/min), and
FD = flow rate of the dilution air (L/min).
Sample this CO concentration until a stable response is obtained.
Adjust the analyzer span control to obtain the desired analyzer
response reading equivalent to the calculated standard concentration.
If substantial adjustment of the analyzer span control is required, it
may be necessary to recheck the zero and span adjustments by repeating
steps 4.4.5 and 4.4.6. Record the CO concentration and the analyzer's
final response.
4.4.7 Generate several additional concentrations (at least three
evenly spaced points across the remaining scale are suggested to verify
linearity) by decreasing FCO or increasing FD. Be sure the total flow
exceeds the analyzer's total flow demand. For each concentration
generated, calculate the exact CO concentration using equation (2).
Record the concentration and the analyzer's stable response for each
concentration. Plot the analyzer responses (vertical or y-axis) versus
the corresponding CO concentrations (horizontal or x-axis). Calculate
the linear regression slope and intercept of the calibration curve and
verify that no point deviates from this line by more than 2 percent of
the highest concentration tested.
4.5 Procedure Using the Multiple-Cylinder Method. Use the procedure
for the dilution method with the following changes:
4.5.1 Use a multi-cylinder, dynamic calibration system such as the
typical one shown in Figure 2.
4.5.2 The flowmeter need not be accurately calibrated, provided the
flow in the output manifold can be verified to exceed the analyzer's
flow demand.
4.5.3 The various CO calibration concentrations required in Steps
4.4.5, 4.4.6, and 4.4.7 are obtained without dilution by selecting zero
air or the appropriate certified standard cylinder.
4.6 Frequency of Calibration. The frequency of calibration, as well
as the number of points necessary to establish the calibration curve
and the frequency of other performance checking, will vary by analyzer.
However, the minimum frequency, acceptance criteria, and subsequent
actions are specified in reference 1, appendix D, ``Measurement Quality
Objectives and Validation Template for CO'' (page 5 of 30). The user's
quality control program should provide guidelines for initial
establishment of these variables and for subsequent alteration as
operational experience is accumulated. Manufacturers of CO analyzers
should include in their instruction/operation manuals information and
guidance as to these variables and on other matters of operation,
calibration, routine maintenance, and quality control.
5.0 Reference
1. QA Handbook for Air Pollution Measurement Systems--Volume II.
Ambient Air Quality Monitoring Program. U.S. EPA. EPA-454/B-08-003
(2008).
BILLING CODE 6560-50-P
[[Page 8201]]
[GRAPHIC] [TIFF OMITTED] TP11FE11.138
[[Page 8202]]
[GRAPHIC] [TIFF OMITTED] TP11FE11.139
BILLING CODE 6560-50-C
PART 53--AMBIENT AIR QUALITY REFERENCE AND EQUIVALENT METHODS
3. The authority citation for part 53 continues to read as follows:
Authority: 42 U.S.C. 7401, et seq.
4. Subpart B of Part 53 is revised to read as follows:
Subpart B--Procedures for Testing Performance Characteristics of
Automated Methods for SO[bdi2], CO, O[bdi3], and NO[bdi2]
Sec.
53.20 General provisions.
53.21 Test conditions.
53.22 Generation of test atmospheres.
53.23 Test procedure.
Appendix A to Subpart B--Optional Forms for Reporting Test Results
Subpart B--Procedures for Testing Performance Characteristics of
Automated Methods for SO[bdi2], CO, O[bdi3], and NO[bdi2]
Sec. 53.20 General provisions.
(a) The test procedures given in this subpart shall be used to test
the performance of candidate automated methods against the performance
requirement specifications given in
[[Page 8203]]
table B-1. A test analyzer representative of the candidate automated
method must exhibit performance better than, or not outside, the
specified limit or limits for each such performance parameter specified
(except range) to satisfy the requirements of this subpart. Except as
provided in paragraph (b) of this section, the measurement range of the
candidate method must be the standard range specified in table B-1 to
satisfy the requirements of this subpart.
(b) Measurement ranges. For a candidate method having more than one
selectable measurement range, one range must be the standard range
specified in table B-1, and a test analyzer representative of the
method must pass the tests required by this subpart while operated in
that range.
(1) Higher ranges. The tests may be repeated for one or more higher
(broader) ranges (i.e., ranges extending to higher concentrations) than
the standard range specified in table B-1, provided that the range does
not extend to concentrations more than four times the upper range limit
of the standard range specified in table B-1. For such higher ranges,
only the tests for range (calibration), noise at 80% of the upper range
limit, and lag, rise and fall time are required to be repeated. For the
purpose of testing a higher range, the test procedure of Sec. 53.23(e)
may be abridged to include only those components needed to test lag,
rise and fall time.
(2) Lower ranges. The tests may be repeated for one or more lower
(narrower) ranges (i.e., ones extending to lower concentrations) than
the standard range specified in table B-1. For methods for some
pollutants, table B-1 specifies special performance limit requirements
for lower ranges. If special low-range performance limit requirements
are not specified in table B-1, then the performance limit requirements
for the standard range apply. For lower ranges for any method, only the
tests for range (calibration), noise at 0% of the measurement range,
lower detectable limit, (and nitric oxide interference for
SO2 UVF methods) are required to be repeated, provided the
tests for the standard range shows the applicable limit specifications
are met for the other test parameters.
(3) If the tests are conducted and passed only for the specified
standard range, any FRM or FEM determination with respect to the method
will be limited to that range. If the tests are passed for both the
specified range and one or more higher or lower ranges, any such
determination will include the additional higher or lower range(s) as
well as the specified standard range. Appropriate test data shall be
submitted for each range sought to be included in a FRM or FEM method
determination under this paragraph (b).
(c) For each performance parameter (except range), the test
procedure shall be initially repeated seven (7) times to yield 7 test
results. Each result shall be compared with the corresponding
performance limit specification in table B-1; a value higher than or
outside the specified limit or limits constitutes a failure. These 7
results for each parameter shall be interpreted as follows:
(1) Zero (0) failures: The candidate method passes the test for the
performance parameter.
(2) Three (3) or more failures: The candidate method fails the test
for the performance parameter.
(3) One (1) or two (2) failures: Repeat the test procedures for the
performance parameter eight (8) additional times yielding a total of
fifteen (15) test results. The combined total of 15 test results shall
then be interpreted as follows:
(i) One (1) or two (2) failures: The candidate method passes the
test for the performance parameter.
(ii) Three (3) or more failures: The candidate method fails the
test for the performance parameter.
(d) The tests for zero drift, span drift, lag time, rise time, fall
time, and precision shall be carried out in a single integrated
procedure conducted at various line voltages and ambient temperatures
specified in Sec. 53.23(e). A temperature-controlled environmental
test chamber large enough to contain the test analyzer is recommended
for this test. The tests for noise, lower detectable limit, and
interference equivalent shall be conducted at any ambient temperature
between 20 [deg]C and 30 [deg]C, at any normal line voltage between 105
and 125 volts, and shall be conducted such that not more than three (3)
test results for each parameter are obtained in any 24-hour period.
