

[Federal Register: July 11, 2007 (Volume 72, Number 132)]
[Proposed Rules]               
[Page 37817-37919]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr11jy07-19]                         
 

[[Page 37817]]

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Part II





Environmental Protection Agency





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40 CFR Part 50



National Ambient Air Quality Standards for Ozone; Proposed Rule


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2005-0172; FRL-8331-5]
RIN 2060-AN24

 
National Ambient Air Quality Standards for Ozone

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: Based on its review of the air quality criteria for ozone 
(O3) and related photochemical oxidants and national ambient 
air quality standards (NAAQS) for O3, EPA proposes to make 
revisions to the primary and secondary NAAQS for O3 to 
provide requisite protection of public health and welfare, 
respectively, and to make corresponding revisions in data handling 
conventions for O3.
    With regard to the primary standard for O3, EPA proposes 
to revise the level of the 8-hour standard to a level within the range 
of 0.070 to 0.075 parts per million (ppm), to provide increased 
protection for children and other ``at risk'' populations against an 
array of O3-related adverse health effects that range from 
decreased lung function and increased respiratory symptoms to serious 
indicators of respiratory morbidity including emergency department 
visits and hospital admissions for respiratory causes, and possibly 
cardiovascular-related morbidity as well as total nonaccidental and 
cardiopulmonary mortality. The EPA also proposes to specify the level 
of the primary standard to the nearest thousandth ppm. The EPA solicits 
comment on alternative levels down to 0.060 ppm and up to and including 
retaining the current 8-hour standard of 0.08 ppm (effectively 0.084 
ppm using current data rounding conventions).
    With regard to the secondary standard for O3, EPA 
proposes to revise the current 8-hour standard with one of two options 
to provide increased protection against O3-related adverse 
impacts on vegetation and forested ecosystems. One option is to replace 
the current standard with a cumulative, seasonal standard expressed as 
an index of the annual sum of weighted hourly concentrations, cumulated 
over 12 hours per day (8 a.m. to 8:00 p.m.) during the consecutive 3-
month period within the O3 season with the maximum index 
value, set at a level within the range of 7 to 21 ppm-hours. The other 
option is to make the secondary standard identical to the proposed 
primary 8-hour standard. The EPA solicits comment on specifying a 
cumulative, seasonal standard in terms of a 3-year average of the 
annual sums of weighted hourly concentrations; on the range of 
alternative 8-hour standard levels for which comment is being solicited 
for the primary standard, including retaining the current secondary 
standard, which is identical to the current primary standard; and on an 
alternative approach to setting a cumulative, seasonal secondary 
standard(s).

DATES: Written comments on this proposed rule must be received by 
October 9, 2007.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2005-0172, by one of the following methods:
     http://www.regulations.gov: Follow the on-line instructions for 

submitting comments.
     E-mail: a-and-r-Docket@epa.gov.
     Fax: 202-566-1741.
     Mail: Docket No. EPA-HQ-OAR-2005-0172, Environmental 
Protection Agency, Mail code 6102T, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460. Please include a total of two copies.
     Hand Delivery: Docket No. EPA-HQ-OAR-2005-0172, 
Environmental Protection Agency, EPA West, Room 3334, 1301 Constitution 
Ave., NW., Washington, DC. Such deliveries are only accepted during the 
Docket's normal hours of operation, and special arrangements should be 
made for deliveries of boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2005-0172. The EPA's policy is that all comments received will be 
included in the public docket without change and may be made available 
online at 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 
http://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
.

    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.
    Public Hearings: The EPA intends to hold public hearings around the 
end of August to early September in several cities across the country, 
and will announce in a separate Federal Register notice the dates, 
times, and addresses of the public hearings on this proposed rule.

FOR FURTHER INFORMATION CONTACT: Dr. David J. McKee, Health and 
Environmental Impacts Division, Office of Air Quality Planning and 
Standards, U.S. Environmental Protection Agency, Mail code C504-06, 
Research Triangle Park, NC 27711; telephone: 919-541-5288; fax: 919-
541-0237; e-mail: mckee.dave@epa.gov.

SUPPLEMENTARY INFORMATION:

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

[[Page 37819]]

you mail to EPA, mark the outside of the disk or CD ROM as CBI and then 
identify electronically within the disk or CD ROM the specific 
information that is claimed as CBI. In addition to one complete version 
of the comment that includes information claimed as CBI, a copy of the 
comment that does not contain the information claimed as CBI must be 
submitted for inclusion in the public docket. Information so marked 
will not be disclosed except in accordance with procedures set forth in 
40 CFR part 2.
    2. Tips for Preparing Your Comments. When submitting comments, 
remember to:
     Identify the rulemaking by docket number and other 
identifying information (subject heading, Federal Register date and 
page number).
     Follow directions--The Agency may ask you to respond to 
specific questions or organize comments by referencing a Code of 
Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree, suggest alternatives, 
and substitute language for your requested changes.
     Describe any assumptions and provide any technical 
information and/or data that you used.
     If you estimate potential costs or burdens, explain how 
you arrived at your estimate in sufficient detail to allow for it to be 
reproduced.
     Provide specific examples to illustrate your concerns, and 
suggest alternatives.
     Explain your views as clearly as possible, avoiding the 
use of profanity or personal threats.
     Make sure to submit your comments by the comment period 
deadline identified.

Availability of Related Information

    A number of documents relevant to this rulemaking are available on 
EPA Web sites. The Air Quality Criteria for Ozone and Related 
Photochemical Oxidants (Criteria Document) (two volumes, EPA/ and EPA/, 
date) is available on EPA's National Center for Environmental 
Assessment Web site. To obtain this document, go to http://www.epa.gov/ncea
, and click on ``Ozone.'' The Staff Paper, human exposure and 

health risk assessments, vegetation exposure and impact assessment, and 
other related technical documents are available on EPA's Office of Air 
Quality Planning and Standards (OAQPS) Technology Transfer Network 
(TTN) Web site. The Staff Paper is available at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html
, and the exposure and risk 

assessments and other related technical documents are available at 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. EPA 

will be making available corrected versions of the final Staff Paper 
and human exposure and health risk assessment technical support 
documents on these same EPA Web sites on or around July 16, 2007. These 
and other related documents are also available for inspection and 
copying in the EPA docket identified above.

Table of Contents

    The following topics are discussed in this preamble:
I. Background
    A. Legislative Requirements
    B. Related Control Requirements
    C. Review of Air Quality Criteria and Standards for 
O3
II. Rationale for Proposed Decision on the Primary Standard
    A. Health Effects Information
    1. Mechanisms
    2. Nature of Effects
    3. Interpretation and Integration of the Health Evidence
    4. O3-Related Impacts on Public Health
    B. Human Exposure and Health Risk Assessments
    1. Exposure Analyses
    2. Quantitative Health Risk Assessment
    C. Conclusions on the Adequacy of the Current Primary Standard
    1. Background
    2. Evidence- and Exposure/Risk-Based Considerations
    3. CASAC Views
    4. Administrator's Proposed Conclusions Concerning Adequacy of 
Current Standard
    D. Conclusions on the Elements of the Primary Standard
    1. Indicator
    2. Averaging Time
    3. Form
    4. Level
    E. Proposed Decision on the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
    A. Vegetation Effects Information
    1. Mechanisms Governing Plant Response to Ozone
    2. Nature of Effects
    3. Adversity of Effects
    B. Biologically Relevant Exposure Indices
    C. Vegetation Exposure and Impact Assessment
    1. Exposure Characterization
    2. Assessment of Risks to Vegetation
    D. Conclusions on the Adequacy of the Current Standard
    1. Background
    2. Evidence- and Exposure/Risk-Based Considerations
    3. CASAC Views
    4. Administrator's Proposed Conclusions Concerning Adequacy of 
Current Standard
    E. Conclusions on the Elements of the Secondary Standard
    1. Indicator
    2. Cumulative, Seasonal Standard
    3. 8-Hour Average Standard
    F. Proposed Decision on the Secondary Standard
V. Creation of Appendix P--Interpretation of the NAAQS for Ozone
    A. Data Completeness
    B. Data Handling and Rounding O3 Conventions
VI. Ambient Monitoring Related to Proposed Revised Standards
VII. Statutory and Executive Order Reviews
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 pollutants'' that ``in his 
judgment, may reasonably be anticipated to endanger public health and 
welfare'' and 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 identifiable effects on public 
health or welfare which may be expected from the presence of [a] 
pollutant in ambient air * * *.''
    Section 109 (42 U.S.C. 7409) directs the Administrator to propose 
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants 
listed under section 108. Section 109(b)(1) defines a primary standard 
as one ``the attainment and maintenance of which in the judgment of the 
Administrator, based on such criteria and allowing an adequate margin 
of safety, are requisite to protect the public health.'' \1\ A 
secondary standard, as defined in section 109(b)(2), must ``specify a 
level of air quality the attainment and maintenance of which, in the 
judgment of the Administrator, based on such criteria, is requisite to 
protect the public welfare from any known or anticipated adverse 
effects associated with the presence of [the] pollutant in the ambient 
air.'' \2\
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    \1\ The legislative history of section 109 indicates that a 
primary standard is to be set at ``the maximum permissible ambient 
air level * * * which will protect the health of any [sensitive] 
group of the population,'' and that for this purpose ``reference 
should be made to a representative sample of persons comprising the 
sensitive group rather than to a single person in such a group'' [S. 
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970)].
    \2\ Welfare effects as defined in section 302(h) (42 U.S.C. 
7602(h)) include, but are not limited to, ``effects on soils, water, 
crops, vegetation, 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 (D.C. Cir. 1981), cert. 
denied, 455 U.S. 1034 (1982). Both kinds of uncertainties are 
components of the risk associated with pollution at levels below those 
at which human health effects can be said to occur with reasonable 
scientific certainty. Thus, in selecting primary standards that include 
an adequate margin of safety, the Administrator is seeking not only to 
prevent pollution levels that have been demonstrated to be harmful but 
also to prevent lower pollutant levels that may pose an unacceptable 
risk of harm, even if the risk is not precisely identified as to nature 
or degree. The CAA does not require the Administrator to establish a 
primary NAAQS at a zero-risk level or at background concentration 
levels, see Lead Industries Association v. EPA, 647 F.2d at 1156 n. 51, 
but rather at a level that reduces risk sufficiently so as to protect 
public health with an adequate margin of safety.
    In addressing the requirement for an adequate margin of safety, EPA 
considers such factors as the nature and severity of the health effects 
involved, the size of the population(s) at risk, and the kind and 
degree of the uncertainties 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) (Breyer, J., concurring 
in part and concurring in judgment).
    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. As discussed by Justice Breyer in Whitman v. 
American Trucking Associations, however, ``this interpretation of Sec.  
109 does not require the EPA to eliminate every health risk, however 
slight, at any economic cost, however great, to the point of 
``hurtling'' industry over ``the brink of ruin,'' or even forcing 
``deindustrialization.'' Id. at 494 (Breyer J., concurring in part and 
concurring in judgment) (citations omitted). Rather, as Justice Breyer 
explained:

    The statute, by its express terms, does not compel the 
elimination of all risk; and it grants the Administrator sufficient 
flexibility to avoid setting ambient air quality standards ruinous 
to industry.
    Section 109(b)(1) directs the Administrator to set standards 
that are ``requisite to protect the public health'' with ``an 
adequate margin of safety.'' But these words do not describe a world 
that is free of all risk--an impossible and undesirable objective. 
(citation omitted). Nor are the words ``requisite'' and ``public 
health'' to be understood independent of context. We consider 
football equipment ``safe'' even if its use entails a level of risk 
that would make drinking water ``unsafe'' for consumption. And what 
counts as ``requisite'' to protecting the public health will 
similarly vary with background circumstances, such as the public's 
ordinary tolerance of the particular health risk in the particular 
context at issue. The Administrator can consider such background 
circumstances when ``deciding what risks are acceptable in the world 
in which we live.'' (citation omitted).
    The statute also permits the Administrator to take account of 
comparative health risks. That is to say, she may consider whether a 
proposed rule promotes safety overall. A rule likely to cause more 
harm to health than it prevents is not a rule that is ``requisite to 
protect the public health.'' For example, as the Court of Appeals 
held and the parties do not contest, the Administrator has the 
authority to determine to what extent possible health risks stemming 
from reductions in tropospheric ozone (which, it is claimed, helps 
prevent cataracts and skin cancer) should be taken into account in 
setting the ambient air quality standard for ozone. (citation 
omitted).
    The statute ultimately specifies that the standard set must be 
``requisite to protect the public health'' ``in the judgment of the 
Administrator,'' Sec.  109(b)(1), 84 Stat. 1680 (emphasis added), a 
phrase that grants the Administrator considerable discretionary 
standard-setting authority.
    The statute's words, then, authorize the Administrator to 
consider the severity of a pollutant's potential adverse health 
effects, the number of those likely to be affected, the distribution 
of the adverse effects, and the uncertainties surrounding each 
estimate. (citation omitted). They permit the Administrator to take 
account of comparative health consequences. They allow her to take 
account of context when determining the acceptability of small risks 
to health. And they give her considerable discretion when she does 
so.
    This discretion would seem sufficient to avoid the extreme 
results that some of the industry parties fear. After all, the EPA, 
in setting standards that ``protect the public health'' with ``an 
adequate margin of safety,'' retains discretionary authority to 
avoid regulating risks that it reasonably concludes are trivial in 
context. Nor need regulation lead to deindustrialization. 
Preindustrial society was not a very healthy society; hence a 
standard demanding the return of the Stone Age would not prove 
``requisite to protect the public health.''
    Although I rely more heavily than does the Court upon 
legislative history and alternative sources of statutory 
flexibility, I reach the same ultimate conclusion. Section 109 does 
not delegate to the EPA authority to base the national ambient air 
quality standards, in whole or in part, upon the economic costs of 
compliance.

Id. at 494-496.
    Section 109(d)(1) of the CAA requires that ``not later than 
December 31, 1980, and at 5-year intervals thereafter, the 
Administrator shall complete a thorough review of the criteria 
published under section 108 and the national ambient air quality 
standards * * * and shall make such revisions in such criteria and 
standards and promulgate such new standards as may be appropriate * * 
*.'' Section 109(d)(2) requires that an independent scientific review 
committee ``shall complete a review of the criteria * * * and the 
national primary and secondary ambient air quality standards * * * and 
shall recommend to the Administrator any new * * * standards and 
revisions of existing criteria and standards as may be appropriate * * 
*.'' This independent review function is performed by the Clean Air 
Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.

B. Related Control Requirements

    States have primary responsibility for ensuring attainment and 
maintenance of ambient air quality standards once EPA has established 
them. Under section 110 of the Act (42 U.S.C. 7410) and related 
provisions, States are to submit, for EPA approval, State 
implementation plans (SIPs) that provide for the attainment and 
maintenance of such standards through control programs directed to 
emission sources. The majority of man-made NOX and VOC 
emissions that contribute to O3 formation in the United 
States come from three types of sources: mobile sources, industrial 
processes (which include consumer and commercial products), and the 
electric

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power industry.\3\ Mobile sources and the electric power industry were 
responsible for 78 percent of annual NOX emissions in 2004. 
That same year, 99 percent of man-made VOC emissions came from 
industrial processes (including solvents) and mobile sources. Emissions 
from natural sources, such as trees, may also comprise a significant 
portion of total VOC emissions in certain regions of the country, 
especially during the O3 season, which are considered 
natural background emissions.
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    \3\ See EPA report, Evaluating Ozone Control Programs in the 
Eastern United States: Focus on the NOX Budget Trading Program, 
2004.
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    EPA has developed new emissions standards for many types of 
stationary sources and for nearly every class of mobile sources in the 
last decade to reduce O3 by decreasing emissions of 
NOX and VOC. These programs complement State and local 
efforts to improve O3 air quality and meet current national 
standards. Under the Federal Motor Vehicle Control Program (FMVCP, see 
title II of the CAA, 42 U.S.C. 7521-7574), EPA has established new 
emissions standards for nearly every type of automobile, truck, bus, 
motorcycle, earth mover, and aircraft engine, and for the fuels used to 
power these engines. EPA also established new standards for the smaller 
engines used in small watercraft, lawn and garden equipment. Recently 
EPA proposed new standards for locomotive and marine diesel engines. 
Benefits from engine standards increase modestly each year as older, 
more-polluting vehicles and engines are replaced with newer, cleaner 
models. In time, these programs will yield substantial emission 
reductions. Benefits from fuel programs generally begin as soon as a 
new fuel is available.
    The reduction of VOC emissions from industrial processes has been 
achieved either directly or indirectly through implementation of 
control technology standards, including maximum achievable control 
technology, reasonably available control technology, and best available 
control technology standards; or are anticipated due to proposed or 
upcoming proposals based on generally available control technology or 
best available controls under provisions related to consumer and 
commercial products. These standards have resulted in VOC emission 
reductions of almost a million tons per year accumulated starting in 
1997 from a variety of sources including combustion sources, coating 
categories, and chemical manufacturing. The EPA is currently working to 
finalize new federal rules, or amendments to existing rules, that will 
establish new nationwide VOC content limits for several categories of 
consumer and commercial products, including aerosol coatings, 
architectural and industrial maintenance coatings, and household and 
institutional commercial products. These rules will take effect in 
2009, and will yield significant new reductions in nationwide VOC 
emissions--about 200,000 tons per year. Additionally, in O3 
nonattainment areas, we anticipate reductions of an additional 25,000 
tons per year following completion of control technique recommendations 
for 3 additional consumer and commercial product categories. These 
emission reductions primarily result from solvent controls and 
typically occur where and when the solvent is used, such as during 
manufacturing processes.
    The power industry is one of the largest emitters of NOX 
in the United States. Power industry emission sources include large 
electric generating units and some large industrial boilers and 
turbines. The EPA's landmark Clean Air Interstate Rule (CAIR), issued 
on March 10, 2005, permanently caps power industry emissions of 
NOX in the eastern United States. The first phase of the cap 
begins in 2009, and a lower second phase cap begins in 2015. By 2015, 
EPA projects that the CAIR and other programs in the Eastern U.S. will 
reduce power industry O3 season NOX emissions in 
that region by about 50 percent and annual NOX emissions by 
about 60 percent from 2003 levels.
    With respect to agricultural sources, the U.S. Department of 
Agriculture (USDA) has approved conservation systems and activities 
that reduce agricultural emissions of NOX and VOC. Current 
practices that may reduce emissions of NOX and VOC include 
engine replacement programs, diesel retrofit programs, manipulation of 
pesticide applications including timing of applications, and animal 
feeding operations waste management techniques. The EPA recognizes that 
USDA has been working with the agricultural community to develop 
conservation systems and activities to control emissions of 
O3 precursors.
    These conservation activities are voluntarily adopted through the 
use of incentives provided to the agricultural producer. In cases where 
the States need these measures to attain the standard, the measures 
could be adopted. The EPA will continue to work with USDA on these 
activities with efforts to identify and/or improve the control 
efficiencies, prioritize the adoption of these conservation systems and 
activities, and ensure that appropriate criteria are used for 
identifying the most effective application of conservation systems and 
activities.
    The EPA will work together with USDA and with States to identify 
appropriate measures to meet the primary and secondary standards, 
including site-specific conservation systems and activities. Based on 
prior experience identifying conservation measures and practices to 
meet the PM NAAQS requirements, the EPA will use a similar process to 
identify measures that could meet the O3 requirements. The 
EPA anticipates that certain USDA-approved conservation systems and 
activities that reduce agricultural emissions of NOX and VOC 
may be able to satisfy the requirements for applicable sources to 
implement reasonably available control measures for purposes of 
attaining the primary and secondary O3 NAAQS.

C. Review of Air Quality Criteria and Standards for O3

    Tropospheric (ground-level) O3 is formed from biogenic 
and anthropogenic precursor emissions. Naturally occurring 
O3 in the troposphere can result from biogenic organic 
precursors reacting with naturally occurring nitrogen oxides 
(NOX) and by stratospheric O3 intrusion into the 
troposphere. Anthropogenic precursors of O3, specifically 
NOX and volatile organic compounds (VOC), originate from a 
wide variety of stationary and mobile sources. Ambient O3 
concentrations produced by these emissions are directly affected by 
temperature, solar radiation, wind speed and other meteorological 
factors.
    The last review of the O3 NAAQS was completed on July 
18, 1997, based on the 1996 O3 CD (U.S. EPA, 1996a) and 1996 
O3 Staff Paper (U.S. EPA, 1996b). EPA revised the primary 
and secondary O3 standards on the basis of the then latest 
scientific evidence linking exposures to ambient O3 to 
adverse health and welfare effects at levels allowed by the 1-hour 
average standards (62 FR 38856). The O3 standards were 
revised by replacing the existing primary 1-hour average standard with 
an 8-hour average O3 standard set at a level of 0.08 ppm, 
which is equivalent to 0.084 ppm using the standard rounding 
conventions. The form of the primary standard was changed to the annual 
fourth-highest daily maximum 8-hour average concentration, averaged 
over three years. The secondary O3 standard was changed by 
making it identical in all respects to the revised primary standard.
    Following promulgation of the revised O3 NAAQS, 
petitions for review were

[[Page 37822]]

filed addressing a broad range of issues. In May 1999, in response to 
those challenges, the U.S. Court of Appeals for the District of 
Columbia Circuit held that EPA's approach to establishing the level of 
the standards in 1997, both for the O3 and for the 
particulate matter (PM) NAAQS promulgated on the same day, effected 
``an unconstitutional delegation of legislative authority.'' American 
Trucking Associations v. EPA, 175 F.3d 1027 (DC Cir., 1999). Although 
the D.C. Circuit stated that ``factors EPA uses in determining the 
degree of public health concern associated with different levels of 
O3 and PM are reasonable,'' it remanded the rule to EPA, 
stating that when EPA considers these factors for potential non-
threshold pollutants ``what EPA lacks is any determinate criterion for 
drawing lines'' to determine where the standards should be set. Id. at 
1034. Consistent with EPA's long-standing interpretation and DC Circuit 
precedent, the court also reaffirmed prior rulings holding that in 
setting the NAAQS, it is ``not permitted to consider the cost of 
implementing those standards.'' Id. at 1040-41. The DC Circuit further 
directed EPA to consider on remand the potential indirect beneficial 
health effects of O3 pollution in shielding the public from 
the effects of solar ultraviolet (UV) radiation, as well as the direct 
adverse health effects of O3 pollution.
    Both sides filed cross appeals on the constitutional and cost 
issues to the United States Supreme Court, and the Court granted 
certiorari. On February 27, 2001, the U.S. Supreme Court issued a 
unanimous decision upholding the EPA's position on both the 
constitutional and the cost issues. Whitman v. American Trucking 
Associations, 531 U.S. at 464, 475-76. On the constitutional issue, the 
Court held that the statutory requirement that NAAQS be ``requisite'' 
to protect public health with an adequate margin of safety sufficiently 
guided EPA's discretion, affirming EPA's approach of setting standards 
that are neither more nor less stringent than necessary. The Supreme 
Court remanded the case to the D.C. Circuit for resolution of any 
remaining issues that had not been addressed by that Court's earlier 
decisions. Id. at 475-76. On March 26, 2002, the D.C. Circuit Court 
rejected all remaining challenges to the NAAQS, holding under 
traditional standard of review that EPA ``engaged in reasoned decision-
making'' in setting the 1997 O3 NAAQS. Whitman v. American 
Trucking Associations, 283 F.3d 355 (DC Cir. 2002).
    In response to the DC Circuit Court's remand to consider the 
potential indirect beneficial health effects of O3 in 
shielding the public from the effects of solar (UV) radiation, on 
November 14, 2001, EPA proposed to leave the 1997 8-hour NAAQS 
unchanged (66 FR 57267). After considering public comment on the 
proposed decision, EPA reaffirmed the 8-hour O3 NAAQS set in 
1997 (68 FR 614). Finally, on April 30, 2004, EPA issued an 8-hour 
implementation rule that, among other things, provided that the 1-hour 
O3 NAAQS would no longer apply to areas one year after the 
effective date of the designation of those areas for the 8-hour NAAQS 
(69 FR 23966).\4\ For most areas, the date that the 1-hour NAAQS no 
longer applied was June 15, 2005. (See 40 CFR 50.9 for details.)
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    \4\ On December 22, 2006, the D.C. Circuit vacated the April 30, 
2004 implementation rule. South Coast Air Quality Management 
District v. EPA, 472 F.3d 882. In March 2007, EPA requested the 
Court to reconsider its decision.
---------------------------------------------------------------------------

    The EPA initiated this current review in September 2000 with a call 
for information (65 FR 57810) for the development of a revised Air 
Quality Criteria Document for O3 and Other Photochemical 
Oxidants (henceforth the ``Criteria Document''). A project work plan 
(U.S. EPA, 2002) for the preparation of the Criteria Document was 
released in November 2002 for CASAC and public review. EPA held a 
series of workshops in mid-2003 on several draft chapters of the 
Criteria Document to obtain broad input from the relevant scientific 
communities. These workshops helped to inform the preparation of the 
first draft Criteria Document (EPA, 2005a), which was released for 
CASAC and public review on January 31, 2005; a CASAC meeting was held 
on May 4-5, 2005 to review the first draft Criteria Document. A second 
draft Criteria Document (EPA, 2005b) was released for CASAC and public 
review on August 31, 2005, and was discussed along with a first draft 
Staff Paper (EPA, 2005c) at a CASAC meeting held on December 6-8, 2005. 
In a February 16, 2006 letter to the Administrator, the CASAC offered 
final comments on all chapters of the Criteria Document (Henderson, 
2006a), and the final Criteria Document (EPA, 2006a) was released on 
March 21, 2006. In a June 8, 2006 letter (Henderson, 2006b) to the 
Administrator, the CASAC offered additional advice to the Agency 
concerning chapter 8 of the final Criteria Document (Integrative 
Synthesis) to help inform the second draft Staff Paper.
    A second draft Staff Paper (EPA, 2006b) was released on July 17, 
2006 and reviewed by CASAC on August 24 and 25, 2006. In an October 24, 
2006 letter to the Administrator, CASAC provided advice and 
recommendations to the Agency concerning the second draft Staff Paper 
(Henderson, 2006c). A final Staff Paper (EPA, 2007) was released on 
January 31, 2007. Around the time of the release of the final Staff 
Paper in January 2007, EPA discovered a small error in the exposure 
model that when corrected resulted in slight increases in the human 
exposure estimates. Since the exposure estimates are an input to the 
lung function portion of the health risk assessment, this correction 
also resulted in slight increases in the lung function risk estimates 
as well. The exposure and risk estimates discussed in this notice 
reflect the corrected estimates, and thus are slightly different than 
the exposure and risk estimates cited in the January 31, 2007 Staff 
Paper.\5\ In a March 26, 2007 letter (Henderson, 2007), CASAC offered 
additional advice to the Administrator with regard to recommendations 
and revisions to the primary and secondary O3 NAAQS.
---------------------------------------------------------------------------

    \5\ EPA plans to make available corrected versions of the final 
Staff Paper and the human exposure and health risk assessment 
technical support documents on or around July 16, 2007 on the EPA 
web site listed in the Availability of Related Information section 
of this notice.
---------------------------------------------------------------------------

    The schedule for completion of this review is governed by a consent 
decree resolving a lawsuit filed in March 2003 by a group of plaintiffs 
representing national environmental and public health organizations, 
alleging that EPA had failed to complete the current review within the 
period provided by statute.\6\ The modified consent decree that governs 
this review, entered by the court on December 16, 2004, provides that 
EPA sign for publication notices of proposed and final rulemaking 
concerning its review of the O3 NAAQS no later than March 
28, 2007 and December 19, 2007, respectively. This consent decree was 
further modified in October 2006 to change these proposed and final 
rulemaking dates to no later than May 30, 2007 and February 20, 2008, 
respectively. These dates for signing the publication notices of 
proposed and final rulemaking were further extended to no later than 
June 20, 2007 and March 12, 2008, respectively.
---------------------------------------------------------------------------

    \6\ American Lung Association v. Whitman (No. 1:03CV00778, 
D.D.C. 2003).
---------------------------------------------------------------------------

    This action presents the Administrator's proposed decisions on the 
review of the current primary and secondary O3 standards. 
Throughout this preamble a number of conclusions, findings, and 
determinations proposed by the Administrator are noted. While

[[Page 37823]]

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/or technical comments on all issues involved with this 
proposal, including all such proposed judgments, conclusions, findings, 
and determinations.

II. Rationale for Proposed Decision on the Primary Standard

    This section presents the rationale for the Administrator's 
proposed decision to revise the existing 8-hour O3 primary 
standard by lowering the level of the standard to within a range from 
0.070 to 0.075 ppm, and to specify the standard to the nearest 
thousandth ppm (i.e., to the nearest parts per billion). As discussed 
more fully below, this rationale is based on a thorough review, in the 
Criteria Document, of the latest scientific information on human health 
effects associated with the presence of O3 in the ambient 
air. This rationale also takes into account and is consistent with: (1) 
Staff assessments of the most policy-relevant information in the 
Criteria Document and staff analyses of air quality, human exposure, 
and health risks, presented in the Staff Paper, upon which staff 
recommendations for revisions to the primary O3 standard are 
based; (2) CASAC advice and recommendations, as reflected in 
discussions of drafts of the Criteria Document and Staff Paper 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.
    In developing this rationale, EPA has drawn upon an integrative 
synthesis of the entire body of evidence, published through early 2006, 
on human health effects associated with the presence of O3 
in the ambient air. As discussed below in section II.A, this body of 
evidence addresses a broad range of health endpoints associated with 
exposure to ambient levels of O3 (EPA, 2006a, chapter 8), 
and includes over one hundred epidemiologic studies conducted in the 
U.S., Canada, and many countries around the world.\7\ In considering 
this evidence, EPA focuses on those health endpoints that have been 
demonstrated to be caused by exposure to O3, or for which 
the Criteria Document judges associations with O3 to be 
causal, likely causal, or for which the evidence is highly suggestive 
that O3 contributes to the reported effects. This rationale 
also draws upon the results of quantitative exposure and risk 
assessments, discussed below in section II.B. Evidence- and exposure/
risk-based considerations that form the basis for the Administrator's 
proposed decisions on the adequacy of the current standard and on the 
elements of the range of proposed alternative standards are discussed 
below in sections II.C and II.D, respectively.
---------------------------------------------------------------------------

    \7\ In its assessment of the epidemiological evidence judged to 
be most relevant to making decisions on the level of the 
O3 primary standard, EPA has placed greater weight on 
U.S. and Canadian epidemiologic studies, since studies conducted in 
other countries may well reflect different demographic and air 
pollution characteristics.
---------------------------------------------------------------------------

    Judgments made in the Criteria Document and Staff Paper about the 
extent to which relationships between various health endpoints and 
short-term exposures to ambient O3 are likely causal have 
been informed by several factors. As discussed below in section II.A, 
these factors include the nature of the evidence (i.e., controlled 
human exposure, epidemiological, and/or toxicological studies) and the 
weight of evidence, which takes into account such considerations as 
biological plausibility, coherence of evidence, strength of 
association, and consistency of evidence.
    In assessing the health effects data base for O3, it is 
clear that human studies provide the most directly applicable 
information for determining causality because they are not limited by 
the uncertainties of dosimetry differences and species sensitivity 
differences, which would need to be addressed in extrapolating animal 
toxicology data to human health effects. Controlled human exposure 
studies provide data with the highest level of confidence since they 
provide human effects data under closely monitored conditions and can 
provide exposure-response relationships. Epidemiological data provide 
evidence of associations between ambient O3 levels and more 
serious acute and chronic health effects (e.g., hospital admissions and 
mortality) that cannot be assessed in controlled human exposure 
studies. For these studies the degree of uncertainty introduced by 
confounding variables (e.g., other pollutants, temperature) and other 
factors affects the level of confidence that the health effects being 
investigated are attributable to O3 exposures, alone and in 
combination with other copollutants.
    In using a weight of evidence approach to inform judgments about 
the degree of confidence that various health effects are likely to be 
caused by exposure to O3, confidence increases as the number 
of studies consistently reporting a particular health endpoint grows 
and as other factors, such as biological plausibility and strength, 
consistency, and coherence of evidence, increase. Conclusions regarding 
biological plausibility, consistency, and coherence of evidence of 
O3-related health effects are drawn from the integration of 
epidemiological studies with mechanistic information from controlled 
human exposure studies and animal toxicological studies. As discussed 
below, this type of mechanistic linkage has been firmly established for 
several respiratory endpoints (e.g., lung function decrements, lung 
inflammation) but remains far more equivocal for cardiovascular 
endpoints (e.g., cardiovascular-related hospital admissions). For 
epidemiological studies, strength of association refers to the 
magnitude of the association and its statistical strength, which 
includes assessment of both effects estimate size and precision. In 
general, when associations yield large relative risk estimates, it is 
less likely that the association could be completely accounted for by a 
potential confounder or some other bias. Consistency refers to the 
persistent finding of an association between exposure and outcome in 
multiple studies of adequate power in different persons, places, 
circumstances and times. For example, the magnitude of effect estimates 
is relatively consistent across recent studies showing association 
between short-term, but not long-term, O3 exposure and 
mortality.
    Based on the information discussed below in sections II.A.1-II.A.3, 
judgments concerning the extent to which relationships between various 
health endpoints and ambient O3 exposures are likely causal 
are summarized below in section II.A.3.c. These judgments reflect the 
nature of the evidence and the overall weight of the evidence, and are 
taken into consideration in the quantitative exposure and risk 
assessments, discussed below in Section II.B.
    To put judgments about health effects that have been demonstrated 
to be caused by exposure to O3, or for which the Criteria 
Document judges associations with O3 to be causal, likely 
causal, or for which the evidence is highly suggestive that 
O3 contributes to the reported effects into a broader public 
health context, EPA has drawn upon the results of the quantitative 
exposure and risk assessments. These assessments provide estimates of 
the likelihood that individuals in particular population groups that 
are at risk for various O3-related physiological health 
effects would experience ``exposures of concern'' and specific health 
endpoints

[[Page 37824]]

under varying air quality scenarios (e.g., just meeting the current or 
alternative standards), as well as characterizations of the kind and 
degree of uncertainties inherent in such estimates.
    In this review, the term ``exposures of concern'' is defined as 
personal exposures while at moderate or greater exertion to 8-hour 
average ambient O3 levels at and above specific benchmark 
levels which represent exposure levels at which O3-related 
health effects are known or can reasonably be inferred to occur in some 
individuals, as discussed below in section II.B.1.\8\ EPA emphasizes 
that although the analysis of ``exposures of concern'' was conducted 
using three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060 
ppm), the concept is more appropriately viewed as a continuum with 
greater confidence and less uncertainty about the existence of health 
effects at the upper end and less confidence and greater uncertainty as 
one considers increasingly lower O3 exposure levels. EPA 
recognizes that there is no sharp breakpoint within the continuum 
ranging from at and above 0.080 ppm down to 0.060 ppm. In considering 
the concept of exposures of concern, it is important to balance 
concerns about the potential for health effects and their severity with 
the increasing uncertainty associated with our understanding of the 
likelihood of such effects at lower O3 levels.
---------------------------------------------------------------------------

    \8\ Exposures of concern were also considered in the last review 
of the O3 NAAQS, and were judged by EPA to be an 
important indicator of the public health impacts of those 
O3-related effects for which information was too limited 
to develop quantitative estimates of risk but which had been 
observed in humans at and above the benchmark level of 0.08 ppm for 
6-to 8-hour exposures * * * including increased nonspecific 
bronchial responsiveness (for example, aggravation of asthma), 
decreased pulmonary defense mechanisms (suggestive of increased 
susceptibility to respiratory infection), and indicators of 
pulmonary inflammation (related to potential aggravation of chronic 
bronchitis or long-term damage to the lungs). (62 FR 38868)
---------------------------------------------------------------------------

    Within the context of this continuum, estimates of exposures of 
concern at discrete benchmark levels provide some perspective on the 
public health impacts of O3-related health effects that have 
been demonstrated in human clinical and toxicological studies but 
cannot be evaluated in quantitative risk assessments, such as lung 
inflammation, increased airway responsiveness, and changes in host 
defenses. They also help in understanding the extent to which such 
impacts have the potential to be reduced by meeting the current and 
alternative standards. These O3-related physiological 
effects are plausibly linked to the increased morbidity seen in 
epidemiological studies (e.g., as indicated by increased medication use 
in asthmatics, school absences in all children, and emergency 
department visits and hospital admissions in people with lung disease). 
Estimates of the number of people likely to experience exposures of 
concern cannot be directly translated into quantitative estimates of 
the number of people likely to experience specific health effects, 
since sufficient information to draw such comparisons is not 
available--if such information were available, these health outcomes 
would have been included in the quantitative risk assessment. Due to 
individual variability in responsiveness, only a subset of individuals 
who have exposures at and above a specific benchmark level can be 
expected to experience such adverse health effects, and susceptible 
subpopulations such as those with asthma are expected to be affected 
more by such exposures than healthy individuals. The amount of weight 
to place on the estimates of exposures of concern at any of these 
benchmark levels depends in part on the weight of the scientific 
evidence concerning health effects associated with O3 
exposures at and above that benchmark level. It also depends on 
judgments about the importance from a public health perspective of the 
health effects that are known or can reasonably be inferred to occur as 
a result of exposures at and above the benchmark level. Such public 
health policy judgments are embodied in the NAAQS standard setting 
criteria (i.e., standards that, in the judgment of the Administrator, 
are requisite to protect public health with an adequate margin of 
safety).
    As discussed below in section II.B.2, the quantitative health risk 
assessment conducted as part of this review includes estimates of risks 
of lung function decrements in asthmatic and all school age children, 
respiratory symptoms in asthmatic children, respiratory-related 
hospital admissions, and non-accidental and cardiorespiratory-related 
mortality associated with recent ambient O3 levels, as well 
as risk reductions and remaining risks associated with just meeting the 
current and various alternative O3 standards in a number of 
example urban areas. There were two parts to this risk assessment: one 
part was based on combining information from controlled human exposure 
studies with modeled population exposure, and the other part was based 
on combining information from community epidemiological studies with 
either monitored or adjusted ambient concentrations levels. This 
assessment not only provided estimates of the potential magnitude of 
O3-related health effects, as well as a characterization of 
the uncertainties and variability inherent in such estimates. This 
assessment also provided insights into the distribution of risks and 
patterns of risk reductions associated with meeting alternative 
O3 standards.
    As discussed below, a substantial amount of new research has been 
conducted since the last review of the O3 NAAQS, with 
important new information coming from epidemiologic studies as well as 
from controlled human exposure, toxicological, and dosimetric studies. 
The newly available research studies evaluated in the Criteria Document 
and the exposure and risk assessments presented in the Staff Paper have 
undergone intensive scrutiny through multiple layers of peer review and 
many opportunities for public review and comment. While important 
uncertainties remain in the qualitative and quantitative 
characterizations of health effects attributable to exposure to ambient 
O3, the review of this information has been extensive and 
deliberate. In the judgment of the Administrator, this intensive 
evaluation of the scientific evidence has provided an adequate basis 
for regulatory decision making. This review also provides important 
input to EPA's research plan for improving our future understanding of 
the effects of ambient O3 at lower levels, especially in at-
risk population groups.