(e) If necessary, all measurement response readings to be recorded
shall be converted to concentration units or adjusted according to the
calibration curve constructed in accordance with Sec. 53.21(b).
(f) All recorder chart tracings (or equivalent data plots),
records, test data and other documentation obtained from or pertinent
to these tests shall be identified, dated, signed by the analyst
performing the test, and submitted.
Note to Sec. 53.20: Suggested formats for reporting the test
results and calculations are provided in Figures B-2, B-3, B-4, B-5,
and B-6 in appendix A to this subpart. Symbols and abbreviations
used in this subpart are listed in table B-5 of appendix A to this
subpart.
Table B-1--Performance Limit Specifications for Automated Methods
--------------------------------------------------------------------------------------------------------------------------------------------------------
SO2 CO
-------------------- O3 -------------------- NO2
Performance parameter Units 1 Lower (Std. Lower (Std. Definitions and test
Std. range 2 range) Std. range 2 range) procedures
range 3 3 range 3 3
--------------------------------------------------------------------------------------------------------------------------------------------------------
1. Range.............................. ppm..................... 0-0.5 < 0.5 0-0.5 0-50 < 50 0-0.5 Sec. 53.23(a).
2. Noise.............................. ppm..................... 0.001 0.0005 0.005 0.2 0.1 0.005 Sec. 53.23(b).
3. Lower detectable limit............. ppm..................... 0.002 0.001 0.010 0.4 0.2 0.010 Sec. 53.23(c).
4. Interference equivalent:
Each interferent.................. ppm..................... minus> minus> minus> minus> minus>
0.005 0.005 0.02 1.0 0.5 0.02
Total, all interferents........... ppm..................... ........ ........ 0.06 ........ ........ 0.04 Sec. 53.23(d).
5. Zero drift, 12 and 24 hour......... ppm..................... minus> minus> minus> minus> minus>
0.004 0.002 0.02 0.5 0.3 0.02
6. Span drift, 24 hour:
20% of upper range limit.......... Percent................. ........ minus> minus> minus>
3.0 20.0 2.0 20.0
80% of upper range limit.......... Percent................. minus> minus> minus>
3.0 5.0 2.0 5.0
7. Lag time........................... Minutes................. 2 2 20 2.0 2.0 20 Sec. 53.23(e).
8. Rise time.......................... Minutes................. 2 2 15 2.0 2.0 15 Sec. 53.23(e).
9. Fall time.......................... Minutes................. 2 2 15 2.0 2.0 15 Sec. 53.23(e).
10. Precision:
20% of upper range limit.......... ppm..................... ........ ........ 0.010 ........ ........ 0.020 Sec. 53.23(e).
Percent................. 2 2 ........ 1.0 1.0 ........ Sec. 53.23(e).
[[Page 8204]]
80% of upper range limit.......... ppm..................... ........ ........ 0.010 ........ ........ 0.030 Sec. 53.23(e).
Percent................. 2 2 ........ 1.0 1.0 ........ Sec. 53.23(e).
--------------------------------------------------------------------------------------------------------------------------------------------------------
1 To convert from parts per million (ppm) to [mu]g/m3 at 25 [deg]C and 760 mm Hg, multiply by M/0.02447, where M is the molecular weight of the gas.
Percent means percent of the upper measurement range limit.
2 Tests for interference equivalent and lag time do not need to be repeated for any lower range provided the test for the standard range shows that the
lower range specification (if applicable) is met for each of these test parameters.
3 For candidate analyzers having automatic or adaptive time constants or smoothing filters, describe their functional nature, and describe and conduct
suitable tests to demonstrate their function aspects and verify that performances for calibration, noise, lag, rise, fall times, and precision are
within specifications under all applicable conditions. For candidate analyzers with operator-selectable time constants or smoothing filters, conduct
calibration, noise, lag, rise, fall times, and precision tests at the highest and lowest settings that are to be included in the FRM or FEM
designation.
4 For nitric oxide interference for the SO2 UVF method, interference equivalent is 0.0003 ppm for the lower range.
Sec. 53.21 Test conditions.
(a) Set-up and start-up of the test analyzer shall be in strict
accordance with the operating instructions specified in the manual
referred to in Sec. 53.4(b)(3). Allow adequate warm-up or
stabilization time as indicated in the operating instructions before
beginning the tests. The test procedures assume that the test analyzer
has a conventional analog measurement signal output that is connected
to a suitable strip chart recorder of the servo, null-balance type.
This recorder shall have a chart width of a least 25 centimeters, chart
speeds up to 10 cm per hour, a response time of 1 second or less, a
deadband of not more than 0.25 percent of full scale, and capability
either of reading measurements at least 5 percent below zero or of
offsetting the zero by at least 5 percent. If the test analyzer does
not have an analog signal output, or if a digital or other type of
measurement data output is used for the tests, an alternative
measurement data recording device (or devices) may be used for
recording the test data, provided that the device is reasonably suited
to the nature and purposes of the tests, and an analog representation
of the analyzer measurements for each test can be plotted or otherwise
generated that is reasonably similar to the analog measurement
recordings that would be produced by a conventional chart recorder
connected to a conventional analog signal output.
(b) Calibration of the test analyzer shall be carried out prior to
conducting the tests described in this subpart. The calibration shall
be as indicated in the manual referred to in Sec. 53.4(b)(3) and as
follows: If the chart recorder or alternative data recorder does not
have below zero capability, adjust either the controls of the test
analyzer or the chart or data recorder to obtain a + 5% offset zero
reading on the recorder chart to facilitate observing negative response
or drift. If the candidate method is not capable of negative response,
the test analyzer (not the data recorder) shall be operated with a
similar offset zero. Construct and submit a calibration curve showing a
plot of recorder scale readings or other measurement output readings
(vertical or y-axis) against pollutant concentrations presented to the
analyzer for measurement (horizontal or x-axis). If applicable, a plot
of base analog output units (volts, millivolts, milliamps, etc.)
against pollutant concentrations shall also be obtained and submitted.
All such calibration plots shall consist of at least seven (7)
approximately equally spaced, identifiable points, including 0 and 90
5 percent of the upper range limit (URL).
(c) Once the test analyzer has been set up and calibrated and the
tests started, manual adjustment or normal periodic maintenance is
permitted only every 3 days. Automatic adjustments which the test
analyzer performs by itself are permitted at any time. The submitted
records shall show clearly when any manual adjustment or periodic
maintenance was made during the tests and describe the specific
operations performed.
(d) If the test analyzer should malfunction during any of the
performance tests, the tests for that parameter shall be repeated. A
detailed explanation of the malfunction, remedial action taken, and
whether recalibration was necessary (along with all pertinent records
and charts) shall be submitted. If more than one malfunction occurs,
all performance test procedures for all parameters shall be repeated.
(e) Tests for all performance parameters shall be completed on the
same test analyzer; however, use of multiple test analyzers to
accelerate testing is permissible for testing additional ranges of a
multi-range candidate method.
Sec. 53.22 Generation of test atmospheres.
(a) Table B-2 specifies preferred methods for generating test
atmospheres and suggested methods of verifying their concentrations.