A. Health Effects Information

    This section outlines key information contained in the Criteria 
Document (chapters 4-8) and in the Staff Paper (chapter 3) on known or 
potential effects on public health which may be expected from the 
presence of O3 in ambient air. The information highlighted 
here summarizes: (1) New information available on potential mechanisms 
for health effects associated with exposure to O3; (2) the 
nature of effects that have been associated directly with exposure to 
O3 and indirectly with the presence of O3 in 
ambient air; (3) an integrative interpretation of the evidence, 
focusing on the biological plausibility and coherence of the evidence; 
and (4) considerations in characterizing the public health impact of 
O3, including the identification of ``at risk'' 
subpopulations.
    The decision in the last review focused primarily on evidence from 
short-term (e.g., 1 to 3 hours) and prolonged ( 6 to 8 hours) 
controlled-exposure studies reporting lung function decrements, 
respiratory symptoms, and respiratory inflammation in humans, as well 
as epidemiology studies reporting excess

[[Page 37825]]

hospital admissions and emergency department (ED) visits for 
respiratory causes. The Criteria Document prepared for this review 
emphasizes a large number of epidemiological studies published since 
the last review with these and additional health endpoints, including 
the effects of acute (short-term and prolonged) and chronic exposures 
to O3 on lung function decrements and enhanced respiratory 
symptoms in asthmatic individuals, school absences, and premature 
mortality. It also emphasizes important new information from 
toxicology, dosimetry, and controlled human exposure studies. 
Highlights of the evidence include:
    (1) Two new controlled human-exposure studies are now available 
that examine respiratory effects associated with prolonged 
O3 exposures at levels below 0.080 ppm, which was the lowest 
exposure level that had been examined in the last review.
    (2) Numerous controlled human-exposure studies have examined 
indicators of O3-induced inflammatory response in both the 
upper respiratory tract (URT) and lower respiratory tract (LRT), while 
other studies have examined changes in host defense capability 
following O3 exposure of healthy young adults and increased 
airway responsiveness to allergens in subjects with allergic asthma and 
allergic rhinitis exposed to O3.
    (3) Animal toxicology studies provide new information regarding 
mechanisms of action, increased susceptibility to respiratory 
infection, and the biological plausibility of acute effects and 
chronic, irreversible respiratory damage.
    (4) Numerous acute exposure epidemiological studies published 
during the past decade offer added evidence of ambient O3-
related lung function decrements and respiratory symptoms in physically 
active healthy subjects and asthmatic subjects, as well as evidence on 
new health endpoints, such as the relationships between ambient 
O3 concentrations and school absenteeism and between ambient 
O3 and cardiac-related physiological endpoints.
    (5) Several additional studies have been published over the last 
decade examining the temporal associations between O3 
exposures and emergency department visits for respiratory diseases and 
on respiratory-related hospital admissions.
    (6) A large number of newly available epidemiological studies have 
examined the effects of acute exposure to PM and O3 on 
mortality, notably including large multicity studies that provide much 
more robust and credible information than was available in the last 
review, as well as recent meta-analyses that have evaluated potential 
sources of heterogeneity in O3-mortality associations.
1. Overview of Mechanisms
    Evidence on possible mechanisms by which exposure to O3 
may result in acute and chronic health effects is discussed in chapters 
5 and 6 of the Criteria Document.\9\ Evidence from dosimetry, 
toxicology, and human exposure studies has contributed to an 
understanding of the mechanisms that help to explain the biological 
plausibility and coherence of evidence for O3-induced 
respiratory health effects reported in epidemiological studies. More 
detailed information about the physiological mechanisms related to the 
respiratory effects of short- and long-term exposure to O3 
can be found in section II.A.3.b.i and II.A.3.b.iii, respectively. In 
the past, however, little information was available to help explain 
potential biological mechanisms which linked O3 exposure to 
premature mortality or cardiovascular effects. As discussed more fully 
in section II.A.3.b.ii below, since the last review an emerging body of 
animal toxicology and human clinical evidence is beginning to suggest 
mechanisms that may mediate acute O3 cardiovascular effects. 
While much is known about mechanisms that play a role in O3-
related respiratory effects, additional research is needed to more 
clearly understand the role that O3 may have in contributing 
to cardiovascular effects.
---------------------------------------------------------------------------

    \9\ While most of the available evidence addresses mechanisms 
for O3, O3 clearly serves as an indicator for 
the total photochemical oxidant mixture found in the ambient air. 
Some effects may be caused by one or more components in the overall 
pollutant mix, either separately or in combination with 
O3.
---------------------------------------------------------------------------

    With regard to the mechanisms related to short-term respiratory 
effects, scientific evidence discussed in the Criteria Document 
(section 5.2) indicates that reactions of O3 with lipids and 
antioxidants in the epithelial lining fluid and the epithelial cell 
membranes of the lung can be the initial step in mediating deleterious 
health effects of O3. This initial step activates a cascade 
of events that lead to oxidative stress, injury, inflammation, airway 
epithelial damage and increased alveolar permeability to vascular 
fluids. Inflammation can be accompanied by increased airway 
responsiveness, which is an increased bronchoconstrictive response to 
airway irritants and allergens. Continued respiratory inflammation also 
can alter the ability to respond to infectious agents, allergens and 
toxins. Acute inflammatory responses to O3 in some healthy 
people are well documented, and precursors to lung injury can become 
apparent within 3 hours after exposure in humans. Repeated respiratory 
inflammation can lead to a chronic inflammatory state with altered lung 
structure and lung function and may lead to chronic respiratory 
diseases such as fibrosis and emphysema (EPA, 2006a, section 8.6.2). 
The severity of symptoms and magnitude of response to acute exposures 
depend on inhaled dose, as well as individual susceptibility to 
O3, as discussed below. At the same O3 dose, 
individuals who are more susceptible to O3 will have a 
larger response than those who are less susceptible; among individuals 
with similar susceptibility, those who receive a larger dose will have 
a larger response to O3.
    The inhaled dose is the product of O3 concentration (C), 
minute ventilation or ventilation rate, and duration of exposure (T), 
or (C x ventilation rate x T). A large body of data regarding the 
interdependent effect of these components of inhaled dose on pulmonary 
responses was assessed in the 1986 and 1996 O3 Criteria 
Documents. In an attempt to describe O3 dose-response 
characteristics, acute responses were modeled as a function of total 
inhaled O3 dose which was generally found to be a better 
predictor of response than O3 concentration, ventilation 
rate, or duration of exposure, alone, or as a combination of any two of 
these factors (EPA 2006a, section 6.2). Predicted O3-induced 
decrements in lung function have been shown to be a function of 
exposure concentration, duration and exercise level for healthy, young 
adults (McDonnell et al., 1997). A meta-analysis of 21 studies (Mudway 
and Kelly, 2004) showed that markers of inflammation and increased 
cellular permeability in healthy subjects are associated with total 
O3 dose.
    The Criteria Document summarizes information on potentially 
susceptible and vulnerable groups in section 8.7. As described there, 
the term susceptibility refers to innate (e.g., genetic or 
developmental) or acquired (e.g., personal risk factors, age) factors 
that make individuals more likely to experience effects with exposure 
to pollutants. A number of population groups have been identified as 
potentially susceptible to health effects as a result of O3 
exposure, including people with existing lung diseases, including 
asthma, children and older adults, and people who have larger than 
normal lung function responses that may be due to genetic 
susceptibility. In addition, some population groups have been 
identified as having increased

[[Page 37826]]

vulnerability to O3-related effects due to increased 
likelihood of exposure while at elevated ventilation rates, including 
healthy children and adults who are active outdoors, for example, 
outdoor workers, and joggers. Taken together, the susceptible and 
vulnerable groups are more commonly referred to as ``at-risk'' groups 
\10\, as discussed more fully below in section II.A.4.b.
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    \10\ In previous Staff Papers and Federal Register notices 
announcing proposed and final decisions on the O3 and 
other NAAQS, EPA has used the phrase ``sensitive population groups'' 
to include both population groups that are at increased risk because 
they are more susceptible and population groups that are at 
increased risk due to increased vulnerability or exposure. In this 
notice, we use the phrase, ``at risk'' populations to include both 
types of population groups.
---------------------------------------------------------------------------

    Based on new evidence from animal, human clinical and 
epidemiological studies the Criteria Document concludes that people 
with preexisting pulmonary disease are likely to be among those at 
increased risk from O3 exposure. Altered physiological, 
morphological and biochemical states typical of respiratory diseases 
like asthma, COPD and chronic bronchitis may render people sensitive to 
additional oxidative burden induced by O3 exposure (EPA 
2006a, section 8.7). Children and adults with asthma are the group that 
has been studied most extensively. Evidence from controlled human 
exposure studies indicates that asthmatics may exhibit larger lung 
function decrements in response to O3 exposure than healthy 
controls. As discussed more fully in section II.A.4.b.ii below, 
asthmatics present a differential response profile for cellular, 
molecular, and biochemical parameters (CD, Figure 8-1) that are altered 
in response to acute O3 exposure. They can have larger 
inflammatory responses, as manifested by larger increases in markers of 
inflammation such as white bloods cells (e.g., PMNs) or inflammatory 
cytokines. Asthmatics, and people with allergic rhinitis, are more 
likely to mount an allergic-type response upon exposure to 
O3, as manifested by increases in white blood cells 
associated with allergy (i.e., eosinophils) and related molecules, 
which increase inflammation in the airways. The increased inflammatory 
and allergic responses also may be associated with the larger late-
phase responses that asthmatics can experience, which can include 
increased bronchoconstrictor responses to irritant substances or 
allergens and additional inflammation. These more serious responses in 
asthmatics and others with lung disease provide biological plausibility 
for the respiratory morbidity effects observed in epidemiological 
studies.
    Children with and without asthma were found to be particularly 
susceptible to O3 effects on lung function and generally 
have greater lung function responses than older people. The American 
Academy of Pediatrics (2004) notes that children and infants are among 
the population groups most susceptible to many air pollutants, 
including O3. This is in part because their lungs are still 
developing. For example, eighty percent of alveoli are formed after 
birth, and changes in lung development continue through adolescence 
(Dietert et al., 2000). Moreover, children have high minute ventilation 
rates and relatively high levels of physical activity which also 
increases their O3 dose (Plunkett et al., 1992). Thus, 
children are at risk due to both their susceptibility and 
vulnerability.
    Looking more broadly at age-related differences in susceptibility, 
several mortality studies have investigated age-related differences in 
O3 effects (EPA, 2006a, section 7.6.7.2), primarily in the 
older adult population. Among the studies that observed positive 
associations between O3 and mortality, a comparison of all 
age or younger age (65 years of age) O3-mortality effect 
estimates to that of the elderly population (>65 years) indicates that, 
in general, the elderly population is more susceptible to O3 
mortality effects. There is supporting evidence of age-related 
differences in susceptibility to O3 lung function effects. 
The Criteria Document concludes that the elderly population (>65 years 
of age) appears to be at greater risk of O3-related 
mortality and hospitalizations compared to all ages or younger 
populations, and children (< 18 years of age) experience other 
potentially adverse respiratory health outcomes with increased 
O3 exposure (EPA, 2006a, section 7.6.7.2).
    Controlled human exposure studies have also indicated a high degree 
of interindividual variability in some of the pulmonary physiological 
parameters, such as lung function decrements. The variable effects in 
individuals have been found to be reproducible, in other words, a 
person who has a large lung function response after exposure to 
O3 will likely have about the same response if exposed again 
to the same dose of O3 (EPA 2006a, p. 6-2). In human 
clinical studies, group mean responses are not representative of this 
segment of the population that has much larger than average responses 
to O3. Recent studies, discussed in section II.A.4.iv below, 
reported a role for genetic polymorphism (i.e., the occurrence together 
in the same population of more than one allele or genetic marker at the 
same locus with the least frequent allele or marker occurring more 
frequently than can be accounted for by mutation alone) in observed 
differences in antioxidant enzymes and genes involved in inflammation 
to modulate pulmonary function and inflammatory responses to 
O3 exposure. These observations suggest a potential role for 
these markers in the innate susceptibility to O3, however, 
the validity of these markers and their relevance in the context of 
prediction to population studies needs additional experimentation.
    Clinical studies that provide information about mechanisms of the 
initial response to O3 (e.g., lung function decrements, 
inflammation, and injury to the lung) also inform the selection of 
appropriate lag times to analyze in epidemiological studies through 
elucidation of the time course of these responses (EPA 2006a, section 
8.4.3). Based on the results of these studies, it would be reasonable 
to expect that lung function decrements could be detected 
epidemiologically within lags of 0 (same day) or 1 to 2 days following 
O3 exposure, given the rapid onset of lung function changes 
and their persistence for 24 to 48 hours among more responsive human 
subjects in clinical studies. Other responses take longer to develop 
and can persist for longer periods of time. For example, although 
asthmatic individuals may begin to experience symptoms soon after 
O3 exposure, it may take anywhere from 1 to 3 days after 
exposure for these subjects to seek medical attention as a result of 
increased airway responsiveness or inflammation that may persist for 2 
to 3 days. This may be reflected by epidemiologic observations of 
significantly increased risk for asthma-related emergency department 
visits or hospital admissions with 1- to 3-day lags, or, perhaps, 
enhanced distributed lag risks (combined across 3 days) for such 
morbidity indicators. Analogously, one might project increased 
mortality within 0 to 3 day lags as a possible consequence of 
O3-induced increases in clotting agents arising from the 
cascade of events, starting with cell injury described above, occurring 
within 12 to 24 hours of O3 exposure. The time course for 
many of these initial responses to O3 is highly variable. 
Moreover these observations pertain only to the initial response to 
O3. Consequent responses can follow. For example, 
J[ouml]rres et al., (1996) found that in subjects with

[[Page 37827]]

asthma and allergic rhinitis, a maximum percent fall in FEV1 
of 27.9% and 7.8%, respectively, occurred 3 days after O3 
exposure when they were challenged with the highest common dose of 
allergen.
2. Nature of Effects
    The Criteria Document provides new evidence that notably enhances 
our understanding of short-term and prolonged exposure effects, 
including effects on lung function, symptoms, and inflammatory effects 
reported in controlled exposure studies. These studies support and 
extend the findings of the previous Criteria Document. There is also a 
significant body of new epidemiological evidence of associations 
between short-term and prolonged exposure to O3 and effects 
such as premature mortality, hospital admissions and emergency 
department visits for respiratory (e.g., asthma) causes. Key 
epidemiological and controlled human exposure studies are summarized 
below and discussed in chapter 3 of the Staff Paper, which is based on 
scientific evidence critically reviewed in chapters 5, 6, and 7 of the 
Criteria Document, as well as the Criteria Document's integration of 
scientific evidence contained in chapter 8.\11\ Conclusions drawn about 
O3-related health effects are based upon the full body of 
evidence from controlled human exposure, epidemiological and 
toxicological data contained in the Criteria Document.
---------------------------------------------------------------------------

    \11\ Health effects discussions are also drawn from the more 
detailed information and tables presented in the Criteria Document's 
annexes.
---------------------------------------------------------------------------

a. Morbidity
    This section summarizes scientific information on the effects of 
inhalation of O3, including public health effects of short-
term, prolonged, and long-term exposures on respiratory morbidity and 
cardiovascular system effects, as discussed in chapters 6, 7 and 8 of 
the Criteria Document and chapter 3 of the Staff Paper. This section 
also summarizes the uncertainty about the potential indirect effects on 
public health associated with changes due to increases in UV-B 
radiation exposure, such as UV-B radiation-related skin cancers, that 
may be associated with reductions in ambient levels of ground-level 
O3, as discussed in chapter 10 of the Criteria Document and 
chapter 3 of the Staff Paper.
i. Effects on the Respiratory System From Short-Term and Prolonged 
O3 Exposures
    Controlled human exposure studies have shown that O3 
induces a variety of health effects, including: lung function 
decrements, respiratory symptoms, increased airway responsiveness, 
respiratory inflammation and permeability, increased susceptibility to 
respiratory infection, and acute morphological effects. Epidemiology 
studies have reported associations between O3 exposures 
(i.e., 1-hour, 8-hour and 24-hour) and a wide range of respiratory-
related health effects including: Pulmonary function decrements; 
respiratory symptoms; increased asthma medication use; increased school 
absences; increased emergency department visits and hospital 
admissions.
(a) Pulmonary Function Decrements, Respiratory Symptoms, and Asthma 
Medication Use
(i) Results From Controlled Human Exposure Studies
    A large number of studies published prior to 1996 that investigated 
short-term O3 exposure health effects on the respiratory 
system from short-term O3 exposures were reviewed in the 
1986 and 1996 Criteria Documents (EPA, 1986, 1996). In the last review, 
0.50 ppm was the lowest O3 concentration at which 
statistically significant reductions in forced vital capacity (FVC) and 
forced expiratory volume in 1 second (FEV1) were reported in 
sedentary subjects. During exercise, spirometric (lung function) and 
symptomatic responses were observed at much lower O3 
exposures. When minute ventilation was considerably increased by 
continuous exercise (CE) during O3 exposures lasting 2 hour 
or less at >= 0.12 ppm, healthy subjects generally experienced 
decreases in FEV1, FVC, and other measures of lung function; 
increases in specific airway resistance (sRaw), breathing frequency, 
and airway responsiveness; and symptoms such as cough, pain on deep 
inspiration, shortness of breath, throat irritation, and wheezing. When 
exposures were increased to 4 to 8 hours in duration, statistically 
significant lung function and symptom responses were reported at 
O3 concentrations as low as 0.08 ppm and at lower minute 
ventilation (i.e., moderate rather than high level exercise) than the 
shorter duration studies.
    The most important observations drawn from studies reviewed in the 
1996 Criteria Document were that: (1) Young healthy adults exposed to 
O3 concentrations >= 0.080 ppm develop significant, 
reversible, transient decrements in pulmonary function if minute 
ventilation or duration of exposure is increased sufficiently; (2) 
children experience similar lung function responses but report lesser 
symptoms from O3 exposure relative to young adults; (3) 
O3-induced lung function responses are decreased in the 
elderly relative to young adults; (4) there is a large degree of 
intersubject variability in physiological and symptomatic responses to 
O3, but responses tend to be reproducible within a given 
individual over a period of several months; (5) subjects exposed 
repeatedly to O3 for several days show an attenuation of 
response upon successive exposures, but this attenuation is lost after 
about a week without exposure; and (6) acute O3 exposure 
initiates an inflammatory response which may persist for at least 18 to 
24 hours post exposure.
    The development of these respiratory effects is time-dependent 
during both exposure and recovery periods, with great overlap for 
development and disappearance of the effects. In healthy human subjects 
exposed to typical ambient O3 levels near 0.120 ppm, lung 
function responses largely resolve within 4 to 6 hours post-exposure, 
but cellular effects persist for about 24 hours. In these healthy 
subjects, small residual lung function effects are almost completely 
gone within 24 hours, while in hyperresponsive subjects, recovery can 
take as much as 48 hours to return to baseline. The majority of these 
responses are attenuated after repeated consecutive exposures, but such 
attenuation to O3 is lost one week post-exposure.
    Since 1996, there have been a number of studies published 
investigating lung function and symptomatic responses that generally 
support the observations previously drawn. Recent studies for acute 
exposures of 1 to 2 hours and 6 to 8 hours in duration are compiled in 
the Staff Paper (Appendix 3C). As summarized in more detail in the 
Staff Paper (section 3.3.1.1), among the more important of the recent 
studies that examined changes in FEV1 in large numbers of 
subjects over a range of 1-2 hours at exposure levels of 0.080 to 0.40 
ppm were studies by McDonnell et al. (1997) and Ultman et al. (2004). 
These studies observed considerable intersubject variability in 
FEV1 decrements, which was consistent with findings in the 
1996 Criteria Document.
    For prolonged exposures (4 to 8 hours) in the range of 0.080 to 
0.160 ppm O3 using moderate intermittent exercise and 
typically using square-

[[Page 37828]]

wave exposure patterns (i.e., a constant exposure level during time of 
exposure), several pre- and post-1996 studies (Folinsbee et al., 1988, 
1994; Horstman et al., 1990; Adams, 2002, 2003a, 2006) have reported 
statistically significant lung function responses and increased 
symptoms in healthy adults with increasing duration of exposure, 
O3 concentration, and minute ventilation. Studies that 
employed triangular exposure patterns (i.e., integrated exposures that 
begin at a low level, rise to a peak, and return to a low level during 
the exposure) (Hazucha et al., 1992; Adams 2003a, 2006) suggest that 
the triangular exposure pattern can potentially lead to greater 
FEV1 decrements and respiratory symptoms than square-wave 
exposures (when the overall O3 doses are equal). These 
results suggest that peak exposures, reflective of the pattern of 
ambient O3 concentrations in some locations, are important 
in terms of O3 toxicology.
    McDonnell (1996) used data from a series of studies to investigate 
the frequency distributions of FEV1 decrements following 6.6 
hour exposures and found statistically significant but relatively small 
group mean decreases in average FEV1 responses (between 5 
and 10 percent) at 0.080 ppm O3.\12\ Notably, about 26 
percent of the 60 exposed subjects had lung function decrements >10 
percent, including about 8 percent of the subjects that experienced 
large decrements (>20 percent) (EPA, 2007, Figure 3-1A). These results 
(which were not corrected for exercise in filtered air responses) 
demonstrate that while average responses may be relatively small at the 
0.080 ppm exposure level, some individuals experience more severe 
effects that may be clinically significant. Similar results at the 
0.080 ppm exposure level (for 6.6 hours during intermittent exercise) 
were seen in more recent studies of 30 healthy young adults by Adams 
(2002, 2006).\13\ In these studies, relatively small but statistically 
significant lung function decrements and respiratory symptom responses 
were found (for both square-wave and triangular exposure patterns), 
with 17 percent of the subjects (5 of 30) experiencing >= 10 percent 
FEV1 decrements (comparing pre- and post-exposures) when the 
results were not corrected for the effects of exercise alone in 
filtered air (EPA, 2007, Figure 3-1B) and with 23 percent of subjects 
(7 of 30) experiencing such effects when the results were corrected 
(EPA, 2007, p. 3-6).\14\
---------------------------------------------------------------------------

    \12\ This study and other studies (Folinsbee et al., 1988; 
Horstman et al., 1990; and McDonnell et al., 1991), conducted in 
EPA's clinical research facility in Chapel Hill, NC, measured ozone 
concentrations to within +/-5 percent or +/-0.004 ppm at the 0.080 
ppm exposure level.
    \13\ These studies, conducted at a facility at the University of 
California, in Davis, CA, reported O3 concentrations to 
be accurate within +/-0.003 ppm over the range of concentrations 
included in these studies.
    \14\ These distributional results presented in the Criteria 
Document and Staff Paper for the Adams studies are based on study 
data that were not included in the publication but were obtained 
from the author.
---------------------------------------------------------------------------

    These studies by Adams (2002, 2006) are notable in that they are 
the only available controlled exposure human studies that examine 
respiratory effects associated with prolonged O3 exposures 
at levels below 0.080 ppm, which was the lowest exposure level that had 
been examined in the last review. The Adams (2006) study investigated a 
range of exposure levels (0.000, 0.040, 0.060, and 0.080 ppm 
O3) using square-wave and triangular exposure patterns. The 
study was designed to examine multiple comparisons of pulmonary 
function (FEV1) and respiratory symptom responses (total 
subjective symptoms (TSS) and pain on deep inspiration (PDI)) between 
these various exposure protocols at six different time points within 
the exposure periods. At the 0.060 ppm exposure level, the author 
reported no statistically significant differences for FEV1 
decrements nor for most respiratory symptoms responses; statistically 
significant responses were reported only for TSS for the triangular 
exposure pattern toward the end of the exposure period, with the PDI 
responses being noted as following a closely similar pattern (Adams, 
2006, p. 131-132). EPA's reanalysis of the data from the Adams (2006) 
study, comparing FEV1 responses pre- and post-exposure at 
the 0.060 ppm exposure level, found small group mean differences from 
responses to filtered air that were statistically significant.\15\ 
Notably, these studies report a small percentage of subjects 
experiencing lung function decrement (>= 10 percent) at the 0.060 ppm 
exposure level.\16\
---------------------------------------------------------------------------

    \15\ Brown, J.S. (2007). EPA Office of Research and Development 
memorandum to Ozone NAAQS Review Docket (OAR-2005-0172); Subject: 
The effects of ozone on lung function at 0.06 ppm in healthy adults, 
June 14, 2007.
    \16\ Based on study data (Adams, 2006) provided by the author, 7 
percent of the subjects (2 of 30 subjects) experienced notable 
FEV1 decrements >= 10 percent) with the square wave 
exposure pattern at the 0.060 ppm exposure level (comparing pre- and 
post-exposures) when the results were corrected for the effects of 
exercise alone in filtered air (EPA, 2007, p. 3-6).
---------------------------------------------------------------------------

(ii) Results of Epidemiological and Field Studies
    A relatively large number of field studies investigating the 
effects of ambient O3 concentrations, in combination with 
other air pollutants, on lung function decrements and respiratory 
symptoms have been published over the last decade that support the 
major findings of the 1996 Criteria Document that lung function 
changes, as measured by decrements in FEV1 or peak 
expiratory flow (PEF), and respiratory symptoms in healthy adults and 
asthmatic children are closely correlated to ambient O3 
concentrations. Pre-1996 field studies focused primarily on children 
attending summer camps and found O3-related impacts on 
measures of lung function, but not respiratory symptoms, in healthy 
children. The newer studies have expanded to evaluate O3-
related effects on outdoor workers, athletes, the elderly, hikers, 
school children, and asthmatics. Collectively, these studies confirm 
and extend clinical observations that prolonged (i.e., 6-8 hour) 
exposure periods, combined with elevated levels of exertion or 
exercise, increase the dose of O3 to the lungs at a given 
ambient exposure level and result in larger lung function effects. The 
results of one large study of hikers (Korrick et al., 1998), which 
reported outcome measures stratified by several factors (e.g., gender, 
age, smoking status, presence of asthma) within a population capable of 
more than normal exertion, provide useful insight. In this study, lung 
function was measured before and after hiking, and individual 
O3 exposures were estimated by averaging hourly 
O3 concentrations from ambient monitors located at the base 
and summit. The mean 8-hour average O3 concentration was 
0.040 ppm (8-hour average concentration range of 0.021 ppm to 0.074 ppm 
O3). Decreased lung function was associated with 
O3 exposure, with the greatest effect estimates reported for 
the subgroup that reported having asthma or wheezing, and for those who 
hiked for longer periods of time.
    Asthma panel studies conducted both in the U.S. and in other 
countries have reported that decrements in PEF are associated with 
routine O3 exposures among asthmatic and healthy persons. 
One large U.S. multicity study, the National Cooperative Inner City 
Asthma Study or NCICAS, (Mortimer et al., 2002) examined O3-
related changes in PEF in 846 asthmatic children from 8 urban areas and 
reported that the incidence of >= 10 percent decrements in morning PEF 
are associated with increases in 8-hour average O3 for a 5-
day cumulative lag, suggesting that O3 exposure may be 
associated with clinically significant changes in PEF in

[[Page 37829]]

asthmatic children; however, no associations were reported with evening 
PEF. The mean 8-hour average O3 was 0.048 ppm across the 8 
cities. Excluding days when 8-hour average O3 was greater 
than 0.080 ppm (less than 5 percent of days), the associations with 
morning PEF remained statistically significant. Mortimer et al. (2002) 
discussed potential biological mechanisms for delayed effects on 
pulmonary function in asthma, which included increased nonspecific 
airway responsiveness secondary to airway inflammation due to 
O3 exposure. Two other panel studies (Romieu et al., 1996, 
1997) carried out simultaneously in northern and southwestern Mexico 
City with mildly asthmatic school children reported statistically 
significant O3-related reductions in PEF, with variations in 
effect depending on lag time and time of day. Mean 1-hour maximum 
O3 concentrations in these locations ranged from 0.190 ppm 
(SD 80) in northern Mexico City to 0.196 ppm (SD 78) in southwestern 
Mexico City. While several studies report statistically significant 
associations between O3 exposure and reduced PEF in 
asthmatics, other studies did not, possibly due to low levels of 
O3 exposure. EPA concludes that these studies collectively 
indicate that O3 may be associated with short-term declines 
in lung function in asthmatic individuals and that the Mortimer et al. 
(2002) study showed statistically significant effect at concentrations 
in the range below 0.080 ppm O3.
    Most of the panel studies which have investigated associations 
between O3 exposure and respiratory symptoms or increased 
use of asthma medication are focused on asthmatic children. Two large 
U.S. studies (Mortimer et al., 2002; Gent et al., 2003) have reported 
associations between ambient O3 concentrations and daily 
symptoms/asthma medication use, even after adjustment for copollutants. 
Results were more mixed, meaning that a greater proportion of studies 
were not both positive and statistically significant, across smaller 
U.S. and international studies that focused on these health endpoints.
    The NCICAS reported morning symptoms in 846 asthmatic children from 
8 U.S. urban areas to be most strongly associated with a cumulative 1-
to 4-day lag of O3 concentrations (Mortimer et al., 2002). 
The NCICAS used standard protocols that included instructing caretakers 
of the subjects to record symptoms (including cough, chest tightness, 
and wheeze) in the daily diary by observing or asking the child. While 
these associations were not statistically significant in several 
cities, when the individual data are pooled from all eight cities, 
statistically significant effects were observed for the incidence of 
symptoms. The authors also reported that the odds ratios remained 
essentially the same and statistically significant for the incidence of 
morning symptoms when days with 8-hour O3 concentrations 
above 0.080 ppm were excluded. These days represented less than 5 
percent of days in the study.
    Gent and colleagues (2003) followed 271 asthmatic children under 
age 12 and living in southern New England for 6 months (April through 
September) using a daily symptom diary. They found that mean 1-hour max 
O3 and 8-hour max O3 concentrations were 0.0586 
ppm (SD 19.0) and 0.0513 ppm (SD 15.5), respectively. The data were 
analyzed for two separate groups of subjects, those who used 
maintenance asthma medications during the follow-up period and those 
who did not. The need for regular medication was considered to be a 
proxy for more severe asthma. Not taking any medication on a regular 
basis and not needing to use a bronchodilator would suggest the 
presence of very mild asthma. Statistically significant effects of 1-
day lag O3 were observed on a variety of respiratory 
symptoms only in the medication user group. Both daily 1-hour max and 
8-hour max O3 concentrations were similarly related to 
symptoms such as chest tightness and shortness of breath. Effects of 
O3, but not PM2.5, remained significant and even 
increased in magnitude in two-pollutant models. Some of the 
associations were noted at 1-hour max O3 levels below 0.060 
ppm. In contrast, no effects were observed among asthmatics not using 
maintenance medication. In terms of person days of follow-up, this is 
one of the larger studies currently available that address symptom 
outcomes in relation to O3, and provides supportive evidence 
for effects of O3 independent of PM2.5. Study 
limitations include the post-hoc nature of the population 
stratification by medication use. Also, the study did not account for 
all of the important meteorological factors that might influence these 
results, such as relative humidity or dew point.
    The multicity study by Mortimer et al. (2002), which provides an 
asthmatic population representative of the United States, and several 
single-city studies indicate a robust association of O3 
concentrations with respiratory symptoms and increased medication use 
in asthmatics. While there are a number of well-conducted, albeit 
relatively smaller, U.S. studies which showed only limited or a lack of 
evidence for symptom increases associated with O3 exposure, 
these studies had less statistical power and/or were conducted in areas 
with relatively low 1-hour maximum average O3 levels, in the 
range of 0.03 to 0.09 ppm. Even so, the evidence has continued to 
expand since 1996 and now is considered to be much stronger than in the 
previous review. The Criteria Document concludes that the asthma panel 
studies, as a group, and the NCICAS in particular, indicate a positive 
association between ambient concentrations and respiratory symptoms and 
increased medication use in asthmatics. The evidence has continued to 
expand since 1996 and now is considered to be much stronger than in the 
previous review of the O3 primary standard.
    School absenteeism is another potential surrogate for the health 
implications of O3 exposure in children. The association 
between school absenteeism and ambient O3 concentrations was 
assessed in two relatively large field studies. Chen et al. (2000) 
examined total daily school absenteeism in about 28,000 elementary 
school students in Nevada over a 2-year period (after adjusting for 
PM10 and CO concentrations) and found that ambient 
O3 concentrations with a distributed lag of 14 days were 
statistically significantly associated with an increased rate of school 
absences. Gilliland et al. (2001) studied O3-related 
absences among about 2,000 4th grade students in 12 southern California 
communities and found statistically significant associations between 8-
hour average O3 concentrations (with a distributed lag out 
to 30 days) and all absence categories, and particularly for 
respiratory causes. Neither PM10 nor NO2 were 
associated with any respiratory or nonrespiratory illness-related 
absences in single pollutant models. The Criteria Document concludes 
that these studies of school absences suggest that ambient 
O3 concentrations, accumulated over two to four weeks, may 
be associated with school absenteeism, and particularly illness-related 
absences, but further replication is needed before firm conclusions can 
be reached regarding the effect of O3 on school absences. In 
addition, more research is needed to help shed light on the 
implications of variation in the duration of the lag structures (i.e., 
1 day, 5 days, 14 days, and 30 days) found both across studies and 
within data sets by health endpoint and exposure metric.

[[Page 37830]]

(b) Increased Airway Responsiveness
    As discussed in more detail in the Criteria Document (section 6.8) 
and Staff Paper (section 3.3.1.1.2), increased airway responsiveness, 
also known as airway hyperresponsiveness (AHR) or bronchial 
hyperreactivity, refers to a condition in which the propensity for the 
airways to bronchoconstrict due to a variety of stimuli (e.g., exposure 
to cold air, allergens, or exercise) becomes augmented. This condition 
is typically quantified by measuring the decrement in pulmonary 
function after inhalation exposure to specific (e.g., antigen, 
allergen) or nonspecific (e.g., methacholine, histamine) 
bronchoconstrictor stimuli. Exposure to O3 causes an 
increase in airway responsiveness as indicated by a reduction in the 
concentration of stimuli required to produce a given reduction in 
FEV1 or airway obstruction. Increased airway responsiveness 
is an important consequence of exposure to O3 because its 
presence means that the airways are predisposed to narrowing on 
inhalation of various stimuli, such as specific allergens, cold air or 
SO2. Statistically significant and clinically relevant 
decreases in pulmonary function have been observed in early phase 
allergen response in subjects with allergic rhinitis after consecutive 
(4-day) 3-hour exposures to 0.125 ppm O3 (Holz et al., 
2002). Similar increased airway responsiveness in asthmatics to house 
dust mite antigen 16 to 18 hours after exposure to a single dose of 
O3 (0.160 ppm for 7.6 hours) was observed. These 
observations, based on O3 exposures to levels much higher 
than the current standard level suggest that O3 exposure may 
be a clinically important factor that can exacerbate the response to 
ambient bronchoconstrictor substances in individuals with preexisting 
allergic asthma or rhinitis. Further, O3 may have an 
immediate impact on the lung function of asthmatics as well as 
contribute to effects that persist for longer periods.
    Kreit et al. (1989) found that O3 can induce increased 
airway responsiveness in asthmatic subjects to O3, who 
typically have increased airway responsiveness at baseline. A 
subsequent study (J[ouml]rres et al., 1996) suggested an increase in 
specific (i.e., allergen-induced) airway reactivity in subjects with 
allergic asthma, and to a lesser extent in subjects with allergic 
rhinitis after short-term exposure to higher O3 levels; 
other studies reported similar results. According to one study 
(Folinsbee and Hazucha, 2000), changes in airway responsiveness after 
O3 exposure resolve more slowly than changes in 
FEV1 or respiratory symptoms. Other studies of repeated 
exposure to O3 suggest that changes in airway responsiveness 
tend to be somewhat less affected by attenuation with consecutive 
exposures than changes in FEV1 (EPA, 2006a, p. 6-31).
    The Criteria Document (section 6.8) concludes that O3 
exposure is linked with increased airway responsiveness. Both human and 
animal studies indicate that increased airway responsiveness is not 
mechanistically associated with inflammation, and does not appear to be 
strongly associated with initial decrements in lung function or 
increases in symptoms. As a result of increased airway responsiveness 
induced by O3 exposure, human airways may be more 
susceptible to a variety of stimuli, including antigens, chemicals, and 
particles. Because asthmatic subjects typically have increased airway 
responsiveness at baseline, enhanced bronchial response to antigens in 
asthmatics raises potential public health concerns as they could lead 
to increased morbidity (e.g., medication usage, school absences, 
emergency room visits, hospital admissions) or to more persistent 
alterations in airway responsiveness (Criteria Document, p. 8-21). As 
such, increased airway responsiveness after O3 exposure 
represents a plausible link between O3 exposure and 
increased hospital admissions.
(c) Respiratory Inflammation and Increased Permeability
    Based on evidence from the previous review, acute inflammatory 
responses in the lung have been observed subsequent to 6.6 hour 
O3 exposures to the lowest tested level--0.080 ppm--in 
healthy adults engaged in moderately high exercise (section 6.9 of the 
Criteria Document and section 3.3.1.3 of the Staff Paper). Some of 
these prior studies suggest that inflammatory responses may be detected 
in some individuals following O3 exposures in the absence of 
O3-induced pulmonary decrements in those subjects. These 
studies also demonstrate that short-term exposures to O3 
also can cause increased permeability in the lungs of humans and 
experimental animals. Inflammatory responses and epithelial 
permeability have been seen to be independent of spirometric responses. 
Not only are the newer lung inflammation and increased cellular 
permeability findings discussed in the Criteria Document (pp. 8-21 to 
8-24) consistent with the previous review, but they provide better 
characterization of the physiological mechanisms by which O3 
causes these effects.
    Lung inflammation and increased permeability, which are distinct 
events controlled by different mechanisms, are two commonly observed 
effects of O3 exposure observed in all of the species 
studied. Increased cellular permeability is a disruption of the lung 
barrier that leads to leakage of serum proteins, influx of 
polymorphonuclear leukocytes (neutrophils or PMNs), release of 
bioactive mediators, and movement of compounds from the airspaces into 
the blood.
    A number of controlled human exposure studies have analyzed 
bronchoalveolar lavage (BAL) and nasal lavage (NL)\17\ fluids and cells 
for markers of inflammation and lung damage (EPA, 2006a, Annex AX6). 
Increased lung inflammation is demonstrated by the presence of 
neutrophils found in BAL fluid in the lungs, which has long been 
accepted as a hallmark of inflammation. It is apparent, however, that 
inflammation within airway tissues may persist beyond the point that 
inflammatory cells are found in the BAL fluid. Soluble mediators of 
inflammation, such as cytokines and arachidonic acid metabolites have 
been measured in the BAL fluid of humans exposed to O3. In 
addition to their role in inflammation, many of these compounds have 
bronchoconstrictive properties and may be involved in increased airway 
responsiveness following O3 exposure. An in vitro study of 
epithelial cells from nonatopic and atopic asthmatics exposed to 0.010 
to 0.100 ppm O3 showed significantly increased permeability 
compared to cells from normal persons. This indicates a potentially 
inherent susceptibility of cells from asthmatic individuals for 
O3-induced permeability.
---------------------------------------------------------------------------

    \17\ Graham and Koren (1990) compared inflammatory mediators 
present in NL and BAL fluids of humans exposed to 0.4 ppm 
O3 for 2 hours and found similar increases in PMNs in 
both fluids, suggesting a qualitative correlation between 
inflammatory changes in the lower airways (BAL) and upper 
respiratory tract (NL).
---------------------------------------------------------------------------

    In the 1996 Criteria Document, assessment of controlled human 
exposure studies indicated that a single, acute (1 to 4 hours) 
O3 exposure (>= 0.080 to 0.100 ppm) of subjects engaged in 
moderate to heavy exercise could induce a number of cellular and 
biochemical changes suggestive of pulmonary inflammation and lung 
permeability (EPA, 2006a, p. 8-22). These changes persisted for at 
least 18 hours. Markers from BAL fluid following both 2-hour and 4-hour 
O3 exposures repeated up to 5 days indicate that there is 
ongoing cellular damage irrespective of attenuation of

[[Page 37831]]

some cellular inflammatory responses of the airways, pulmonary 
function, and symptom scores (EPA, 2006a, p. 8-22). Acute airway 
inflammation was shown in Devlin et al. (1990) to occur among adults 
exposed to 0.080 ppm O3 for 6.6 hours with exercise. McBride 
et al. (1994) reported that asthmatic subjects were more sensitive than 
non-asthmatics to upper airway inflammation for O3 exposures 
that did not affect pulmonary function (EPA, 2006a, p. 6-33). However, 
the public health significance of these changes is not entirely clear.
    The studies reporting inflammatory responses and markers of lung 
injury have clearly demonstrated that there is significant variation in 
response of subjects exposed, especially to 6.6 hours O3 
exposures at 0.080 and 0.100 ppm. To provide some perspective on the 
public health impact for these effects, the Staff Paper (section 
3.3.1.1.3) notes that one study (Devlin et al., 1991) showed that 
roughly 10 to 50 percent of the 18 young healthy adult subjects 
experienced notable increases (i.e., >= 2 fold increase) in most of the 
inflammatory and cellular injury indicators analyzed, associated with 
6.6-hour exposures at 0.080 ppm. Similar, although in some cases 
higher, fractions of the population of 10 healthy adults tested saw > 2 
fold increases associated with 6.6-hour exposures to 0.100 ppm. The 
authors of this study expressed the view that ``susceptible 
subpopulations such as the very young, elderly, and people with 
pulmonary impairment or disease may be even more affected'' (Devlin et 
al., 1991).
    Since 1996, a substantial number of human exposure studies have 
been published which have provided important new information on lung 
inflammation and epithelial permeability. Mudway and Kelly (2004) 
examined O3-induced inflammatory responses and epithelial 
permeability with a meta-analysis of 21 controlled human exposure 
studies and showed that an influx in neutrophils and protein in healthy 
subjects is associated with total O3 dose (product of 
O3 concentration, exposure duration, and minute ventilation) 
(EPA, 2006a, p. 6-34). Results of the analysis suggest that the time 
course for inflammatory responses (including recruitment of neutrophils 
and other soluble mediators) is not clearly established, but there is 
evidence that attenuation profiles for many of these parameters are 
different (EPA, 2006a, p. 8-22).
    The Criteria Document (chapter 8) concludes that interaction of 
O3 with lipid constituents of epithelial lining fluid (ELF) 
and cell membranes and the induction of oxidative stress is implicated 
in injury and inflammation. Alterations in the expression of cytokines, 
chemokines, and adhesion molecules, indicative of an ongoing oxidative 
stress response, as well as injury repair and regeneration processes, 
have been reported in animal toxicology and human in vitro studies 
evaluating biochemical mediators implicated in injury and inflammation. 
While antioxidants in ELF confer some protection, O3 
reactivity is not eliminated at environmentally relevant exposures 
(Criteria Document, p. 8-24). Further, antioxidant reactivity with 
O3 is both species-specific and dose-dependent.
(d) Increased Susceptibility to Respiratory Infection
    As discussed in more detail in the Criteria Document (sections 
5.2.2, 6.9.6, and 8.4.2), short-term exposures to O3 have 
been shown to impair physiological defense capabilities in experimental 
animals by depressing alveolar macrophage (AM) functions and by 
altering the mucociliary clearance of inhaled particles and microbes 
resulting in increased susceptibility to respiratory infection. Short-
term O3 exposures also interfere with the clearance process 
by accelerating clearance for low doses and slowing clearance for high 
doses. Animal toxicological studies have reported that acute 
O3 exposures suppress alveolar phagocytosis and immune 
system functions. Dysfunction of host defenses and subsequent increased 
susceptibility to bacterial lung infection in laboratory animals has 
been induced by short-term exposures to O3 levels as low as 
0.080 ppm.
    A single controlled human exposure study reviewed in the 1996 
Criteria Document reported that exposure to 0.080 to 0.100 ppm 
O3 for 6.6 hours (with moderate exercise) induced decrements 
in the ability of AMs to phagocytose microorganisms (EPA, 2006a, p. 8-
26). Integrating the recent animal study results with human exposure 
evidence available in the 1996 Criteria Document, the Criteria Document 
concludes that available evidence indicates that short-term 
O3 exposures have the potential to impair host defenses in 
humans, primarily by interfering with AM function. Any impairment in AM 
function may lead to decreased clearance of microorganisms or nonviable 
particles. Compromised AM functions in asthmatics may increase their 
susceptibility to other O3 effects, the effects of 
particles, and respiratory infections (EPA, 2006a, p. 8-26).
(e) Morphological Effects
    The 1996 Criteria Document found that short-term O3 
exposures cause similar alterations in lung morphology in all 
laboratory animal species studied, including primates. As discussed in 
the Staff Paper (section 3.3.1.1.5), cells in the centriacinar region 
(CAR) of the lung (the segment between the last conducting airway and 
the gas exchange region) have been recognized as a primary target of 
O3-induced damage (epithelial cell necrosis and remodeling 
of respiratory bronchioles), possibly because epithelium in this region 
receives the greatest dose of O3 delivered to the lower 
respiratory tract. Following chronic O3 exposure, structural 
changes have been observed in the CAR, the region typically affected in 
most chronic airway diseases of the human lung (EPA, 2006a, p. 8-24).
    Ciliated cells in the nasal cavity and airways, as well as Type I 
cells in the gas-exchange region, are also identified as targets. While 
short-term O3 exposures can cause epithelial cell 
proliferation and fibrolitic changes in the CAR, these changes appear 
to be transient with recovery time after exposure, depending on species 
and O3 dose. The potential impacts of repeated short-term 
and chronic morphological effects of O3 exposure are 
discussed below in the section on effects from long-term exposures. 
Long-term or prolonged exposure has been found to cause chronic lesions 
similar to early lesions of respiratory bronchiolitis, which have the 
potential to progress to fibrotic lung disease (Criteria Document, p. 
8-25).
    Recent studies continue to show that short-term and sub-chronic 
exposures to O3 cause similar alterations in lung structure 
in a variety of experimental animal species. For example, a series of 
new studies that used infant rhesus monkeys and simulated seasonal 
ambient exposure (0.5 ppm 8 hours/day for 5 days, every 14 days for 11 
episodes) reported remodeling in the distal airways; abnormalities in 
tracheal basement membrane; eosinophil accumulation in conducting 
airways; and decrements in airway innervation (Criteria Document, p. 8-
25). Based on evidence from animal toxicological studies, short-term 
and sub-chronic exposures to O3 can cause morphological 
changes in the respiratory systems, particularly in the CAR, of a 
number of laboratory animal species (EPA, 2006a, section 5.2.4).

[[Page 37832]]

(f) Emergency Department Visits/Hospital Admissions for Respiratory 
Causes
    Increased summertime emergency department visits and hospital 
admissions for respiratory causes have been associated with ambient 
exposures to O3. As discussed in section 3.3.1.1.6 of the 
Staff Paper, numerous studies conducted in various locations in the 
U.S. and Canada consistently have shown a relationship between ambient 
O3 levels and increased incidence of emergency department 
visits and hospital admissions for respiratory causes, even after 
controlling for modifying factors, such as weather and copollutants. 
Such associations between elevated ambient O3 during summer 
months and increased hospital admissions have a plausible biological 
basis in the human and animal evidence of functional, symptomatic, and 
physiologic effects discussed above and in the increased susceptibility 
to respiratory infections observed in laboratory animals.
    In the last review of the O3 NAAQS, the Criteria 
Document evaluated emergency department visits and hospital admissions 
as possible outcomes following exposure to O3 (EPA, 2006a, 
section 7.3). The evidence was limited for emergency department visits, 
but results of several studies generally indicated that short-term 
exposures to O3 were associated with respiratory emergency 
department visits. The strongest and most consistent evidence, at both 
lower levels (i.e., below 0.120 ppm 1-hour max O3) and at 
higher levels (above 0.120 ppm 1-hour max O3), was found in 
the group of studies which investigated summertime\18\ daily hospital 
admissions for respiratory causes in different eastern North American 
cities. These studies consistently demonstrated that ambient 
O3 levels were associated with increased hospital admissions 
and accounted for about one to three excess respiratory hospital 
admissions per million persons with each 0.100 ppm increase in 1-hour 
max O3, after adjustment for possible confounding effects of 
temperature and copollutants. Overall, the 1996 Criteria Document 
concluded that there was strong evidence that ambient O3 
exposures can cause significant exacerbations of preexisting 
respiratory disease in the general public. Excess respiratory-related 
hospital admissions associated with O3 exposures for the New 
York City area (based on Thurston et al., 1992) were included in the 
quantitative risk assessment in the prior review and are included in 
the current assessment along with estimates for respiratory-related 
hospital admissions in Cleveland, Detroit, and Los Angeles based on 
more recent studies (Staff Paper, chapter 5). Significant uncertainties 
and the difficulty of obtaining reliable baseline incidence numbers 
resulted in emergency department visits not being used in the 
quantitative risk assessment in either the last or the current 
O3 NAAQS review.
---------------------------------------------------------------------------

    \18\ Discussion of the reasons for focusing on warm season 
studies is found in the section 2.A.3.a below.
---------------------------------------------------------------------------

    In the past decade, a number of studies have examined the temporal 
pattern associations between O3 exposures and emergency 
department visits for respiratory causes (EPA, 2006a, section 7.3.2). 
These studies are summarized in the Criteria Document (chapter 7 Annex) 
and some are shown in Figure 1 (in section II.A.3). Respiratory causes 
for emergency department visits include asthma, bronchitis, emphysema, 
pneumonia, and other upper and lower respiratory infections, such as 
influenza, but asthma visits typically dominate the daily incidence 
counts. Most studies report positive associations. Among studies with 
adequate controls for seasonal patterns, many reported at least one 
significant positive association involving O3.
    In reviewing evidence for associations between emergency department 
visits for asthma and short-term O3 exposures, the Criteria 
Document notes that in general, O3 effect estimates from 
summer only analyses tended to be positive and larger compared to 
results from cool season or all year analyses (Figure 7-8, EPA, 2006a, 
p. 7-68). Several of the studies reported significant associations 
between O3 concentrations and emergency department visits 
for respiratory causes, in particular asthma. However, inconsistencies 
were observed which were at least partially attributable to differences 
in model specifications and analysis approach among various studies. 
For example, ambient O3 concentrations, length of the study 
period, and statistical methods used to control confounding by seasonal 
patterns and copollutants appear to affect the observed O3 
effect on emergency department visits. Thus, the Criteria Document has 
concluded that stratified analyses by season generally supported a 
positive association between O3 concentrations and emergency 
department visits for asthma in the warm season.
    Hospital admissions studies focus specifically on unscheduled 
admissions because unscheduled hospital admissions occur in response to 
unanticipated disease exacerbations and are more likely than scheduled 
admissions to be affected by variations in environmental factors, such 
as daily O3 levels. Results of a fairly large number of 
these studies published during the past decade are summarized in 
Criteria Document (chapter 7 Annex), and results of U.S. and Canadian 
studies are shown in Figure 1 below (in section II.A.3). As a group, 
these hospital admissions studies tend to be larger geographically and 
temporally than the emergency department visit studies and provide 
results that are generally more consistent. The strongest associations 
of respiratory hospital admissions with O3 concentrations 
were observed using short lag periods, in particular for a 0-day lag 
(same day exposure) and a 1-day lag (previous day exposure). Most 
studies in the United States and Canada indicated positive, 
statistically significant associations between ambient O3 
concentrations and respiratory hospital admissions in the warm season. 
However, not all studies found a statistically significant relationship 
with O3, possibly because of very low ambient O3 
levels. Analyses for confounding using multipollutant regression models 
suggest that copollutants generally do not confound the association 
between O3 and respiratory hospitalizations. Ozone effect 
estimates were robust to PM adjustment in all-year and warm-season only 
data.
    Overall, the Criteria Document concludes that positive and robust 
associations were found between ambient O3 concentrations 
and various respiratory disease hospitalization outcomes, when focusing 
particularly on results of warm-season analyses. Recent studies also 
generally indicate a positive association between O3 
concentrations and emergency department visits for asthma during the 
warm season (EPA, 2006a, p. 7-175). These positive and robust 
associations are supported by the human clinical, animal toxicological, 
and epidemiological evidence for lung function decrements, increased 
respiratory symptoms, airway inflammation, and increased airway 
responsiveness. Taken together, the overall evidence supports a causal 
relationship between acute ambient O3 exposures and 
increased respiratory morbidity outcomes resulting in increased 
emergency department visits and hospitalizations during the warm season 
(EPA, 2006a, p. 8-77).

[[Page 37833]]

ii. Effects on the Respiratory System of Long-Term O3 
Exposures
    The 1996 Criteria Document concluded that there was insufficient 
evidence from the limited number of studies to determine whether long-
term O3 exposures resulted in chronic health effects at 
ambient levels observed in the U.S. However, the aggregate evidence 
suggested that O3 exposure, along with other environmental 
factors, could be responsible for health effects in exposed 
populations. Animal toxicological studies carried out in the 1980's and 
1990's demonstrated that long-term exposures can result in a variety of 
morphological effects, including permanent changes in the small airways 
of the lungs, including remodeling of the distal airways and CAR and 
deposition of collagen, possibly representing fibrotic changes. These 
changes result from the damage and repair processes that occur with 
repeated exposure. Fibrotic changes were also found to persist after 
months of exposure providing a potential pathophysiologic basis for 
changes in airway function observed in children in some recent 
epidemiological studies. It appears that variable seasonal ambient 
patterns of exposure may be of greater concern than continuous daily 
exposures.
    Several studies published since 1996 have investigated lung 
function changes over seasonal time periods (EPA, 2006a, section 
7.5.3). The Criteria Document (p. 7-114) summarizes these studies 
collectively indicate that seasonal O3 exposure is 
associated with smaller growth-related increases in lung function in 
children than they would have experienced living in areas with lower 
O3 levels and that there is some limited, as yet uncertain, 
evidence that seasonal O3 also may affect lung function in 
young adults, although the uncertainty about the role of copollutants 
makes it difficult to attribute the effects to O3 alone.
    Lung capacity grows during childhood and adolescence as body size 
increases, reaches a maximum during the twenties, and then begins to 
decline steadily and progressively with age. Long-term exposure to air 
pollution has long been thought to contribute to slower growth in lung 
capacity, diminished maximally attained capacity, and/or more rapid 
decline in lung capacity with age (EPA, 2006a, section 7.5.4). 
Toxicological findings evaluated in the 1996 Criteria Document 
demonstrated that repeated daily exposure of rats to an episodic 
profile of O3 caused small, but significant, decrements in 
growth-related lung function that were consistent with early indicators 
of focal fibrogenesis in the proximal alveolar region, without overt 
fibrosis. Because O3 at sufficient concentrations is a 
strong respiratory irritant and has been shown to cause inflammation 
and restructuring of the respiratory airways, it is plausible that 
long-term O3 exposures might have a negative impact on 
baseline lung function, particularly during childhood when these 
exposures might have long-term risks.
    Several epidemiological studies published since 1996 have examined 
the relationship between lung function development and long-term 
O3 exposure. The most extensive and robust study of 
respiratory effects in relation to long-term air pollution exposures 
among children in the U.S. is the Children's Health Study carried out 
in 12 communities of southern California starting in 1993. One analysis 
(Peters et al., 1999a) examined the relationship between long-term 
O3 exposures and self-reports of respiratory symptoms and 
asthma in a cross sectional analysis and found a limited relationship 
between outcomes of current asthma, bronchitis, cough and wheeze and a 
0.040 ppm increase in 1-hour max O3 (EPA, 2006a, p. 7-115). 
Another analysis (Peters et al., 1999b) examined the relationship 
between lung function at baseline and levels of air pollution in the 
community. They reported evidence that annual mean O3 levels 
were associated with decreases in FVC, FEV1, PEF and forced 
expiratory flow (FEF25-75) (the latter two being 
statistically significant) among females but not males. In a separate 
analysis (Gauderman et al., 2000) of 4th, 7th, and 10th grade students, 
a longitudinal analysis of lung function development over four years 
found no association with O3 exposure. The Children's Health 
Study enrolled a second cohort of more than 1500 fourth graders in 1996 
(Gauderman et al., 2002). While the strongest associations with 
negative lung function growth were observed with acid vapors in this 
cohort, children from communities with higher 4-year average 
O3 levels also experienced smaller increases in various lung 
function parameters. The strongest relationship with O3 was 
with PEF. Specifically, children from the least-polluted community had 
a small but statistically significant increase in PEF as compared to 
those from the most-polluted communities. In two-pollutant models, only 
8-hour average O3 and NO2 were significant joint 
predictors of FEV1 and maximal midexpiratory flow (MMEF). 
Although results from the second cohort of children are supportive of a 
weak association, the definitive 8-year follow-up analysis of the first 
cohort (Gauderman et al., 2004a) provides little evidence that long-
term exposure to ambient O3 at current levels is associated 
with significant deficits in the growth rate of lung function in 
children. Avol et al. (2001) examined children who had moved away from 
participating communities in southern California to other states with 
improved air quality. They found that a negative, but not statistically 
significant, association was observed between O3 and lung 
function parameters. Collectively, the results of these reports from 
the children's health cohorts provide little evidence to support an 
impact of long-term O3 exposures on lung function 
development.
    Evidence for a significant relationship between long-term 
O3 exposures and decrements in maximally attained lung 
function was reported in a nationwide study of first year Yale students 
(Kinney et al., 1998; Galizia and Kinney, 1999) (EPA, 2006a, p. 7-120). 
Males had much larger effect estimates than females, which might 
reflect higher outdoor activity levels and correspondingly higher 
O3 exposures during childhood. A similar study of college 
freshmen at University of California at Berkeley also reported 
significant effects of long-term O3 exposures on lung 
function (K[uuml]nzli et al., 1997; Tager et al., 1998). In a 
comparison of students whose city of origin was either Los Angeles or 
San Francisco, long-term O3 exposures were associated with 
significant changes in mid- and end-expiratory flow measures, which 
could be considered early indicators for pathologic changes that might 
progress to COPD.
    There have been a few studies that investigated associations 
between long-term O3 exposures and the onset of new cases of 
asthma (EPA, 2006a, section 7.5.6). The Adventist Health and Smog 
(AHSMOG) study cohort of about 4,000 was drawn from nonsmoking, non-
Hispanic white adult Seventh Day Adventists living in California (Greer 
et al., 1993; McDonnell et al., 1999). During the ten-year follow-up in 
1987, a statistically significant increased relative risk of asthma 
development was observed in males, compared to a nonsignificant 
relative risk in females (Greer et al., 1993). In the 15-year follow-up 
in 1992, it was reported that for males, there was a statistically 
significant increased relative risk of developing asthma associated 
with 8-hour average O3 exposures, but there was no evidence 
of an association in females. Consistency of results in the two studies 
with different follow-up

[[Page 37834]]

times provides supportive evidence of the potential for an association 
between long-term O3 exposure and asthma incidence in adult 
males; however, representativeness of this cohort to the general U.S. 
population may be limited (EPA, 2006a, p. 7-125).
    In a similar study (McConnell et al., 2002) of incident asthma 
among children (ages 9 to 16 at enrollment), annual surveys of 3,535 
children initially without asthma were used to identify new-onset 
asthma cases as part of the Children's Health Study. Six high-
O3 and six low-O3 communities were identified 
where the children resided. There were 265 children who reported new-
onset asthma during the follow-up period. Although asthma risk was no 
higher for all residents of the six high-O3 communities 
versus the six low-O3 communities, asthma risk was 3.3 times 
greater for children who played three or more sports as compared with 
children who played no sports within the high-O3 
communities. This association was absent in the communities with lower 
O3 concentrations. No other pollutants were found to be 
associated with new-onset asthma (EPA, 2006a, p. 7-125). Playing sports 
may result in extended outdoor activity and exposure occurring during 
periods when O3 levels are higher. It should be noted, 
however, that the results of the Children's Health Study were based on 
a small number of new-onset asthma cases among children who played 
three or more sports. Future replication of these findings in other 
cohorts would help determine whether a causal interpretation is 
appropriate.
    In animal toxicology studies, the progression of morphological 
effects reported during and after a chronic exposure in the range of 
0.50 to 1.00 ppm O3 is complex, with inflammation peaking 
over the first few days of exposure, then dropping, then plateauing, 
and finally, largely disappearing (EPA, 2006a, section 5.2.4.4). By 
contrast, fibrotic changes in the tissue increase very slowly over 
months of exposure, and, after exposure ceases, the changes sometimes 
persist or increase. Epithelial hyperplasia peaks soon after the 
inflammatory response but is usually maintained in both the nose and 
lungs with continuous exposure; it also does not return to pre-exposure 
levels after the end of exposure. Patterns of exposure in this same 
concentration range determine effects, with 18 months of daily 
exposure, causing less morphologic damage than exposures on alternating 
months. This is important as environmental O3 exposure is 
typically seasonal. Long-term studies by Plopper and colleagues (Evans 
et al., 2003; Schelegle et al., 2003; Chen et al., 2003; Plopper and 
Fanucchi, 2000) investigated infant rhesus monkeys exposed to 
simulated, seasonal O3 and demonstrated: (1) Remodeling in 
the distal airways, (2) abnormalities in tracheal basement membrane; 
(3) eosinophil accumulation in conducting airways; and (4) decrements 
in airway innervation (EPA, 2006a, p. 5-45). These findings provide 
additional information regarding possible injury-repair processes 
occurring with long-term O3 exposures suggesting that these 
processes are only partially reversible and may progress following 
cessation of O3 exposure. Further, these processes may lead 
to nonreversible structural damage to lung tissue; however, there is 
still too much uncertainty to characterize the significance of these 
findings to human exposure profiles and effect levels (EPA, 2006a, p. 
8-25).
    In summary, in the past decade, important new longitudinal studies 
have examined the effect of chronic O3 exposure on 
respiratory health outcomes. Limited evidence from recent long-term 
morbidity studies have suggested in some cases that chronic exposure to 
O3 may be associated with seasonal declines in lung function 
or reduced lung function development, increases in inflammation, and 
development of asthma in children and adults. Seasonal decrements or 
smaller increases in lung function measures have been reported in 
several studies; however, the extent to which these changes are 
transient remains uncertain. While there is supportive evidence from 
animal studies involving effects from chronic exposures, large 
uncertainties still remain as to whether current ambient levels and 
exposure patterns might cause these same effects in human populations. 
The Criteria Document concludes that epidemiological studies of new 
asthma development and longer-term lung function declines remain 
inconclusive at present (EPA, 2006a, p. 7-134).
iii. Effects on the Cardiovascular System of O3 Exposure
    At the time of the 1997 review, the possibility of O3-
induced cardiovascular effects was largely unrecognized. Since then, a 
very limited body of evidence from animal, controlled human exposure 
and epidemiologic studies has emerged that provides evidence for some 
potential plausible mechanisms for how O3 exposures might 
exert cardiovascular system effects, however much needs to be done to 
substantiate these potential mechanisms. Possible mechanisms may 
involve O3-induced secretions of vasoconstrictive substances 
and/or effects on neuronal reflexes that may result in increased 
arterial blood pressure and/or altered electrophysiologic control of 
heart rate or rhythm. Some animal toxicology studies have shown 
O3-induced decreases in heart rate, mean arterial pressure, 
and core temperature. One controlled human exposure study that 
evaluated effects of O3 exposure on cardiovascular health 
outcomes found no significant O3-induced differences in ECG 
or blood pressure in healthy or hypertensive subjects but did observe a 
significant O3-induced increase the alveolar-to-arterial 
PO2 gradient and heart rate in both groups resulting in an 
overall increase in myocardial work and impairment in pulmonary gas 
exchange (Gong et al., 1998). In another controlled human exposure 
study, inhalation of a mixture of PM2.5 and O3 by 
healthy subjects increased brachial artery vasoconstriction and 
reactivity (Brook et al., 2002).
    The evidence from a few animal studies also includes potential 
direct effects such as O3-induced release from lung 
epithelial cells of platelet activating factor (PAF) that may 
contribute to blood clot formation that would have the potential to 
increase the risk of serious cardiovascular outcomes (e.g., heart 
attack, stroke, mortality). Also, interactions of O3 with 
surfactant components in epithelial lining fluid of the lung may result 
in production of oxysterols and reactive oxygen species that may 
exhibit PAF-like activity contributing to clotting and also may exert 
cytotoxic effects on lung and heart muscle cells.
    Epidemiologic panel and field studies that examined associations 
between O3 and various cardiac physiologic endpoints have 
yielded limited evidence suggestive of a potential association between 
acute O3 exposure and altered heart rate variability, 
ventricular arrhythmias, and incidence of heart attacks. A number of 
epidemiological studies have also reported associations between short-
term exposures and hospitalization for cardiovascular diseases. As 
shown in Figure 7-13 of the Criteria Document, many of the studies 
reported negative or inconsistent associations. Some other studies, 
especially those that examined the relationship when O3 
exposures were higher, have found robust positive associations between 
O3 and cardiovascular hospital admissions (EPA, 2006a, p. 7-
82). For example, one study reported a positive association between 
O3 and cardiovascular hospital admissions in Toronto, Canada 
in a summer-only analysis (Burnett et al.,

[[Page 37835]]

1997b). The results were robust to adjustment for various PM indices, 
whereas the PM effects diminished when adjusting for gaseous 
pollutants. Other studies stratified their analysis by temperature, 
i.e., by warm days versus cool days. Several analyses using warm season 
days consistently produced positive associations.
    The epidemiologic evidence for cardiovascular morbidity is much 
weaker than for respiratory morbidity, with only one of several U.S./
Canadian studies showing statistically significant positive 
associations of cardiovascular hospitalizations with warm-season 
O3 concentrations. Most of the available European and 
Australian studies, all of which conducted all-year O3 
analyses, did not find an association between short-term O3 
concentrations and cardiovascular hospitalizations. Overall, the 
currently available evidence is inconclusive regarding an association 
between cardiovascular hospital admissions and ambient O3 
exposure (EPA, 2006a, p. 7-83).
    In summary, based on the evidence from animal toxicology, human 
controlled exposure, and epidemiologic studies, from the Criteria 
Document concludes that this generally limited body of evidence is 
suggestive that O3 can directly and/or indirectly contribute 
to cardiovascular-related morbidity, but that much needs to be done to 
more fully integrate links between ambient O3 exposures and 
adverse cardiovascular outcomes (EPA, 2006a, p. 8-77).
b. Mortality
i. Mortality and Short-Term O3 Exposure
    The 1996 Criteria Document concluded that an association between 
daily mortality and O3 concentration for areas with high 
O3 levels (e.g., Los Angeles) was suggested. However, due to 
a very limited number of studies available at that time, there was 
insufficient evidence to conclude that the observed association was 
likely causal.
    The current Criteria Document includes results from numerous 
epidemiological analyses of the relationship between O3 and 
mortality. Additional single city analyses have also been conducted 
since 1996, however, the most pivotal studies in EPA's (and CASAC's) 
finding of increased support for the relationship between premature 
mortality and O3 is in part related to differences in study 
design--limiting analyses to warm seasons, better control for 
copollutants, particularly PM, and use of multicity designs (both time 
series and meta-analytic designs). Key findings are available from 
multi-city time-series studies that report associations between 
O3 and mortality. These studies include analyses using data 
from 90 U.S. cities in the National Mortality, Morbidity and Air 
Pollution (NMMAPS) study (Dominici et al., 2003) and from 95 U.S. 
communities in an extension to the NMMAPS analyses (Bell et al., 2004).
    The original 90-city NMMAPS analysis, with data from 1987 to 1994, 
was primarily focused on investigating effects of PM10 on 
mortality. A significant association was reported between mortality and 
24-hour average O3 concentrations in analyses using all 
available data as well as in the warm season only analyses (Dominici et 
al., 2003). The estimate using all available data was about half that 
for the summer-only data at a lag of 1-day. The extended NMMAPS 
analysis included data from 95 U.S. cities and included an additional 6 
years of data, from 1987-2000 (Bell et al., 2004). Significant 
associations were reported between O3 and mortality in 
analyses using all available data. The effect estimate for increased 
mortality was approximately 0.5 percent per 0.020 ppm change in 24-hour 
average O3 measured on the same day, and approximately 1.04 
percent per 0.020 ppm change in 24-hour average O3 in a 7-
day distributed lag model (EPA, 2006a, p. 7-88). In analyses using only 
data from the warm season, the results were not significantly different 
from the full-year results. The authors also report that O3-
mortality associations were robust to adjustment for PM (EPA, 2006a, p. 
7-100). Using a subset of the NMMAPS data set, Huang et al. (2005) 
focused on associations between cardiopulmonary mortality and 
O3 exposure (24-hour average) during the summer season only. 
The authors report an approximate 1.47 percent increase per 0.020 ppm 
change in O3 concentration measured on the same day and an 
approximate 2.52 percent increase per 0.020 ppm change in O3 
concentration using a 7-day distributed lag model. These findings 
suggest that the effect of O3 on mortality is immediate but 
also persists for several days.
    As discussed below in section II.A.3.a, confounding by weather, 
especially temperature, is complicated by the fact that higher 
temperatures are associated with the increased photochemical activities 
that are important for O3 formation. Using a case-crossover 
study design, Schwartz (2005) assessed associations between daily 
maximum concentrations and mortality, matching case and control periods 
by temperature, and using data only from the warm season. The reported 
effect estimate of approximately 0.92 percent change in mortality per 
0.040 ppm O3 (1-hour maximum) was similar to time-series 
analysis results with adjustment for temperature (approximately 0.76 
percent per 0.040 ppm O3), suggesting that associations 
between O3 and mortality were robust to the different 
adjustment methods for temperature.
    An initial publication from APHEA, a European multi-city study, 
reported statistically significant associations between daily maximum 
O3 concentrations and mortality in four cities in a full 
year analysis (Toulomi et al., 1997). An extended analysis was done 
using data from 23 cities throughout Europe (Gryparis et al., 2004). In 
this report, a positive but not statistically significant association 
was found between mortality and 1-hour daily maximum O3 in a 
full year analysis. Gryparis et al. (2004) noted that there was a 
considerable seasonal difference in the O3 effect on 
mortality; thus, the small effect for the all-year data might be 
attributable to inadequate adjustment for confounding by seasonality. 
Focusing on analyses using summer measurements, the authors report 
statistically significant associations with total mortality, 
cardiovascular mortality and with respiratory mortality (EPA, 2006a, p. 
7-93, 7-99).
    Numerous single-city analyses have also reported associations 
between mortality and short-term O3 exposure, especially for 
those analyses using warm season data. As shown in Figure 7-21 of the 
Criteria Document, the results of recent publications show a pattern of 
positive, often statistically significant associations between short-
term O3 exposure and mortality during the warm season. In 
considering results from year-round analyses, there remains a pattern 
of positive results but the findings are less consistent. In most 
single-city analyses, effect estimates were not substantially changed 
with adjustment for PM (EPA, 2006a, Figure 7-22).
    In addition, several meta-analyses have been conducted on the 
relationship between O3 and mortality. As described in 
section 7.4.4 of the Criteria Document, these analyses reported fairly 
consistent and positive combined effect estimates ranging from 
approximately 1.5 to 2.5 percent increase in mortality for a 
standardized change in O3 (EPA, 2006a, Figure 7-20). Three 
recent meta-analyses evaluated potential sources of heterogeneity in 
O3-mortality associations (Bell et al., 2005; Ito et al., 
2005; Levy et al., 2005). The

[[Page 37836]]

Criteria Document (p. 7-96) observes common findings across all three 
analyses, in that all reported that effect estimates were larger in 
warm season analyses, reanalysis of results using default convergence 
criteria in generalized additive models (GAM) did not change the effect 
estimates, and there was no strong evidence of confounding by PM. Bell 
et al. (2005) and Ito et al. (2005) both provided suggestive evidence 
of publication bias, but O3-mortality associations remained 
after accounting for that potential bias. The Criteria Document 
concludes that the ``positive O3 effects estimates, along 
with the sensitivity analyses in these three meta-analyses, provide 
evidence of a robust association between ambient O3 and 
mortality'' (EPA, 2006a, p. 7-97).
    Most of the single-pollutant model estimates from single-city 
studies range from 0.5 to 5 percent excess deaths per standardized 
increments. Corresponding summary estimates in large U.S. multi-city 
studies ranged between 0.5 to 1 percent with some studies noting 
heterogeneity across cities and studies (EPA, 2006a, p. 7-110).
    Finally, from those studies that included assessment of 
associations with specific causes of death, it appears that effect 
estimates for associations with cardiovascular mortality are larger 
than those for total mortality. The meta-analysis by Bell et al. (2005) 
observed a slightly larger effect estimate for cardiovascular mortality 
compared to mortality from all causes. The effect estimate for 
respiratory mortality was approximately one-half that of cardiovascular 
mortality in the meta-analysis. However, other studies have observed 
larger effect estimates for respiratory mortality compared to 
cardiovascular mortality. The apparent inconsistency regarding the 
effect size of O3-related respiratory mortality may be due 
to reduced statistical power in this subcategory of mortality (EPA, 
2006a, p. 7-108).
    In summary, many single- and multi-city studies observed positive 
associations of ambient O3 concentrations with total 
nonaccidental and cardiopulmonary mortality. The Criteria Document 
finds that the results from U.S. multi-city time-series studies provide 
the strongest evidence to date for O3 effects on acute 
mortality. Recent meta-analyses also indicate positive risk estimates 
that are unlikely to be confounded by PM; however, future work is 
needed to better understand the influence of model specifications on 
the risk coefficient (EPA, 2006a, p. 7-175). A meta-analysis that 
examined specific causes of mortality found that the cardiovascular 
mortality risk estimates were higher than those for total mortality. 
For cardiovascular mortality, the Criteria Document (Figure 7-25, p. 7-
106) suggests that effect estimates are consistently positive and more 
likely to be larger and statistically significant in warm season 
analyses. The findings regarding the effect size for respiratory 
mortality have been less consistent, possibly because of lower 
statistical power in this subcategory of mortality. The Criteria 
Document (p. 8-78) concludes that these findings are highly suggestive 
that short-term O3 exposure directly or indirectly 
contribute to non-accidental and cardiopulmonary-related mortality, but 
additional research is needed to more fully establish underlying 
mechanisms by which such effects occur.\19\
---------------------------------------------------------------------------

    \19\ In commenting on the Criteria Document, the CASAC Ozone 
Panel raised questions about the implications of these time-series 
results in a policy context, emphasizing that ``* * * while the 
time-series study design is a powerful tool to detect very small 
effects that could not be detected using other designs, it is also a 
blunt tool'' (Henderson, 2006b). They note that ``* * * not only is 
the interpretation of these associations complicated by the fact 
that the day-to-day variation in concentrations of these pollutants 
is, to a varying degree, determined by meteorology, the pollutants 
are often part of a large and highly correlated mix of pollutants, 
only a very few of which are measured'' (Henderson, 2006b). Even 
with these uncertainties, the CASAC Ozone Panel, in its review of 
the Staff Paper, found ``* * * premature total non-accidental and 
cardiorespiratory mortality for inclusion in the quantitative risk 
assessment to be appropriate.'' (Henderson, 2006b).
---------------------------------------------------------------------------

ii. Mortality and Long-Term O3 Exposure
    Little evidence was available in the last review on the potential 
for associations between mortality and long-term exposure to 
O3. In the Harvard Six City prospective cohort analysis, the 
authors report that mortality was not associated with long-term 
exposure to O3 (Dockery et al., 1993). The authors note that 
the range of O3 concentrations across the six cities was 
small, which may have limited the power of the study to detect 
associations between mortality and O3 levels (EPA, 2006a, p. 
7-127).
    As discussed in section 7.5.8 of the Criteria Document, in this 
review there are results available from three prospective cohort 
studies: the American Cancer Society (ACS) study (Pope et al., 2002), 
the Adventist Health and Smog (AHSMOG) study (Beeson et al., 1998; 
Abbey et al., 1999), and the U.S. Veterans Cohort study (Lipfert et 
al., 2000, 2003). In addition, a major reanalysis report includes 
evaluation of data from the Harvard Six City cohort study (Krewski et 
al., 2000).\20\ This reanalysis also includes additional evaluation of 
data from the initial ACS cohort study report that had only reported 
results of associations between mortality and long-term exposure to 
fine particles and sulfates (Pope et al., 1995). This reanalysis was 
discussed in the Staff Paper (section 3.3.2.2) but not in the Criteria 
Document.
---------------------------------------------------------------------------

    \20\ This reanalysis report and the original prospective cohort 
study findings are discussed in more detail in section 8.2.3 of the 
Air Quality Criteria for Particulate Matter (EPA, 2004).
---------------------------------------------------------------------------

    In this reanalysis of data from the previous Harvard Six City 
prospective cohort study, the investigators replicated and validated 
the findings of the original studies, and the report included 
additional quantitative results beyond those available in the original 
report (Krewski et al., 2000). In the reanalysis of data from the 
Harvard Six Cities study, the effect estimate for the association 
between long-term O3 concentrations and mortality was 
negative and nearly statistically significant (relative risk = 0.87, 95 
percent CI: 0.76, 1.00).
    The ACS study is based on health data from a large prospective 
cohort of approximately 500,000 adults and air quality data from about 
150 U.S. cities. The initial report (Pope et al., 1995) focused on 
associations with fine particles and sulfates, for which significant 
associations had been reported in the earlier Harvard Six Cities study 
(Dockery et al., 1993). As part of the major reanalysis of these data, 
results for associations with other air pollutants were also reported, 
and the authors report that no significant associations were found 
between O3 and all-cause mortality. However, a significant 
association was reported for cardiopulmonary mortality in the warm 
season (Krewski et al., 2000). The ACS II study (Pope et al., 2002) 
reported results of associations with an extended data base; the 
mortality records for the cohort had been updated to include 16 years 
of follow-up (compared with 8 years in the first report) and more 
recent air quality data were included in the analyses. Similar to the 
earlier reanalysis, a marginally significant association was observed 
between long-term exposure to O3 and cardiopulmonary 
mortality in the warm season. No other associations with mortality were 
observed in both the full-year and warm season analyses.
    The Adventist Health and Smog (AHSMOG) cohort includes about 6,000 
adults living in California. In two studies from this cohort, a 
significant association has been reported between long-term 
O3 exposure and increased risk of lung cancer mortality 
among males only (Beeson et al., 1998; Abbey

[[Page 37837]]

et al., 1999). No significant associations were reported between long-
term O3 exposure and mortality from all causes or 
cardiopulmonary causes. Due to the small numbers of lung cancer deaths 
(12 for males, 18 for females) and the precision of the effect estimate 
(i.e., the wide confidence intervals), the Criteria Document discussed 
concerns about the plausibility of the reported association with lung 
cancer (EPA, 2006a, p. 7-130).
    The U.S. Veterans Cohort study (Lipfert et al., 2000, 2003) of 
approximately 50,000 middle-aged males diagnosed with hypertension, 
reported some positive associations between mortality and peak 
O3 exposures (95th percentile level for several years of 
data). The study included numerous analyses using subsets of exposure 
and mortality follow-up periods which spanned the years 1960 to 1996. 
In the results of analyses using deaths and O3 exposure 
estimates concurrently across the study period, there were positive, 
statistically significant associations between peak O3 and 
mortality (EPA, 2006a, p. 7-129).
    Overall, the Criteria Document concludes that consistent 
associations have not been reported between long-term O3 
exposure and all-cause, cardiopulmonary or lung cancer mortality (EPA, 
2006a, p. 7-130).
c. Role of Ground-Level O3 in Solar Radiation-Related Human 
Health Effects
    Beyond the direct health effects attributable to inhalation 
exposure to O3 in the ambient air discussed above, the 
Criteria Document also assesses potential indirect effects related to 
the presence of O3 in the ambient air by considering the 
role of ground-level O3 in mediating human health effects 
that may be directly attributable to exposure to solar ultraviolet 
radiation (UV-B). The Criteria Document (chapter 10) focuses this 
assessment on three key factors, including those factors that govern 
(1) UV-B radiation flux at the earth's surface, (2) human exposure to 
UV-B radiation, and (3) human health effects due to UV-B radiation. In 
so doing, the Criteria Document provides a thorough analysis of the 
current understanding of the relationship between reducing ground-level 
O3 concentrations and the potential impact these reductions 
might have on increasing UV-B surface fluxes and indirectly 
contributing to UV-B related health effects.
    There are many factors that influence UV-B radiation penetration to 
the earth's surface, including latitude, altitude, cloud cover, surface 
albedo, PM concentration and composition, and gas phase pollution. Of 
these, only latitude and altitude can be defined with small uncertainty 
in any effort to assess the changes in UV-B flux that may be 
attributable to any changes in tropospheric O3 as a result 
of any revision to the O3 NAAQS. Such an assessment of UV-B 
related health effects would also need to take into account human 
habits, such as outdoor activities (including age- and occupation-
related exposure patterns), dress and skin care to adequately estimate 
UV-B exposure levels. However, little is known about the impact of 
these factors on individual exposure to UV-B.
    Moreover, detailed information does not exist regarding other 
factors that are relevant to assessing changes in disease incidence, 
including: Type (e.g., peak or cumulative) and time period (e.g., 
childhood, lifetime, current) of exposures related to various adverse 
health outcomes (e.g., damage to the skin, including skin cancer; 
damage to the eye, such as cataracts; and immune system suppression); 
wavelength dependency of biological responses; and interindividual 
variability in UV-B resistance to such health outcomes. Beyond these 
well recognized adverse health effects associated with various 
wavelengths of UV radiation, the Criteria Document (section 10.2.3.6) 
also discusses protective effects of UV-B radiation. Recent reports 
indicate the necessity of UV-B in producing vitamin D, and that vitamin 
D deficiency can cause metabolic bone disease among children and 
adults, and may also increase the risk of many common chronic diseases 
(e.g., type I diabetes and rheumatoid arthritis) as well as the risk of 
various types of cancers. Thus, the Criteria Document concludes that 
any assessment that attempts to quantify the consequences of increased 
UV-B exposure on humans due to reduced ground-level O3 must 
include consideration of both negative and positive effects. However, 
as with other impacts of UV-B on human health, this beneficial effect 
of UV-B radiation has not been studied in sufficient detail to allow 
for a credible health benefits or risk assessment. In conclusion, the 
effect of changes in surface-level O3 concentrations on UV-
induced health outcomes cannot yet be critically assessed within 
reasonable uncertainty (Criteria Document, p. 10-36).
    The Agency last considered indirect effects of O3 in the 
ambient air in its 2003 final response to a remand of the Agency's 1997 
decision to revise the O3 NAAQS. In so doing, based on the 
available information in the last review, the Administrator determined 
that the information linking (a) Changes in patterns of ground-level 
O3 concentrations likely to occur as a result of programs 
implemented to attain the 1997 O3 NAAQS to (b) changes in 
relevant exposures to UV-B radiation of concern to public health was 
too uncertain at that time to warrant any relaxation in the level of 
public health protection previously determined to be requisite to 
protect against the demonstrated direct adverse respiratory effects of 
exposure to O3 in the ambient air (68 FR 614). At that time, 
the more recent information on protective effects of UV-B radiation was 
not available, such that only adverse UV-B-related effects could be 
considered. Taking into consideration the more recent information 
available in this review, the Criteria Document and Staff Paper 
conclude that the effect of changes in ground-level O3 
concentrations, likely to occur as a result of revising the 
O3 NAAQS, on UV-induced health outcomes, including whether 
these changes would ultimately result in increased or decreased 
incidence of UV-B-related diseases, cannot yet be critically assessed. 
EPA requests comment on available studies or data that would be 
relevant to conducting a critical assessment with reasonable certainty 
of UV-induced health outcomes and how evidence of UV-induced health 
outcomes might inform the Agency's review of the primary O3 
standard.
3. Interpretation and Integration of Health Evidence
    As discussed below, in assessing the new health evidence, the 
Criteria Document integrates findings from experimental (e.g., 
toxicological, dosimetric and controlled human exposure) and 
epidemiological studies, to make judgments about the extent to which 
causal inferences can be made about observed associations between 
health endpoints and exposure to O3. In evaluating the 
evidence from epidemiological studies, the EPA focuses on well-
recognized criteria, including: The strength of reported associations, 
including the magnitude and precision of reported effect estimates and 
their statistical significance; the robustness of reported 
associations, or stability in the effect estimates after considering 
factors such as alternative models and model specification, potential 
confounding by co-pollutants, and issues related to the consequences of 
exposure measurement error; potential aggregation bias in pooling data; 
and the consistency of the effects associations as observed by looking 
across results of multiple- and