Only one means of establishing the concentration of a test atmosphere
is normally required, provided that that means is adequately accurate
and credible. If the method of generation can produce accurate,
reproducible concentrations, verification is optional. If the method of
generation is not reproducible or reasonably quantifiable, then
establishment of the concentration by some credible verification method
is required.
(b) The test atmosphere delivery system shall be designed and
constructed so as not to significantly alter the test atmosphere
composition or concentration during the period of the test. The system
shall be vented to insure that test atmospheres are presented to the
test analyzer at very nearly atmospheric pressure. The delivery system
shall be fabricated from borosilicate glass, FEP Teflon, or other
material that is inert with regard to the gas or gases to be used.
(c) The output of the test atmosphere generation system shall be
sufficiently stable to obtain stable response readings from the test
analyzer during the required tests. If a permeation device is used for
generation of a test atmosphere, the device, as well as the air passing
over it, shall be controlled to 0.1 [deg]C.
(d) All diluent air shall be zero air free of contaminants likely
to react with the test atmospheres or cause a detectable response on
the test analyzer.
(e) The concentration of each test atmosphere used shall be
quantitatively established and/or verified before or during each series
of tests. Samples for verifying test concentrations shall be
[[Page 8205]]
collected from the test atmosphere delivery system as close as feasible
to the sample intake port of the test analyzer.
(f) The accuracy of all flow measurements used to calculate test
atmosphere concentrations shall be documented and referenced to a
primary flow rate or volume standard (such as a spirometer, bubble
meter, etc.). Any corrections shall be clearly shown. All flow
measurements given in volume units shall be standardized to 25 [deg]C.
and 760 mm Hg.
(g) Schematic drawings, photos, descriptions, and other information
showing complete procedural details of the test atmosphere generation,
verification, and delivery system shall be provided. All pertinent
calculations shall be clearly indicated.
Table B-2--Test Atmospheres
----------------------------------------------------------------------------------------------------------------
Test gas Generation Verification
----------------------------------------------------------------------------------------------------------------
Ammonia............................ Permeation device. Similar to system Indophenol method, reference 3.
described in references 1 and 2.
Carbon dioxide..................... Cylinder of zero air or nitrogen Use NIST-certified standards
containing CO2 as required to obtain whenever possible. If NIST
the concentration specified in table standards are not available, obtain
B-3. 2 standards from independent
sources which agree within 2
percent, or obtain one standard and
submit it to an independent
laboratory for analysis, which must
agree within 2 percent of the
supplier's nominal analysis.
Carbon monoxide.................... Cylinder of zero air or nitrogen Use an FRM CO analyzer as described
containing CO as required to obtain in reference 8.
the concentration specified in table
B-3.
Ethane............................. Cylinder of zero air or nitrogen Gas chromatography, ASTM D2820,
containing ethane as required to reference 10. Use NIST-traceable
obtain the concentration specified gaseous methane or propane
in table B-3. standards for calibration.
Ethylene........................... Cylinder of pre-purified nitrogen Do.
containing ethylene as required to
obtain the concentration specified
in table B-3.
Hydrogen chloride.................. Cylinder \1\ of pre-purified nitrogen Collect samples in bubbler
containing approximately 100 ppm of containing distilled water and
gaseous HCl. Dilute with zero air to analyze by the mercuric thiocyanate
concentration specified in table B-3. method, ASTM (D612), p. 29,
reference 4.
Hydrogen sulfide................... Permeation device system described in Tentative method of analysis for H2S
references 1 and 2. content of the atmosphere, p. 426,
reference 5.
Methane............................ Cylinder of zero air containing Gas chromatography ASTM D2820,
methane as required to obtain the reference 10. Use NIST-traceable
concentration specified in table B-3. methane standards for calibration.
Nitric oxide....................... Cylinder \1\ of pre-purified nitrogen Gas phase titration as described in
containing approximately 100 ppm NO. reference 6, section 7.1.
Dilute with zero air to required
concentration.
Nitrogen dioxide................... 1. Gas phase titration as described 1. Use an FRM NO2 analyzer
in reference 6. calibrated with a gravimetrically
calibrated permeation device.
2. Permeation device, similar to 2. Use an FRM NO2 analyzer
system described in reference 6. calibrated by gas-phase titration
as described in reference 6.
Ozone.............................. Calibrated ozone generator as Use an FEM ozone analyzer calibrated
described in reference 9. as described in reference 9.
Sulfur dioxide..................... 1. Permeation device as described in Use an SO2 FRM or FEM analyzer as
references 1 and 2. described in reference 7.
2. Dynamic dilution of a cylinder ....................................
containing approximately 100 ppm SO2
as described in Reference 7.
Water.............................. Pass zero air through distilled water Measure relative humidity by means
at a fixed known temperature between of a dew-point indicator,
20[deg] and 30[deg] C such that the calibrated electrolytic or piezo
air stream becomes saturated. Dilute electric hygrometer, or wet/dry
with zero air to concentration bulb thermometer.
specified in table B-3.
Xylene............................. Cylinder of pre-purified nitrogen Use NIST-certified standards
containing 100 ppm xylene. Dilute whenever possible. If NIST
with zero air to concentration standards are not available, obtain
specified in table B-3. 2 standards from independent
sources which agree within 2
percent, or obtain one standard and
submit it to an independent
laboratory for analysis, which must
agree within 2 percent of the
supplier's nominal analysis.
Zero air........................... 1. Ambient air purified by ....................................
appropriate scrubbers or other
devices such that it is free of
contaminants likely to cause a
detectable response on the analyzer.
2. Cylinder of compressed zero air ....................................
certified by the supplier or an
independent laboratory to be free of
contaminants likely to cause a
detectable response on the analyzer.
----------------------------------------------------------------------------------------------------------------
\1\ Use stainless steel pressure regulator dedicated to the pollutant measured.
Reference 1. O'Keefe, A. E., and Ortaman, G. C. ``Primary Standards for Trace Gas Analysis,'' Anal. Chem. 38,
760 (1966).
Reference 2. Scaringelli, F. P., A. E. Rosenberg, E*, and Bell, J. P., ``Primary Standards for Trace Gas
Analysis.'' Anal. Chem. 42, 871 (1970).
Reference 3. ``Tentative Method of Analysis for Ammonia in the Atmosphere (Indophenol Method)'', Health Lab
Sciences, vol. 10, No. 2, 115-118, April 1973.
Reference 4. 1973 Annual Book of ASTM Standards, American Society for Testing and Materials, 1916 Race St.,
Philadelphia, PA.
Reference 5. Methods for Air Sampling and Analysis, Intersociety Committee, 1972, American Public Health
Association, 1015.
Reference 6. 40 CFR 50 Appendix F, ``Measurement Principle and Calibration Principle for the Measurement of
Nitrogen Dioxide in the Atmosphere (Gas Phase Chemiluminescence).''
Reference 7. 40 CFR 50 Appendix A-1, ``Measurement Principle and Calibration Procedure for the Measurement of
Sulfur Dioxide in the Atmosphere (Ultraviolet Fluorscence).''