[[Page 37838]]

single-city studies conducted by different investigators in different 
places and times. Consideration is also given to evaluating 
concentration-response relationships observed in epidemiological 
studies to inform judgments about the potential for threshold levels 
for O3-related effects. Integrating more broadly across 
epidemiological and experimental evidence, the Criteria Document also 
focuses on the coherence and plausibility of observed O3-
related health effects to reach judgments about the extent to which 
causal inferences can be made about observed associations between 
health endpoints and exposure to O3 in the ambient air.
a. Assessment of Evidence From Epidemiological Studies
    Key elements of the evaluation of epidemiological studies are 
briefly summarized below.
    (1) The strength of associations most directly refers to the 
magnitude of the reported relative risk estimates. Taking a broader 
view, the Criteria Document draws upon the criteria summarized in a 
recent report from the U.S. Surgeon General, which define strength of 
an association as ``the magnitude of the association and its 
statistical strength'' which includes assessment of both effect 
estimate size and precision, which is related to the statistical power 
of the study (CDC, 2004). In general, when associations are strong in 
terms of yielding large relative risk estimates, it is less likely that 
the association could be completely accounted for by a potential 
confounder or some other source of bias, whereas with associations that 
yield small relative risk estimates it is especially important to 
consider potential confounding and other factors in assessing 
causality. Effect estimates between O3 and some of the 
health outcomes are generally small in size and could thus be 
characterized as weak. For example, effect estimates for associations 
with mortality generally range from 0.5 to 5 percent increases per 
0.040 ppm increase in 1-hour maximum O3 or equivalent, 
whereas associations for hospitalization range up to 50 percent 
increases per standardized O3 increment. However, the 
Criteria Document notes that there are large multicity studies that 
find small associations between short-term O3 exposure and 
mortality or morbidity and have done so with great precision due to the 
statistical power of the studies (EPA, 2006a, p. 8-40). That is, the 
power of the studies allows the authors to reliably distinguish even 
weak relationships from the null hypothesis with statistical 
confidence.
    (2) In evaluating the robustness of associations, the Criteria 
Document (sections 7.1.3 and 8.4.4.3) and Staff Paper (section 3.4.2) 
have primarily considered the impact of exposure error, potential 
confounding by copollutants, and alternative models and model 
specifications.
    In time-series and panel studies, the temporal (e.g., daily or 
hourly) changes in ambient O3 concentrations measured at 
centrally-located ambient monitoring stations are generally used to 
represent a community's exposure to ambient O3. In 
prospective cohort or cross-sectional studies, air quality data 
averaged over a period of months to years are used as indicators of a 
community's long-term exposure to ambient O3 and other 
pollutants. In both types of analyses, exposure error is an important 
consideration, as actual exposures to individuals in the population 
will vary across the community.
    Ozone concentrations measured at central ambient monitoring sites 
may explain, at least partially, the variance in individual exposures 
to ambient O3; however, this relationship is influenced by 
various factors related to building ventilation practices and personal 
behaviors. Further, the pattern of exposure misclassification error and 
the influence of confounders may differ across the outcomes of interest 
as well as in susceptible populations. As discussed in the Criteria 
Document (section 3.9), only a limited number of studies have examined 
the relationship between ambient O3 concentrations and 
personal exposures to ambient O3. One of the strongest 
predictors of the relationship between ambient concentrations and 
personal exposures appears to be time spent outdoors. The strongest 
relationships were observed in outdoor workers (Brauer and Brook, 1995, 
1997; O'Neill et al., 2004). Statistically significant correlations 
between ambient concentrations and personal exposures were also 
observed for children, who likely spend more time outdoors in the warm 
season (Linn et al., 1996; Xue et al., 2005). There is some concern 
about the extent to which ambient concentrations are representative of 
personal O3 exposures of another particularly susceptible 
group of individuals, the debilitated elderly, since those who suffer 
from chronic cardiovascular or respiratory conditions may tend to 
protect themselves more than healthy individuals from environmental 
threats by reducing their exposure to both O3 and its 
confounders, such as high temperature and PM. Studies by Sarnat et al. 
(2001, 2005) that included this susceptible group reported mixed 
results for associations between ambient O3 concentrations 
and personal exposures to O3. Collectively, these studies 
observed that the daily averaged personal O3 exposures tend 
to be well correlated with ambient O3 concentrations despite 
the substantial variability that existed among the personal 
measurements. These studies provide supportive evidence that ambient 
O3 concentrations from central monitors may serve as valid 
surrogate measures for mean personal exposures experienced by the 
population, which is of most relevance for time-series studies. A 
better understanding of the relationship between ambient concentrations 
and personal exposures, as well as of the other factors that affect 
relationship will improve the interpretation of concentration-
population health response associations observed.
    The Criteria Document (section 7.1.3.1) also discusses the 
potential influence of exposure error on epidemiologic study results. 
Zeger et al. (2000) outlined the components to exposure measurement 
error, finding that ambient exposure can be assumed to be the product 
of the ambient concentration and an attenuation factor (i.e., building 
filter) and that panel studies and time-series studies that use ambient 
concentrations instead of personal exposure measurements will estimate 
a health risk that is attenuated by that factor. Navidi et al. (1999) 
used data from a children's cohort study to compare effect estimates 
from a simulated ``true'' exposure level to results of analyses from 
O3 exposures determined by several methods, finding that 
O3 exposures based on the use of ambient monitoring data 
overestimate the individual's O3 exposure and thus generally 
result in O3 effect estimates that are biased downward (EPA, 
2006a, p. 7-8). Similarly, in a reanalysis of a study by Burnett et al. 
(1994) on the acute respiratory effects of ambient air pollution, Zidek 
et al. (1998) reported that accounting for measurement error, as well 
as making a few additional changes to the analysis, resulted in 
qualitatively similar conclusions, but the effects estimates were 
considerably larger in magnitude (EPA, 2006a, p. 7-8). A simulation 
study by Sheppard et al. (2005) also considered attenuation of the risk 
based on personal behavior, their microenvironment, and the qualities 
of the pollutant in time-series studies. Of particular interest is 
their finding that risk estimates were not further attenuated in time-
series studies even when the correlations between personal exposures 
and ambient

[[Page 37839]]

concentrations were weak. In addition to overestimation of exposure and 
the resulting underestimation of effects, the use of ambient 
O3 concentrations may obscure the presence of thresholds in 
epidemiologic studies (EPA, 2006a, p. 7-9).
    As discussed in the Criteria Document (section 3.9), using ambient 
concentrations to determine exposure generally overestimates true 
personal O3 exposures by approximately 2- to 4-fold in 
available studies, resulting in attenuated risk estimates. The 
implication is that the effects being estimated occur at fairly low 
exposures and the potency of O3 is greater than these 
effects estimates indicate. As very few studies evaluating 
O3 health effects with personal O3 exposure 
measurements exist in the literature, effect estimates determined from 
ambient O3 concentrations must be evaluated and used with 
caution to assess the health risks of O3. In the absence of 
available data on personal O3 exposure, the use of routinely 
monitored ambient O3 concentrations as a surrogate for 
personal exposures is not generally expected to change the principal 
conclusions from O3 epidemiologic studies. Therefore, 
population health risk estimates derived using ambient O3 
levels from currently available observational studies, with appropriate 
caveats about personal exposure considerations, remain useful. The 
Criteria Document recommends caution in the quantitative use of effect 
estimates calculated using ambient O3 concentrations as they 
may lead to underestimation of the potency of O3. However, 
the Staff Paper observes that the use of these risk estimates for 
comparing relative risk reductions between alternative ambient 
O3 standards considered in the risk assessment (discussed 
below in section II.B.2) is less likely to suffer from this concern.
    Confounding occurs when a health effect that is caused by one risk 
factor is attributed to another variable that is correlated with the 
causal risk factor; epidemiological analyses attempt to adjust or 
control for potential confounders. Copollutants (e.g., PM, CO, 
SO2 and NO2) can meet the criteria for potential 
confounding in O3-health associations if they are potential 
risk factors for the health effect under study and are correlated with 
O3. Effect modifiers include variables that may influence 
the health response to the pollutant exposure (e.g., co-pollutants, 
individual susceptibility, smoking or age). Both are important 
considerations for evaluating effects in a mixture of pollutants, but 
for confounding, the emphasis is on controlling or adjusting for 
potential confounders in estimating the effects of one pollutant, while 
the emphasis for effect modification is on identifying and assessing 
the effects for different modifiers. The Criteria Document (p. 7-148) 
observes that O3 is generally not highly correlated with 
other criteria pollutants (e.g., PM10, CO, SO2 
and NO2), but may be more highly correlated with secondary 
fine particles, especially during the summer months, and that the 
degree of correlation between O3 and other pollutants may 
vary across seasons. For example, positive associations are observed 
between O3 and pollutants such as fine particles during the 
warmer months, but negative correlations may be observed during the 
cooler months (EPA, 2006a, p. 7-17). Thus, the Criteria Document 
(section 7.6.4) pays particular attention to the results of season-
specific analyses and studies that assess effects of PM in potential 
confounding of O3-health relationships. The Criteria 
Document also discussed the limitations of commonly used multipollutant 
models that include the difficulty in interpreting results where the 
copollutants are highly colinear, or where correlations between 
pollutants change by season (EPA, 2006a, p. 7-150). This is 
particularly the situation where O3 and a copollutant, such 
as sulfates, are formed under the same atmospheric condition; in such 
cases multipollutant models would produce unstable and possibly 
misleading results (EPA, 2006a, p. 7-152).
    For mortality, the results from numerous multi-city and single-city 
studies indicate that O3-mortality associations do not 
appear to be substantially changed in multipollutant models including 
PM10 or PM2.5 (EPA, 2006a, p. 7-101; Figure 7-
22). Focusing on results of warm season analyses, effect estimates for 
O3-mortality associations are fairly robust to adjustment 
for PM in multipollutant models (EPA, 2006a, p. 7-102; Figure 7-23). 
The Criteria Document concludes that in the few multipollutant analyses 
conducted for these endpoints, copollutants generally do not confound 
the relationship between O3 and respiratory hospitalization 
(EPA, 2006a, p. 7-79 to 7-80; Figure 7-12). Multipollutant models were 
not used as commonly in studies of relationships between respiratory 
symptoms or lung function with O3, but the Criteria Document 
reports that results of available analyses indicate that such 
associations generally were robust to adjustment for PM2.5 
(EPA, 2006a, p. 7-154). For example, in a large multi-city study of 
asthmatic children (Mortimer et al., 2002), the O3 effect 
was attenuated, but there was still a positive association; in Gent et 
al. (2003), effects of O3, but not PM2.5, 
remained statistically significant and even increased in magnitude in 
two-pollutant models (EPA, 2006a, p. 7-53). Considering this body of 
studies, the Criteria Document concludes: ``Multipollultant regression 
analyses indicated that O3 risk estimates, in general, were 
not sensitive to the inclusion of copollutants, including 
PM2.5 and sulfate. These results suggest that the effects of 
O3 on respiratory health outcomes appear to be robust and 
independent of the effects of other copollutants (EPA, 2006a, p. 7-
154).''
    The Criteria Document observes that another challenge of time-
series epidemiological analysis is assessing the relationship between 
O3 and health outcomes while avoiding bias due to 
confounding by other time-varying factors, particularly seasonal trends 
and weather variables (EPA, 2006a, p. 7-14). These variables are of 
particular interest because O3 concentrations have a well-
characterized seasonal pattern and are also highly correlated with 
changes in temperature, such that it can be difficult to distinguish 
whether effects are associated with O3 or with seasonal or 
weather variables in statistical analyses.
    The Criteria Document (section 7.1.3.4) discusses statistical 
modeling approaches that have been used to adjust for time-varying 
factors, highlighting a series of analyses that were done in a Health 
Effects Institute-funded reanalysis of numerous time-series studies. 
While the focus of these reanalyses was on associations with PM, a 
number of investigators also examined the sensitivity of O3 
coefficients to the extent of adjustment for temporal trends and 
weather factors. In addition, several recent studies, including U.S. 
multi-city studies (Bell et al., 2005; Huang et al., 2005; Schwartz et 
al., 2005) and a meta-analysis study (Ito et al., 2005), evaluated the 
effect of model specification on O3-mortality associations. 
As discussed in the Criteria Document (section 7.6.3.1), these studies 
generally report that associations reported with O3 are not 
substantially changed with alternative modeling strategies for 
adjusting for temporal trends and meteorologic effects. In the meta-
analysis by Ito et al. (2005), a separate multi-city analysis was 
presented that found that alternative adjustments for weather resulted 
in up to 2-fold difference in the O3 effect estimate. 
Significant confounding can occur when strong seasonal cycles are 
present, suggesting

[[Page 37840]]

that season-specific results are more generally robust than year-round 
results in such cases. A number of epidemiological studies have 
conducted season-specific analyses, and have generally reported 
stronger and more precise effect estimates for O3 
associations in the warm season than in analyses conducted in the cool 
seasons or over the full year.
    (3) Consistency refers to the persistent finding of an association 
between exposure and outcome in multiple studies of adequate power in 
different persons, places, circumstances and times (CDC, 2004). In 
considering results from multi-city studies and single-city studies in 
different areas, the Criteria Document (p. 8-41) observes general 
consistency in effects of short-term O3 exposure on 
mortality, respiratory hospitalization and other respiratory health 
outcomes. The variations in effects that are observed may be 
attributable to differences in relative personal exposure to 
O3, as well as varying concentrations and composition of 
copollutants present in different regions. Thus, the Criteria Document 
(p. 8-41) concludes that ``consideration of consistency or 
heterogeneity of effects is appropriately understood as an evaluation 
of the similarity or general concordance of results, rather than an 
expectation of finding quantitative results with a very narrow range.''
    (4) The Staff Paper recognizes that it is likely that there are 
biological thresholds for different health effects in individuals or 
groups of individuals with similar innate characteristics and health 
status. For O3 exposure, individual thresholds would 
presumably vary substantially from person to person due to individual 
differences in genetic susceptibility, pre-existing disease conditions 
and possibly individual risk factors such as diet or exercise levels 
(and could even vary from one time to another for a given person). 
Thus, it would be difficult to detect a distinct threshold at the 
population level below which no individual would experience a given 
effect, especially if some members of a population are unusually 
sensitive even down to very low concentrations (EPA, 2004, p. 9-43, 9-
44).
    Some studies have tested associations between O3 and 
health outcomes after removal of days with higher O3 levels 
from the data set; such analyses do not necessarily indicate the 
presence or absence of a threshold, but provide some information on 
whether the relationship is found using only lower-concentration data. 
For example, using data from 95 U.S. cities, Bell et al. (2004) found 
that the effect estimate for an association between short-term 
O3 exposure and mortality was little changed when days 
exceeding 0.060 ppm (24-hour average) were excluded in the analysis. 
Bell et al. (2006) found no difference in estimated effect even when 
all days with 24-hour O3 concentrations <0.020 ppm were 
excluded (EPA, 2006a, p. 8-43). Using data from 8 U.S. cities, Mortimer 
and colleagues (2002) also reported that associations between 
O3 and both lung function and respiratory symptoms remained 
statistically significant and of the same or greater magnitude in 
effect size when concentrations greater than 0.080 ppm (8-hour average) 
were excluded (EPA, 2006a, p. 7-46). Several single-city studies also 
report similar findings of associations that remain or are increased in 
magnitude and statistical significance when data at the upper end of 
the concentration range are removed (EPA, 2006a, section 7.6.5).
    Other time-series epidemiological studies have used statistical 
modeling approaches to evaluate whether thresholds exist in 
associations between short-term O3 exposure and mortality. 
As discussed in section 7.6.5 of the Criteria Document, one European 
multi-city study included evaluation of the shape of the concentration-
response curve, and observed no deviation from a linear function across 
the range of O3 measurements from the study (Gryparis et 
al., 2004; EPA, 2006a, p. 7-154). Several single-city studies also 
observed a monotonic increase in associations between O3 and 
morbidity that suggest that no population threshold exists (EPA, 2006a, 
p. 7-159).
    On the other hand, a study in Korea used several different modeling 
approaches and reported that a threshold model provided the best fit 
for the data. The results suggested a potential threshold level of 
about 0.045 ppm (1-hour maximum concentration; < 0.035 ppm, 8-hour 
average) for an association between mortality and short-term 
O3 exposure during the summer months (Kim et al., 2004; EPA, 
2006a, p. 8-43). The authors reported larger effect estimates for the 
association for data above the potential threshold level, suggesting 
that an O3-mortality association might be underestimated in 
the non-threshold model. A threshold analysis recently reported by Bell 
et al. (2006) for 98 U.S. communities, including the same 95 
communities in Bell et al. (2004), indicated that if a population 
threshold existed for mortality, it would likely fall below a 24-hour 
average O3 concentration of 0.015 ppm (<0.025 ppm, 8-hour 
average). In addition, Burnett and colleagues (1997a,b) plotted the 
relationships between air pollutant concentrations and both respiratory 
and cardiovascular hospitalization, and it appears in these results 
that the associations with O3 are found in the concentration 
range above about 0.030 ppm (1-hour maximum; < 0.025 ppm, 8-hour 
average). Vedal and colleagues (2003) reported a significant 
association between O3 and mortality in British Columbia 
where O3 concentrations were quite low (mean 1-hour maximum 
concentration of 0.0273 ppm). The authors did not specifically test for 
threshold levels, but the fact that the association was found in an 
area with such low O3 concentrations suggests that any 
potential threshold level would be quite low in this data set.
    In summary, the Criteria Document finds that, taken together, the 
available evidence from clinical and epidemiological studies suggests 
that no clear conclusion can now be reached with regard to possible 
threshold levels for O3-related effects (EPA, 2006a, p. 8-
44). Thus, the available epidemiological evidence neither supports nor 
refutes the existence of thresholds at the population level for effects 
such as increased hospital admissions and premature mortality. There 
are limitations in epidemiological studies that make discerning 
thresholds in populations difficult, including low data density in the 
lower concentration ranges, the possible influence of exposure 
measurement error, and interindividual differences in susceptibility to 
O3-related effects in populations. There is the possibility 
that thresholds for individuals may exist in reported associations at 
fairly low levels within the range of air quality observed in the 
studies but not be detectable as population thresholds in 
epidemiological analyses.
b. Biological Plausibility and Coherence of Evidence
    The body of epidemiological studies discussed in the Staff Paper 
emphasizes the role of O3 in association with a variety of 
adverse respiratory and cardiovascular effects. While recognizing a 
variety of plausible mechanisms, there exists a general consensus 
suggesting that O3 could, either directly or through 
initiation, interfere with basic cellular oxidation processes 
responsible for inflammation, reduced antioxidant capacity, 
atherosclerosis and other effects. Reasoning that O3 
influences cellular chemistry through basic oxidative properties (as 
opposed to a unique chemical interaction), other reactive oxidizing 
species (ROS) in the

[[Page 37841]]

atmosphere acting either independently or in combination with 
O3 may also contribute to a number of adverse respiratory 
and cardiovascular health effects. Consequently, the role of 
O3 should be considered more broadly as O3 
behaves as a generator of numerous oxidative species in the atmosphere.
    In considering the biological plausibility of reported 
O3-related effects, the Staff Paper (section 3.4.6) 
considers this broader question of health effects of pollutant mixtures 
containing O3. The potential for O3-related 
enhancements of PM formation, particle uptake, and exacerbation of PM-
induced cardiovascular effects underscores the importance of 
considering contributions of O3 interactions with other 
often co-occurring air pollutants to health effects due to 
O3-containing pollutant mixes. The Staff Paper summarizes 
some examples of important pollutant mixture effects from studies that 
evaluate interactions of O3 with other co-occurring 
pollutants, as discussed in chapters 4, 5, and 6 of the Criteria 
Document.
    All of the types of interactive effects of O3 with other 
co-occurring gaseous and nongaseous viable and nonviable PM components 
of ambient air mixes noted above argue that O3 acts not only 
alone but that O3 also is a surrogate indicator for air 
pollution mixes which may enhance the risk of adverse effects due to 
O3 acting in combination with other pollutants. Viewed from 
this perspective, those epidemiologic findings of morbidity and 
mortality associations, with ambient O3 concentrations 
extending to quite low levels in many cases, become more understandable 
and plausible.
    The Criteria Document integrates epidemiological studies with 
mechanistic information from controlled human exposure studies and 
animal toxicological studies to draw conclusions regarding the 
coherence of evidence and biological plausibility of O3-
related health effects to reach judgments about the causal nature of 
observed associations. As summarized below, coherence and biological 
plausibility are discussed for each of the following types of 
O3-related effects: short-term effects on the respiratory 
system, effects on the cardiovascular system, effects related to long-
term O3 exposure, and short-term mortality-related health 
endpoints.
i. Coherence and Plausibility of Short-Term Effects on the Respiratory 
System
    Acute respiratory morbidity effects that have been associated with 
short-term exposure to O3 include such health endpoints as 
decrements in lung function, increased airway responsiveness, airway 
inflammation, increased permeability related to epithelial injury, 
immune system effects, emergency department visits for respiratory 
diseases, and hospitalization due to respiratory illness.
    Recent epidemiological studies have supported evidence available in 
the previous O3 NAAQS review on associations between ambient 
O3 exposure and decline in lung function for children. The 
Criteria Document (p. 8-34) concludes that exposure to ambient 
O3 has a significant effect on lung function and is 
associated with increased respiratory symptoms and medication use, 
particularly in asthmatics. Short-term exposure to O3 has 
also been associated with more severe morbidity endpoints, such as 
emergency department visits and hospital admissions for respiratory 
cases, including specific respiratory illness (e.g., asthma) (EPA, 
2006a, sections 7.3.2 and 7.3.3). In addition, a few epidemiological 
studies have reported positive associations between short-term 
O3 exposure and respiratory mortality, though the 
associations are not generally statistically significant (EPA, 2006a, 
p. 7-108).
    Considering the evidence from epidemiological studies, the results 
described above provide evidence for coherence in O3-related 
effects on the respiratory system. Effect estimates from U.S. and 
Canadian studies are shown in Figure 1, where it can be seen that 
mostly positive associations have been reported with respiratory 
effects ranging from respiratory symptoms, such as cough or wheeze, to 
hospitalization for various respiratory diseases, and there is 
suggestive evidence for associations with respiratory mortality. Many 
of the reported associations are statistically significant, 
particularly in the warm season. In Figure 1, the central effect 
estimate is indicated by a square for each result, with the vertical 
bar representing the 95 percent confidence interval around the 
estimate. In the discussions that follow, an individual study result is 
considered to be statistically significant if the 95 percent confidence 
interval does not include zero.\21\ Positive effect estimates indicate 
increases in the health outcome with O3 exposure. In 
considering these results as a whole, it is important to consider not 
only whether statistical significance at the 95 percent confidence 
level is reported in individual studies but also the general pattern of 
results, focusing in particular on studies with greater statistical 
power that report relatively more precise results.
---------------------------------------------------------------------------

    \21\ Results for studies of respiratory symptoms are presented 
as odds ratios; an odds ratio of 1.0 is equivalent to no effect, and 
thus is presented as equivalent to the zero effect estimate line.
---------------------------------------------------------------------------

BILLING CODE 6560-50-P

[[Page 37842]]

[GRAPHIC] [TIFF OMITTED] TP11JY07.000

BILLING CODE 6560-50-C
    Considering also evidence from toxicological, chamber, and field 
studies, the Criteria Document (section 8.6) discusses biological 
plausibility and coherence of evidence for acute O3-induced 
respiratory health effects. Inhalation of O3 for several 
hours while subjects are physically active can elicit both acute 
adverse pathophysiological changes and subjective respiratory tract 
symptoms (EPA, 2006a, section 8.4.2). Acute pulmonary responses 
observed in healthy humans exposed to O3 at ambient 
concentrations include: decreased inspiratory capacity; mild 
bronchoconstriction; rapid, shallow breathing during exercise; 
subjective symptoms of tracheobronchial airway irritation, including 
cough and pain on deep inspiration; decreases in measures of lung 
function; and increased airway resistance. The severity of symptoms and 
magnitude of response depends on inhaled dose, individual O3 
sensitivity, and the degree of attenuation or enhancement of response 
resulting from previous O3 exposures. Lung function studies 
of several animal species acutely exposed to relatively low 
O3 levels (0.25 to 0.4 ppm) show responses similar to those 
observed in humans, including increased breathing frequency, decreased 
tidal volume, increased resistance, and decreased FVC. Alterations in 
breathing pattern return to normal within hours of exposure, and 
attenuation in functional responses

[[Page 37843]]

following repeated O3 exposures is similar to those observed 
in humans.
    Physiological and biochemical alterations investigated in 
controlled human exposure and animal toxicology studies tend to support 
certain hypotheses of underlying pathological mechanisms which lead to 
the development of respiratory-related effects reported in epidemiology 
studies (e.g., increased hospitalization and medication use). Some of 
these are: (a) Decrements in lung function, (b) bronchoconstriction, 
(c) increased airway responsiveness, (d) airway inflammation, (e) 
epithelial injury, (f) immune system activation, (g) host defense 
impairment, and (h) sensitivity of individuals, which depends on at 
least a person's age, disease status, genetic susceptibility, and the 
degree of attenuation present due to prior exposures. The time 
sequence, magnitude, and overlap of these complex events, both in terms 
of development and recovery, illustrate the inherent difficulty of 
interpreting the biological plausibility of O3-induced 
cardiopulmonary health effects (EPA, 2006a, p. 8-48).
    The interaction of O3 with airway epithelial cell 
membranes and ELF to form lipid ozonation products and ROS is supported 
by numerous human, animal and in vitro studies. Ozonation products and 
ROS initiate a cascade of events that lead to oxidative stress, injury, 
inflammation, airway epithelial damage and increased epithelial damage 
and increased alveolar permeability to vascular fluids. Repeated 
respiratory inflammation can lead to a chronic inflammatory state with 
altered lung structure and lung function and may lead to chronic 
respiratory diseases such as fibrosis and emphysema (EPA, 2006a, 
section 8.6.2). Continued respiratory inflammation also can alter the 
ability to respond to infectious agents, allergens and toxins. Acute 
inflammatory responses to O3 are well documented, and lung 
injury can become apparent within 3 hours after exposure in humans.
    Taken together, the Criteria Document concludes that the evidence 
from experimental human and animal toxicology studies indicates that 
acute O3 exposure is causally associated with respiratory 
system effects, including O3-induced pulmonary function 
decrements, respiratory symptoms, lung inflammation, and increased lung 
permeability, airway hyperresponsiveness, increased uptake of nonviable 
and viable particles, and consequent increased susceptibility to PM-
related toxic effects and respiratory infections (EPA, 2006a, p. 8-48).
ii. Coherence and Plausibility of Effects on the Cardiovascular System
    There is very limited experimental evidence of animals and humans 
that has evaluated possible mechanisms or physiological pathways by 
which acute O3 exposures may induce cardiovascular system 
effects. Ozone induces lung injury, inflammation, and impaired 
mucociliary clearance, with a host of associated biochemical changes 
all leading to increased lung epithelial permeability. As noted above 
in section II.A.2.b, the generation of lipid ozonation products and ROS 
in lung tissues can influence pulmonary hemodynamics, and ultimately 
the cardiovascular system. Other potential mechanisms by which 
O3 exposure may be associated with cardiovascular disease 
outcomes have been described. Laboratory animals exposed to relatively 
high O3 concentrations (>=0.5 ppm) demonstrate tissue edema 
in the heart and lungs. Ozone-induced changes in heart rate, edema of 
heart tissue, and increased tissue and serum levels of ANF found with 
8-hour 0.5 ppm O3 exposure in animal toxicology studies 
(Vesely et al., 1994a, b, c) also raise the possibility of potential 
cardiovascular effects of acute ambient O3 exposures.
    Animal toxicology studies have found both transient and persistent 
ventilatory responses with and without progressive decreases in heart 
rate (Arito et al., 1997). Observations of O3-induced 
vasoconstriction in a controlled human exposure study by Brook et al. 
(2002) suggests another possible mechanism for O3-related 
exacerbations of preexisting cardiovascular disease. One controlled 
human study (Gong et al., 1998) evaluated potential cardiovascular 
health effects of O3 exposure. The overall results did not 
indicate acute cardiovascular effects of O3 in either the 
hypertensive or control subjects. The authors observed an increase in 
rate-pressure product and heart rate, a decrement for FEV1, 
and a >10 mm Hg increase in the alveolar/arterial pressure difference 
for O2 following O3 exposure. Foster et al. 
(1993) demonstrated that even in relatively young healthy adults, 
O3 exposure can cause ventilation to shift away from the 
well-perfused basal lung. This effect of O3 on ventilation 
distribution may persist beyond 24-hours post-exposure (Foster et al., 
1997). These findings suggest that O3 may exert 
cardiovascular effects indirectly by impairing alveolar-arterial 
O2 transfer and potentially reducing O2 supply to 
the myocardium. Ozone exposure may increase myocardial work and impair 
pulmonary gas exchange to a degree that could perhaps be clinically 
important in persons with significant preexisting cardiovascular 
impairment.
    As noted above in section II.A.2.b, a limited number of new 
epidemiological studies have reported associations between short-term 
O3 exposure and effects on the cardiovascular system. Among 
these studies, three were population-based and involved relatively 
large cohorts; two of these studies evaluated associations between 
O3 and heart rate variability (HRV) and the other study 
evaluated the association between O3 levels and the relative 
risk of myocardial infarction (MI). Such studies may offer more 
informative results based on their large subject-pool and design. 
Results from these three studies were suggestive of an association 
between O3 exposure and the cardiovascular endpoints 
studied. In other recent studies on the incidence of MI and some more 
subtle cardiovascular health endpoints, such as changes in HRV or 
cardiac arrhythmia, some but not all studies reported associations with 
short-term exposure to O3 (EPA, 2006a, section 7.2.7.1). 
From these studies, the Criteria Document concludes that the ``current 
evidence is rather limited but suggestive of a potential effect on HRV, 
ventricular arrhythmias, and MI incidence'' (EPA, 2006a, p. 7-65).
    An increasing number of studies have evaluated the association 
between O3 exposure and cardiovascular hospital admissions. 
As discussed in section 7.3.4 of the Criteria Document, many reported 
negative or inconsistent associations, whereas other studies, 
especially those that examined the relationship when O3 
exposures were higher, have found positive and robust associations 
between O3 and cardiovascular hospital admissions. The 
Criteria Document finds that the overall evidence from these studies 
remains inconclusive regarding the effect of O3 on 
cardiovascular hospitalizations (EPA, 2006a, p. 7-83).
    The Criteria Document notes that the suggestive positive 
epidemiologic findings of O3 exposure on cardiac autonomic 
control, including effects on HRV, ventricular arrhythmias and MI, and 
reported associations between O3 exposure and cardiovascular 
hospitalizations generally in the warm season gain credibility and 
scientific support from the results of experimental animal toxicology 
and human clinical studies, which are indicative of plausible pathways 
by which O3 may exert cardiovascular effects (EPA, 2006a, 
section 8.6.1).

[[Page 37844]]

iii. Coherence and Plausibility of Effects Related to Long-Term 
O3 Exposure
    Human chamber studies can not evaluate effects of long-term 
exposures to O3; there is some evidence available from 
toxicological studies. While early animal toxicology studies of long-
term O3 exposures were conducted using continuous exposures, 
more recent studies have focused on exposures which mimic diurnal and 
seasonal patterns and more realistic O3 exposure levels 
(EPA, 2006a, p. 8-50). Studies of monkeys that compared these two 
exposure scenarios found increased airway pathology only with the 
latter design. Persistent and irreversible effects reported in chronic 
animal toxicology studies suggest that additional complementary human 
data are needed from epidemiologic studies (EPA, 2006a, p. 8-50).
    There is limited evidence from human studies for long-term 
O3-induced effects on lung function. As discussed in section 
8.6.2 of the Criteria Document, previous epidemiological studies have 
provided only inconclusive evidence for either mortality or morbidity 
effects of long-term O3 exposure. The Criteria Document 
observes that the inconsistency in findings may be due to a lack of 
precise exposure information, the possibility of selection bias, and 
the difficulty of controlling for confounders (EPA, 2006a, p. 8-50). 
Several new longitudinal epidemiology studies have evaluated 
associations between long-term O3 exposures and morbidity 
and mortality and suggest that these long-term exposures may be related 
to changes in lung function in children; however, little evidence is 
available to support a relationship between chronic O3 
exposure and mortality or lung cancer incidence (EPA, 2006a, p. 8-50).
    The Criteria Document (p. 8-51) concludes that evidence from animal 
toxicology studies strongly suggests that chronic O3 
exposure is capable of damaging the distal airways and proximal 
alveoli, resulting in lung tissue remodeling leading to apparent 
irreversible changes. Such structural changes and compromised pulmonary 
function caused by persistent inflammation may exacerbate the 
progression and development of chronic lung disease. Together with the 
limited evidence available from epidemiological studies, these findings 
offer some insight into potential biological mechanisms for suggested 
associations between long-term or seasonal exposures to O3 
and reduced lung function development in children which have been 
observed in epidemiologic studies (EPA, 2006a, p. 8-51).
iv. Coherence and Plausibility of Short-Term Mortality-Related Health 
Endpoints
    An extensive epidemiological literature on air pollution related 
mortality risk estimates from the U.S., Canada, and Europe is discussed 
in the Criteria Document (sections 7.4 and 8.6.3). These single- and 
multi-city mortality studies coupled with meta-analyses generally 
indicate associations between acute O3 exposure and elevated 
risk for all-cause mortality, even after adjustment for the influence 
of season and PM. Several single-city studies that specifically 
evaluated the relationship between O3 exposure and 
cardiopulmonary mortality also reported results suggestive of a 
positive association (EPA, 2006a, p. 8-51). These mortality studies 
suggest a pattern of effects for causality that have biologically 
plausible explanations, but our knowledge regarding potential 
underlying mechanisms is very limited at this time and requires further 
research. Most of the physiological and biochemical parameters 
investigated in human and animal studies suggest that O3-
induced biochemical effects are relatively transient and attenuate over 
time. The Criteria Document (p. 8-52) hypothesizes a generic pathway of 
O3-induced lung damage, potentially involving oxidative lung 
damage with subsequent inflammation and/or decline in lung function 
leading to respiratory distress in some sensitive population groups 
(e.g., asthmatics), or other plausible pathways noted below that may 
lead to O3-related contributions to cardiovascular effects 
that ultimately increase risk of mortality.
    The third National Health and Nutrition Examination Follow-up data 
analysis indicates that about 20 percent of the adult population has 
reduced FEV1 values, suggesting impaired lung function in 
some portion of the population. Most of these individuals have COPD, 
asthma or fibrotic lung disease (Manino et al., 2003), which are 
associated with persistent low-grade inflammation. Furthermore, 
patients with COPD are at increased risk for cardiovascular disease. 
Also, lung disease with underlying inflammation may be linked to low-
grade systemic inflammation associated with atherosclerosis, 
independent of cigarette smoking (EPA, 2006a, p. 8-52). Lung function 
decrements in persons with cardiopulmonary disease have been associated 
with inflammatory markers, such as C-reactive protein (CRP) in the 
blood. At a population level it has been found that individuals with 
the lowest FEV1 values have the highest levels of CRP, and 
those with the highest FEV1 values have the lowest CRP 
levels (Manino et al., 2003; Sin and Man, 2003). This complex series of 
physiological and biochemical reactions following O3 
exposure may tilt the biological homeostasis mechanisms which could 
lead to adverse health effects in people with compromised 
cardiopulmonary systems.
    Of much interest are several other types of newly available data 
that support reasonable hypotheses that may help to explain the 
findings of O3-related increases in cardiovascular mortality 
observed in some epidemiological studies. These include the direct 
effect of O3 on increasing PAF in lung tissue that can then 
enter the general circulation and possibly contribute to increased risk 
of blood clot formation and the consequent increased risk of MI, 
cerebrovascular events (stroke), or associated cardiovascular-related 
mortality. Ozone reactions with cholesterol in lung surfactant to form 
epoxides and oxysterols that are cytotoxic to lung and heart muscles 
and that contribute to atherosclerotic plaque formation in arterial 
walls represent another potential pathway. Stimulation of airway 
irritant receptors may lead to increases in tissue and serum levels of 
ANF, changes in heart rate, and edema of heart tissue. A few new field 
and panel studies of human adults have reported associations between 
ambient O3 concentrations and changes in cardiac autonomic 
control (e.g., HRV, ventricular arrhythmias, and MI). These represent 
plausible pathways that may lead to O3-related contributions 
to cardiovascular effects that ultimately increase the risk of 
mortality.
    In addition, O3-induced increases in lung permeability 
allow more ready entry for inhaled PM into the blood stream, and 
O3 exposure may increase the risk of PM-related 
cardiovascular effects. Furthermore, increased ambient O3 
levels contribute to ultrafine PM formation in the ambient air and 
indoor environments. Thus, the contributions of elevated ambient 
O3 concentrations to ultrafine PM formation and human 
exposure, along with the enhanced uptake of inhaled fine particles, 
consequently may contribute to exacerbation of PM-induced 
cardiovascular effects in addition to those more directly induced by 
O3 (EPA, 2006a, p. 8-53).
c. Summary
    Judgments concerning the extent to which relationships between 
various health endpoints and ambient O3

[[Page 37845]]

exposures are likely causal are informed by the conclusions and 
discussion in the Criteria Document as discussed above and summarized 
in section 3.7.5 of the Staff Paper. These judgments reflect the nature 
of the evidence and overall weight of the evidence, and are taken into 
consideration in the quantitative risk assessment discussed below in 
section II.B.2.
    For example, there is a very high level of confidence that 
O3 induces lung function decrements in healthy adults and 
children due in part to the dozens of controlled human exposure and 
epidemiological studies consistently showing such effects. The Criteria 
Document (p. 8-74) states that these studies provide clear evidence of 
causality for associations between short-term O3 exposures 
and statistically significant declines in lung function in children, 
asthmatics and adults who exercise outdoors. An increase in respiratory 
symptoms (e.g., cough, shortness of breath) has been observed in 
controlled human exposure studies of short-term O3 
exposures, and significant associations between ambient O3 
exposures and a wide variety of symptoms have been reported in 
epidemiology studies (EPA, 2006a, p. 8-75). Aggregate population time-
series studies showing robust associations with respiratory hospital 
admissions and emergency department visits are strongly supported by 
human clinical, animal toxicologic, and epidemiologic evidence for 
O3-related lung function decrements, respiratory symptoms, 
airway inflammation, and airway hyperreactivity. The Criteria Document 
(p. 8-77) concludes that, taken together, the overall evidence supports 
the inference of a causal relationship between acute ambient 
O3 exposures and increased respiratory morbidity outcomes 
resulting in increased emergency department visits and hospitalizations 
during the warm season. Further, recent epidemiologic evidence has been 
characterized in the Criteria Document (p. 8-78) as highly suggestive 
that O3 directly or indirectly contributes to non-accidental 
and cardiopulmonary-related mortality.
4. O3-Related Impacts on Public Health
    The following discussion draws from chapters 6 and 7 and section 
8.7 of the Criteria Document and section 3.6 of the Staff Paper to 
characterize factors which modify responsiveness to O3, 
subpopulations potentially at risk for O3-related health 
effects, the adversity of O3-related effects, and the size 
of the at-risk subpopulations in the U.S. These considerations are all 
important elements in characterizing the potential public health 
impacts associated with exposure to ambient O3.
a. Factors That Modify Responsiveness to Ozone
    There are numerous factors that can modify individual 
responsiveness to O3. These include: influence of physical 
activity; age; gender and hormonal influences; racial, ethnic and 
socioeconomic status (SES) factors; environmental factors; and oxidant-
antioxidant balance. These factors are discussed in more detail in 
section 6.5 of the Criteria Document.
    It is well established that physical activity increases an 
individual's minute ventilation and will thus increase the dose of 
O3 inhaled (EPA, 2006a, section 6.5.4). Increased physical 
activity results in deeper penetration of O3 into more 
distal regions of the lungs, which are more sensitive to acute 
O3 response and injury. This will result in greater lung 
function decrements for acute exposures of individuals during increased 
physical activity. Research has shown that respiratory effects are 
observed at lower O3 concentrations if the level of exertion 
is increased and/or duration of exposure and exertion are extended. 
Predicted O3-induced decrements in lung function have been 
shown to be a function of exposure concentration, duration and exercise 
level for healthy, young adults (McDonnell et al., 1997).
    Most of the studies investigating the influence of age have used 
lung function decrements and symptoms as measures of response. For 
healthy adults, lung function and symptom responses to O3 
decline as age increases. The rate of decline in O3 
responsiveness appears greater in those 18 to 35 years old compared to 
those 35 to 55 years old, while there is very little change after age 
55. In one study (Seal et al., 1996) analyzing a large data set, a 5.4% 
decrement in FEV1 was estimated for 20 year old individuals exposed to 
0.12 ppm O3, whereas similar exposure of 35 year old 
individuals were estimated to have a 2.6% decrement. While healthy 
children tend not to report respiratory symptoms when exposed to low 
levels of O3, for subjects 18 to 36 years old symptom 
responses induced by O3 tend to decrease with increasing age 
(McDonnell et al., 1999).
    Limited evidence of gender differences in response to O3 
exposure has suggested that females may be predisposed to a greater 
susceptibility to O3. Lower plasma and NL fluid levels of 
the most prevalent antioxidant, uric acid, in females relative to males 
may be a contributing factor. Consequently, reduced removal of 
O3 in the upper airways may promote deeper penetration. 
However, most of the evidence on gender differences appears to be 
equivocal, with one study (Hazucha et al., 2003) suggesting that 
physiological responses of young healthy males and females may be 
comparable (EPA, 2006a, section 6.5.2).
    A few studies have suggested that ethnic minorities might be more 
responsive to O3 than Caucasian population groups (EPA, 
2006a, section 6.5.3). This may be more the result of a lack of 
adequate health care and socioeconomic status (SES) than any 
differences in sensitivity to O3. The limited data 
available, which have investigated the influence of race, ethnic or 
other related factors on responsiveness to O3, prevent 
drawing any clear conclusions at this time.
    Few human studies have examined the potential influence of 
environmental factors such as the sensitivity of individuals who 
voluntarily smoke tobacco (i.e., smokers) and the effect of high 
temperatures. New controlled human exposure studies have confirmed that 
smokers are less responsive to O3 than nonsmokers; however, 
time course of development and recovery of these effects, as well as 
reproducibility, was not different from nonsmokers (EPA, 2006a, section 
6.5.5). Influence of ambient temperature on pulmonary effects induced 
by O3 has been studied very little, but additive effects of 
heat and O3 exposure have been reported.
    Antioxidants, which scavenge free radicals and limit lipid 
peroxidation in the ELF, are the first line of defense against 
oxidative stress. Ozone exposure leads to absorption of O3 
in the ELF with subsequent depletion of antioxidant in the nasal ELF, 
but concentration and antioxidant enzyme activity in ELF or plasma do 
not appear related to O3 responsiveness (EPA 2006a, section 
6.5.6). Controlled studies of dietary antioxidant supplements have 
shown some protective effects on lung function decrements but not on 
symptoms and airway inflammatory responses. Dietary antioxidant 
supplements have provided some protection to asthmatics by attenuating 
post-exposure airway hyperresponsiveness. Animal studies have also 
supported the protective effects of ELF antioxidants.
b. At-Risk Subgroups for O3-Related Effects
    Several characteristics may increase the extent to which a 
population group shows increased susceptibility or vulnerability. 
Information on potentially susceptible and vulnerable groups is 
summarized in section 8.7 of the

[[Page 37846]]

Criteria Document. As described there, the term susceptibility refers 
to innate (e.g., genetic or developmental) or acquired (e.g., personal 
risk factors, age) factors that make individuals more likely to 
experience effects with exposure to pollutants. A number of population 
groups have been identified as potentially susceptible to health 
effects as a result of O3 exposure, including people with 
existing lung diseases, including asthma, children and older adults, 
and people who have larger than normal lung function responses that may 
be due to genetic susceptibility. In addition, some population groups 
have been identified as having increased vulnerability to 
O3-related effects due to increased likelihood of exposure 
while at elevated ventilation rates, including healthy children and 
adults who are active outdoors, for example, outdoor workers, and 
joggers. Taken together, the susceptible and vulnerable groups make up 
``at-risk'' groups.\22\
---------------------------------------------------------------------------

    \22\ In the Staff Paper and documents from previous 
O3 NAAQS reviews, ``at-risk'' groups have also been 
called ``sensitive'' groups, to mean both groups with greater 
inherent susceptibility and those more likely to be exposed.
---------------------------------------------------------------------------

i. Active People
    A large group of individuals at risk from O3 exposure 
consists of outdoor workers and children, adolescents, and adults who 
engage in outdoor activities involving exertion or exercise during 
summer daylight hours when ambient O3 concentrations tend to 
be higher. This conclusion is based on a large number of controlled-
human exposure studies and several epidemiologic field/panel studies 
which have been conducted with healthy children and adults and those 
with preexisting respiratory diseases (EPA 2006a, sections 6.2, 6.3, 
7.2, and 8.4.4). The controlled human exposure studies show a clear 
O3 exposure-response relationship with increasing 
spirometric and symptomatic response as exercise level increases. 
Furthermore, O3-induced response increases as time of 
exposure increases. Studies of outdoor workers and others who 
participate in outdoor activities indicate that extended exposures to 
O3 at elevated exertion levels can produce marked effects on 
lung function, as discussed above in section IIA.2 (Brauer et al., 
1996; H[ouml]ppe et al., 1995; Korrick et al., 1998; McConnell et al., 
2002).
    These field studies with subjects at elevated exertion levels 
support the extensive evidence derived from controlled human exposure 
studies. The majority of human chamber studies have examined the 
effects of O3 exposure in subjects performing continuous or 
intermittent exercise for variable periods of time. Significant 
O3-induced respiratory responses have been observed in 
clinical studies of exercising individuals. The epidemiologic studies 
discussed above also indicate that prolonged exposure periods, combined 
with elevated levels of exertion or exercise, may magnify O3 
effects on lung function. Thus, outdoor workers and others who 
participate in higher exertion activities outdoors during the time of 
day when high peak O3 concentrations occur appear to be 
particularly vulnerable to O3 effects on respiratory health. 
Although these studies show a wide variability of response and 
sensitivity among subjects and the factors contributing to this 
variability continue to be incompletely understood, the effect of 
increased exertion is consistent. It should be noted that this wide 
variability of response and sensitivity among subjects may be in part 
due to the wide range of other highly reactive photochemical oxidants 
coexisting with O3 in the ambient air.
ii. People With Lung Disease
    People with preexisting pulmonary disease are likely to be among 
those at increased risk from O3 exposure. Altered 
physiological, morphological and biochemical states typical of 
respiratory diseases like asthma, COPD and chronic bronchitis may 
render people sensitive to additional oxidative burden induced by 
O3 exposure. At the time of the last review, it was 
concluded that this group was at greater risk because the impact of 
O3-induced responses on already-compromised respiratory 
systems would noticeably impair an individual's ability to engage in 
normal activity or would be more likely to result in increased self-
medication or medical treatment. At that time there was little evidence 
that people with pre-existing disease were more responsive than healthy 
individuals in terms of the magnitude of pulmonary function decrements 
or symptomatic responses. The new results from controlled exposure and 
epidemiologic studies continue to indicate that individuals with 
preexisting pulmonary disease are a sensitive subpopulation for 
O3 health effects.
    Several clinical studies reviewed in the 1996 Criteria Document on 
atopic and asthmatic subjects had suggested but not clearly 
demonstrated enhanced responsiveness to acute O3 exposure 
compared to healthy subjects. The majority of the newer studies 
reviewed in Chapter 6 of the Criteria Document indicate that asthmatics 
are as sensitive as, if not more sensitive than, normal subjects in 
manifesting O3-induced pulmonary function decrements. In one 
key study (Horstman et al., 1995), the FEV1 decrement observed in the 
asthmatics was significantly larger than in the healthy subjects (19% 
versus 10%, respectively). There was also a notable tendency for a 
greater O3-induced decrease in FEF25-75 in 
asthmatics relative to the healthy subjects (24% versus 15%, 
respectively). A significant positive correlation in asthmatics was 
also reported between O3-induced spirometric responses and 
baseline lung function, i.e., responses increased with severity of 
disease.
    Asthmatics present a differential response profile for cellular, 
molecular, and biochemical parameters (Criteria Document, Figure 8-1) 
that are altered in response to acute O3 exposure. Ozone-
induced increases in neutrophils, IL-8 and protein were found to be 
significantly higher in the BAL fluid from asthmatics compared to 
healthy subjects, suggesting mechanisms for the increased sensitivity 
of asthmatics (Basha et al., 1994; McBride et al., 1994; Scannell et 
al., 1996; Hiltermann et al., 1999; Holz et al., 1999; Bosson et al., 
2003). Neutrophils, or PMNs, are the white blood cell most associated 
with inflammation. IL-8 is an inflammatory cytokine with a number of 
biological effects, primarily on neutrophils. The major role of this 
cytokine is to attract and activate neutrophils. Protein in the airways 
is leaked from the circulatory system, and is a marker for increased 
cellular permeability.
    Bronchial constriction following provocation with O3 
and/or allergens presents a two-phase response. The early response is 
mediated by release of histamine and leukotrienes that leads to 
contraction of smooth muscle cells in the bronchi, narrowing the lumen 
and decreasing the airflow. In people with allergic airway disease, 
including people with rhinitis and asthma, these mediators also cause 
accumulation of eosinophils in the airways (Bascom et al., 1990; Jorres 
et al., 1996; Peden et al., 1995 and 1997; Frampton et al., 1997a; 
Michelson et al., 1999; Hiltermann et al., 1999; Holz et al., 2002; 
Vagaggini et al., 2002). In asthma, the eosinophil, which increases 
inflammation and allergic responses, is the cell most frequently 
associated with exacerbations of the disease. A study by Bosson et al. 
(2003) evaluated the difference in O3-induced bronchial 
epithelial cytokine expression between healthy and asthmatic subjects. 
After O3 exposure the epithelial expression of IL-5 and GM-
CSF increased significantly in

[[Page 37847]]

asthmatics, compared to healthy subjects. Asthma is associated with 
Th2-related airway response (allergic response), and IL-5 is an 
important Th2-related cytokine. The O3-induced increase in 
IL-5, and also in GM-CSF, which affects the growth, activation and 
survival of eosinophils, may indicate an effect on the Th2-related 
airway response and on airway eosinophils. The authors reported that 
the O3-induced Th2-related cytokine responses that were 
found within the asthmatic group may indicate a worsening of their 
asthmatic airway inflammation and thus suggest a plausible link to 
epidemiological data indicating O3-associated increases in 
bronchial reactivity and hospital admissions.
    The accumulation of eosinophils in the airways of asthmatics is 
followed by production of mucus and a late-phase bronchial constriction 
and reduced airflow. In a study of 16 intermittent asthmatics, 
Hiltermann et al. (1999) found that there was a significant inverse 
correlation between the O3-induced change in the percentage 
of eosinophils in induced sputum and the change in PC20, the 
concentration of methacholine causing a 20% decrease in 
FEV1. Characteristic O3-induced inflammatory 
airway neutrophilia at one time was considered a leading mechanism of 
airway hyperresponsiveness. However, Hiltermann et al. (1999) 
determined that the O3-induced change in percentage 
neutrophils in sputum was not significantly related to the change in 
PC20. These results are consistent with the results of Zhang 
et al. (1995), which found neutrophilia in a murine model to be only 
coincidentally associated with airway hyperresponsiveness, i.e., there 
was no cause and effect relationship. (Criteria Document, AX 6-26). 
Hiltermann et al. (1999) concluded that the results point to the role 
of eosinophils in O3-induced airway hyperresponsiveness. 
Increases in O3-induced nonspecific airway responsiveness 
incidence and duration could have important clinical implications for 
asthmatics.
    Two studies (J[ouml]rres et al., 1996; Holz et al., 2002) observed 
increased airway responsiveness to O3 exposure with 
bronchial allergen challenge in subjects with preexisting allergic 
airway disease. J[ouml]rres et al. (1996) found that O3 
causes an increased response to bronchial allergen challenge in 
subjects with allergic rhinitis and mild allergic asthma. The subjects 
were exposed to 0.25 ppm O3 for 3 hours with IE. Airway 
responsiveness to methacholine was determined 1 hour before and after 
exposure; responsiveness to allergen was determined 3 hours after 
exposure. Statistically significant decreases in FEV1 
occurred in subjects with allergic rhinitis (13.8%) and allergic asthma 
(10.6%), and in healthy controls (7.3%). Methacholine responsiveness 
was statistically increased in asthmatics, but not in subjects with 
allergic rhinitis or healthy controls. Airway responsiveness to an 
individual's historical allergen (either grass and birch pollen, house 
dust mite, or animal dander) was significantly increased after 
O3 exposure when compared to FA exposure. In subjects with 
asthma and allergic rhinitis, a maximum percent fall in FEV1 
of 27.9% and 7.8%, respectively, occurred 3 days after O3 
exposure when they were challenged with of the highest common dose of 
allergen. The authors concluded that subjects with asthma or allergic 
rhinitis, without asthma, could be at risk if a high O3 
exposure is followed by a high dose of allergen. Holz et al. (2002) 
reported an early phase lung function response in subjects with 
rhinitis after a consecutive 4-day exposure to 0.125 ppm O3 
that resulted in a clinically relevant (>20%) decrease in FEV1. Ozone-
induced exacerbation of airway responsiveness persists longer and 
attenuates more slowly than O3-induced lung function 
decrements and respiratory symptom responses and can have important 
clinical implications for asthmatics.
    A small number of in vitro studies corroborate the differences in 
the responses of asthmatic and healthy subject generally found in 
controlled human exposure studies. In vitro studies (Schierhorn et al., 
1999) of nasal mucosal biopsies from atopic and nonatopic subjects 
exposed to 0.1 ppm O3 found significant differences in 
release of IL-4, IL-6, IL-8, and TNF-[alpha]. Another study by 
Schierhorn et al. (2002) found significant differences in the 
O3-induced release of the neuropeptides neurokinin A and 
substance P for allergic patients in comparison to nonallergic 
controls, suggesting increased activation of sensory nerves by 
O3 in the allergic tissues. Another study by Bayram et al. 
(2002) using in vitro culture of bronchial epithelial cells recovered 
from atopic and nonatopic asthmatics also found significant increases 
in epithelial permeability in response to O3 exposure.
    The new data on airway responsiveness, inflammation, and various 
molecular markers of inflammation and bronchoconstriction indicate that 
people with asthma and allergic rhinitis (with or without asthma) 
comprise susceptible groups for O3-induced adverse effects. 
This body of evidence indicates that human clinical and epidemiological 
panel studies of lung function decrements and respiratory symptoms that 
evaluate only healthy, non-asthmatic subjects likely underestimate the 
effects of O3 exposure on asthmatics and other susceptible 
populations. The effects of O3 on lung function, 
inflammation, and increased airway responsiveness demonstrated in 
subjects with asthma and other allergic airway diseases, provide 
plausible mechanisms underlying the more serious respiratory morbidity 
effects, such as emergency department visits and hospital admissions, 
and respiratory mortality effects.
    A number of epidemiological studies have been conducted using 
asthmatic study populations. The majority of epidemiological panel 
studies that evaluated respiratory symptoms and medication use related 
to O3 exposures focused on children. These studies suggest 
that O3 exposure may be associated with increased 
respiratory symptoms and medication use in children with asthma. Other 
reported effects include respiratory symptoms, lung function 
decrements, and emergency department visits, as discussed in the 
Criteria Document (section 7.6.7.1). Strong evidence from a large 
multi-city study (Mortimer et al., 2002), along with support from 
several single-city studies suggest that O3 exposure may be 
associated with increased respiratory symptoms and medication use in 
children with asthma. With regard to ambient O3 levels and 
increased hospital admissions and emergency department visits for 
asthma and other respiratory causes, strong and consistent evidence 
establishes a correlation between O3 exposure and increased 
exacerbations of preexisting respiratory disease for 1-hour maximum 
O3 concentrations <0.12 ppm. As discussed in the Criteria 
Document, section 7.3, several hospital admission and emergency 
department visit studies in the U.S., Canada, and Europe have reported 
positive associations between increase in O3 and increased 
risk of emergency department visits and hospital admissions for asthma 
and other respiratory diseases, especially during the warm season. 
Finally, from epidemiological studies that included assessment of 
associations with specific causes of death, some studies have observed 
larger effects estimates for respiratory mortality and others have 
observed larger effects estimates for cardiovascular mortality. The 
apparent inconsistency regarding the effect size of O3-
related respiratory mortality may be due to reduced statistical power 
in this

[[Page 37848]]

subcategory of mortality (EPA, 2006a, p. 7-108).
    Newly available reports from controlled human exposure studies (see 
chapter 6 in the Criteria Document) utilized subjects with preexisting 
cardiopulmonary diseases such as COPD, asthma, allergic rhinitis, and 
hypertension. The data generated from these studies that evaluated 
changes in spirometry did not find clear differences between filtered 
air and O3 exposure in COPD subjects. However, the new data 
on airway responsiveness, inflammation, and various molecular markers 
of inflammation and bronchoconstriction indicate that people with 
atopic asthma and allergic rhinitis comprise susceptible groups for 
O3-induced adverse health effects.
    Although controlled human exposure studies have not found evidence 
of larger spirometric changes in people with COPD relative to healthy 
subjects, this may be due to the fact that most people with COPD are 
older adults who would not be expected to have such changes based on 
their age. However, in section 8.7.1, the Criteria Document notes that 
new epidemiological evidence indicates that people with COPD may be 
more likely to experience other effects, including emergency room 
visits, hospital admissions, or premature mortality. For example, 
results from an analysis of five European cities indicated strong and 
consistent O3 effects on unscheduled respiratory hospital 
admissions, including COPD (Anderson et al., 1997). Also, an analysis 
of a 9-year data set for the whole population of the Netherlands 
provided risk estimates for more specific causes of mortality, 
including COPD (Hoek et al., 2000, 2001; reanalysis, Hoek, 2003); a 
positive, but nonsignificant, excess risk of COPD-related mortality was 
found to be associated with short-term O3 concentrations. 
Moreover, as indicated by Gong et al. (1998), the effects of 
O3 exposure on alveolar-arterial oxygen gradients may be 
more pronounced in patients with preexisting obstructive lung diseases. 
Relative to healthy elderly subjects, COPD patients have reduced gas 
exchange and low SaO2. Any inflammatory or edematous responses due to 
O3 delivered to the well-ventilated regions of the COPD lung 
could further inhibit gas exchange and reduce oxygen saturation. In 
addition, O3-induced vasoconstriction could also acutely 
induce pulmonary hypertension. Inducing pulmonary vasoconstriction and 
hypertension in these patients would perhaps worsen their condition, 
especially if their right ventricular function was already compromised 
(EPA, 2006a, section 6.10).
iii. Children and Older Adults
    Supporting evidence exists for heterogeneity in the effects of 
O3 by age. As discussed in section 6.5.1 of the Criteria 
Document, children, adolescents, and young adults (< 18 yrs of age) 
appear, on average, to have nearly equivalent spirometric responses to 
O3, but have greater responses than middle-aged and older 
adults when exposed to comparable O3 doses. Symptomatic 
responses to O3 exposure, however, do not appear to occur in 
healthy children, but are observed in asthmatic children, particularly 
those who use maintenance medications. For adults (>17 yrs of age) 
symptoms gradually decrease with increasing age. In contrast to young 
adults, the diminished symptomatic responses in children and the 
diminished symptomatic and spirometric responses in older adults 
increases the likelihood that these groups continue outdoor activities 
leading to greater O3 exposure and dose.
    As described in the section 7.6.7.2 of the Criteria Document, many 
epidemiological field studies focused on the effect of O3 on 
the respiratory health of school children. In general, children 
experienced decrements in pulmonary function parameters, including PEF, 
FEV1, and FVC. Increases in respiratory symptoms and asthma 
medication use were also observed in asthmatic children. In one German 
study, children with and without asthma were found to be particularly 
susceptible to O3 effects on lung function. Approximately 
20% of the children, both with and without asthma, experienced a 
greater than 10% change in FEV1, compared to only 5% of the 
elderly population and athletes (Hoppe et al., 2003).
    The American Academy of Pediatrics (2004) notes that children and 
infants are among the population groups most susceptible to many air 
pollutants, including O3. This is in part because their 
lungs are still developing. For example, eighty percent of alveoli are 
formed after birth, and changes in lung development continue through 
adolescence (Dietert et al., 2000). Children are also likely to spend 
more time outdoors than adults, which results in increased exposure to 
air pollutants (Wiley et al., 1991a,b). Moreover, children have high 
minute ventilation rates and high levels of physical activity which 
also increases their dose (Plunkett et al., 1992).
    Several mortality studies have investigated age-related differences 
in O3 effects (EPA, 2006a, section 7.6.7.2). Older adults 
are also often classified as being particularly susceptible to air 
pollution. The basis for increased O3 sensitivity among the 
elderly is not known, but one hypothesis is that it may be related to 
changes in the respiratory tract lining fluid antioxidant defense 
network (Kelly et al., 2003). (EPA 2006a, p. 8-60) Older adults have 
lower baseline lung function than younger people, and are also more 
likely to have preexisting lung and heart disease. Increased 
susceptibility of older adults to O3 health effects is most 
clearly indicated in the newer mortality studies. Among the studies 
that observed positive associations between O3 and 
mortality, a comparison of all age or younger age (< =65 years of age) 
O3-mortality effect estimates to that of the elderly 
population (>65 years) indicates that, in general, the elderly 
population is more susceptible to O3 mortality effects. The 
meta-analysis by Bell et al. (2005) found a larger mortality effect 
estimate for the elderly than for all ages. In the large U.S. 95 
communities study (Bell et al., 2004), mortality effect estimates were 
slightly higher for those aged 65 to 74 years, compared to individuals 
less than 65 years and 75 years or greater. The absolute effect of 
O3 on premature mortality may be substantially greater in 
the elderly population because of higher rates of preexisting 
respiratory and cardiac diseases. The Criteria Document concludes that 
the elderly population (>65 years of age) appear to be at greater risk 
of O3-related mortality and hospitalizations compared to all 
ages or younger populations (EPA, 2006a, p. 7-177).
    The Criteria Document notes that, collectively, there is supporting 
evidence of age-related differences in susceptibility to O3 
lung function effects. The elderly population (>65 years of age) appear 
to be at increased risk of O3-related mortality and 
hospitalizations, and children (< 18 years of age) experience other 
potentially adverse respiratory health outcomes with increased 
O3 exposure (EPA, 2006a, section 7.6.7.2).
iv. People With Increased Responsiveness to Ozone
    New animal toxicology studies using various strains of mice and 
rats have identified O3-sensitive and resistant strains and 
illustrated the importance of genetic background in determining 
O3 susceptibility (EPA, 2006a, section 8.7.4). Controlled 
human exposure studies have also indicated a high degree of variability 
in some of the pulmonary physiological parameters. The variable effects 
in individuals have

[[Page 37849]]

been found to be reproducible, in other words, a person who has a large 
lung function response after exposure to O3 will likely have 
about the same response if exposed again to the same dose of 
O3. In human clinical studies, group mean responses are not 
representative of this segment of the population that has much larger 
than average responses to O3. Recent studies of asthmatics 
by David et al. (2003) and Romieu et al. (2004) reported a role for 
genetic polymorphism in observed differences in antioxidant enzymes and 
genes involved in inflammation to modulate pulmonary function and 
inflammatory responses to O3 exposure.\23\
---------------------------------------------------------------------------

    \23\ Similar to animal toxicology studies referred above, a 
polymorphism in a specific proinflammatory cytokine gene has been 
implicated in O3-induced lung function changes in 
healthy, mild asthmatics and individuals with rhinitis. These 
observations suggest a potential role for these markers in the 
innate susceptibility to O3, however, the validity of 
these markers and their relevance in the context of prediction to 
population studies needs additional experimentation.
---------------------------------------------------------------------------

    Biochemical and molecular parameters extensively evaluated in these 
experiments were used to identify specific loci on chromosomes and, in 
some cases, to relate the differential expression of specific genes to 
biochemical and physiological differences observed among these species. 
Utilizing O3-sensitive and O3-resistant species, 
it has been possible to identify the involvement of increased airway 
reactivity and inflammation processes in O3 susceptibility. 
However, most of these studies were carried out using relatively high 
doses of O3, making the relevance of these studies 
questionable in human health effects assessment. The genes and genetic 
loci identified in these studies may serve as useful biomarkers and, 
ultimately, can likely be integrated with epidemiological studies.
v. Other Population Groups
    There is limited, new evidence supporting associations between 
short-term O3 exposures and a range of effects on the 
cardiovascular system. Some but not all, epidemiological studies have 
reported associations between short-term O3 exposures and 
the incidence of MI and more subtle cardiovascular health endpoints, 
such as changes in HRV and cardiac arrhythmia. Others have reported 
associations with hospitalization or emergency department visits for 
cardiovascular diseases, although the results across the studies are 
not consistent. Studies also report associations between short-term 
O3 exposure and mortality from cardiovascular or 
cardiopulmonary causes. The Criteria Document concludes that current 
cardiovascular effects evidence from some field studies is rather 
limited but supportive of a potential effect of short-term 
O3 exposure and HRV, cardiac arrhythmia, and MI incidence 
(EPA, 2006a, p. 7-65). In the Criteria Document's evaluation of studies 
of hospital admissions for cardiovascular disease (EPA 2006a, section 
7.3.4), it is concluded that evidence from this growing group of 
studies is generally inconclusive regarding an association with 
O3 in studies conducted during the warm season (EPA 2006a, 
p. 7-83). This body of evidence suggests that people with heart disease 
may be at increased risk from short-term exposures to O3; 
however, more evidence is needed to conclude that people with heart 
disease are a susceptible population.
    Other groups that might have enhanced sensitivity to O3, 
but for which there is currently very little evidence, include groups 
based on race, gender and SES, and those with nutritional deficiencies, 
which presents factors which modify responsiveness to O3.
c. Adversity of Effects
    In making judgments as to when various O3-related 
effects become regarded as adverse to the health of individuals, the 
Administrator has looked to guidelines published by the American 
Thoracic Society (ATS) and the advice of CASAC. While recognizing that 
perceptions of ``medical significance'' and ``normal activity'' may 
differ among physicians, lung physiologists and experimental subjects, 
the ATS (1985) \24\ defined adverse respiratory health effects as 
``medically significant physiologic changes generally evidenced by one 
or more of the following: (1) Interference with the normal activity of 
the affected person or persons, (2) episodic respiratory illness, (3) 
incapacitating illness, (4) permanent respiratory injury, and/or (5) 
progressive respiratory dysfunction.'' During the 1997 review, it was 
concluded that there was evidence of causal associations from 
controlled human exposure studies for effects in the first of these 
five ATS-defined categories, evidence of statistically significant 
associations from epidemiological studies for effects in the second and 
third categories, and evidence from animal toxicology studies, which 
could be extrapolated to humans only with a significant degree of 
uncertainty, for the last two categories.
---------------------------------------------------------------------------

    \24\ In 2000, the American Thoracic Society (ATS) published an 
official statement on ``What Constitutes an Adverse Health Effect of 
Air Pollution?'' (ATS, 2000), which updated its earlier guidance 
(ATS, 1985). Overall, the new guidance does not fundamentally change 
the approach previously taken to define adversity, nor does it 
suggest a need at this time to change the structure or content of 
the tables describing gradation of severity and adversity of effects 
described below.
---------------------------------------------------------------------------

    For ethical reasons, clear causal evidence from controlled human 
exposure studies still covers only effects in the first category. 
However, for this review there are results from epidemiological 
studies, upon which to base judgments about adversity, for effects in 
all of the categories. Statistically significant and robust 
associations have been reported in epidemiology studies falling into 
the second and third categories. These more serious effects include 
respiratory events (e.g., triggering asthma attacks) that may require 
medication (e.g., asthma), but not necessarily hospitalization, as well 
as respiratory hospital admissions and emergency department visits for 
respiratory causes. Less conclusive, but still positive associations 
have been reported for school absences and cardiovascular hospital 
admissions. Human health effects for which associations have been 
suggested through evidence from epidemiological and animal toxicology 
studies, but have not been conclusively demonstrated still fall 
primarily into the last two categories. In the last review of the 
O3 standard, evidence for these more serious effects came 
from studies of effects in laboratory animals. Evidence from animal 
studies evaluated in this Criteria Document strongly suggests that 
O3 is capable of damaging the distal airways and proximal 
alveoli, resulting in lung tissue remodeling leading to apparently 
irreversible changes. Recent advancements of dosimetry modeling also 
provide a better basis for extrapolation from animals to humans. 
Information from epidemiological studies provides supporting, but 
limited evidence of irreversible respiratory effects in humans than was 
available in the prior review. Moreover, the findings from single-city 
and multi-city time-series epidemiology studies and meta-analyses of 
these epidemiology studies are highly suggestive of an association 
between short-term O3 exposure and mortality particularly in 
the warm season.
    While O3 has been associated with effects that are 
clearly adverse, application of these guidelines, in particular to the 
least serious category of effects related to ambient O3 
exposures, involves judgments about which medical experts on the CASAC 
panel and public commenters have expressed diverse views in the past. 
To help frame such judgments, EPA staff have defined specific ranges of 
functional responses

[[Page 37850]]

(e.g., decrements in FEV1 and airway responsiveness) and 
symptomatic responses (e.g., cough, chest pain, wheeze), together with 
judgments as to the potential impact on individuals experiencing 
varying degrees of severity of these responses, that have been used in 
previous NAAQS reviews. These ranges of pulmonary responses and their 
associated potential impacts are summarized in Tables 3-2 and 3-3 of 
the Staff Paper.
    For active healthy people, moderate levels of functional responses 
(e.g., FEV1 decrements of >=10% but <20%, lasting up to 24 
hours) and/or moderate symptomatic responses (e.g., frequent 
spontaneous cough, marked discomfort on exercise or deep breath, 
lasting up to 24 hours) would likely interfere with normal activity for 
relatively few responsive individuals. On the other hand, EPA staff 
determined that large functional responses (e.g., FEV1 
decrements >=20%, lasting longer than 24 hours) and/or severe 
symptomatic responses (e.g., persistent uncontrollable cough, severe 
discomfort on exercise or deep breath, lasting longer than 24 hours) 
would likely interfere with normal activities for many responsive 
individuals. EPA staff determined that these would be considered 
adverse under ATS guidelines. In the context of standard setting, CASAC 
indicated that a focus on the mid to upper end of the range of moderate 
levels of functional responses (e.g., FEV1 decrements >=15% 
but < 20%) is appropriate for estimating potentially adverse lung 
function decrements in active healthy people. However, for people with 
lung disease, even moderate functional (e.g., FEV1 
decrements >=10% but <20%, lasting up to 24 hours) or symptomatic 
responses (e.g., frequent spontaneous cough, marked discomfort on 
exercise or with deep breath, wheeze accompanied by shortness of 
breath, lasting up to 24 hours) would likely interfere with normal 
activity for many individuals, and would likely result in more frequent 
use of medication. For people with lung disease, large functional 
responses (e.g., FEV1 decrements >=20%, lasting longer than 
24 hours) and/or severe symptomatic responses (e.g., persistent 
uncontrollable cough, severe discomfort on exercise or deep breath, 
persistent wheeze accompanied by shortness of breath, lasting longer 
than 24 hours) would likely interfere with normal activity for most 
individuals and would increase the likelihood that these individuals 
would seek medical treatment. In the context of standard setting, the 
CASAC indicated (Henderson, 2006c) that a focus on the lower end of the 
range of moderate levels of functional responses (e.g., FEV1 
decrements >=10%) is most appropriate for estimating potentially 
adverse lung function decrements in active healthy people.
    In judging the extent to which these impacts represent effects that 
should be regarded as adverse to the health status of individuals, an 
additional factor that has been considered in previous NAAQS reviews is 
whether such effects are experienced repeatedly during the course of a 
year or only on a single occasion. While some experts would judge 
single occurrences of moderate responses to be a ``nuisance,'' 
especially for healthy individuals, a more general consensus view of 
the adversity of such moderate responses emerges as the frequency of 
occurrence increases.
    The new guidance builds upon and expands the 1985 definition of 
adversity in several ways. There is an increased focus on quality of 
life measures as indicators of adversity. There is also a more specific 
consideration of population risk. Exposure to air pollution that 
increases the risk of an adverse effect to the entire population is 
adverse, even though it may not increase the risk of any individual to 
an unacceptable level. For example, a population of asthmatics could 
have a distribution of lung function such that no individual has a 
level associated with significant impairment. Exposure to air pollution 
could shift the distribution to lower levels that still do not bring 
any individual to a level that is associated with clinically relevant 
effects. However, this would be considered to be adverse because 
individuals within the population would have diminished reserve 
function, and therefore would be at increased risk if affected by 
another agent.
    Of the various effects of O3 exposure that have been 
studied, many would meet the ATS definition of adversity. Such effects 
include, for example, any detectible level of permanent lung function 
loss attributable to air pollution, including both reductions in lung 
growth or acceleration of the age-related decline of lung function; 
exacerbations of disease in individuals with chronic cardiopulmonary 
diseases; reversible loss of lung function in combination with the 
presence of symptoms; as well as more serious effects such as those 
requiring medical care including hospitalization and, obviously, 
mortality.
d. Size of At-Risk Subpopulations
    Although O3-related health risk estimates may appear to 
be small, their significance from an overall public health perspective 
is determined by the large numbers of individuals in the subpopulations 
potentially at-risk for O3-related health effects discussed 
above. For example, a population of concern includes people with 
respiratory disease, including approximately 11 percent of U.S. adults 
and 13 percent of children who have been diagnosed with asthma and 6 
percent of adults with chronic obstructive pulmonary disease (chronic 
bronchitis and/or emphysema) in 2002 and 2003 (Table 8-4 in the 
Criteria Document, section 8.7.5.2). More broadly, individuals with 
preexisting cardiopulmonary disease may constitute an additional 
population of concern, with potentially tens of millions of people 
included in each disease category. In addition, subpopulations based on 
age group also comprise substantial segments of the population that may 
be potentially at risk for O3-related health impacts. Based 
on U.S. census data from 2003, about 26 percent of the U.S. population 
are under 18 years of age and 12 percent are 65 years of age or older. 
Hence, large proportions of the U.S. population are included in age 
groups include those most likely to have increased susceptibility to 
the health effects of O3 and or those with the highest 
ambient O3 exposures.
    The Criteria Document (section 8.7.5.2) notes that the health 
statistics data illustrate what is known as the ``pyramid'' of effects. 
At the top of the pyramid, there are approximately 2.5 millions deaths 
from all causes per year in the U.S. population, with about 100,000 
deaths from chronic lower respiratory diseases. For respiratory health 
diseases, there are nearly 4 million hospital discharges per year, 14 
million emergency department visits, 112 million ambulatory care 
visits, and an estimated 700 million restricted activity days per year 
due to respiratory conditions from all causes per year. Applying small 
risk estimates for the O3-related contribution to such 
health effects with relatively large baseline levels of health outcomes 
can result in quite large public health impacts related to ambient 
O3 exposure. Thus, even a small percentage reduction in 
O3 health impacts on cardiopulmonary diseases would reflect 
a large number of avoided cases. In considering this information 
together with the concentration-response relationships that have been 
observed between exposure to O3 and various health 
endpoints, the Criteria

[[Page 37851]]

Document (section 8.7.5.2) concludes that exposure to ambient 
O3 likely has a significant impact on public health in the 
U.S.