Reference 8. 40 CFR 50 Appendix C, ``Measurement Principle and Calibration Procedure for the Measurement of
Carbon Monoxide in the Atmosphere'' (Non-Dispersive Infrared Photometry)''.
[[Page 8206]]
Reference 9. 40 CFR 50 Appendix D, ``Measurement Principle and Calibration Procedure for the Measurement of
Ozone in the Atmosphere''.
Reference 10. ``Standard Test Method for C, through C5 Hydrocarbons in the Atmosphere by Gas Chromatography'', D
2820, 1987 Annual Book of Aston Standards, vol 11.03, American Society for Testing and Materials, 1916 Race
St., Philadelphia, PA 19103.
Sec. 53.23 Test procedures.
(a) Range--(1) Technical definition. The nominal minimum and
maximum concentrations that a method is capable of measuring.
Note to Sec. 53.23(a)(1): The nominal range is given as the
lower and upper range limits in concentration units, for example, 0-
0.5 parts per million (ppm).
(2) Test procedure. Determine and submit a suitable calibration
curve, as specified in Sec. 53.21(b), showing the test analyzer's
measurement response over at least 95 percent of the required or
indicated measurement range.
Note to Sec. 53.23(a)(2): A single calibration curve for each
measurement range for which an FRM or FEM designation is sought will
normally suffice.
(b) Noise--(1) Technical definition. Spontaneous, short duration
deviations in measurements or measurement signal output, about the mean
output, that are not caused by input concentration changes. Measurement
noise is determined as the standard deviation of a series of
measurements of a constant concentration about the mean and is
expressed in concentration units.
(2) Test procedure. (i) Allow sufficient time for the test analyzer
to warm up and stabilize. Determine measurement noise at each of two
fixed concentrations, first using zero air and then a pollutant test
gas concentration as indicated below. The noise limit specification in
table B-1 shall apply to both of these tests.
(ii) For an analyzer with an analog signal output, connect an
integrating-type digital meter (DM) suitable for the test analyzer's
output and accurate to three significant digits, to determine the
analyzer's measurement output signal.
Note to Sec. 53.23(b)(2): Use of a chart recorder in addition
to the DM is optional.
(iii) Measure zero air with the test analyzer for 60 minutes.
During this 60-minute interval, record twenty-five (25) test analyzer
concentration measurements or DM readings at 2-minute intervals. (See
Figure B-2 in appendix A of this subpart.)
(iv) If applicable, convert each DM test reading to concentration
units (ppm) or adjust the test readings (if necessary) by reference to
the test analyzer's calibration curve as determined in Sec. 53.21(b).
Label and record the test measurements or converted DM readings as
r1, r2, r3 * * * ri * * *
r25.
(v) Calculate measurement noise as the standard deviation, S, as
follows:
[GRAPHIC] [TIFF OMITTED] TP11FE11.140
where i indicates the i-th test measurement or DM reading in ppm.
(vi) Let S at 0 ppm be identified as S0; compare
S0 to the noise limit specification given in table B-1.
(vii) Repeat steps in Paragraphs (b)(2)(iii) through (v) of this
section using a pollutant test atmosphere concentration of 80 5 percent of the URL instead of zero air, and let S at 80
percent of the URL be identified as S80. Compare
S80 to the noise limit specification given in table B-1 of
this subpart.
(viii) Both S0 and S80 must be less than or
equal to the table B-1 noise limit specification to pass the test for
the noise parameter.
(c) Lower detectable limit--(1) Technical definition. The minimum
pollutant concentration that produces a measurement or measurement
output signal of at least twice the noise level.
(2) Test procedure. (i) Allow sufficient time for the test analyzer
to warm up and stabilize. Measure zero air and record the stable
measurement reading in ppm as BZ. (See Figure B-3 in
appendix A of this subpart.)
(ii) Generate and measure a pollutant test concentration equal to
the value for the lower detectable limit specified in table B-1.
Note to Sec. 53.23(c)(2): If necessary, the test concentration
may be generated or verified at a higher concentration, then
quantitatively and accurately diluted with zero air to the final
required test concentration.
(iii) Record the test analyzer's stable measurement reading, in
ppm, as BL.
(iv) Determine the lower detectable limit (LDL) test result as LDL
= BL - BZ. Compare this LDL value with the noise
level, S0, determined in Sec. 53.23(b), for the 0
concentration test atmosphere. LDL must be equal to or higher than 2 x
S0 to pass this test.
(d) Interference equivalent--(1) Technical definition. Positive or
negative measurement response caused by a substance other than the one
being measured.
(2) Test procedure. The test analyzer shall be tested for all
substances likely to cause a detectable response. The test analyzer
shall be challenged, in turn, with each potential interfering agent
(interferent) specified in table B-3. In the event that there are
substances likely to cause a significant interference which have not
been specified in table B-3, these substances shall also be tested, in
a manner similar to that for the specified interferents, at a
concentration substantially higher than that likely to be found in the
ambient air. The interference may be either positive or negative,
depending on whether the test analyzer's measurement response is
increased or decreased by the presence of the interferent. Interference
equivalents shall be determined by mixing each interferent, one at a
time, with the pollutant at an interferent test concentration not lower
than the test concentration specified in table B-3 (or as otherwise
required for unlisted interferents), and comparing the test analyzer's
measurement response to the response caused by the pollutant alone.
Known gas-phase reactions that might occur between a listed interferent
and the pollutant are designated by footnote 3 in table B-3. In these
cases, the interference equivalent shall be determined without mixing
with the pollutant.
(i) Allow sufficient time for warm-up and stabilization of the test
analyzer.
(ii) For a candidate method using a prefilter or scrubber device
based upon a chemical reaction to derive part of its specificity and
which device requires periodic service or maintenance, the test
analyzer shall be ``conditioned'' prior to conducting each interference
test series. This requirement includes conditioning for the
NO2 converter in chemiluminescence NO/NO2/
NOX analyzers and for the ozone scrubber in UV-absorption
ozone analyzers. Conditioning is as follows:
(A) Service or perform the indicated maintenance on the scrubber or
prefilter device, as if it were due for such maintenance, as directed
in the manual referred to in Sec. 53.4(b)(3).
(B) Before testing for each potential interferent, allow the test
analyzer to sample through the prefilter or scrubber device a test
atmosphere containing the interferent at a concentration not lower than
the value specified in table B-3 (or, for unlisted potential
interferents, at a concentration substantially higher than likely to be
found in ambient air). Sampling shall be at the normal flow rate and
shall be continued for 6 continuous hours prior to the interference
test series. Conditioning for all applicable interferents prior to any
of
[[Page 8207]]
the interference tests is permissible. Also permissible is simultaneous
conditioning with multiple interferents, provided no interferent
reactions are likely to occur in the conditioning system.
(iii) Generate three test atmosphere streams as follows:
(A) Test atmosphere P: Pollutant test concentration.
(B) Test atmosphere I: Interferent test concentration.
(C) Test atmosphere Z: Zero air.
(iv) Adjust the individual flow rates and the pollutant or
interferent generators for the three test atmospheres as follows:
(A) The flow rates of test atmospheres I and Z shall be equal.