B. Human Exposure and Health Risk Assessments

    To put judgments about health effects that are adverse for 
individuals into a broader public health context, EPA has developed and 
applied models to estimate human exposures and health risks. This 
broader context includes consideration of the size of particular 
population groups at risk for various effects, the likelihood that 
exposures of concern will occur for individuals in such groups under 
varying air quality scenarios, estimates of the number of people likely 
to experience O3-related effects, the variability in 
estimated exposures and risks, and the kind and degree of uncertainties 
inherent in assessing the exposures and risks involved.
    As discussed below there are a number of important uncertainties 
that affect the exposure and health risk estimates. It is also 
important to note that there have been significant improvements in both 
the exposure and health risk model. CASAC expressed the view that the 
exposure analysis represents a state-of-the-art modeling approach and 
that the health risk assessment was ``well done, balanced and 
reasonably communicated'' (Henderson, 2006c). While recognizing and 
considering the kind and degree of uncertainties in both the exposure 
and health risk estimates, the Staff Paper judged that the quality of 
the estimates is such that they are suitable to be used as an input to 
the Administrator's decisions on the O3 primary standard 
(Staff Paper, p. 6-20--6-21).
    In modeling exposures and health risks associated with just meeting 
the current and alternative O3 standards, EPA has simulated 
air quality to represent conditions just meeting these standards based 
on O3 air quality patterns in several recent years and on 
how the shape of the O3 air quality distribution has changed 
over time based on historical trends in monitored O3 air 
quality data. As described in the Staff Paper (section 4.5.8) and 
discussed below, recent O3 air quality distributions have 
been statistically adjusted to simulate just meeting the current and 
selected alternative standards. These simulations do not reflect any 
consideration of specific control programs or strategies designed to 
achieve the reductions in emissions required to meet the specified 
standards. Further, these simulations do not represent predictions of 
when, whether, or how areas might meet the specified standards.\25\
---------------------------------------------------------------------------

    \25\ Modeling that projects whether and how areas might attain 
alternative standards in a future year is presented in the 
Regulatory Impact Analysis being prepared in connection with this 
rulemaking.
---------------------------------------------------------------------------

    As noted in section I.C above, around the time of the release of 
the final Staff Paper in January 2007, EPA discovered a small error in 
the exposure model that when corrected resulted in slight increases in 
the simulated exposures. Since the exposure estimates are an input to 
the lung function portion of the health risk assessment, this 
correction also resulted in slight increases in the lung function risk 
estimates as well. The exposure and risk estimates discussed in this 
notice reflect the corrected estimates, and thus are slightly different 
than the exposure and risk estimates cited in the January 31, 2007 
Staff Paper.\26\
---------------------------------------------------------------------------

    \26\ EPA plans to make available corrected versions of the final 
Staff Paper, and human exposure and health risk assessment technical 
support documents on or around July 16, 2007 on the EPA web site 
listed in the Availability of Related Information section of this 
notice.
---------------------------------------------------------------------------

1. Exposure Analyses
a. Overview
    The EPA conducted exposure analyses using a simulation model to 
estimate O3 exposures for the general population, school age 
children (ages 5-18), and school age children with asthma living in 12 
U.S. metropolitan areas representing different regions of the country 
where the current 8-hour O3 standard is not met. The 
emphasis on children reflects the finding of the last O3 
NAAQS review that children are an important at-risk group. The 12 
modeled areas combined represent a significant fraction of the U.S. 
urban population, 89 million people, including 18 million school age 
children of whom approximately 2.6 million have asthma. The selection 
of urban areas to include in the exposure analysis took into 
consideration the location of O3 epidemiological studies, 
the availability of ambient O3 data, and the desire to 
represent a range of geographic areas, population demographics, and 
O3 climatology. These selection criteria are discussed 
further in chapter 5 of the Staff Paper. The geographic extent of each 
modeled area consists of the census tracts in the combined statistical 
area (CSA) as defined by OMB (OMB, 2005).\27\
---------------------------------------------------------------------------

    \27\ The 12 CSAs modeled are: Atlanta-Sandy Springs-Gainesville, 
GA-AL; Boston-Worcester-Manchester, MA-NH; Chicago-Naperville-
Michigan City, IL-IN-WI; Cleveland-Akron-Elyria, OH; Detroit-Warren-
Flint, MI; Houston-Baytown-Huntsville, TX; Los Angeles-Long Beach-
Riverside, CA; New York-Newark-Bridgeport, NY-NJ-CT-PA; 
Philadelphia-Camden-Vineland, PA-NJ-DE-MD; Sacramento-Arden-Arcade-
Truckee, CA-NV; St. Louis-St. Charles-Farmington, MO-IL; Washington-
Baltimore-N. Virginia, DC-MD-VA-WV.
---------------------------------------------------------------------------

    Exposure estimates were developed using a probabilistic exposure 
model that is designed to explicitly model the numerous sources of 
variability that affect people's exposures. As discussed below, the 
model estimates population exposures by simulating human activity 
patterns, air conditioning prevalence, air exchange rates, and other 
factors. The modeled exposure estimates were developed for three recent 
years of ambient O3 concentrations (2002, 2003, and 2004), 
as well as for O3 concentrations adjusted to simulate 
conditions associated with just meeting the current NAAQS and various 
alternative 8-hour standards based on the three year period 2002-
2004.\28\ This exposure assessment is more fully described and 
presented in the Staff Paper and in a technical support document, Ozone 
Population Exposure Analysis for Selected Urban Areas (US EPA, 2006b; 
hereafter Exposure Analysis TSD). The scope and methodology for this 
exposure assessment were developed over the last few years with 
considerable input from the CASAC Ozone Panel and the public.\29\
---------------------------------------------------------------------------

    \28\ All 12 of the CSAs modeled did not meet the current 
O3 NAAQS for the three year period examined.
    \29\ The general approach used in the current exposure 
assessment was described in the draft Health Assessment Plan (EPA, 
2005a) that was released to the CASAC and general public in April 
2005 and was the subject of a consultation with the CASAC 
O3 Panel on May 5, 2005. In October 2005, OAQPS released 
the first draft of the Staff Paper containing a chapter discussing 
the exposure analyses and first draft of the Exposure Analyses TSD 
for CASAC consultation and public review on December 8, 2005. In 
July 2006, OAQPS released the second draft of the Staff Paper and 
second draft of the Exposure Analyses TSD for CASAC review and 
public comment which was held by the CASAC O3 Panel on 
August 24-25, 2006.
---------------------------------------------------------------------------

    The goals of the O3 exposure assessment were: (1) To 
provide estimates of the size of at-risk populations exposed to various 
levels associated with recent O3 concentrations, and with 
just meeting the current O3 NAAQS and alternative 
O3 standards, in specific urban areas; (2) to provide 
distributions of exposure estimates over the entire range of ambient 
O3 concentrations as an important input to the lung function 
risk assessment summarized below in section II.B.2; (3) to develop a 
better understanding of the influence of various inputs and assumptions 
on the exposure estimates; and (4) to gain insight into the 
distribution of exposures and patterns of exposure

[[Page 37852]]

reductions associated with meeting alternative O3 standards.
    EPA recognizes that there are many sources of variability and 
uncertainty inherent in the inputs to this assessment and that there is 
uncertainty in the resulting O3 exposure estimates. With 
respect to variability, the exposure modeling approach accounts for 
variability in ambient O3 levels, demographic 
characteristics, physiological attributes, activity patterns, and 
factors affecting microenvironmental (e.g., indoor) concentrations. In 
EPA's judgment, the most important uncertainties affecting the exposure 
estimates are related to the modeling of human activity patterns over 
an O3 season, the modeling of variations in ambient 
concentrations near roadways, and the modeling of air exchange rates 
that affect the amount of O3 that penetrates indoors. 
Another important uncertainty that affects the estimation of how many 
exposures are associated with moderate or greater exertion, is the 
characterization of energy expenditure for children engaged in various 
activities. As discussed in more detail in the Staff Paper (section 
4.3.4.7), the uncertainty in energy expenditure values carries over to 
the uncertainty of the modeled breathing rates, which are important 
since they are used to classify exposures occurring at moderate or 
greater exertion which are the relevant exposures since O3-
related effects observed in clinical studies only are observed when 
individuals are engaged in some form of exercise. The uncertainties in 
the exposure model inputs and the estimated exposures have been 
assessed using quantitative uncertainty and sensitivity analyses. 
Details are discussed in the Staff Paper (section 4.6) and in a 
technical memorandum describing the exposure modeling uncertainty 
analysis (Langstaff, 2007).
b. Scope and Key Components
    Population exposures to O3 are primarily driven by 
ambient outdoor concentrations, which vary by time of day, location, 
and peoples' activities. Outdoor O3 concentration estimates 
used in the exposure assessment are provided by measurements and 
statistical adjustments to the measured concentrations. The current 
exposure analysis allows comparisons of population exposures to 
O3 within each urban area, associated with current 
O3 levels and with O3 levels just meeting several 
potential alternative air quality standards or scenarios. Human 
exposure, regardless of the pollutant, depends on where individuals are 
located and what they are doing. Inhalation exposure models are useful 
in realistically estimating personal exposures to O3 based 
on activity-specific breathing rates, particularly when recognizing 
that large scale population exposure measurement studies have not been 
conducted that are representative of the overall population or at-risk 
subpopulations.
    The model EPA used to simulate O3 population exposure is 
the Air Pollutants Exposure Model (APEX), the human inhalation exposure 
model within the Total Risk Integrated Methodology (TRIM) framework 
(EPA, 2006c,d). APEX is conceptually based on the probabilistic NAAQS 
exposure model for O3 (pNEM/O3) used in the last 
O3 NAAQS review. Since that time, the model has been 
restructured, improved, and expanded to reflect conceptual advances in 
the science of exposure modeling and newer input data available for the 
model. Key improvements to algorithms include replacement of the cohort 
approach with a probabilistic sampling approach focused on individuals, 
accounting for fatigue and oxygen debt after exercise in the 
calculation of breathing rates, and a new approach for construction of 
longitudinal activity patterns for simulated persons. Major 
improvements to data input to the model include updated air exchange 
rates, more recent census and commuting data, and a greatly expanded 
daily time-activities database.
    APEX is a probabilistic model designed to explicitly model the 
numerous sources of variability that affect people's exposures. APEX 
simulates the movement of individuals through time and space and 
estimates their exposures to O3 in indoor, outdoor, and in-
vehicle microenvironments. The exposure model takes into account the 
most significant factors contributing to total human O3 
exposure, including the temporal and spatial distribution of people and 
O3 concentrations throughout an urban area, the variation of 
O3 levels within each microenvironment, and the effects of 
exertion on breathing rate in exposed individuals. A more detailed 
description of APEX and its application is presented in chapter 4 of 
the Staff Paper and associated technical documents (EPA, 2006b, c, d).
    Several methods have been used to evaluate the APEX model and to 
characterize the uncertainty of the model estimates. These include 
conducting model evaluation, sensitivity analyses, and a detailed 
uncertainty analysis for one urban area. These are discussed fully in 
the Staff Paper (section 4.6) and in Langstaff (2007). The uncertainty 
of model structure was judged to be of lesser importance than the 
uncertainties of the model inputs and parameters. Model structure 
refers to the algorithms in APEX designed to simulate the processes 
that result in people's exposures, for example, the way that APEX 
models exposures to individuals when they are near roads. The 
uncertainties in the model input data (e.g., measurement error, ambient 
concentrations, air exchange rates, and activity pattern data) have 
been assessed individually, and their impact on the uncertainty in the 
modeled exposure estimates was assessed in a unified quantitative 
analysis with results expressed in the form of estimated confidence 
ranges around the estimated measures of exposure. This uncertainty 
analysis was conducted for one urban area (Boston) using the observed 
2002 O3 concentrations and 2002 concentrations adjusted to 
simulate just meeting the current standard, with the expectation that 
the results would be similar for other cities and years. One 
significant source of uncertainty, due to limitations in the database 
used to model peoples' daily activities, was not included in the 
unified analysis, and was assessed through separate sensitivity 
analyses. This analysis indicates that the uncertainty of the exposure 
results is relatively small. For example, 95 percent uncertainty 
intervals were calculated for the APEX estimates of the percent of 
children or asthmatic children with exposures above 0.060, 0.070, or 
0.080 ppm under moderate exertion, for two air quality scenarios 
(current 2002 and 2002 adjusted to simulate just meeting the current 
standard) in Boston (Tables 26 and 27 in Langstaff, 2007). The 95 
percent uncertainty intervals for this set of 12 exposure estimates 
indicate the possibility of underpredictions of the exposure estimates 
ranging from 3 to 25 percent of the modeled estimates, and 
overpredictions ranging from 4 to 11 percent of the estimates. For 
example, APEX estimates the percent of asthmatic children with 
exposures above 0.070 ppm under moderate exertion to be 24 percent, for 
Boston 2002 O3 concentrations adjusted to simulate just 
meeting the current standard. The 95 percent uncertainty interval for 
this estimate is 23-30 percent, or -4 to +25 percent of the estimate. 
These uncertainty intervals do not include the uncertainty engendered 
by limitations of the activity database, which is in the range of one 
to ten percent.
    The exposure periods modeled here are the O3 seasons in 
2002, 2003, and

[[Page 37853]]

2004. The O3 season in each area includes the period of the 
year where elevated O3 levels tend to be observed and for 
which routine hourly O3 monitoring data are available. 
Typically this period spans from March or April through September or 
October, or in some areas, spanning the entire year. Three years were 
modeled to reflect the substantial year-to-year variability that occurs 
in O3 levels and related meteorological conditions, and 
because the standard is specified in terms of a three-year period. The 
year-to-year variability observed in O3 levels is due to a 
combination of different weather patterns and the variation in 
emissions of O3 precursors. Nationally, 2002 was a 
relatively high year with respect to the 4th highest daily maximum 8-
hour O3 levels observed in urban areas across the U.S. (EPA, 
2007, Figure 2-16), with the mean of the distribution of O3 
levels for the urban monitors being in the upper third among the years 
1990 through 2006. In contrast, on a national basis, 2004 is the lowest 
year on record through 2006 for this same air quality statistic, and 8-
hour daily maximum O3 levels observed in most, but not all 
of the 12 urban areas included in the exposure and risk analyses were 
relatively low compared to other recent years. The 4th highest daily 
maximum 8-hour O3 levels observed in 2003 in the 12 urban 
areas and nationally generally were between those observed in 2002 and 
2004.
    Regulatory scenarios examined include the current 0.08 ppm, average 
of the 4th daily maximum 8-hour averages over a three year period 
standard; standards with the same form but with alternative levels of 
0.080, 0.074, 0.070, and 0.064 ppm; standards specified as the average 
of the 3rd highest daily maximum 8-hour averages over a three year 
period with alternative levels of 0.084 and 0.074 ppm; and a standard 
specified as the average of the 5th highest daily maximum 8-hour 
averages over a three year period with a level of 0.074 ppm.\30\ The 
current standard uses a rounding convention that allows areas to have 
an average of the 4th daily maximum 8-hour averages as high as 0.084 
ppm and still meet the standard. All alternative standards analyzed 
were intended to reflect improved precision in the measurement of 
ambient concentrations, where the precision would extend to three 
instead of two decimal places (in ppm).
---------------------------------------------------------------------------

    \30\ The current O3 standard is 0.08 ppm, but the 
current rounding convention specifies that the average of the 4th 
daily maximum 8-hour average concentrations over a three-year period 
must be at 0.084 ppm or lower to be in attainment of the standard. 
When EPA staff selected alternative standards to analyze, it was 
presumed that the same type of rounding convention would be used, 
and thus alternative standards of 0.084, 0.074, 0.064 ppm were 
chosen.
---------------------------------------------------------------------------

    The current standard and all alternative standards were modeled 
using a quadratic rollback approach to adjust the hourly concentrations 
observed in 2002-2004 to yield a design value \31\ corresponding to the 
standard being analyzed. The quadratic rollback technique reduces 
higher concentrations more than lower concentrations near ambient 
background levels.\32\ This procedure was considered in a sensitivity 
analysis in the last review of the O3 standard and has been 
shown to be more realistic than a linear, proportional rollback method, 
where all of the ambient concentrations are reduced by the same factor.
---------------------------------------------------------------------------

    \31\ A design value is a statistic that describes the air 
quality status of a given area relative to the level of the NAAQS. 
Design values are often based on multiple years of data, consistent 
with specification of the NAAQS in Part 50 of the CFR. For the 
current O3 NAAQS, the 3-year average of the annual 4th-
highest daily maximum 8-hour average concentrations, based on the 
monitor within (or downwind of) an urban area yielding the highest 
3-year average, is the design value.
    \32\ The quadratic rollback approach and evaluation of this 
approach are described by Johnson (1997), Duff et al. (1998) and 
Rizzo (2005, 2006).
---------------------------------------------------------------------------

c. Exposure Estimates and Key Observations
    The exposure assessment, which provides estimates of the number of 
people exposed to different levels of ambient O3 while at 
specified exertion levels \33\ serve two purposes. First, the entire 
range of modeled personal exposures to ambient O3 is an 
essential input to the portion of the health risk assessment based on 
exposure-response functions from controlled human exposure studies, 
discussed in the next section. Second, estimates of personal exposures 
to ambient O3 concentrations at and above specific benchmark 
levels provide some perspective on the public health impacts of health 
effects that we cannot currently evaluate in quantitative risk 
assessments that may occur at current air quality levels, and the 
extent to which such impacts might be reduced by meeting the current 
and alternative standards. This is especially true when there are 
exposure levels at which we know or can reasonably infer that specific 
O3-related health effects are occurring. We refer to 
exposures at and above these benchmark concentrations as ``exposures of 
concern.''
---------------------------------------------------------------------------

    \33\ As discussed above in Section II.A., O3 health 
responses observed in human clinical studies are associated with 
exposures while engaged in moderate or greater exertion and, 
therefore, these are the exposure measures of interest. The level of 
exertion of individuals engaged in particular activities is measured 
by an equivalent ventilation rate (EVR), ventilation normalized by 
body surface area (BSA, in m\2\), which is calculated as VE/BSA, 
where VE is the ventilation rate (liters/minute). Moderate and 
greater exertion levels were defined as EVR > 13 liters/min-m\2\ 
(Whitfield et al., 1996) to correspond to the exertion levels 
measured in most subjects studied in the controlled human exposure 
studies that reported health effects associated with 6.6 hour 
O3 exposures.
---------------------------------------------------------------------------

    EPA emphasizes that, although the analysis of ``exposures of 
concern'' was conducted using three discrete benchmark levels (i.e., 
0.080, 0.070, and 0.060 ppm), the concept is more appropriately viewed 
as a continuum with greater confidence and less uncertainty about the 
existence of health effects at the upper end and less confidence and 
greater uncertainty as one considers increasingly lower O3 
exposure levels. EPA recognizes that there is no sharp breakpoint 
within the continuum ranging from at and above 0.080 ppm down to 0.060 
ppm. In considering the concept of exposures of concern, it is 
important to balance concerns about the potential for health effects 
and their severity with the increasing uncertainty associated with our 
understanding of the likelihood of such effects at lower O3 
levels.
    Within the context of this continuum, estimates of exposures of 
concern at discrete benchmark levels provide some perspective on the 
public health impacts of O3-related health effects that have 
been demonstrated in human clinical and toxicological studies but 
cannot be evaluated in quantitative risk assessments, such as lung 
inflammation, increased airway responsiveness, and changes in host 
defenses. They also help in understanding the extent to which such 
impacts have the potential to be reduced by meeting the current and 
alternative standards. In the selection of specific benchmark 
concentrations for this analysis, we first considered the exposure 
level of 0.080 ppm, at which there is a substantial amount of clinical 
evidence demonstrating a range of O3-related health effects 
including lung inflammation and airway responsiveness in healthy 
individuals. Thus, as in the last review, this level was selected as a 
benchmark level for this assessment of exposures of concern. Evidence 
newly available in this review is the basis for identifying additional, 
lower benchmark levels of 0.070 and 0.060 ppm for this assessment.
    More specifically, as discussed above in section II.A.2, evidence 
available from controlled human exposure and epidemiology studies 
indicates that people with asthma have larger and more serious effects 
than healthy individuals, including lung function, respiratory 
symptoms, increased airway

[[Page 37854]]

responsiveness, and pulmonary inflammation, which has been shown to be 
a more sensitive marker than lung function responses. Further, a 
substantial new body of evidence from epidemiology studies shows 
associations with serious respiratory morbidity and cardiopulmonary 
mortality effects at O3 levels that extend below 0.080 ppm. 
Additional, but very limited new evidence from controlled human 
exposure studies shows lung function decrements and respiratory 
symptoms in healthy subjects at an O3 exposure level of 
0.060 ppm. The selected benchmark level of 0.070 ppm reflects the new 
information that asthmatics have larger and more serious effects than 
healthy people and therefore controlled human exposure studies done 
with healthy subjects may underestimate effects in this group, as well 
as the substantial body of epidemiological evidence of associations 
with O3 levels below 0.080 ppm. The selected benchmark level 
of 0.060 ppm additionally reflects the very limited new evidence from 
controlled human exposure studies that show lung function decrements 
and respiratory symptoms in some healthy subjects at the 0.060 ppm 
exposure level, recognizing that asthmatics are likely to have more 
serious responses and that lung function is not likely to be as 
sensitive a marker for O3 effects as is lung inflammation.
    The estimates of exposures of concern were reported in terms of 
both ``people exposed'' (the number and percent of people who 
experience a given level of O3 concentrations, or higher, at 
least one time during the O3 season in a given year) and 
``occurrences of exposure'' (the number of times a given level of 
pollution is experienced by the population of interest, expressed in 
terms of person-days of occurrences). Estimating exposures of concern 
is important because it provides some indication of the potential 
public health impacts of a range of O3-related health 
outcomes, such as lung inflammation, increased airway responsiveness, 
and changes in host defenses. These particular health effects have been 
demonstrated in controlled human exposure studies of healthy 
individuals to occur at levels as low as 0.080 ppm O3, but 
have not been evaluated at lower levels in controlled human exposure 
studies. EPA has not included these effects in the quantitative risk 
assessment due to a lack of adequate information on the exposure-
response relationships.
    The 1997 O3 NAAQS review estimated exposures associated 
with 1-hour heavy exertion, 1-hour moderate exertion, and 8-hour 
moderate exertion for children, outdoor workers, and the general 
population. EPA's analysis in the 1997 Staff Paper showed that exposure 
estimates based on the 8-hour moderate exertion scenario for children 
yielded the largest number of children experiencing exposures at or 
above exposures of concern. Consequently, EPA has chosen to focus on 
the 8-hour moderate and greater exertion exposures in all and asthmatic 
school age children in the current exposure assessment. While outdoor 
workers and other adults who engage in moderate or greater exertion for 
prolonged durations while outdoors during the day in areas experiencing 
elevated O3 concentrations also are at risk for experiencing 
exposures associated with O3-related health effects, EPA did 
not focus on quantitative estimates for these populations due to the 
lack of information about the number of individuals who regularly work 
or exercise outdoors. Thus, the exposure estimates presented here and 
in the Staff Paper are most useful for making relative comparisons 
across alternative air quality scenarios and do not represent the total 
exposures in all children or other groups within the general population 
associated with the air quality scenarios.
    Population exposures to O3 were estimated in 12 urban 
areas for 2002, 2003, and 2004 air quality, and also using 
O3 concentrations adjusted to just meet the current and 
several alternative standards. The estimates of 8-hour exposures of 
concern at and above benchmark levels of 0.080, 0.070, and 0.060 ppm 
aggregated across all 12 areas are shown in Table 1 for air quality 
scenarios just meeting the current and four alternative 8-hour average 
standards.\34\ Table 1 provides estimates of the number and percent of 
school age children and asthmatic school age children exposed, with 
daily 8-hour maximum exposures at or above each O3 benchmark 
level of exposures of concern, while at intermittent moderate or 
greater exertion and based on O3 concentrations observed in 
2002 and 2004. Table 1 summarizes estimates for 2002 and 2004, because 
these years reflect years that bracket relatively higher and lower 
O3 levels, with year 2003 generally containing O3 
levels in between when considering the 12 urban areas modeled. This 
table also reports the percent change in the number of persons exposed 
when a given alternative standard is compared with the current 
standard.
---------------------------------------------------------------------------

    \34\ The full range of quantitative exposure estimates 
associated with just meeting the current and alternative 
O3 standards are presented in chapter 4 and Appendix 4A 
of the Staff Paper.
---------------------------------------------------------------------------

    Key observations important in comparing exposure estimates 
associated with just meeting the current NAAQS and alternative 
standards under consideration include:
    (1) As shown in Table 6-1 of the Staff Paper, the patterns of 
exposure in terms of percentages of the population exceeding a given 
exposure level are very similar for the general population and for 
asthmatic and all school age (5-18) children, although children are 
about twice as likely to be exposed, based on the percent of the 
population exposed, at any given level.
    (2) As shown in Table 1 below, the number and percentage of 
asthmatic and all school-age children aggregated across the 12 urban 
areas estimated to experience 1 or more exposures of concern decline 
from simulations of just meeting the current standard to simulations of 
alternative 8-hour standards by varying amounts depending on the 
benchmark level, the population subgroup considered, and the year 
chosen. For example, the estimated percentage of school age children 
experiencing one or more exposures >= 0.070 ppm, while engaged in 
moderate or greater exertion, during an O3 season is about 
18 percent of this population when the current standard is met using 
the 2002 simulation; this is reduced to about 12, 4, 1, and 0.2 percent 
of children upon meeting alternative standards of 0.080, 0.074, 0.070, 
and 0.064 ppm, respectively (all specified in terms of the 4th highest 
daily maximum 8-hour average), using the 2002 simulation.

[[Page 37855]]



 Table 1.--Number and Percent of All and Asthmatic School Age Children in 12 Urban Areas Estimated to Experience
   8-Hour Ozone Exposures Above 0.080, 0.070, and 0.060 ppm While at Moderate or Greater Exertion, One or More
 Times Per Season and the Number of Occurrences Associated with Just Meeting Alternative 8-Hour Standards Based
                                on Adjusting 2002 and 2004 Air Quality Data\1, 2\
----------------------------------------------------------------------------------------------------------------
                                     All children, ages 5-18 aggregate for      Asthmatic children, ages 5-18
                       8-Hour air      12 urban areas, number of children   Aggregate for 12 urban areas, number
Benchmark levels of      quality      exposed (% of all) [%reduction from    of children exposed (% of group) [%
    exposures of      standards\3\             current standard]              reduction from current standard]
   concern (ppm)          (ppm)     ----------------------------------------------------------------------------
                                            2002                2004               2002               2004
----------------------------------------------------------------------------------------------------------------
0.080..............           0.084  700,000 (4%)......  30,000 (0%)......  110,000 (4%).....  0 (0%)
                              0.080  290,000 (2%) [70%]  10,000 (0%) [67%]  50,000 (2%) [54%]  0 (0%)
                              0.074  60,000 (0%) [91%].  0 (0%) [100%]....  10,000 (0%) [91%]  0 (0%)
                              0.070  10,000 (0%) [98%].  0 (0%) [100%]....  0 (0%) [100%]....  0 (0%)
                              0.064  0 (0%) [100%].....  0 (0%) [100%]....  0 (0%) [100%]....  0 (0%)
----------------------------------------------------------------------------------------------------------------
0.070..............           0.084  3,340,000 (18%)...  260,000 (1%).....  520,000 (20%)....  40,000 (1%)
                              0.080  2,160,000 (12%)     100,000 (1%)       330,000 (13%)      10,000 (0%) [75%]
                                      [35%].              [62%].             [36%].
                              0.074  770,000 (4%) [77%]  20,000 (0%) [92%]  120,000 (5%)       0 (0%) [100%]
                                                                             [77%].
                              0.070  270,000 (1%) [92%]  0 (0%) [100%]....  50,000 (2%) [90%]  0 (0%) [100%]
                              0.064  30,000 (0.2%)       0 (0%) [100%]....  10,000 (0.2%)      0 (0%) [100%]
                                      [99%].                                 [98% ].
----------------------------------------------------------------------------------------------------------------
0.060..............           0.084  7,970,000 (44%)...  1,800,000 (10%)..  1,210,000 (47%)..  270,000 (11%)
                              0.080  6,730,000 (37%)     1,050,000 (6%)     1,020,000 (40%)    150,000 (6%)
                                      [16%].              [42%].             [16%].             [44%]
                              0.074  4,550,000 (25%)     350,000 (2%)       700,000 (27%)      50,000 (2%) [81%]
                                      [43%].              [80%].             [42%].
                              0.070  3,000,000 (16%)     110,000 (1%)       460,000 (18%)      10,000 (1%) [96%]
                                      [62%].              [94%].             [62%].
                              0.064  950,000 (5%) [88%]  10,000 (0%) [99%]  150,000 (6%)       0 (0%) [100%]
                                                                             [88%].
----------------------------------------------------------------------------------------------------------------
\1\ Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate >= 13 l-min/
  m\2\.
\2\ Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago,
  Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC).
  Estimates are for the ozone season which is all year in Houston, Los Angeles and Sacramento and March or April
  to September or October for the remaining urban areas.
\3\ All standards summarized here have the same form as the current 8-hour standard which is specified as the 3-
  year average of the annual 4th highest daily maximum 8-hour average concentrations must be at or below the
  concentration level specified. As described in the Staff Paper (section 4.5.8), recent O3 air quality
  distributions have been statistically adjusted to simulate just meeting the current and selected alternative
  standards. These simulations do not represent predictions of when, whether, or how areas might meet the
  specified standards.

    (3) Substantial year-to-year variability in exposure estimates is 
observed over the three-year modeling period. For example, the 
estimated number of school age children experiencing one or more 
exposures >=0.070 ppm during an O3 season when the current 
standard is met in the 12 urban areas included in the analysis is 3.3, 
1.0, or 0.3 million for the 2002, 2003, and 2004 simulations, 
respectively.
    (4) There is substantial variability observed across the 12 urban 
areas in the percent of the population subgroups estimated to 
experience exposures of concern. For example, when 2002 O3 
concentrations are simulated to just meet the current standard, the 
aggregate 12 urban area estimate is 18 percent of all school age 
children are estimated to experience O3 exposures (>=0.070 
ppm (Table 1 below), while the range of exposure estimates in the 12 
urban areas considered separately for all children range from 1 to 38 
percent (EPA, 2007, Exhibit 2, p. 4-48). There was also variability in 
exposure estimates among the modeled areas when using the 2004 air 
quality simulation for the same scenario; however it was reduced and 
ranged from 0 to 7 percent in the 12 urban areas (EPA, 2007, Exhibit 8, 
p. 4-60).
    (5) Of particular note, as discussed above in section II.A. of this 
notice, high inter-individual variability in responsiveness means that 
only a subset of individuals in these groups who are exposed at and 
above a given benchmark level would actually be expected to experience 
such adverse health effects.
    (6) In considering these observations, it is important to take into 
account the variability, uncertainties, and limitations associated with 
this assessment, including the degree of uncertainty associated with a 
number of model inputs and uncertainty in the model itself, as 
discussed above.
2. Quantitative Health Risk Assessment
    This section discusses the approach used to develop quantitative 
health risk estimates associated with exposures to O3 
building upon a more limited risk assessment that was conducted during 
the last review.\35\ As part of the last review, EPA conducted a health 
risk assessment that produced risk estimates for the number and percent 
of children and outdoor workers experiencing lung function and 
respiratory symptoms associated with O3 exposures for 9 
urban areas.\36\ The risk assessment for the last review also included 
risk estimates for excess respiratory-related hospital admissions 
related to O3 concentrations for New York City. In the last 
review, the risk estimates played a significant role in both the staff 
recommendations and in the proposed and final decisions to revise the 
O3 standards. The health risk assessment conducted for the 
current review builds upon the methodology and lessons learned from the 
prior review.
---------------------------------------------------------------------------

    \35\ The methodology, scope, and results from the risk 
assessment conducted in the last review are described in Chapter 6 
of the 1996 Staff Paper (EPA, 1996) and in several technical reports 
(Whitfield et al., 1996; Whitfield, 1997) and publication (Whitfield 
et al., 1998).
    \36\ The 9 urban study areas included in the exposure and risk 
analyses conducted during the last review were: Chicago, Denver, 
Houston, Los Angeles, Miami, New York City, Philadephia, St. Louis, 
and Washington, DC.
---------------------------------------------------------------------------

a. Overview
    The updated health risk assessment conducted as part of this review 
includes estimates of (1) Risks of lung function decrements in all and 
asthmatic school age children, respiratory symptoms in asthmatic 
children, respiratory-related hospital admissions, and non-accidental 
and cardiorespiratory-related mortality associated with recent ambient 
O3 levels; (2) risk reductions and remaining

[[Page 37856]]

risks associated with just meeting the current 8-hour O3 
NAAQS; and (3) risk reductions and remaining risks associated with just 
meeting various alternative 8-hour O3 NAAQS in a number of 
example urban areas. This risk assessment is more fully described and 
presented in the Staff Paper (EPA, 2007, chapter 5) and in a technical 
support document (TSD), Ozone Health Risk Assessment for Selected Urban 
Areas (Abt Associates, 2006, hereafter referred to as ``Risk Assessment 
TSD''). The scope and methodology for this risk assessment were 
developed over the last few years with considerable input from the 
CASAC O3 Panel and the public.\37\ The information contained 
in these documents included specific criteria for the selection of 
health endpoints, studies, and locations to include in the assessment. 
In a peer review letter sent by CASAC to the Administrator documenting 
its advice in October 2006 (Henderson, 2006c), the CASAC O3 
Panel concluded that the risk assessment was ``well done, balanced, and 
reasonably communicated'' and that the selection of health endpoints 
for inclusion in the quantitative risk assessment was appropriate.
---------------------------------------------------------------------------

    \37\ The general approach used in the current risk assessment 
was described in the draft Health Assessment Plan (EPA, 2005a) that 
was released to the CASAC and general public in April 2005 and was 
the subject of a consultation with the CASAC O3 Panel on 
May 5, 2005. In October 2005, OAQPS released the first draft of the 
Staff Paper containing a chapter discussing the risk assessment and 
first draft of the Risk Assessment TSD for CASAC consultation and 
public review on December 8, 2005. In July 2006, OAQPS released the 
second draft of the Staff Paper and second draft of the Risk 
Assessment TSD for CASAC review and public comment which was held by 
the CASAC O3 Panel on August 24-25, 2006.
---------------------------------------------------------------------------

    The goals of the risk assessment are: (1) To provide estimates of 
the potential magnitude of several morbidity effects and mortality 
associated with current O3 levels, and with meeting the 
current and alternative 8-hour O3 standards in specific 
urban areas; (2) to develop a better understanding of the influence of 
various inputs and assumptions on the risk estimates; and (3) to gain 
insights into the distribution of risks and patterns of risk reductions 
associated with meeting alternative O3 standards. The health 
risk assessment is intended to be dependent on and reflect the overall 
weight and nature of the health effects evidence discussed above in 
section II.A and in more detail in the Criteria Document and Staff 
Paper. While not independent of the overall evaluation of the health 
effects evidence, the quantitative health risk assessment provides 
additional insights regarding the relative public health implications 
associated with just meeting the current and several alternative 8-hour 
standards.
    The risk assessment covers a variety of health effects for which 
there is adequate information to develop quantitative risk estimates. 
However, as noted by CASAC (Henderson, 2007) and in the Staff Paper, 
there are a number of health endpoints (e.g., increased lung 
inflammation, increased airway responsiveness, impaired host defenses, 
increased medication usage for asthmatics, increased emergency 
department visits for respiratory causes, and increased school 
absences) for which there currently is insufficient information to 
develop quantitative risk estimates, but which are important to 
consider in assessing the overall public health impacts associated with 
exposures to O3. These additional health endpoints are 
discussed above in section II.A.2 and are also taken into account in 
considering the level of exposures of concern in populations 
particularly at risk, discussed above in this notice.
    There are two parts to the health risk assessment: one based on 
combining information from controlled human exposure studies with 
modeled population exposure and the other based on combining 
information from community epidemiological studies with either 
monitored or adjusted ambient concentrations levels. Both parts of the 
risk assessment were implemented within a new probabilistic version of 
TRIM.Risk, the component of EPA's Total Risk Integrated Methodology 
(TRIM) model framework that estimates human health risks.
    EPA recognizes that there are many sources of uncertainty and 
variability in the inputs to this assessment and that there is 
significant variability and uncertainty in the resulting O3 
risk estimates. As discussed in chapters 2, 5, and 6 of the Staff 
Paper, there is significant year-to-year and city-to-city variability 
related to the air quality data that affects both the controlled human 
exposure studies-based and epidemiological studies-based parts of the 
risk assessment. There are also uncertainties associated with the air 
quality adjustment procedure used to simulate just meeting the current 
and selected alternative standards In the prior review, different 
statistical approaches using alternative functional forms (i.e., 
quadratic, proportional, Weibull) were used to reflect how 
O3 air quality concentrations have historically changed. 
Based on sensitivity analyses conducted in the prior review, the choice 
of alternative air quality adjustment procedures had only a modest 
impact on the risk estimates (EPA, 2007, p. 6-20). With respect to 
uncertainties about estimated background concentrations, as discussed 
below and in the Staff Paper (EPA 2007b, section 5.4.3), alternative 
assumptions about background levels have a variable impact depending on 
the location, standard, and health endpoint analyzed.
    With respect to the lung function part of the health risk 
assessment, key uncertainties include uncertainties in the exposure 
estimates, discussed above, and uncertainties associated with the shape 
of the exposure-response relationship, especially at levels below 0.08 
ppm, 8-hour average, where only very limited data are available down to 
0.04 ppm and there is an absence of data below 0.04 ppm (EPA, 2007, pp. 
6-20--6-21). Concerning the part of the risk assessment based on 
effects reported in epidemiological studies, important uncertainties 
include uncertainties (1) Surrounding estimates of the O3 
coefficients for concentration-response relationships used in the 
assessment, (2) involving the shape of the concentration-response 
relationship and whether or not a population threshold or non-linear 
relationship exists within the range of concentrations examined in the 
studies, (3) related to the extent to which concentration-response 
relationships derived from studies in a given location and time when 
O3 levels were higher or behavior and /or housing conditions 
were different provide accurate representations of the relationships 
for the same locations with lower air quality distributions and/or 
different behavior and/or housing conditions, and (4) concerning the 
possible role of co-pollutants which also may have varied between the 
time of the studies and the current assessment period. An important 
additional uncertainty for the mortality risk estimates is the extent 
to which the associations reported between O3 and non-
accidental and cardiorespiratory mortality actually reflect causal 
relationships.
    As discussed below, some of these uncertainties have been addressed 
quantitatively in the form of estimated confidence ranges around 
central risk estimates; others are addressed through separate 
sensitivity analyses (e.g., the influence of alternative estimates for 
policy-relevant background levels) or are characterized qualitatively. 
For both parts of the health risk assessment, statistical uncertainty 
due to sampling error has been characterized and is expressed in terms 
of 95 percent credible intervals. EPA recognizes that these credible 
intervals do not reflect all of the uncertainties noted above.

[[Page 37857]]

b. Scope and Key Components
    The current health risk assessment is based on the information 
evaluated in the final Criteria Document. The risk assessment includes 
several categories of health effects and estimates risks associated 
with just meeting the current and alternative 8-hour O3 
NAAQS and with several individual recent years of air quality (i.e., 
2002, 2003, and 2004). The risk assessment considers the same 
alternative air quality scenarios that were examined in the human 
exposure analyses described above. Risk estimates were developed for up 
to 12 urban areas selected to illustrate the public health impacts 
associated with these air quality scenarios.\38\ As discussed above in 
section II.B.1, the selection of urban areas was largely determined by 
identifying areas in the U.S. which represented a range of geographic 
areas, population demographics, and climatology; with an emphasis on 
areas that do not meet the current 8-hour O3 NAAQS and which 
included the largest areas with O3 nonattainment problems. 
The selection criteria also included whether or not there were 
acceptable epidemiological studies available that reported 
concentration-response relationships for the health endpoints selected 
for inclusion in the assessment.
---------------------------------------------------------------------------

    \38\ The 12 urban areas are the same urban areas evaluated in 
the exposure analysis discussed in the prior section. However, for 
most of the health endpoints based on findings from epidemiological 
studies, the geographic areas and populations examined in the health 
risk assessment were limited to those counties included in the 
original epidemiological studies that served as the basis for the 
concentration-response relationships.
---------------------------------------------------------------------------

    The short-term exposure related health endpoints selected for 
inclusion in the quantitative risk assessment include those for which 
the final Criteria Document and or Staff Paper concluded that the 
evidence as a whole supports the general conclusion that O3, 
acting alone and/or in combination with other components in the ambient 
air pollution mix, is either clearly causal or is judged to be likely 
causal. Some health effects met this criterion of likely causality, but 
were not included in the risk assessment for other reasons, such as 
insufficient exposure-response data or lack of baseline incidence data.
    As discussed in the section above describing the exposure analysis, 
in order to estimate the health risks associated with just meeting the 
current and alternative 8-hour O3 NAAQS, it is necessary to 
estimate the distribution of hourly O3 concentrations that 
would occur under any given standard. Since compliance is based on a 3-
year average, the amount of control has been applied to each year of 
data (i.e., 2002 to 2004) to estimate risks for a single O3 
season or single warm O3 season, depending on the health 
effect, based on a simulation that adjusted each of these individual 
years so that the three year period would just meet the specified 
standard.
    Consistent with the risk assessment approach used in the last 
review, the risk estimates developed for both recent air quality levels 
and just meeting the current and selected alternative 8-hour standards 
represent risks associated with O3 levels attributable to 
anthropogenic sources and activities (i.e., risk associated with 
concentrations above ``policy-relevant background''). Policy-relevant 
background O3 concentrations used in the O3 risk 
assessment were defined in chapter 2 of the Staff Paper (EPA, 2007, pp. 
2-48--2-55) as the O3 concentrations that would be observed 
in the U.S. in the absence of anthropogenic emissions of precursors 
(e.g., VOC, NOX, and CO) in the U.S., Canada, and Mexico. 
The results of a global tropospheric O3 model (GEOS-CHEM) 
have been used to estimate monthly background daily diurnal profiles 
for each of the 12 urban areas for each month of the O3 
season using meteorology for the year 2001. Based on the results of the 
GEOS-CHEM model, the Criteria Document indicates that background 
O3 concentrations are generally predicted to be in the range 
of 0.015 to 0.035 ppm in the afternoon, and they are generally lower 
under conditions conducive to man-made O3 episodes.\39\
---------------------------------------------------------------------------

    \39\ EPA notes that the estimated level of policy-relevant 
background O3 used in the prior risk assessment was a 
single concentration of 0.04 ppm, which was the midpoint of the 
range of levels for policy-relevant background that was provided in 
the 1996 Criteria Document.
---------------------------------------------------------------------------

    This approach of estimating risks in excess of background is judged 
to be more relevant to policy decisions regarding ambient air quality 
standards than risk estimates that include effects potentially 
attributable to uncontrollable background O3 concentrations. 
Sensitivity analyses examining the impact of alternative estimates for 
background on lung function and mortality risk estimates have been 
developed and are included in the Staff Paper and Risk Assessment TSD 
and key observations are discussed below. Further, CASAC noted the 
difficulties and complexities associated with available approaches to 
estimating policy-relevant background concentrations (Henderson, 2007). 
Recognizing these complexities, EPA requests comments on the new 
approach used in this review for estimating these levels as an input to 
the health risk assessment.\40\
---------------------------------------------------------------------------

    \40\ Recognizing the importance of this issue, EPA intends to 
conduct additional sensitivity analyses related to policy-relevant 
background and its implications for the risk assessment.
---------------------------------------------------------------------------

    In the first part of the current risk assessment, lung function 
decrement, as measured by FEV1, is the only health response 
that is based on data from controlled human exposure studies. As 
discussed above, there is clear evidence of a causal relationship 
between lung function decrements and O3 exposures for school 
age children engaged in moderate exertion based on numerous controlled 
human exposure and summer camp field studies conducted by various 
investigators. Risk estimates have been developed for O3-
related lung function decrements (measured as changes in 
FEV1) for all school age children (ages 5 to 18) and a 
subset of this group, asthmatic school age children (ages 5 to 18), 
whose average exertion over an 8-hour period was moderate or greater. 
The exposure period and exertion level were chosen to generally match 
the exposure period and exertion level used in the controlled human 
exposure studies that were the basis for the exposure-response 
relationships. A combined data set including individual level data from 
the Folinsbee et al. (1988), Horstman et al. (1990), and McDonnell et 
al. (1991) studies, used in the previous risk assessment, and more 
recent data from Adams (2002, 2003, 2006) have been used to estimate 
probabilistic exposure-response relationships for 8-hour exposures 
under different definitions of lung function response (i.e., >=10, 15, 
and 20 percent decrements in FEV1). As discussed in the 
Staff Paper (EPA, 2007, p. 5-27), while these specific controlled human 
exposure studies only included healthy adults aged 18-35, findings from 
other controlled human exposure studies and summer camp field studies 
involving school age children in at least six different locations in 
the northeastern United States, Canada, and Southern California 
indicated changes in lung function in healthy children similar to those 
observed in healthy adults exposed to O3 under controlled 
chamber conditions.
    Consistent with advice from CASAC (Henderson, 2006c), EPA has 
considered both linear and logistic functional forms in estimating the 
probabilistic exposure-response relationships for lung function 
responses. A Bayesian Markov Chain Monte Carlo approach, described in 
more detail in the Risk Assessment TSD, has been used that incorporates 
both model uncertainty and uncertainty due

[[Page 37858]]

to sample size in the combined data set that served as the basis for 
the assessment. EPA has chosen a model reflecting a 90 percent 
weighting on a logistic form and a 10 percent weighting on a linear 
form as the base case for the current risk assessment. The basis for 
this choice is that the logistic form provides a very good fit to the 
combined data set, but a linear model cannot be entirely ruled out 
since there are only very limited data (i.e., 30 subjects) at the two 
lowest exposure levels (i.e., 0.040 and 0.060 ppm). EPA has conducted a 
sensitivity analysis which examines the impact on the lung function 
risk estimates of two alternative choices, an 80 percent logistic/20 
percent linear split and a 50 percent logistic/50 percent linear split.
    As noted above, risk estimates have been developed for three 
measures of lung function response (i.e., >=10, 15, and 20 percent 
decrements in FEV1). However, the Staff Paper and risk 
estimates summarized below focus on FEV1 decrements >=15 
percent for all school age children and >=10 percent for asthmatic 
school age children, consistent with the advice from CASAC (Henderson, 
2006c) that these levels of response represent indicators of adverse 
health effects in these populations. The Risk Assessment TSD and Staff 
Paper present the broader range of risk estimates including all three 
measures of lung function response.
    Developing risk estimates for lung function decrements involved 
combining probabilistic exposure-response relationships based on the 
combined data set from several controlled human exposure studies with 
population exposure distributions for all and asthmatic school age 
children associated with recent air quality and air quality simulated 
to just meet the current and alternative 8-hour O3 NAAQS 
based on the results from the exposure analysis described in the 
previous section. The risk estimates have been developed for 12 large 
urban areas for the O3 season.\41\ These 12 urban areas 
include approximately 18.3 million school age children, of which 2.6 
million are asthmatic school age children.\42\
---------------------------------------------------------------------------

    \41\ As discussed above in section II.B.1, the urban areas were 
defined using the consolidated statistical areas definition and the 
total population residing in the 12 urban areas was approximately 
88.5 million people.
    \42\ For 9 of the 12 urban areas, the O3 season is 
defined as a period running from March or April to September or 
October. In 3 of the urban areas (Houston, Los Angeles, and 
Sacramento), the O3 season is defined as the entire year.
---------------------------------------------------------------------------

    In addition to uncertainties arising from sample size 
considerations, which are quantitatively characterized and presented as 
95 percentile credible intervals, there are additional uncertainties 
and caveats associated with the lung function risk estimates. These 
include uncertainties about the shape of the exposure-response 
relationship, particularly at levels below 0.080 ppm, and about policy-
relevant background levels, for which sensitivity analyses have been 
conducted. Additional important caveats and uncertainties concerning 
the lung function portion of the health risk assessment include: (1) 
The uncertainties and limitations associated with the exposure 
estimates discussed above and (2) the inability to account for some 
factors which are known to affect the exposure-response relationships 
(e.g., assigning healthy and asthmatic children the same responses as 
observed in healthy adult subjects and not adjusting response rates to 
reflect the increase and attenuation of responses that have been 
observed in studies of lung function responses upon repeated 
exposures). A more complete discussion of assumptions and uncertainties 
is contained in chapter 5 of the Staff Paper and in the Risk Assessment 
TSD (Abt Associates, 2006).
    The second part of the risk assessment is based on health effects 
observed in epidemiological studies. Based on a review of the evidence 
evaluated in the Criteria Document and Staff Paper, as well as the 
criteria discussed in chapter 5 of the Staff Paper, the following 
categories of health endpoints associated with short-term exposures to 
ambient O3 concentrations were included in the risk 
assessment: respiratory symptoms in moderate to severe asthmatic 
children, hospital admissions for respiratory causes, and non-
accidental and cardiorespiratory mortality. As discussed above, there 
is strong evidence of a causal relationship for the respiratory 
morbidity endpoints included in the current risk assessment. With 
respect to nonaccidental and cardiorespiratory mortality, the Criteria 
Document concludes that there is strong evidence which is highly 
suggestive of a causal relationship between nonaccidental and 
cardiorespiratory-related mortality and O3 exposures during 
the warm O3 season. As discussed in the Staff Paper (chapter 
5), EPA also recognizes that for some of the effects observed in 
epidemiological studies, such as increased respiratory-related hospital 
admissions and nonaccidental and cardiorespiratory mortality, 
O3 may be serving as an indicator for reactive oxidant 
species in the overall photochemical oxidant mix and that these other 
constituents may be responsible in whole or part for the observed 
effects.
    Risk estimates for each health endpoint category were only 
developed for areas that were the same or close to the location where 
at least one concentration-response function for the health endpoint 
had been estimated.\43\ Thus, for respiratory symptoms in moderate to 
severe asthmatic children only the Boston urban area was included and 
four urban areas were included for respiratory-related hospital 
admissions. Nonaccidental mortality risk estimates were developed for 
12 urban areas and 8 urban areas were included for cardiorespiratory 
mortality.
---------------------------------------------------------------------------

    \43\ The geographic boundaries for the urban areas included in 
this portion of the risk assessment were generally matched to the 
geographic boundaries used in the epidemiological studies that 
served as the basis for the concentration-response functions. In 
most cases, the urban areas were defined as either a single county 
or a few counties for this portion of the risk assessment.
---------------------------------------------------------------------------

    The concentration-response relationships used in the assessment are 
based on findings from human epidemiological studies that have relied 
on fixed-site ambient monitors as a surrogate for actual ambient 
O3 exposures. In order to estimate the incidence of a 
particular health effect associated with recent air quality in a 
specific county or set of counties attributable to ambient 
O3 exposures in excess of background, as well as the change 
in incidence corresponding to a given change in O3 levels 
resulting from just meeting the current or alternative 8-hour 
O3 standards, three elements are required for this part of 
the risk assessment. These elements are: (1) Air quality information 
(including recent air quality data for O3 from ambient 
monitors for the selected location, estimates of background 
O3 concentrations appropriate for that location, and a 
method for adjusting the recent data to reflect patterns of air quality 
estimated to occur when the area just meets a given O3 
standard); (2) relative risk-based concentration-response functions 
that provide an estimate of the relationship between the health 
endpoints of interest and ambient O3 concentration; and (3) 
annual or seasonal baseline health effects incidence rates and 
population data, which are needed to provide an estimate of the 
seasonal baseline incidence of health effects in an area before any 
changes in O3 air quality.
    A key component in the portion of the risk assessment based on 
epidemiological studies is the set of concentration-response functions 
which provide estimates of the relationships

[[Page 37859]]

between each health endpoint of interest and changes in ambient 
O3 concentrations. Studies often report more than one 
estimated concentration-response function for the same location and 
health endpoint. Sometimes models include different sets of co-
pollutants and/or different lag periods between the ambient 
concentrations and reported health responses. For some health 
endpoints, there are studies that estimated multi-city and single-city 
O3 concentration-response functions. While the Risk 
Assessment TSD and chapter 5 of the Staff Paper present a more 
comprehensive set of risk estimates, EPA has focused on estimates based 
on multi-city studies where available. The advantages of relying more 
heavily on concentration-response functions based on multi-city studies 
include: (1) More precise effect estimates due to larger data sets, 
reducing the uncertainty around the estimated coefficient; (2) greater 
consistency in data handling and model specification that can eliminate 
city-to-city variation due to study design; and (3) less likelihood of 
publication bias or exclusion of reporting of negative or 
nonsignificant findings. Where studies reported different effect 
estimates for varying lag periods, consistent with the Criteria 
Document, single day lag periods of 0 to 1 days were used for 
associations with respiratory hospital admissions and mortality. For 
mortality associated with exposure to O3 which may result 
over a several day period after exposure, distributed lag models, which 
take into account the contribution to mortality effects over several 
days, were used where available.
    One of the most important elements affecting uncertainties in the 
epidemiological-based portion of the risk assessment is the 
concentration-response relationships used in the assessment. The 
uncertainty resulting from the statistical uncertainty associated with 
the estimate of the O3 coefficient in the concentration-
response function was characterized either by confidence intervals or 
by Bayesian credible intervals around the corresponding point estimates 
of risk. Confidence and credible intervals express the range within 
which the true risk is likely to fall if the only uncertainty 
surrounding the O3 coefficient involved sampling error. 
Other uncertainties, such as differences in study location, time period 
(i.e., the years in which the study was conducted), and model 
uncertainties are not represented by the confidence or credible 
intervals presented, but were addressed by presenting estimates for 
different urban areas, by including risk estimates based on studies 
using different time periods and models, where available, and/or are 
discussed throughout section 5.3 of the Staff Paper. Because 
O3 effects observed in the epidemiological studies have been 
more clearly and consistently shown for warm season analyses, all 
analyses for this portion of the risk assessment were carried out for 
the same time period, April through September.
    The Criteria Document finds that no definitive conclusion can be 
reached with regard to the existence of population thresholds in 
epidemiological studies (Criteria Document, pp. 8-44). EPA recognizes, 
however, the possibility that thresholds for individuals may exist for 
reported associations at fairly low levels within the range of air 
quality observed in the studies, but not be detectable as population 
thresholds in epidemiological analyses. Based on the Criteria 
Document's conclusions, EPA judged and CASAC concurred, that there is 
insufficient evidence to support use of potential population threshold 
levels in the quantitative risk assessment. However, EPA recognizes 
that there is increasing uncertainty about the concentration-response 
relationship at lower concentrations which is not captured by the 
characterization of the statistical uncertainty due to sampling error. 
Therefore, the risk estimates for respiratory symptoms in moderate to 
severe asthmatic children, respiratory-related hospital admissions, and 
premature mortality associated with exposure to O3 must be 
considered in light of uncertainties about whether or not these 
O3-related effects occur in these populations at very low 
O3 concentrations.
    With respect to variability within this portion of the risk 
assessment, there is variability among concentration-response functions 
describing the relation between O3 and both respiratory-
related hospital admissions and nonaccidental and cardiorespiratory 
mortality across urban areas. This variability is likely due to 
differences in population (e.g., age distribution), population 
activities that affect exposure to O3 (e.g., use of air 
conditioning), levels and composition of co-pollutants, baseline 
incidence rates, and/or other factors that vary across urban areas. The 
current risk assessment incorporates some of the variability in key 
inputs to the analysis by using location-specific inputs (e.g., 
location-specific concentration-response functions, baseline incidence 
rates, and air quality data). Although spatial variability in these key 
inputs across all U.S. locations has not been fully characterized, 
variability across the selected locations is imbedded in the analysis 
by using, to the extent possible, inputs specific to each urban area.
c. Risk Estimates and Key Observations
    The Staff Paper (chapter 5) and Risk Assessment TSD present risk 
estimates associated with just meeting the current and several 
alternative 8-hour standards, as well as three recent years of air 
quality as represented by 2002, 2003, and 2004 monitoring data. As 
discussed in the exposure analysis section above, there is considerable 
city-to-city and year-to-year variability in the O3 levels 
during this period, which results in significant variability in both 
portions of the health risk assessment.
    In the 1997 risk assessment, risks for lung function decrements 
associated with 1-hour heavy exertion, 1-hour moderate exertion, and 8-
hour moderate exertion exposures were estimated. Since the 8-hour 
moderate exertion exposure scenario for children clearly resulted in 
the greatest health risks in terms of lung function decrements, EPA has 
chosen to include only the 8-hour moderate exertion exposures in the 
current risk assessment for this health endpoint. Thus, the risk 
estimates presented here and in the Staff Paper are most useful for 
making relative comparisons across alternative air quality scenarios 
and do not represent the total risks for lung function decrements in 
children or other groups within the general population associated with 
any of the air quality scenarios. Thus, some outdoor workers and adults 
engaged in moderate exertion over multi-hour periods (e.g., 6-8-hour 
exposures) also would be expected to experience similar lung function 
decrements. However, the percentage of each of these other 
subpopulations expected to experience these effects is expected to be 
smaller than all school age children who tend to spend more hours 
outdoors while active based on the exposure analyses conducted during 
the prior review.
    Table 2 presents a summary of the risk estimates for lung function 
decrements for the current standard and several alternative 8-hour 
standard levels with the same form as the current 8-hour standard. The 
estimates are for the aggregate number and percent of all school age 
children across 12 urban areas and the aggregate number and percent of 
asthmatic school age children

[[Page 37860]]

across 5 urban areas \44\ who are estimated to have at least 1 moderate 
or greater lung function response (defined as FEV1 >=15 
percent in all children and >=10 percent in asthmatic children) 
associated with 8-hour exposures to O3 while engaged in 
moderate or greater exertion on average over the 8-hour period. The 
lung function risk estimates summarized in Table 2 illustrate the year-
to-year variability in both remaining risk associated with a relatively 
high year (i.e., based on adjusting 2002 O3 air quality 
data) and relatively low year (based on adjusting 2004 O3 
air quality data) as well as the year-to-year variability in the risk 
reduction estimated to occur associated with various alternative 
standards relative to just meeting the current standard. For example, 
it is estimated that about 610,000 school age children (3.2 percent of 
school age children) would experience 1 or more moderate lung function 
decrements for the 12 urban areas associated with O3 levels 
just meeting the current standard based on 2002 air quality data 
compared to 230,000 (1.2 percent of children) associated with just 
meeting the current standard based on 2004 air quality data.
---------------------------------------------------------------------------

    \44\ Due to time constraints, lung function risk estimates for 
asthmatic school age children were developed for only 5 of the 12 
urban areas, and the areas were selected to represent different 
geographic regions. The 5 areas were: Atlanta, Chicago, Houston, Los 
Angeles, and New York City.

    Table 2.--Number and Percent of All and Asthmatic School Age Children in Several Urban Areas Estimated To
 Experience Moderate or Greater Lung Function Responses 1 or More Times per Season Associated With 8-Hour Ozone
Exposures Associated With Just Meeting Alternative 8-Hour Standards Based on Adjusting 2002 and 2004 Air Quality
                                                  Data \1,\ \2\
----------------------------------------------------------------------------------------------------------------
                                    All children, ages 5-18, FEV1 >=15      Asthmatic children, ages 5-18, FEV1
                                  percent, aggregate for 12 urban areas,    >=10 percent, aggregate for 5 urban
                                  number of children affected (% of all)   areas, number of children affected (%
8-Hour air quality standards \3\    [% reduction from current standard]     of group) [% reduction from current
                                 ----------------------------------------                standard]
                                                                         ---------------------------------------
                                         2002                2004                2002                2004]
----------------------------------------------------------------------------------------------------------------
0.084 ppm (Current standard)....  610,000 (3.3%)....  230,000 (1.2%)....  130,000 (7.8%)....  70,000 (4.2%).
0.080 ppm.......................  490,000 (2.7%)      180,000 (1.0%)      NA \4\............  NA.
                                   [20% reduction].    [22% reduction].
0.074 ppm.......................  340,000 (1.9%)      130,000 (0.7%)      90,000 (5.0%) [31   40,000 (2.7%) [43%
                                   [44% reduction].    [43% reduction].    % reduction].       reduction].
0.070 ppm.......................  260,000 (1.5%)      100,000 (0.5%)      NA................  NA.
                                   [57% reduction].    [57% reduction].
0.064 ppm.......................  180,000 (1.0%)      70,000 (0.4%) [70%  50,000 (3.0%) [62%  20,000 (1.5%) [71%
                                   [70% reduction].    reduction].         reduction].         reduction].
----------------------------------------------------------------------------------------------------------------
\1\ Associated with exposures while engaged in moderate or greater exertion which is defined as having an 8-hour
  average equivalent ventilation rate >=13 l-min/m \2\.
\2\ Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston,
  Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and
  Washington, DC) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, New York). Estimates are for the O3
  season which is all year in Houston, Los Angeles and Sacramento and March or April to September or October for
  the remaining urban areas.
\3\ All standards summarized here have the same form as the current 8-hour standard which is specified as the 3-
  year average of the annual 4th highest daily maximum 8-hour average concentrations must be at or below the
  stated concentration level. As described in the Staff Paper (section 4.5.8), recent O3 air quality
  distributions have been statistically adjusted to simulate just meeting the current and selected alternative
  standards. These simulations do not represent predictions of when, whether, or how areas might meet the
  specified standards
\4\ NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic
  school age children population.

    As discussed in the Staff Paper, a child may experience multiple 
occurrences of a lung function response during the O3 
season. For example, upon meeting the current 8-hour standard, the 
median estimates are that about 610,000 children would experience a 
moderate or greater lung function response 1 or more times for the 
aggregate of the 12 urban areas over a single O3 season 
(based on the 2002 simulation), and that there would be almost 3.2 
million total occurrences. Thus, on average it is estimated that there 
would be about 5 occurrences per O3 season per responding 
child for air quality just meeting the current 8-hour standard across 
the 12 urban areas. While the estimated number of occurrences per 
O3 season is lower when based on the 2004 simulation than 
for the 2002 simulation, the estimated number of occurrences per 
responding child is similar. EPA recognizes that some children in the 
population might have only 1 or 2 occurrences while others may have 6 
or more occurrences per O3 season. Risk estimates based on 
adjusting 2003 air quality to simulate just meeting the current and 
alternative 8-hour standards are intermediate to the estimates 
presented in Table 2 above in this notice and are presented in the 
Staff Paper (chapter 5) and Risk Assessment TSD.
    For just meeting the current 8-hour standard, Table 5-8 in the 
Staff Paper shows that median estimates across the 12 urban areas for 
all school age children experiencing 1 or more moderate lung function 
decrements ranges from 0.9 to 5.4 percent based on the 2002 simulation 
and from 0.8 to 2.2 percent based on the 2004 simulation. Risk 
estimates for each urban area included in the assessment, for each of 
the three years analyzed, and for additional alternative standards are 
presented in chapter 5 of the Staff Paper and in the Risk Assessment 
TSD.
    For just meeting the current 8-hour standard, the median estimates 
across the 5 urban areas for asthmatic school age children range from 
3.4 to 10.9 percent based on the 2002 simulation and from 3.2 to 6.9 
percent based on the 2004 simulation.
    Key observations important in comparing estimated lung function 
risks associated with attainment of the current NAAQS and alternative 
standards under consideration include:
    (1) As discussed above, there is significant year to year 
variability in the range of median estimates of the number of school 
age children (ages 5-18) estimated to experience at least one 
FEV1 decrement >=15 percent due to 8-hour O3 
exposures across the 12 urban

[[Page 37861]]

areas analyzed, and similarly across the 5 urban areas analyzed for 
asthmatic school age children (ages 5-18) estimated to experience at 
least one FEV1 decrement >=10 percent, when the current and 
alternative 8-hour standards are just met.
    (2) For asthmatic school age children, the median estimates of 
occurrences of FEV1 decrements >=10% range from 52,000 to 
nearly 510,000 responses associated with just meeting the current 
standard (based on the 2002 simulation) and range from 61,000 to about 
240,000 occurrences (based on the 2004 simulation). These risk 
estimates would be reduced to a range of 14,000 to about 275,000 
occurrences (2002 simulation) and to about 18,000 to nearly 125,000 
occurrences (2004 simulation) upon just meeting the most stringent 
alternative 8-hour standard (0.064 ppm, 4th highest). The average 
number of occurrences per asthmatic child in an O3 season 
ranged from about 6 to 11 associated with just meeting the current 
standard (2002 simulation). The average number of occurrences per 
asthmatic child ranged from 4 to 12 upon meeting the most stringent 
alternative examined (0.064 ppm, 4th-highest) based on the 2002 
simulation. The number of occurrences per asthmatic child is similar 
for the scenarios based on the 2004 simulation.
    As discussed above, several epidemiological studies have reported 
increased respiratory morbidity outcomes (e.g., respiratory symptoms in 
moderate to severe asthmatic children, respiratory-related hospital 
admissions) and increased nonaccidental and cardiorespiratory mortality 
associated with exposure to ambient O3 concentrations. The 
results and key observations from this portion of the risk assessment 
are presented below:
    (1) Estimates for increased respiratory symptoms (i.e., chest 
tightness, shortness of breath, and wheeze) in moderate/severe 
asthmatic children (ages 0-12) were developed for the Boston urban area 
only. The median estimated number of days involving chest tightness 
(using the concentration-response relationship with only O3 
in the model) is about 6,100 (based on the 2002 simulation) and about 
4,500 (based on the 2004 simulation) upon meeting the current 8-hour 
standard and this is reduced to about 4,600 days (2002 simulation) and 
3,100 days (2004 simulation) upon meeting the most stringent 
alternative examined (0.064 ppm, 4th-highest daily maximum 8-hour 
average). This corresponds to 11 percent (2002 simulation) and 8 
percent (2004 simulation) of total incidence of chest tightness upon 
meeting the current 8-hour standard and to about 8 percent (2002 
simulation) and 5.5 percent (2004 simulation) of total incidence of 
chest tightness upon meeting a 0.064 ppm, 4th-highest daily maximum 8-
hour average standard. Similar patterns of effects and reductions in 
effects are observed for each of the respiratory symptoms examined.
    (2) The Staff Paper and Risk Assessment TSD present unscheduled 
hospital admission risk estimates for respiratory illness and asthma in 
New York City associated with short-term exposures to O3 
concentrations in excess of background levels from April through 
September for several recent years (2002, 2003, and 2004) and upon just 
meeting the current and alternative 8-hour standards based on 
simulating O3 levels using 2002-2004 O3 air 
quality data. For total respiratory illness, EPA estimates about 6.4 
cases per 100,000 relevant population (2002 simulation) and about 4.6 
cases per 100,000 relevant population (2004 simulation), which 
represents 1.5 percent (2002 simulation) and 1.0 percent (2004 
simulation) of total incidence or about 510 cases (2002 simulation) and 
about 370 cases (2004 simulation) upon just meeting the current 8-hour 
standard. For asthma-related hospital admissions, which are a subset of 
total respiratory illness admissions, the estimates are about 5.5 cases 
per 100,000 relevant population (2002 simulation) and about 3.9 cases 
per 100,000 relevant population (2004 simulation), which represents 
about 3.3 percent (2002 simulation) and 2.4 percent (2004 simulation) 
of total incidence or about 440 cases (2002) and about 310 cases (2004) 
for this same air quality scenario.
    For increasingly more stringent alternative 8-hour standards, there 
is a gradual reduction in respiratory illness cases per 100,000 
relevant population from 6.4 cases per 100,000 upon just meeting the 
current 8-hour standard to 4.6 cases per 100,000 under the most 
stringent 8-hour standard (i.e., 0.064 ppm, average 4th-highest daily 
maximum) analyzed based on the 2002 simulation. Similarly, based on the 
2004 simulation there is a gradual reduction from 4.6 cases per 100,000 
relevant population upon just meeting the current 8-hour standard to 
3.0 cases per 100,000 under the 0.064 ppm, average 4th-highest daily 
maximum standard.
    Additional respiratory-related hospital admission estimates for 
three other locations are provided in the Risk Assessment TSD. EPA 
notes that the concentration-response functions for each of these 
locations examined different outcomes in different age groups (e.g., > 
age 30 in Los Angeles, > age 64 in Cleveland and Detroit, vs. all ages 
in New York City), making comparison of the risk estimates across the 
areas very difficult.
    (3) Based on the median estimates for incidence for nonaccidental 
mortality (based on the Bell et al. (2004) 95 cities concentration-
response function), meeting the most stringent standard (0.064 ppm) is 
estimated to reduce mortality by 40 percent of what it would be 
associated with just meeting the current standard (based on the 2002 
simulation). The patterns for cardiorespiratory mortality are similar. 
The aggregate O3-related cardiorespiratory mortality upon 
just meeting the most stringent standard shown is estimated to be about 
42 percent of what it would be upon just meeting the current standard, 
using simulated O3 concentrations that just meet the current 
and alternative 8-hour standards based on the 2002 simulation. Using 
the 2004 simulation, the corresponding reductions show a similar 
pattern but are somewhat greater.
    (4) Much of the contribution to the risk estimates for non-
accidental and cardiorespiratory mortality upon just meeting the 
current 8-hour standard is associated with 24-hour O3 
concentrations between background and 0.040 ppm. Based on examining 
relationships between 24-hour concentrations averaged across the 
monitors within an urban area and 8-hour daily maximum concentrations, 
8-hour daily maximum levels at the highest monitor in an urban area 
associated with these averaged 24-hour levels are generally about twice 
as high as the 24-hour levels. Thus, most O3-related 
nonaccidental mortality is estimated to occur when O3 
concentrations are between background and when the highest monitor in 
the urban area is at or below 0.080 ppm, 8-hour average concentration.
    The discussion below highlights additional observations and 
insights from the O3 risk assessment, together with 
important uncertainties and limitations.
    (1) As discussed in the Staff Paper (section 5.4.5) EPA has greater 
confidence in relative comparisons in risk estimates between 
alternative standards than in the absolute magnitude of risk estimates 
associated with any particular standard.
    (2) Significant year-to-year variability in O3 
concentrations combined with the use of a 3-year design value to 
determine the amount of air quality adjustment to be applied to each 
year analyzed, results in significant year-to-year variability in the 
annual health risk

[[Page 37862]]

estimates upon just meeting the current and potential alternative 8-
hour standards.
    (3) There is noticeable city-to-city variability in estimated 
O3-related incidence of morbidity and mortality across the 
12 urban areas analyzed for both recent years of air quality and for 
air quality adjusted to simulate just meeting the current and selected 
potential alternative standards. This variability is likely due to 
differences in air quality distributions, differences in exposure 
related to many factors including varying activity patterns and air 
exchange rates, differences in baseline incidence rates, and 
differences in susceptible populations and age distributions across the 
12 urban areas.
    (4) With respect to the uncertainties about estimated policy-
relevant background concentrations, as discussed in the Staff Paper 
(section 5.4.3), alternative assumptions about background levels had a 
variable impact depending on the health effect considered and the 
location and standard analyzed in terms of the absolute magnitude and 
relative changes in the risk estimates. There was relatively little 
impact on either absolute magnitude or relative changes in lung 
function risk estimates due to alternative assumptions about background 
levels. With respect to O3-related non-accidental mortality, 
while notable differences (i.e., greater than 50 percent)\45\ were 
observed for nonaccidental mortality in some areas, particularly for 
more stringent standards, the overall pattern of estimated reductions, 
expressed in terms of percentage reduction relative to the current 
standard, was significantly less impacted.
---------------------------------------------------------------------------

    \45\ For example, assuming lower background levels resulted in 
increased estimates of non-accidental mortality incidence per 
100,000 that were often 50 to 100 percent greater than the base case 
estimates; assuming higher background levels resulted in decreased 
estimates of non-accidental mortality incidence per 100,000 that 
were less than the base case estimates by 50 percent or more in many 
of the areas.
---------------------------------------------------------------------------

C. Conclusions on the Adequacy of the Current Primary Standard

1. Background
    The initial issue to be addressed in the current review of the 
primary O3 standard is whether, in view of the advances in 
scientific knowledge and additional information, the existing standard 
should be revised. In evaluating whether it is appropriate to retain or 
revise the current standard, 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 O3 
standard. Evidence-based considerations include the assessment of 
evidence from controlled human exposure, animal toxicological, field, 
and epidemiological studies for a variety of health endpoints. For 
those endpoints based on epidemiological studies, greater weight has 
been placed on associations with health endpoints that are causal or 
likely causal based on an integrative synthesis of the entire body of 
evidence, including not only all available epidemiological evidence but 
also evidence from animal toxicological and controlled human exposure 
studies. Less weight has been placed on evidence of associations that 
were judged to be only suggestive of possible causal relationships. 
Consideration of quantitative exposure- and risk-based information 
draws from the results of the exposure and risk assessments described 
above. More specifically, estimates of the magnitude of O3-
related exposures and risks associated with recent air quality levels, 
as well as the exposure and risk reductions likely to be associated 
with just meeting the current 8-hour primary O3 NAAQS, have 
been considered.
    In this review, a series of general questions frames the approach 
to reaching a decision on the adequacy of the current standard, such as 
the following: (1) To what extent does newly available information 
reinforce or call into question evidence of associations of 
O3 exposures with effects identified in the last review?; 
(2) to what extent has evidence of new effects and/or at-risk 
populations become available since the last review?; (3) to what extent 
have important uncertainties identified in the last review been reduced 
and have new uncertainties emerged?; (4) to what extent does newly 
available information reinforce or call into question any of the basic 
elements of the current standards?
    The question of whether the available evidence supports 
consideration of a standard that is more protective than the current 
standard includes consideration of: (1) Whether there is evidence that 
associations, especially likely causal associations, extend to ambient 
O3 concentration levels that are as low as or lower than had 
previously been observed, and the important uncertainties associated 
with that evidence; (2) the extent to which exposures of concern and 
health risks are estimated to occur in areas upon meeting the current 
standard and the important uncertainties associated with the estimated 
exposures and risks; and (3) the extent to which the O3-
related health effects indicated by the evidence and the exposure and 
risk assessments are considered important from a public health 
perspective, taking into account the nature and severity of the health 
effects, the size of the at-risk populations, and the kind and degree 
of the uncertainties associated with these considerations.
    The current primary O3 standard is an 8-hour standard, 
which was set at a level of 0.08 ppm,\46\ with a form of the annual 
fourth-highest daily maximum 8-hour average concentration, averaged 
over three years. This standard was chosen to provide protection to the 
public, especially children and other at-risk populations, against a 
wide range of O3-induced health effects. As an introduction 
to this discussion of the adequacy of the current O3 
standard, it is useful to summarize the key factors that formed the 
basis of the decision in the last review to revise the averaging time, 
level, and form of the then current 1-hour standard.
---------------------------------------------------------------------------

    \46\ If the standard were to be specified to the nearest 
thousandth ppm, the current 0.08 ppm 8-hour standard would be 
equivalent to a standard set at 0.084 ppm, reflecting the data 
rounding conventions that are part of the definition of the current 
8-hour standard.
---------------------------------------------------------------------------

    In the last review, the key factor in deciding to revise the 
averaging time of the primary standard was evidence from controlled 
human exposure studies of healthy young adult subjects exposed for 1 to 
8 hours to O3. The best documented health endpoints in these 
studies were decrements in indices of lung function, such as forced 
expiratory volume in 1 second (FEV1), and respiratory 
symptoms, such as cough and chest pain on deep inspiration. For short-
term exposures of 1 to 3 hours, group mean FEV1 decrements were 
statistically significant for O3 concentrations only at and 
above 0.12 ppm, and only when subjects engaged in very heavy exertion. 
By contrast, evidence available in the prior review showed that 
prolonged exposures of 6 to 8 hours produced statistically significant 
group mean FEV1 decrements at the lowest O3 
concentrations evaluated in those studies, 0.080 ppm, even when 
experimental subjects were engaged in more realistic intermittent 
moderate exertion levels. The health significance of this newer 
evidence led to the conclusion in the 1997 final decision that the 8-
hour averaging time is more directly associated with health effects of 
concern at lower O3 concentrations than is the 1-hour 
averaging time.

[[Page 37863]]

    Based on the available evidence of O3-related health 
effects, the following factors were of particular importance in the 
last review in informing the selection of the level and form of a new 
8-hour standard: (1) Quantitative estimates of O3-related 
risks to active children, who were judged to be an at-risk subgroup of 
concern, in terms of transient and reversible respiratory effects 
judged to be adverse, including moderate to large decreases in lung 
function and moderate to severe pain on deep inspiration, and the 
uncertainty and variability in such estimates; (2) consideration of 
both the estimated percentages, total numbers of children, and number 
of times they were likely to experience such effects; (3) 
epidemiological evidence of associations between ambient O3 
and increased respiratory hospital admissions, and quantitative 
estimates of percentages and total numbers of asthma-related admissions 
in one example urban area that were judged to be indicative of a 
pyramid of much larger effects, including respiratory-related hospital 
admissions, emergency department visits, doctor visits, and asthma 
attacks and related increased medication use; (4) quantitative 
estimates of the number of ``exposures of concern\47\'' (defined as 
exposures >= 0.080 ppm for 6 to 8 hour) that active children are likely 
to experience, and the uncertainty and variability in such estimates; 
(5) the judgment that such exposures are an important indicator of 
public health impacts of O3-related effects for which 
information is too limited to develop quantitative risk estimates, 
including increased nonspecific bronchial responsiveness (e.g., related 
to aggravation of asthma), decreased pulmonary defense mechanisms 
(suggestive of increased susceptibility to respiratory infection), and 
indicators of pulmonary inflammation (related to potential aggravation 
of chronic bronchitis or long-term damage to the lungs); (6) the 
broader public health perspective of the number of people living in 
areas that would breathe cleaner air as a result of the revised 
standard; (7) consideration of the relative seriousness of various 
health effects and the relative degree of certainty in both the 
likelihood that people will experience various health effects and their 
medical significance; (8) the relationship of a standard level to 
estimated ``background'' levels associated with nonanthropogenic 
sources of O3; and (9) CASAC's advice and recommendations. 
Additional factors considered in selecting the form of the standard 
included balancing the public health implications of the estimated 
number of times in an O3 season that the standard level 
might be exceeded in an area that is in attainment with the standard 
with the year-to-year stability of the air quality statistic, which can 
be particularly affected by years with unusual meteorology. A more 
stable air quality statistic serves to avoid disruptions to ongoing 
control programs that could result from moving into and out of 
attainment, thereby interrupting the public health protection afforded 
by such control programs.
---------------------------------------------------------------------------

    \47\ In the last review, ``exposures of concern'' referred to 
exposures at and above 0.08 ppm, 8-hour average, at which a range of 
health effects have been observed in controlled human studies, but 
for which data were too limited to allow for quantitative risk 
assessment. (62 FR 38860, July 18, 1997).
---------------------------------------------------------------------------

    In reaching a final decision in the last review, the Administrator 
was mindful that O3 exhibits a continuum of effects, such 
that there is no discernible threshold above which public health 
protection requires that no exposures be allowed or below which all 
risks to public health can be avoided. The final decision reflected a 
recognition that important uncertainties remained, for example with 
regard to interpreting the role of other pollutants co-occurring with 
O3 in observed associations, understanding biological 
mechanisms of O3-related health effects, and estimating 
human exposures and quantitative risks to at-risk populations for these 
health effects.
2. Evidence- and Exposure/Risk-Based Considerations in the Staff Paper
    The Staff Paper (section 6.3.1) considers the evidence presented in 
the Criteria Document as discussed above in section II.A as a basis for 
evaluating the adequacy of the current O3 standard, 
recognizing that important uncertainties remain. The extensive body of 
human clinical, toxicological, and epidemiological evidence serves as 
the basis for the judgments about O3-related health effects 
discussed above, including judgments about causal relationships with a 
range of respiratory morbidity effects, including lung function 
decrements, increased respiratory symptoms, airway inflammation, 
increased airway responsiveness, and respiratory-related 
hospitalizations and emergency department visits in the warm season, 
and about the evidence being highly suggestive that O3 
directly or indirectly contributes to non-accidental and 
cardiopulmonary-related mortality.
    These judgments take into account important uncertainties that 
remain in interpreting this evidence. For example, with regard to the 
utility of time-series epidemiological studies to inform judgments 
about a NAAQS for an individual pollutant, such as O3, 
within a mix of highly correlated pollutants, such as the mix of 
oxidants produced in photochemical reactions in the atmosphere, the 
Staff Paper notes that there are limitations especially at ambient 
O3 concentrations below levels at which O3-
related effects have been observed in controlled human exposure 
studies. The Staff Paper (section 3.4.5) also recognizes that the 
available epidemiological evidence neither supports nor refutes the 
existence of thresholds at the population level for effects such as 
increased hospital admissions and premature mortality. There are 
limitations in epidemiological studies that make discerning thresholds 
in populations difficult, including low data density in the lower 
concentration ranges, the possible influence of exposure measurement 
error, and variability in susceptibility to O3-related 
effects in populations.
    While noting these limitations in the interpretation of the 
findings from the epidemiological studies, the Staff Paper (section 
3.4.5) concludes that if a population threshold level does exist, it 
would likely be well below the level of the current O3 
standard and possibly within the range of background levels. As 
discussed above in section II.A.3.a, this conclusion is supported by 
several epidemiological studies that have explored the question of 
potential thresholds directly, either using a statistical curve-fitting 
approach to evaluate whether linear or non-linear models fit the data 
better using sub-sets of the data, where days over or under a specific 
cutpoint (e.g., 0.080 ppm or even lower O3 levels) were 
excluded and then evaluating the association for statistical 
significance. In addition to direct consideration of the 
epidemiological studies, findings from controlled human exposure 
studies discussed above in section II.A.2.a.i(a)(i) indicate that 
prolonged exposures produced statistically significant group mean 
FEV1 decrements and symptoms in healthy adult subjects at 
levels down to at least 0.060 ppm, with a small percentage of subjects 
experiencing notable effects (e.g., >10 percent FEV1 
decrement, pain on deep inspiration). Controlled human exposure studies 
evaluated in the last review also found significant responses in 
indicators of lung inflammation and cell injury at 0.080 ppm in healthy 
adult subjects. The effects in these controlled human exposure studies 
were observed in healthy young adult subjects, and it is likely that 
more serious responses, and