(B) The concentration of the pollutant in test atmosphere P shall
be adjusted such that when P is mixed (diluted) with either test
atmosphere I or Z, the resulting concentration of pollutant shall be as
specified in table B-3.
(C) The concentration of the interferent in test atmosphere I shall
be adjusted such that when I is mixed (diluted) with test atmosphere P,
the resulting concentration of interferent shall be not less than the
value specified in table B-3 (or as otherwise required for unlisted
potential interferents).
(D) To minimize concentration errors due to flow rate differences
between I and Z, it is recommended that, when possible, the flow rate
of P be from 10 to 20 times larger than the flow rates of I and Z.
(v) Mix test atmospheres P and Z by passing the total flow of both
atmospheres through a (passive) mixing component to insure complete
mixing of the gases.
(vi) Sample and measure the mixture of test atmospheres P and Z
with the test analyzer. Allow for a stable measurement reading, and
record the reading, in concentration units, as R (see Figure B-3).
(vii) Mix test atmospheres P and I by passing the total flow of
both atmospheres through a (passive) mixing component to insure
complete mixing of the gases.
(viii) Sample and measure this mixture of P and I with the test
analyzer. Record the stable measurement reading, in concentration
units, as RI.
(ix) Calculate the interference equivalent (IE) test result as:
IE = RI - R.
IE must be within the limits (inclusive) specified in table B-1 for
each interferent tested to pass the interference equivalent test.
(x) Follow steps (iii) through (ix) of this section, in turn, to
determine the interference equivalent for each listed interferent as
well as for any other potential interferents identified.
(xi) For those potential interferents which cannot be mixed with
the pollutant, as indicated by footnote (3) in table B-3, adjust the
concentration of test atmosphere I to the specified value without being
mixed or diluted by the pollutant test atmosphere. Determine IE as
follows:
(A) Sample and measure test atmosphere Z (zero air). Allow for a
stable measurement reading and record the reading, in concentration
units, as R.
(B) Sample and measure the interferent test atmosphere I. If the
test analyzer is not capable of negative readings, adjust the analyzer
(not the recorder) to give an offset zero. Record the stable reading in
concentration units as RI, extrapolating the calibration
curve, if necessary, to represent negative readings.
(C) Calculate IE = RI - R. IE must be within the limits
(inclusive) specified in table B-1 for each interferent tested to pass
the interference equivalent test.
(xii) Sum the absolute value of all the individual interference
equivalent test results. This sum must be equal to or less than the
total interferent limit given in table B-1 to pass the test.
BILLING CODE 6560-50-P
[[Page 8208]]
[GRAPHIC] [TIFF OMITTED] TP11FE11.141
[[Page 8209]]
[GRAPHIC] [TIFF OMITTED] TP11FE11.142
BILLING CODE 6560-50-C
(e) Zero drift, span drift, lag time, rise time, fall time, and
precision--(1) Technical definitions--(i) Zero drift. The change in
measurement response to
[[Page 8210]]
zero pollutant concentration over 12- and 24-hour periods of continuous
unadjusted operation.
(ii) Span drift. The percent change in measurement response to an
up-scale pollutant concentration over a 24-hour period of continuous
unadjusted operation.
(iii) Lag time. The time interval between a step change in input
concentration and the first observable corresponding change in
measurement response.
(iv) Rise time. The time interval between initial measurement
response and 95 percent of final response after a step increase in
input concentration.
(v) Fall time. The time interval between initial measurement
response and 95 percent of final response after a step decrease in
input concentration.
(vi) Precision. Variation about the mean of repeated measurements
of the same pollutant concentration, expressed as one standard
deviation.
(2) Tests for these performance parameters shall be accomplished
over a period of seven (7) or fifteen (15) test days. During this time,
the line voltage supplied to the test analyzer and the ambient
temperature surrounding the analyzer shall be changed from day to day,
as required in paragraph(e)(4) of this section. One test result for
each performance parameter shall be obtained each test day, for seven
(7) or fifteen (15) test days, as determined from the test results of
the first seven days. The tests for each test day are performed in a
single integrated procedure.
(3) The 24-hour test day may begin at any clock hour. The first
approximately 12 hours of each test day are required for testing 12-
hour zero drift. Tests for the other parameters shall be conducted any
time during the remaining 12 hours.
(4) Table B-4 of this section specifies the line voltage and room
temperature to be used for each test day. The applicant may elect to
specify a wider temperature range (minimum and maximum temperatures)
than the range specified in table B-4 and to conduct these tests over
that wider temperature range in lieu of the specified temperature
range. If the test results show that all test parameters of this
section Sec. 53.23(e) are passed over this wider temperature range, a
subsequent FRM or FEM designation for the candidate method based in
part on this test shall indicate approval for operation of the method
over such wider temperature range. The line voltage and temperature
shall be changed to the specified values (or to the alternative, wider
temperature values, if applicable) at the start of each test day (i.e.,
at the start of the 12-hour zero test). Initial adjustments (day zero)
shall be made at a line voltage of 115 volts (rms) and a room
temperature of 25 [deg]C.
(5) The tests shall be conducted in blocks consisting of 3 test
days each until 7 (or 15, if necessary) test results have been
obtained. (The final block may contain fewer than three test days.)
Test days need not be contiguous days, but during any idle time between
tests or test days, the test analyzer must operate continuously and
measurements must be recorded continuously at a low chart speed (or
equivalent data recording) and included with the test data. If a test
is interrupted by an occurrence other than a malfunction of the test
analyzer, only the block during which the interruption occurred shall
be repeated.
(6) During each test block, manual adjustments to the electronics,
gas, or reagent flows or periodic maintenance shall not be permitted.
Automatic adjustments that the test analyzer performs by itself are
permitted at any time.
(7) At least 4 hours prior to the start of the first test day of
each test block, the test analyzer may be adjusted and/or serviced
according to the periodic maintenance procedures specified in the
manual referred to in Sec. 53.4(b)(3). If a new block is to
immediately follow a previous block, such adjustments or servicing may
be done immediately after completion of the day's tests for the last
day of the previous block and at the voltage and temperature specified
for that day, but only on test days 3, 6, 9, and 12.
Note to Sec. 53.23(e)(7): If necessary, the beginning of the
test days succeeding such maintenance or adjustment may be delayed
as required to complete the service or adjustment operation.
(8) All measurement response readings to be recorded shall be
converted to concentration units or adjusted (if necessary) according
to the calibration curve. Whenever a test atmosphere is to be measured
but a stable reading is not required, the test atmosphere shall be
sampled and measured long enough to cause a change in measurement
response of at least 10% of full scale. Identify all readings and other
pertinent data on the strip chart (or equivalent test data record).
(See Figure B-1 illustrating the pattern of the required readings.)
Table B-4--Line Voltage and Room Temperature Test Conditions
--------------------------------------------------------------------------------------------------------------------------------------------------------
Line Room
Test day voltage,\1\ temperature,\2\ Comments
rms [deg]C
--------------------------------------------------------------------------------------------------------------------------------------------------------
0................................ 115 25 Initial set-up and adjustments.
1................................ 125 20 .......................................................................................
2................................ 105 20 .......................................................................................
3................................ 125 30 Adjustments and/or periodic maintenance permitted at end of tests.
4................................ 105 30 .......................................................................................
5................................ 125 20 .......................................................................................
6................................ 105 20 Adjustments and/or periodic maintenance permitted at end of tests.
7................................ 125 30 Examine test results to ascertain if further testing is required.
8................................ 105 30 .......................................................................................
9................................ 125 20 Adjustments and/or periodic maintenance permitted at end of tests.
10............................... 105 20 .......................................................................................
11............................... 125 30 .......................................................................................
12............................... 105 30 Adjustments and/or periodic maintenance permitted at end of tests.
13............................... 125 20 .......................................................................................
14............................... 105 20 .......................................................................................
15............................... 125 30 .......................................................................................
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Voltage specified shall be controlled to 1 volt.
\2\ Temperatures shall be controlled to 1 [deg]C.
[[Page 8211]]
BILLING CODE 6560-60-P
[GRAPHIC] [TIFF OMITTED] TP11FE11.143
BILLING CODE 6560-60-C
(9) Test procedure. (i) Arrange to generate pollutant test
atmospheres as follows. Test atmospheres A0, A20,
and A80 shall be maintained consistent during the tests and
reproducible from test day to test day.
------------------------------------------------------------------------
Test atmosphere Pollutant concentration (percent)
------------------------------------------------------------------------
A0................................ Zero air.
A20............................... 205 of the upper range
limit.
A30............................... 305 of the upper range
limit.
A80............................... 805 of the upper range
limit.
A90............................... 905 of the upper range
limit.
------------------------------------------------------------------------
(ii) For steps within paragraphs (e)(9)(xxv) through (e)(9)(xxxi)
of this section, a chart speed of at least 10 centimeters per hour (or
equivalent resolution for a digital representation) shall be used to
clearly show changes in measurement responses. The actual chart speed,
chart speed changes, and time checks shall be clearly marked on the
chart.
(iii) Test day 0. Allow sufficient time for the test analyzer to
warm up and stabilize at a line voltage of 115 volts and a room
temperature of 25 [deg]C. Adjust the zero baseline to 5 percent of
chart (see Sec. 53.21(b)) and recalibrate, if necessary. No further
adjustments shall be made to the analyzer until the end of the tests on
the third, sixth, ninth, or twelfth test day.
(iv) Measure test atmosphere A0 until a stable
measurement reading is obtained and record this reading (in
[[Page 8212]]
ppm) as Z'n, where n = 0 (see Figure B-4 in appendix A of this
subpart).
(v) [Reserved]
(vi) Measure test atmosphere A80. Allow for a stable
measurement reading and record it as S'n, where n = 0.
(vii) The above readings for Z'0 and S'0
should be taken at least four (4) hours prior to the beginning of test
day 1.
(viii) At the beginning of each test day, adjust the line voltage
and room temperature to the values given in table B-4 of this subpart
(or to the corresponding alternative temperature if a wider temperature
range is being tested).
(ix) Measure test atmosphere A0 continuously for at
least twelve (12) continuous hours during each test day.
(x) After the 12-hour zero drift test (step ix) is complete, sample
test atmosphere A0. A stable reading is not required.
(xi) Measure test atmosphere A20 and record the stable
reading (in ppm) as P1. (See Figure B-4 in appendix A.)
(xii) Sample test atmosphere A30; a stable reading is
not required.
(xiii) Measure test atmosphere A20 and record the stable
reading as P2.
(xiv) Sample test atmosphere A0; a stable reading is not
required.
(xv) Measure test atmosphere A20 and record the stable
reading as P3.
(xvi) Sample test atmosphere A30; a stable reading is
not required.
(xvii) Measure test atmosphere A20 and record the stable
reading as P4.
(xviii) Sample test atmosphere A0; a stable reading is
not required.
(xix) Measure test atmosphere A20 and record the stable
reading as P5.
(xx) Sample test atmosphere A30; a stable reading is not
required.
(xxi) Measure test atmosphere A20 and record the stable
reading as P6.
(xxii) Measure test atmosphere A80 and record the stable
reading as P7.
(xxiii) Sample test atmosphere A90; a stable reading is
not required.
(xxiv) Measure test atmosphere A80 and record the stable
reading as P8. Increase the chart speed to at least 10
centimeters per hour.
(xxv) Measure test atmosphere A0. Record the stable
reading as L1.
(xxvi) Quickly switch the test analyzer to measure test atmosphere
A80 and mark the recorder chart to show, or otherwise
record, the exact time when the switch occurred.
(xxvii) Measure test atmosphere A80 and record the
stable reading as P9.
(xxviii) Sample test atmosphere A90; a stable reading is
not required.
(xxix) Measure test atmosphere A80 and record the stable
reading as P10.
(xxx) Measure test atmosphere A0 and record the stable
reading as L2.
(xxxi) Measure test atmosphere A80 and record the stable
reading as P11.
(xxxii) Sample test atmosphere A90; a stable reading is
not required.
(xxxiii) Measure test atmosphere A80 and record the
stable reading as P12.
(xxxiv) Repeat steps within paragraphs (e)(9)(viii) through
(e)(9)(xxxiii) of this section, each test day.
(xxxv) If zero and span adjustments are made after the readings are
taken on test days 3, 6, 9, or 12, complete all adjustments; then
measure test atmospheres A0 and A80. Allow for a
stable reading on each, and record the readings as Z'n and S'n,
respectively, where n = the test day number (3, 6, 9, or 12). These
readings must be made at least 4 hours prior to the start of the next
test day.
(10) Determine the results of each day's tests as follows. Mark the
recorder chart to show readings and determinations.
(i) Zero drift. (A) Determine the 12-hour zero drift by examining
the strip chart pertaining to the 12-hour continuous zero air test.
Determine the minimum (Cmin.) and maximum (Cmax.) measurement readings
(in ppm) during this period of 12 consecutive hours, extrapolating the
calibration curve to negative concentration units if necessary.
Calculate the 12-hour zero drift (12ZD) as 12ZD = Cmax.--Cmin. (See
Figure B-5 in appendix A.)
(B) Calculate the 24-hour zero drift (24ZD) for the n-th test day
as 24ZDn = Zn - Zn-1, or 24ZDn = Zn - Z'n-1 if zero adjustment was made
on the previous test day, where Zn = \1/2\(L1+L2)
for L1 and L2 taken on the n-th test day.
(C) Compare 12ZD and 24ZD to the zero drift limit specifications in
table B-1. Both 12ZD and 24ZD must be within the specified limits
(inclusive) to pass the test for zero drift.
(ii) Span drift.
(A) Calculate the span drift (SD) as:
[GRAPHIC] [TIFF OMITTED] TP11FE11.144
or if a span adjustment was made on the previous test day,
[GRAPHIC] [TIFF OMITTED] TP11FE11.145
where
[GRAPHIC] [TIFF OMITTED] TP11FE11.146
n indicates the n-th test day, and i indicates the i-th measurement
reading on the n-th test day.
(B) SD must be within the span drift limits (inclusive) specified
in table B-1 to pass the test for span drift.
(iii) Lag time. Determine, from the strip chart (or alternative
test data record), the elapsed time in minutes between the change in
test concentration (or mark) made in step (xxvi) and the first
observable (two times the noise level) measurement response. This time
must be equal to or less than the lag time limit specified in table B-1
to pass the test for lag time.
(iv) Rise time. Calculate 95 percent of measurement reading
P9 and determine, from the recorder chart (or alternative
test data record), the elapsed time between the first observable (two
times noise level) measurement response and a response equal to 95
percent of the P9 reading. This time must be equal to or
less than the rise time limit specified in table B-1 to pass the test
for rise time.
(v) Fall time. Calculate five percent of (P10 -
L2) and determine, from the strip chart (or alternative test
record), the elapsed time in minutes between the first observable
decrease in measurement response following reading P10 and a
response equal to L2 + five percent of (P10 -
L2). This time must be equal to or less than the fall time
limit specification in table B-1 to pass the test for fall time.
(vi) Precision. Calculate precision (both P20 and
P80) for each test day as follows:
(A)
[GRAPHIC] [TIFF OMITTED] TP11FE11.147
(B)
[GRAPHIC] [TIFF OMITTED] TP11FE11.148
(C) Both P20 and P80 must be equal to or less
than the precision limits specified in table B-1 to pass the test for
precision.
Table B-5--Symbols and Abbreviations
------------------------------------------------------------------------
------------------------------------------------------------------------
BL............................... Analyzer reading at the specified LDL
test concentration for the LDL test.
Bz............................... Analyzer reading at 0 concentration
for the LDL test.
DM............................... Digital meter.
Cmax............................. Maximum analyzer reading during the
12ZD test period.
Cmin............................. Minimum analyzer reading during the
12ZD test period.
i................................ Subscript indicating the i-th
quantity in a series.
IE............................... Interference equivalent.
L1............................... First analyzer zero reading for the
24ZD test.
[[Page 8213]]
L2............................... Second analyzer zero reading for the
24ZD test.
n................................ Subscript indicating the test day
number.
P................................ Analyzer reading for the span drift
and precision tests.
Pi............................... The i-th analyzer reading for the
span drift and precision tests.
P20.............................. Precision at 20 percent of URL.
P80.............................. Precision at 80 percent of URL.
ppb.............................. Parts per billion of pollutant gas
(usually in air), by volume.
ppm.............................. Parts per million of pollutant gas
(usually in air), by volume.
R................................ Analyzer reading of pollutant alone
for the IE test.
RI............................... Analyzer reading with interferent
added for the IE test.
ri............................... The i-th analyzer or DM reading for
the noise test.
S................................ Standard deviation of the noise test
readings.
S0............................... Noise value (S) measured at 0
concentration.
S80.............................. Noise value (S) measured at 80
percent of the URL.
Sn............................... Average of P7 * * * P12 for the n-th
test day of the SD test.
S'n.............................. Adjusted span reading on the n-th
test day.
SD............................... Span drift
URL.............................. Upper range limit of the analyzer's
measurement range.
Z................................ Average of L1 and L2 readings for the
24ZD test.
Zn............................... Average of L1 and L2 readings on the
n-th test day for the 24ZD test.
Z'n.............................. Adjusted analyzer zero reading on the
n-th test day for the 24ZD test.
ZD............................... Zero drift.
12ZD............................. 12-hour zero drift.
24ZD............................. 24-hour zero drift.
------------------------------------------------------------------------
Appendix A to Subpart B of Part 53--Optional Forms for Reporting Test
Results
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BILLING CODE 6560-50-C
PART 58--AMBIENT AIR QUALITY SURVEILLANCE
5. The authority citation for part 58 continues to read as follows:
Authority: 42 U.S.C. 7403, 7410, 7601(a), 7611, and 7619.
Subpart B--[Amended]
6. Section 58.10, is amended by adding paragraph (a)(7) to read as
follows:
Sec. 58.10 Annual monitoring network plan and periodic network
assessment.
(a) * * *
(7) A plan for establishing CO monitoring sites in accordance with
the requirements of appendix D to this part shall be submitted to the
Administrator by July 1, 2012. The plan shall provide for all required
monitoring stations to be operational by January 1, 2013.
* * * * *
7. Section 58.13 is amended by adding paragraph (e) to read as
follows:
Sec. 58.13 Monitoring network completion.
* * * * *
(e) The network of CO monitors must be physically established no
later than January 1, 2013, and at that time, must be operating under
all of the requirements of this part, including the requirements of
appendices A, C, D, and E to this part.
8. Appendix D to Part 58 is amended by revising section 4.2 to read
as follows:
Appendix D to Part 58--Network Design Criteria for Ambient Air Quality
Monitoring
* * * * *
4.2 Carbon Monoxide (CO) Design Criteria.
[[Page 8219]]
4.2.1 General Requirements. (a) One CO monitor is required to
operate co-located with any required near-road NO2
monitor, as required in Section 4.3.2 of this part, in CBSAs having
a population of 1,000,000 or more persons. Continued operation of
existing, but non-required SLAMS CO sites using an FRM or FEM is
required until discontinuation is approved by the EPA Regional
Administrator, per section Sec. 58.14 of this part.
4.2.2 Regional Administrator Required Monitoring.
(a) The Regional Administrators, in collaboration with states,
may require additional CO monitors above the minimum number of
monitors required in 4.2.1 of this part, where the minimum
monitoring requirements are not sufficient to meet monitoring
objectives. The Regional Administrator may require, at his/her
discretion, additional monitors in situations where data or other
information suggest that CO concentrations may be approaching or
exceeding the NAAQS. Such situations include, but are not limited
to, (1) Characterizing impacts on ground-level concentrations due to
stationary CO sources, (2) characterizing CO concentrations in urban
downtown areas or urban street canyons, and (3) characterizing CO
concentrations in areas that are subject to high ground level CO
concentrations particularly due or enhanced by topographical and
meteorological impacts.
(b) The Regional Administrator and the responsible State or
local air monitoring agency should work together to design and/or
maintain the most appropriate CO network to address the data needs
for an area, and include all monitors under this provision in the
annual monitoring network plan.
4.2.3 CO Monitoring Spatial Scales. (a) Microscale and middle
scale measurements are the most useful site classifications for CO
monitoring sites since most people have the potential for exposure
on these scales. Carbon monoxide maxima occur primarily in areas
near major roadways and intersections with high traffic density and
often in areas with poor atmospheric ventilation.
(1) Microscale--Microscale measurements typically represent
areas in close proximity to major roadways, within street canyons,
over sidewalks, and in some cases, point and area sources. Emissions
from roadways result in high ground level CO concentrations at the
microscale, where concentration gradients generally exhibit a marked
decrease with increasing downwind distance from major roads, or
within urban downtown areas including urban street canyons.
Emissions from stationary point and area sources, and non-road
sources may, under certain plume conditions, result in high ground
level concentrations at the microscale.
(2) Middle scale--Middle scale measurements are intended to
represent areas with dimensions from 100 meters to 0.5 kilometer. In
certain cases, middle scale measurements may apply to areas that
have a total length of several kilometers, such as ``line'' emission
source areas. This type of emission sources areas would include air
quality along a commercially developed street or shopping plaza,
freeway corridors, parking lots and feeder streets.
* * * * *
9. Appendix E to Part 58 is amended by revising sections 2 and
6.2(a), 6.2(b), 6.2(c), and Table E-4 to read as follows:
Appendix E to Part 58--Probe and Monitoring Path Siting Criteria for
Ambient Air Quality Monitoring
* * * * *
2. Horizontal and Vertical Placement
The probe or at least 80 percent of the monitoring path must be
located between 2 and 15 meters above ground level for all ozone and
sulfur dioxide monitoring sites, and for neighborhood or larger
spatial scale Pb, PM10, PM10-2.5,
PM2.5, NO2, and carbon monoxide sites. Middle
scale PM10-2.5 sites are required to have sampler inlets
between 2 and 7 meters above ground level. Microscale Pb,
PM10, PM10-2.5, and PM2.5 sites are
required to have sampler inlets between 2 and 7 meters above ground
level. Microscale near-road NO2 monitoring sites are
required to have sampler inlets between 2 and 7 meters above ground
level. The inlet probes for microscale carbon monoxide monitors that
are being used to measure concentrations near roadways must be
between 2 and 7 meters above ground level. The probe or at least 90
percent of the monitoring path must be at least 1 meter vertically
or horizontally away from any supporting structure, walls, parapets,
penthouses, etc., and away from dusty or dirty areas. If the probe
or a significant portion of the monitoring path is located near the
side of a building or wall, then it should be located on the
windward side of the building relative to the prevailing wind
direction during the season of highest concentration potential for
the pollutant being measured.
* * * * *
6. * * *
6.2 Spacing for Carbon Monoxide Probes and Monitoring Paths. (a)
Near-road or urban street canyon CO monitoring microscale sites are
intended to provide a measurement of the influence of the immediate
source on the pollution exposure on the adjacent area. In order to
provide some reasonable consistency and comparability in the air
quality data from microscale sites, the CO monitor probe shall be as
near as practicable to the outside nearest edge of the traffic lanes
of the target road segment; but shall not be located at a distance
greater than 50 meters, in the horizontal, from the outside nearest
edge of the traffic lanes of the target road segment.
(b) Downtown urban area or urban street canyon (microscale) CO
monitor inlet probes must be located at least 10 meters from an
intersection and preferably at a midblock location. Midblock
locations are preferable to intersection locations because
intersections represent a much smaller portion of downtown space
than do the streets between them. Pedestrian exposure is probably
also greater in street canyon/corridors than at intersections.
(c) In determining the minimum separation between a neighborhood
scale monitoring site and a specific roadway, the presumption is
made that measurements should not be substantially influenced by any
one roadway. Computations were made to determine the separation
distance, and Table E-2 of this appendix provides the required
minimum separation distance between roadways and a probe or 90
percent of a monitoring path. Probes or monitoring paths that are
located closer to roads than this criterion allows should not be
classified as neighborhood scale, since the measurements from such a
site would closely represent the middle scale. Therefore, sites not
meeting this criterion should be classified as middle scale.
* * * * *
Table E-4 of Appendix E to Part 58--Summary of Probe and Monitoring Path Siting Criteria
--------------------------------------------------------------------------------------------------------------------------------------------------------
Horizontal and
vertical distance from Distance from trees to Distance from
Scale (maximum Height from ground to supporting structures probe, inlet or 90% of roadways to probe,
Pollutant monitoring path probe, inlet or 80% of \2\ to probe, inlet or monitoring path \1\ inlet or monitoring
length, meters) monitoring path \1\ 90% of monitoring path (meters) path \1\ (meters)
\1\ (meters)
--------------------------------------------------------------------------------------------------------------------------------------------------------
SO2 3,4,5,6....................... Middle (300 m)....... 2-15 >1 >10 N/A.
Neighborhood Urban,
and Regional (1 km).
[[Page 8220]]
CO 4,5,7.......................... Micro, middle (300 m) 2-7: 2-15 >1 >10 2-10 for downtown
Neighborhood (1 km).. urban area or street
canyon microscale;
<=50 for near-road
microscale; see
Table E-2 of this
appendix for middle
and neighborhood
scales.
O3 3,4,5.......................... Middle (300 m)....... 2-15 >1 >10 See Table E-1 of this
Neighborhood, Urban, appendix for all
and Regional (1 km). scales.
NO2 3,4,5......................... Micro (Near-road [50- 2-7 (micro); 2-15 (all >1 >10 <=50 meters for near-
300]). other scales) road microscale;
Middle (300m)........ See Table E-1 of this
Neighborhood, Urban, appendix for all
and Regional (1 km). other scales.
Ozone precursors (for PAMS) 3,4,5. Neighborhood and 2-15 >1 >10 See Table E-4 of this
Urban (1 km). appendix for all
scales.
PM,Pb 3,4,5,6,8................... Micro: Middle, 2-7 (micro); >2 (all scales, >10 (all scales) 2-10 (micro); see
Neighborhood, Urban 2-7 (middle PM10 2.5); horizontal distance Figure E-1 of this
and Regional. 2-15 (all other only) appendix for all
scales) other scales.
--------------------------------------------------------------------------------------------------------------------------------------------------------
N/A--Not applicable.
\1\ Monitoring path for open path analyzers is applicable only to middle or neighborhood scale CO monitoring, middle, neighborhood, urban, and regional
scale NO2 monitoring, and all applicable scales for monitoring SO2,O3, and O3 precursors.
\2\ When probe is located on a rooftop, this separation distance is in reference to walls, parapets, or penthouses located on roof.
\3\ Should be >20 meters from the drip-line of tree(s) and must be 10 meters from the drip-line when the tree(s) act as an obstruction.
\4\ Distance from sampler, probe, or 90% of monitoring path to obstacle, such as a building, must be at least twice the height the obstacle protrudes
above the sampler, probe, or monitoring path. Sites not meeting this criterion may be classified as middle scale (see text).
\5\ Must have unrestricted airflow 270 degrees around the probe or sampler; 180 degrees if the probe is on the side of a building or a wall.
\6\ The probe, sampler, or monitoring path should be away from minor sources, such as furnace or incineration flues. The separation distance is
dependent on the height of the minor source's emission point (such as a flue), the type of fuel or waste burned, and the quality of the fuel (sulfur,
ash, or lead content). This criterion is designed to avoid undue influences from minor sources.
\7\ For microscale CO monitoring sites in downtown areas or street canyons (not at near-road NO2 monitoring sites), the probe must be >10 meters from a
street intersection and preferably at a midblock location.
\8\ Collocated monitors must be within 4 meters of each other and at least 2 meters apart for flow rates greater than 200 liters/min or at least 1 meter
apart for samplers having flow rates less than 200 liters/min to preclude airflow interference.
* * * * *
[FR Doc. 2011-2404 Filed 2-10-11; 8:45 am]
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