[[Page 37864]]

responses at lower levels, would occur in people with asthma and other 
respiratory diseases. These physiological effects have been linked to 
aggravation of asthma and increased susceptibility to respiratory 
infection, potentially leading to increased medication use, increased 
school and work absences, increased visits to doctors' offices and 
emergency departments, and increased hospital admissions. The 
observations provide additional support for the conclusion in the Staff 
Paper that the associations observed in the epidemiological studies, 
particularly for respiratory-related effects and potentially for 
cardiovascular effects, extend down to O3 levels well below 
the current standard (i.e., 0.084 ppm) (EPA, 2007, p. 6-7).
    As discussed above in section II.A and in the Staff Paper (section 
3.7), the newly available information reinforces the judgments about 
the likelihood of causal relationships between O3 exposure 
and respiratory effects observed in the last review and broadens the 
evidence of O3-related associations to include additional 
respiratory-related endpoints, newly identified cardiovascular-related 
health endpoints, and mortality. Newly available evidence also has 
shown that people with asthma are likely to experience more serious 
effects than people who do not have asthma (section II.A.4.b.ii above). 
The Staff Paper also concludes that substantial progress has been made 
since the last review in advancing the understanding of potential 
mechanisms by which ambient O3, alone and in combination 
with other pollutants, is causally linked to a range of respiratory-
related health endpoints, and may be causally linked to a range of 
cardiovascular-related health endpoints. Thus, the Staff Paper (section 
6.3.6) finds strong support in the evidence developed since the last 
review, for consideration of an O3 standard that is at least 
as protective as the current standard and finds no support for 
consideration of an O3 standard that is less protective than 
the current standard. This conclusion is consistent with the advice and 
recommendations of CASAC and with the views expressed by all interested 
parties who provided comments on drafts of the Staff Paper. While CASAC 
and some commenters supported revising the current standard to provide 
increased public health protection and other commenters supported 
retaining the current standard, no one who provided comments supported 
a standard that would be less protective than the current standard.
a. Evidence-Based Considerations
    In looking more specifically at the controlled human exposure and 
epidemiological evidence (which is summarized in chapter 3 and Appendix 
3B of the Staff Paper), the Staff Paper first notes that controlled 
human exposure studies provide the clearest and most compelling 
evidence for an array of human health effects that are directly 
attributable to acute exposures to O3 per se. Evidence from 
such human studies, together with animal toxicological studies, help to 
provide biological plausibility for health effects observed in 
epidemiological studies. In considering the available evidence, the 
Staff Paper focuses on studies that examined health effects that have 
been demonstrated to be caused by exposure to O3, or for 
which the Criteria Document judges associations with O3 to 
be causal or likely causal, or for which the evidence is highly 
suggestive that O3 contributes to the reported effects. In 
considering the epidemiological evidence as a basis for reaching 
conclusions about the adequacy of the current standard, the Staff Paper 
focuses on studies reporting effects in the warm season, for which the 
effect estimates are more consistently positive and statistically 
significant than those from all-year studies. The Staff Paper (section 
6.3.1.1) considers the extent to which such studies provide evidence of 
associations that extend down to ambient O3 concentrations 
below the level of the current standard, which would thereby call into 
question the adequacy of the current standard. In so doing, the Staff 
Paper notes, as discussed above, that if a population threshold level 
does exist for an effect observed in such studies, it would likely be 
at a level well below the level of the current standard. The Staff 
Paper (section 6.3.1.1) also attempts to characterize whether the area 
in which a study was conducted likely would or would not have met the 
current standard during the time of the study, although it recognizes 
that the confidence that would appropriately be placed on the 
associations observed in any given study, or on the extent to which the 
association would likely extend down to relatively low O3 
concentrations, is not dependent on this distinction. Further, the 
Staff Paper considered studies that examined subsets of data that 
include only days with ambient O3 concentrations below the 
level of the current O3 standard, or below even lower 
O3 concentrations, and continue to report statistically 
significant associations. The Staff Paper (section 6.3.1.1) judges that 
such studies are directly relevant to considering the adequacy of the 
current standard, particularly in light of reported responses to 
O3 at levels below the current standard found in controlled 
human exposure studies.
i. Lung Function, Respiratory Symptoms, and Other Respiratory Effects
    Health effects for which the Criteria Document continues to find 
clear evidence of causal associations with short-term O3 
exposures include lung function decrements, respiratory symptoms, 
pulmonary inflammation, and increased airway responsiveness. In the 
last review, these O3-induced effects were demonstrated with 
statistical significance down to the lowest level tested in controlled 
human exposure studies at that time (i.e., 0.080 ppm). As discussed in 
chapter 3 of the Staff Paper, and in section II.A.2.a.i.(a)(i) above, 
two new studies are notable in that they are the only controlled human 
exposure studies that examined respiratory effects, including lung 
function decrements and respiratory symptoms, in healthy adults at 
lower exposure levels than had previously been examined. EPA's 
reanalysis of the data from the most recent study shows small group 
mean decrements in lung function responses to be statistically 
significant at the 0.060 ppm exposure level, while the author's 
analysis did not yield statistically significant lung function 
responses but did yield some statistically significant respiratory 
symptom responses toward the end of the exposure period. Notably, these 
studies report a small percentage of subjects experiencing lung 
function decrements (>= 10 percent) at the 0.060 ppm exposure level. 
These studies provide very limited evidence of O3-related 
lung function decrements and respiratory symptoms at this lower 
exposure level.
    The Staff Paper (section 3.3.1.1.1) notes that evidence from 
controlled human exposures studies indicates that people with moderate-
to-severe asthma have somewhat larger decreases in lung function in 
response to O3 relative to healthy individuals and that lung 
function responses in people with asthma appear to be affected by 
baseline lung function (i.e., magnitude of responses increases with 
increasing disease severity). As discussed in the Criteria Document 
(p.8-80), this newer information expands our understanding of the 
physiological basis for increased sensitivity in people with asthma and 
other airway diseases, recognizing that

[[Page 37865]]

people with asthma present a different response profile for cellular, 
molecular, and biochemical responses than people who do not have 
asthma. New evidence indicates that some people with asthma have 
increased occurrence and duration of nonspecific airway responsiveness, 
which is an increased bronchoconstrictive response to airway irritants. 
Controlled human exposure studies also indicate that some people with 
allergic asthma and rhinitis have increased airway responsiveness to 
allergens following O3 exposure. Exposures to O3 
exacerbated lung function decrements in people with pre-existing 
allergic airway disease, with and without asthma. Ozone-induced 
exacerbation of airway responsiveness persists longer and attenuates 
more slowly than O3-induced lung function decrements and 
respiratory symptom responses and can have important clinical 
implications for asthmatics.
    The Staff Paper (p.6-10) also concludes that newly available human 
exposure studies suggest that some people with asthma also have 
increased inflammatory responses, relative to non-asthmatic subjects, 
and that this inflammation may take longer to resolve. The new data on 
airway responsiveness, inflammation, and various molecular markers of 
inflammation and bronchoconstriction indicate that people with asthma 
and allergic rhinitis (with or without asthma) comprise susceptible 
groups for O3-induced adverse effects. This body of evidence 
qualitatively informs the Staff Paper's (pp.6-10 to 6-11) evaluation of 
the adequacy of the current O3 standard in that it indicates 
that human clinical and epidemiological panel studies of lung function 
decrements and respiratory symptoms that evaluate only healthy, non-
asthmatic subjects likely underestimate the effects of O3 
exposure on asthmatics and other susceptible populations.
    The Staff Paper (p.6-11) notes that in addition to the experimental 
evidence of lung function decrements, respiratory symptoms, and other 
respiratory effects in healthy and asthmatic populations discussed 
above, epidemiological studies have reported associations of lung 
function decrements and respiratory symptoms in several locations 
(Appendix 3B; also Figure 3-4 for respiratory symptoms). As discussed 
in the Staff Paper (section 3.3.1.1.1) and above, two large U.S. panel 
studies which together followed over 1000 asthmatic children on a daily 
basis (Mortimer et al., 2002, the National Cooperative Inner-City 
Asthma Study, or NCICAS; and Gent et al., 2003), as well as several 
smaller U.S. and international studies, have reported robust 
associations between ambient O3 concentrations and measures 
of lung function and daily symptoms (e.g., chest tightness, wheeze, 
shortness of breath) in children with moderate to severe asthma and 
between O3 and increased asthma medication use. Overall, the 
multi-city NCICAS (2002), Gent et al. (2003), and several other single-
city studies indicate a robust positive association between ambient 
O3 concentrations and increased respiratory symptoms and 
increased medication use in asthmatics.
    In considering the large number of single-city epidemiological 
studies reporting lung function or respiratory symptoms in healthy or 
asthmatic populations (Staff Paper, Appendix 3B), the Staff Paper (p.6-
11) notes that most such studies that reported positive and often 
statistically significant associations in the warm season were 
conducted in areas that likely would not have met the current standard. 
In considering the large multi-city NCICAS (Mortimer et al., 2002), the 
Staff Paper notes that the 98th percentile 8-hour daily maximum 
O3 concentrations at the monitor reporting the highest 
O3 concentrations in each of the study areas ranged from 
0.084 ppm to >0.10 ppm. However, the authors indicate that less than 5 
percent of the days in the eight urban areas had 8-hour daily 
O3 concentrations exceeding 0.080 ppm. Moreover, the authors 
observed that when days with 8-hour average O3 levels 
greater than 0.080 ppm were excluded, similar effect estimates were 
seen compared to estimates which included all of the days. There are 
also a few other studies in which the relevant air quality statistics 
provide some indication that lung function and respiratory symptom 
effects may be occurring in areas that likely would have met the 
current standard (EPA, 2007, p.6-12).
ii. Respiratory Hospital Admissions and Emergency Department Visits
    At the time of the last review, many time-series studies indicated 
positive associations between ambient O3 and increased 
respiratory hospital admissions and emergency room visits, providing 
strong evidence for a relationship between O3 exposure and 
increased exacerbations of preexisting lung disease at O3 
levels below the level of the then current 1-hour standard (EPA 2007, 
section 3.3.1.1.6). Analyses of data from studies conducted in the 
northeastern U.S. indicated that O3 air pollution was 
consistently and strongly associated with summertime respiratory 
hospital admissions.
    Since the last review, new epidemiological studies have evaluated 
the association between short-term exposures to O3 and 
unscheduled hospital admissions for respiratory causes. Large multi-
city studies, as well as many studies from individual cities, have 
reported positive and often statistically significant O3 
associations with total respiratory hospitalizations as well as asthma- 
and COPD-related hospitalizations, especially in studies analyzing the 
O3 effect during the summer or warm season. Analyses using 
multipollutant regression models generally indicate that copollutants 
do not confound the association between O3 and respiratory 
hospitalizations and that the O3 effect estimates were 
robust to PM adjustment in all-year and warm-season only data. The 
Criteria Document (p.8-77) concludes that the evidence supports a 
causal relationship between acute O3 exposures and increased 
respiratory-related hospitalizations during the warm season.
    In looking specifically at U.S. and Canadian respiratory 
hospitalization studies that reported positive and often statistically 
significant associations (and that either did not use GAM or were 
reanalyzed to address GAM-related problems), the Staff Paper (p.6-12) 
notes that many such studies were conducted in areas that likely would 
not have met the current O3 standard, with many providing 
only all-year effect estimates, and with some reporting a statistically 
significant association in the warm season. Of the studies that provide 
some indication that O3-related respiratory hospitalizations 
may be occurring in areas that likely would have met the current 
standard, the Staff Paper notes that some are all-year studies, whereas 
others reported statistically significant warm-season associations.
    Emergency department visits for respiratory causes have been the 
focus of a number of new studies that have examined visits related to 
asthma, COPD, bronchitis, pneumonia, and other upper and lower 
respiratory infections, such as influenza, with asthma visits typically 
dominating the daily incidence counts. Among studies with adequate 
controls for seasonal patterns, many reported at least one significant 
positive association involving O3. However, inconsistencies 
were observed which were at least partially attributable to differences 
in model specifications and analysis approach among various studies. In 
general, O3 effect estimates from summer-only analyses 
tended to be positive and larger compared to results from cool season 
or all-year analyses. Almost all of the studies that reported

[[Page 37866]]

statistically significant effect estimates were conducted in areas that 
likely would not have met the current standard. The Criteria Document 
(section 7.3.2) concluded that analyses stratified by season generally 
supported a positive association between O3 concentrations 
and emergency department visits for asthma in the warm season. These 
studies provide evidence of effects in areas that likely would not have 
met the current standard and evidence of associations that likely 
extend down to relatively low ambient O3 concentrations.
iii. Mortality
    The 1996 Criteria Document concluded that an association between 
daily mortality and O3 concentrations for areas with high 
O3 levels (e.g., Los Angeles) was suggested. However, due to 
a very limited number of studies available at that time, there was 
insufficient evidence to conclude that the observed association was 
likely causal, and thus the possibility that O3 exposure may 
be associated with mortality was not relied upon in the 1997 decision 
on the O3 primary standard.
    Since the last review, as described above, the body of evidence 
with regard to O3-related health effects has been expanded 
by animal, human clinical, and epidemiological studies and now includes 
biologically plausible mechanisms by which O3 may affect the 
cardiovascular system. In addition, there is stronger information 
linking O3 to serious morbidity outcomes, such as 
hospitalization, that are associated with increased mortality. Thus, 
there is now a coherent body of evidence that describes a range of 
health outcomes from lung function decrements to hospitalization and 
premature mortality.
    Newly available large multi-city studies (Bell et al., 2004; Huang 
et al.,2005; and Schwartz 2005) designed specifically to examine the 
effect of O3 and other pollutants on mortality have provided 
much more robust and credible information. Together these studies have 
reported significant associations between O3 and mortality 
that were robust to adjustment for PM and different adjustment methods 
for temperature and suggest that the effect of O3 on 
mortality is immediate but also persists for several days. One recent 
multi-city study (Bell et al., 2006) examined the shape of the 
concentration-response function for the O3-mortality 
relationship in 98 U.S. urban communities for the period 1987 to 2000 
specifically to evaluate whether a ``safe'' threshold level exists. 
Results from various analytic methods all indicated that any threshold, 
if it exists, would likely occur at very low concentrations, far below 
the level of the current O3 NAAQS and nearing background 
levels.
    New data are also available from several single-city studies 
conducted world-wide, as well as from several meta-analyses that have 
combined information from multiple studies. Three recent meta-analyses 
evaluated potential sources of heterogeneity in O3-mortality 
associations. All three analyses reported common findings, including 
effect estimates that were statistically significant and larger in warm 
season analyses. Reanalysis of results using default GAM criteria did 
not change the effect estimates, and there was no strong evidence of 
confounding by PM. The Criteria Document (p.7-175) finds that the 
majority of these studies suggest that there is an elevated risk of 
total nonaccidental mortality associated with acute exposure to 
O3, especially in the summer or warm season when 
O3 levels are typically high, with somewhat larger effect 
estimate sizes for associations with cardiovascular mortality.
    Overall, the Criteria Document (p.8-78) finds that the results from 
U.S. multi-city time-series studies, along with the meta-analyses, 
provide relatively strong evidence for associations between short-term 
O3 exposure and all-cause mortality even after adjustment 
for the influence of season and PM. The results of these analyses 
indicate that copollutants generally do not appear to substantially 
confound the association between O3 and mortality. In 
addition, several single-city studies observed positive associations of 
ambient O3 concentrations with total nonaccidental and 
cardiopulmonary mortality.
    Finally, from those studies that included assessment of 
associations with specific causes of death, it appears that effect 
estimates for associations with cardiovascular mortality are larger 
than those for total mortality; effect estimates for respiratory 
mortality are less consistent in size, possibly due to reduced 
statistical power in this subcategory of mortality. For cardiovascular 
mortality, the Criteria Document (p.7-106) suggests that effect 
estimates are consistently positive and more likely to be larger and 
statistically significant in warm season analyses. The Criteria 
Document (p.8-78) concludes that these findings are highly suggestive 
that short-term O3 exposure directly or indirectly 
contributes to nonaccidental and cardiopulmonary-related mortality, but 
additional research is needed to more fully establish underlying 
mechanisms by which such effects occur.
b. Exposure- and Risk-Based Considerations
    As discussed above in section II.B, the Staff Paper also estimated 
quantitative exposures and health risks associated with recent air 
quality levels and with air quality that meets the current standard to 
help inform judgments about whether or not the current standard 
provides adequate protection of public health. In so doing, it 
presented the important uncertainties and limitations associated with 
the exposure and risk assessments (discussed above in section II.B and 
more fully in chapters 4 and 5 of the Staff Paper).
    The Staff Paper (and the CASAC) also recognized that the exposure 
and risk analyses could not provide a full picture of the O3 
exposures and O3-related health risks posed nationally. The 
Staff Paper did not have sufficient information to evaluate all 
relevant at-risk groups (e.g., outdoor workers) or all O3-
related health outcomes (e.g., increased medication use, school 
absences, and emergency department visits that are part of the broader 
pyramid of effects discussed above in section II.A.4.d), and the scope 
of the Staff Paper analyses was generally limited to estimating 
exposures and risks in 12 urban areas across the U.S., and to only five 
or just one area for some health effects included in the risk 
assessment. Thus, national-scale public health impacts of ambient 
O3 exposures are clearly much larger than the quantitative 
estimates of O3-related incidences of adverse health effects 
and the numbers of children likely to experience exposures of concern 
associated with recent air quality or air quality that just meets the 
current or alternative standards. On the other hand, inter-individual 
variability in responsiveness means that only a subset of individuals 
in each group estimated to experience exposures exceeding a given 
benchmark exposure of concern level would actually be expected to 
experience such adverse health effects.
    As described above in section II.B, the Staff Paper estimated 
exposures and risks for the three most recent years (2002-2004) for 
which data were available at the time of the analyses. Within this 3-
year period, 2002 was a year with relatively higher O3 
levels in most, but not all, areas and simulation of just meeting the 
current standard based on 2002 air quality data provides a generally 
more upper-end estimate of exposures and risks, while 2004 was a year 
with relatively lower O3 levels in


[[Continued on page 37867]]


From the Federal Register Online via GPO Access [wais.access.gpo.gov]
]                         
 
[[pp. 37867-37916]] National Ambient Air Quality Standards for Ozone

[[Continued from page 37866]]

[[Page 37867]]

most, but not all, areas and simulation of just meeting the current 
standard using 2004 air quality data provides a generally more lower-
end estimate of exposures and risks.
i. Exposure Assessment Results
    As discussed above in section II.B.1, the Staff Paper estimates 
personal exposures to ambient O3 levels at and above 
specific benchmark levels to provide some perspective on the public 
health impacts of health effects that cannot currently be evaluated in 
quantitative risk assessments but that may occur at current air quality 
levels, and the extent to which such impacts might be reduced by 
meeting the current and alternative standards. As described in greater 
detail in section II.B.1.c above, the Staff Paper refers to exposures 
at and above these benchmark levels as ``exposures of concern.'' The 
Staff Paper notes that exposures of concern, and the health outcomes 
they represent, likely occur across a range of O3 exposure 
levels, such that there is no one exposure level that addresses all 
relevant public health concerns. Therefore, with the concurrence of the 
CASAC, the Staff Paper estimated exposures of concern not only at 0.080 
ppm O3, a level at which there are demonstrated effects, but 
also at 0.070 and 0.060 ppm O3. The Staff Paper recognized 
that there will be varying degrees of concern about exposures at each 
of these levels, based in part on the population subgroups experiencing 
them. Given that there is clear evidence of inflammation, increased 
airway responsiveness, and changes in host defenses in healthy people 
exposed to 0.080 ppm O3 and reason to infer that such 
effects will continue at lower exposure levels, but with increasing 
uncertainty about the extent to which such effects occur at lower 
O3 concentrations, the Staff Paper, and the discussion 
below, focuses on exposures of concern at or above benchmark levels of 
0.070 and 0.060 ppm O3 for purposes of evaluating the 
adequacy of the current standard.
    The exposure estimates presented in the Staff Paper are for the 
number and percent of all school age children and asthmatic school age 
children exposed, and the number of person-days (occurrences) of 
exposures, with daily 8-hour maximum exposures at or above several 
benchmark levels while at intermittent moderate or greater exertion. As 
shown in the Table 1 in this notice, the percent of population exposed 
at any given level is very similar for all and asthmatic school age 
children. Substantial year-to-year variability in exposure estimates is 
observed, ranging to over an order of magnitude at the current standard 
level, in estimates of the number of children and, as shown in Table 6-
1a and b of the Staff Paper, the number of occurrences of exposures of 
concern at both of these benchmark levels. The Staff Paper states that 
it is appropriate to consider not just the average estimates across all 
years, but also to consider public health impacts in year with 
relatively higher O3 levels. The Staff Paper also notes that 
there is substantial city-to-city variability in these estimates, and 
notes that it is appropriate to consider not just the aggregate 
estimates across all cities, but also to consider the public health 
impacts in cities that receive relatively less protection upon meeting 
the current standard.
    As discussed in the Staff Paper (EPA, 2007b, see section 6.3.1.2), 
about 50 percent of asthmatic or all school age children, representing 
nearly 1.3 million asthmatic children and about 8.5 million school age 
children in the 12 urban areas examined, are estimated to experience 
exposures of concern at or above the 0.070 ppm benchmark level (i.e., 
these individuals are estimated to experience 8-hour O3 
exposures at or above 0.070 ppm while engaged in moderate or greater 
exertion 1 or more times during the O3 season) associated 
with 2002 O3 air quality levels. In contrast, about 17 
percent of asthmatic and all school age children are estimated to 
experience exposures of concern at or above the 0.070 ppm benchmark 
level associated with 2004 O3 air quality levels. Just 
meeting the current standard results in an aggregate estimate of about 
20 percent of asthmatic or 18 percent or all school age children likely 
to experience exposures of concern at or above the 0.070 ppm benchmark 
level using the 2002 simulation. The exposure estimates for this 
benchmark level range up to about 40 percent of asthmatic or all school 
age children in the single city with the least degree of protection 
from this standard. Just meeting the current standard based on the 2004 
simulation, results in an aggregate estimate of about 1 percent of 
asthmatic or all school age children experiencing exposures at the 0.07 
ppm benchmark level.
    At the benchmark level of 0.060 ppm, about 70 percent of all or 
asthmatic school age children are estimated to experience exposures of 
concern at this benchmark level for the aggregate of the 12 urban areas 
associated with 2002 O3 levels. Just meeting the current 
standard would result in an aggregate estimate of about 45 percent of 
asthmatic or all school age children likely to experience exposures of 
concern at or above the 0.060 ppm benchmark level using the 2002 
simulation. The exposure estimates for this benchmark level range up to 
nearly 70 percent of all or asthmatic school age children in the single 
city with the least degree of protection associated with just meeting 
the current standard using the 2002 simulation. The Staff Paper 
indicates an aggregate estimate of about 10 percent of asthmatic or all 
school age children would experience exposures at or above the 0.06 ppm 
benchmark level associated with just meeting the current standard using 
the 2004 simulation.
ii. Risk Assessment Results
    As described in more detail in section II.B.2 above and in chapters 
5 and 6 of the Staff Paper, risk estimates have been developed for 
several important health endpoints, including: (1) Lung function 
decrements (i.e., >=15 percent and >=20 percent reductions in 
FEV1) in all school age children for 12 urban areas; (2) 
lung function decrements (i.e., >=10 percent and >=20 percent 
reductions in FEV1) in asthmatic school age children for 5 
urban areas (a subset of the 12 urban areas); (3) respiratory symptoms 
(i.e., chest tightness, shortness of breath, wheeze) in moderate to 
severe asthmatic children for the Boston area; (4) respiratory-related 
hospital admissions for 3 urban areas; and (5) nonaccidental and 
cardiorespiratory mortality for 12 urban areas for three recent years 
(2002 to 2004) and for just meeting the current standard using a 2002 
simulation and a 2004 simulation.
    With regard to estimates of moderate lung function decrements, as 
shown in Tables 6-2 of the Staff Paper, meeting the current standard 
substantially reduces the estimated number of school age children 
experiencing one or more occurrences of FEV1 decrements >=15 
percent for the 12 urban areas, going from about 1.3 million children 
(7 percent of children) under 2002 air quality to about 610,000 (3 
percent of children) based on the 2002 simulation, and from about 
620,000 children (3 percent of children) to about 230,000 (1 percent of 
children) using the 2004 simulation. In asthmatic children, the 
estimated number of children experiencing one or more occurrences of 
FEV1 decrements >=10 percent for the 5 urban areas goes from 
about 250,000 children (16 percent of asthmatic children) under 2002 
air quality to about 130,000 (8 percent of asthmatic children) using 
the 2002 simulation, and from about 160,000 (10 percent of asthmatic 
children) to about 70,000 (4 percent of asthmatic children) using the 
2004 simulation. Thus, even when the

[[Page 37868]]

current standard is met, about 4 to 8 percent of asthmatic school age 
children are estimated to experience one or more occurrences of 
moderate lung function decrements, resulting in about 1 million 
occurrences (using the 2002 simulation) and nearly 700,000 occurrence 
(using the 2004 simulation) in just 5 urban areas. Moreover, the 
estimated number of occurrences of moderate or greater lung function 
decrements per child is on average approximately 6 to 7 in all children 
and 8 to 10 in asthmatic children in an O3 season, even when 
the current standard is met, depending on the year used to simulate 
meeting the current standard. In the 1997 review of the O3 
standard a general consensus view of the adversity of such moderate 
responses emerged as the frequency of occurrences increases, with the 
judgment that repeated occurrences of moderate responses, even in 
otherwise healthy individuals, may be considered adverse since they may 
well set the stage for more serious illness.
    With regard to estimates of large lung function decrements, the 
Staff Paper notes that FEV1 decrements 20 percent 
would likely interfere with normal activities in many healthy 
individuals, therefore single occurrences would be considered to be 
adverse. In people with asthma, large lung function responses would 
likely interfere with normal activities for most individuals and would 
also increase the likelihood that these individuals would use 
additional medication or seek medical treatment. Not only would single 
occurrences be considered to be adverse to asthmatic individuals under 
the ATS definition, but they also would be cause for medical concern. 
While the current standard reduces the occurrences of large lung 
function decrements in all children and asthmatic children from about 
60 to 70%, in a year with relatively higher O3 levels 
(2002), there are estimated to be about 500,000 occurrences in all 
school children across the entire 12 urban areas, and about 40,000 
occurrences in asthmatic children across just 5 urban areas. As noted 
above, it is clear that even when the current standard is met over a 
three-year period, O3 levels in each year can vary 
considerably, as evidenced by relatively large differences between risk 
estimates based on 2002 to 2004 air quality. The Staff Paper expressed 
the view that it was appropriate to consider this yearly variation in 
O3 levels allowed by the current standard in judging the 
extent to which impacts on members of at-risk groups in a year with 
relatively higher O3 levels remains of concern from a public 
health perspective.
    With regard to other O3-related health effects, as shown 
in Tables 6-4 through 6-6 of the Staff Paper, the estimated risks of 
respiratory symptom days in moderate to severe asthmatic children, 
respiratory-related hospital admissions, and non-accidental and 
cardiorespiratory mortality, respectively, are not reduced to as great 
an extent by meeting the current standard as are lung function 
decrements. For example, just meeting the current standard reduces the 
estimated average incidence of chest tightness in moderate to severe 
asthmatic children living in the Boston urban area by 11 to 15%, based 
on 2002 and 2004 simulations, respectively, resulting in an estimated 
incidence of about 23,000 to 31,000 per 100,000 children attributable 
to O3 exposure (Table 6-4). Just meeting the current 
standard is estimated to reduce the incidence of respiratory-related 
hospital admissions in the New York City urban area by about 16 to 18%, 
based on 2002 and 2004 simulations, respectively, resulting in an 
estimated incidence per 100,000 population of 4.6 to 6.4, respectively 
(Table 6-5). Across the 12 urban areas, the estimates of non-accidental 
mortality incidence per 100,000 relevant population range from 0.4 to 
2.6 (for 2002) and 0.5 to 1.5 (for 2004) (Table 6-6). Meeting the 
current standard results in a reduction of the estimated incidence per 
100,000 population to a range of 0.3 to 2.4 based on the 2002 
simulation and a range of 0.3 to 1.2 based on the 2004 simulation. 
Estimates for cardiorespiratory mortality show similar patterns.
    In considering the estimates of the proportion of population 
affected and the number of occurrences of the health effects that are 
included in the risk assessment, the Staff Paper notes that these 
limited estimates are indicative of a much broader array of 
O3-related health endpoints that are part of a ``pyramid of 
effects'' that include various indicators of morbidity that could not 
be included in the risk assessment (e.g., school absences, increased 
medication use, emergency department visits) and which primarily affect 
members of at-risk groups. While the Staff Paper had sufficient 
information to estimate and consider the number of symptom days in 
children with moderate to severe asthma, it recognized that there are 
many other effects that may be associated with symptom days, such as 
increased medication use, school and work absences, or visits to 
doctors' offices, for which there was not sufficient information to 
estimate risks but which are important to consider in assessing the 
adequacy of the current standard. The same is true for more serious, 
but less frequent effects. The Staff Paper estimated hospital 
admissions, but there was not sufficient information to estimate 
emergency department visits in a quantitative risk assessment. 
Consideration of such unquantified risks in the Staff Paper reinforces 
the Staff Paper conclusion that consideration should be given to 
revising the standard so as to provide increased public health 
protection, especially for at-risk groups such as people with asthma or 
other lung diseases, as well as children and older adults, particularly 
those active outdoors, and outdoor workers.
c. Summary
    Based on the available information and taking into account the 
views of CASAC and public comments, the Staff Paper initially notes 
that all parties commenting on the NAAQS review agree that the standard 
should be at least as protective as the current standard, as no party 
suggested it should be revised to provide less protection. The Staff 
Paper concludes that the overall body of evidence clearly calls into 
question the adequacy of the current standard in protecting at-risk 
groups, notably including asthmatic children and other people with lung 
disease, as well as all children and older adults, especially those 
active outdoors, and outdoor workers,\48\ against an array of adverse 
health effects that range from decreased lung function to serious 
indicators of respiratory morbidity including emergency department 
visits and hospital admissions for respiratory causes, nonaccidental 
mortality, and possibly cardiovascular effects. The available 
information provides strong support for consideration of an 
O3 standard that would provide increased health protection 
for these at-risk groups. The Staff Paper also concludes that risks 
projected to remain upon meeting the current standard, based on the 
exposure and risk estimates discussed above and in more detail in the 
Staff Paper, are indicative of risks to at-risk groups that can be 
judged to be important from a public health perspective, which 
reinforces the Staff Paper conclusion that consideration should be 
given to revising the level of the standard so as to provide increased

[[Page 37869]]

public health protection (EPA, 2007, section 6.3.6).
---------------------------------------------------------------------------

    \48\ In defining at-risk groups this way we are including both 
groups with greater inherent sensitivity and those more likely to be 
exposed.
---------------------------------------------------------------------------

3. CASAC Views
    In its letter to the Administrator, the CASAC O3 Panel, 
with full endorsement of the chartered CASAC, unanimously concluded 
that there is ``no scientific justification for retaining'' the current 
primary O3 standard, and the current standard ``needs to be 
substantially reduced to protect human health, particularly in 
sensitive subpopulations'' (Henderson, 2006c, pp. 1-2). In its 
rationale for this conclusion, the CASAC Panel concluded that ``new 
evidence supports and build-upon key, health-related conclusions drawn 
in the 1997 Ozone NAAQS review'' (id., p. 3). The Panel points to 
studies discussed in chapter 3 and Appendix 3B of the Staff Paper in 
noting that several new single-city studies and large multi-city 
studies have provided more evidence for adverse health effects at 
concentrations lower than the current standard, and that these 
epidemiological studies are backed-up by evidence from controlled human 
exposure studies. The Panel specifically noted evidence from the recent 
Adams (2006) study that reported statistically significant decrements 
in the lung function of healthy, moderately exercising adults at a 
0.080 ppm exposure level, and importantly, also reported adverse lung 
function effects in some healthy individuals at 0.060 ppm. The Panel 
concluded that these results indicate that the current standard ``is 
not sufficiently health-protective with an adequate margin of safety,'' 
noting that that while similar studies in sensitive groups such as 
asthmatics have yet to be conducted, ``people with asthma, and 
particularly children, have been found to be more sensitive and to 
experience larger decrements in lung function in response to 
O3 exposures than would healthy volunteers (Mortimer et al., 
2002)'' (Henderson, 2006c, p. 4).
    The CASAC Panel also highlighted a number of O3-related 
adverse health effects, that are associated with exposure to ambient 
O3, below the level of the current standard, based on a 
broad range of epidemiological studies (Henderson, 2006c). These 
adverse health effects include increases in school absenteeism, 
respiratory hospital emergency department visits among asthmatics and 
patients with other respiratory diseases, hospitalizations for 
respiratory illnesses, symptoms associated with adverse health effects 
(including chest tightness and medication usage), and premature 
mortality (nonaccidental, cardiorespiratory deaths) reported at 
exposure levels well below the current standard. ``The CASAC considers 
each of these findings to be an important indicator of adverse health 
effects'' (Henderson, 2006c).
    The CASAC Panel expressed the view that more emphasis should be 
placed on the subjects in controlled human exposure studies with 
FEV1 decrements greater than 10 percent, which can be 
clinically significant, rather than on the relatively small average 
decrements. The Panel also emphasized significant O3-related 
inflammatory responses and markers of injury to the epithelial lining 
of the lung that are independent of spirometric responses. Further, the 
Panel expressed the view that the Staff Paper did not place enough 
emphasis on serious morbidity (e.g., hospital admissions) and mortality 
observed in epidemiology studies. On the basis of the large amount of 
recent data evaluating adverse health effects at levels at and below 
the current O3 standard, it was the unanimous opinion of the 
CASAC Panel that the current primary O3 standard is not 
adequate to protect human health, that the relevant scientific data do 
not support consideration of retaining the current standard, and that 
the current standard needs to be substantially reduced to be protective 
of human health, particularly in sensitive subpopulations (Henderson, 
2006c, pp. 4-5).
    Further, the CASAC letter noted that ``there is no longer 
significant scientific uncertainty regarding the CASAC's conclusion 
that the current 8-hour primary NAAQS must be lowered'' (Henderson, 
2006c, p. 5). The Panel noted that a ``large body of data clearly 
demonstrates adverse human health effects at the current level'' of the 
standard, such that ``[R]etaining this standard would continue to put 
large numbers of individuals at risk for respiratory effects and/or 
significant impact on quality of life including asthma exacerbations, 
emergency room visits, hospital admissions and mortality'' (Henderson, 
2006c). The Panel also noted that ``scientific uncertainty does exist 
with regard to the lower level of O3 exposure that would be 
fully protective of human health,'' concluding that ``it is possible 
that there is no threshold for an O3-induced impact on human 
health and that some adverse events may occur at policy-relevant 
background'' (Henderson, 2006c, p.5).
4. Administrator's Proposed Conclusions Concerning Adequacy of Current 
Standard
    Based on the large body of evidence concerning the public health 
impacts of O3 pollution, including significant new evidence 
concerning effects at O3 concentrations below the level of 
the current standard, the Administrator proposes that the current 
standard does not protect public health with an adequate margin of 
safety and should be revised to provide additional public health 
protection. In considering whether the primary standard should be 
revised, the Administrator has carefully considered the conclusions 
contained in the Criteria Document, the rationale and recommendations 
contained in the Staff Paper, the advice and recommendations from the 
CASAC, and public comments to date. The Administrator notes that 
evidence of a range of respiratory-related morbidity effects seen in 
the last review has been considerably strengthened, both through 
toxicological and controlled human exposure studies as well as through 
many new panel and epidemiological studies.
    In addition, new evidence from controlled human exposure and 
epidemiological studies identifies people with asthma as an important 
susceptible population for which estimates of respiratory effects in 
the general population likely underestimate the magnitude or importance 
of these effects. New evidence about mechanisms of toxicity more 
completely explains the biological plausibility of O3-
induced respiratory effects and is beginning to suggest mechanisms that 
may link O3 exposure to cardiovascular effects. Further, 
there is now relatively strong evidence for associations between 
O3 and total nonaccidental and cardiopulmonary mortality, 
even after adjustment for the influence of season and PM. Relative to 
the information that was available to inform the Agency's 1997 decision 
to set the current standard, the newly available evidence increases the 
Administrator's confidence that respiratory morbidity effects such as 
lung function decrements and respiratory symptoms are causally related 
to O3 exposures, that indicators of respiratory morbidity 
such as emergency department visits and hospital admissions are 
causally related to O3 exposures, and that the evidence is 
highly suggestive that O3 exposures during the O3 
season contribute to premature mortality.
    The Administrator judges that there is important new evidence 
demonstrating that exposures to O3 at levels below the level 
of the current standard are associated with a broad array of adverse 
health effects, especially in at-risk populations. These at-risk 
populations include people with asthma or other lung diseases who are 
likely to experience more serious effects from

[[Page 37870]]

exposure to O3. As discussed in section II.A.4 above, these 
groups also include children and older adults with increased 
susceptibility, as well as those who are likely to be vulnerable as a 
result of spending a lot of time outdoors engaged in physical activity, 
especially active children and outdoor workers.
    Examples of this important new evidence include demonstration of 
O3-induced lung function effects and respiratory symptoms in 
some healthy individuals down to the previously observed exposure level 
of 0.080 ppm, as well as very limited new evidence at exposure levels 
well below the level of the current standard. In addition, there is now 
epidemiological evidence of statistically significant O3-
related associations with lung function and respiratory symptom 
effects, respiratory-related emergency department visits and hospital 
admissions, and increased mortality, in areas that likely would have 
met the current standard. There are also many epidemiological studies 
done in areas that likely would not have met the current standard but 
which nonetheless report statistically significant associations that 
generally extend down to ambient O3 concentrations that are 
below the level of the current standard. Further, there are a few 
studies that have examined subsets of data that include only days with 
ambient O3 concentrations below the level of the current 
standard, or below even much lower O3 concentrations, and 
continue to report statistically significant associations with 
respiratory morbidity outcomes and mortality. The Administrator 
recognizes that the evidence from controlled human exposure studies, 
together with animal toxicological studies, provides considerable 
support for the biological plausibility of the respiratory morbidity 
associations observed in the epidemiological studies and for concluding 
that the associations extend below the level of the current standard.
    Based on the strength of the currently available evidence of 
adverse health effects, and on the extent to which the evidence 
indicates that such effects result from exposures to ambient 
O3 concentrations below the level of the current standard, 
the Administrator judges that the current standard does not protect 
public health with an adequate margin of safety and that the standard 
should be revised to provide such protection, especially for at-risk 
groups, against a broad array of adverse health effects.
    In reaching this judgment, the Administrator has also considered 
the results of both the exposure and risk assessments conducted for 
this review, to provide some perspective on the extent to which at-risk 
groups would likely experience ``exposures of concern'' \49\ and on the 
potential magnitude of the risk of experiencing various adverse health 
effects when recent air quality data (from 2002 to 2004) are used to 
simulate meeting the current standard and alternative standards in a 
number of urban areas in the U.S.\50\ In considering the exposure 
assessment results, the Administrator is relying on analyses that 
define exposures of concern by three benchmark exposure levels: 0.080, 
0.070, and 0.060 ppm. Estimates of exposures of concern in at-risk 
groups at and above these benchmark levels, using O3 air 
quality data in 2002 and 2004, provide some indication of the potential 
magnitude of the incidence of health outcomes that cannot currently be 
evaluated in a quantitative risk assessment, such as increased airway 
responsiveness, increased pulmonary inflammation, including increased 
cellular permeability, and decreased pulmonary defense mechanisms. 
These physiological effects have been demonstrated to occur in healthy 
people at O3 exposures as low as 0.080 ppm, the lowest level 
tested. They are associated with aggravation of asthma, increased 
medication use, increased school and work absences, increased 
susceptibility to respiratory infection, increased visits to doctors' 
offices and emergency departments, increased admissions to hospitals, 
and possibly to cardiovascular system effects and chronic effects such 
as chronic bronchitis or long-term damage to the lungs that can lead to 
reduced quality of life.
---------------------------------------------------------------------------

    \49\ As discussed in section II.B.1.c above, ``exposures of 
concern'' are estimates of personal exposures while at moderate or 
greater exertion to 8-hour average ambient O3 levels at 
and above specific benchmark levels which represent exposure levels 
at which O3-related health effects are known or can with 
varying degrees of certainty be inferred to occur in some 
individuals. Estimates of exposures of concern provide some 
perspective on the public health impacts of health effects that may 
occur in some individuals at recent air quality levels but cannot be 
evaluated in quantitative risk assessments, and the extent to which 
such impacts might be reduced by meeting the current and alternative 
standards.
    \50\ As described in the Staff Paper (section 4.5.8) and 
discussed above, recent O3 air quality distributions have 
been statistically adjusted to simulate just meeting the current and 
selected alternative standards. These simulations do not represent 
predictions of when, whether, or how areas might meet the specified 
standards.
---------------------------------------------------------------------------

    In considering these various benchmark levels for exposures of 
concern, the Administrator has focused primarily on estimated exposures 
at and above the 0.070 ppm benchmark level as an important surrogate 
measure for potentially more serious health effects in at-risk groups 
such as people with asthma. This judgment is based on the strong 
evidence of effects in healthy people at the 0.080 ppm exposure level 
and the new evidence that people with asthma are likely to experience 
larger and more serious effects than healthy people at the same level 
of exposure. In the Administrator's view, this evidence does not 
support a focus on exposures at and above the benchmark level of 0.080 
ppm O3, as it would not adequately account for the increased 
risk of harm from exposure for members of at-risk groups, especially 
people with asthma. The Administrator also judges that the evidence of 
demonstrated effects is too limited to support a primary focus on 
exposures down to the lowest benchmark level considered of 0.060 ppm. 
The Administrator particularly notes that although the analysis of 
``exposures of concern'' was conducted to estimate exposures at and 
above three discrete benchmark levels (0.080, 0.070, and 0.060 ppm), 
the concept is appropriately viewed as a continuum. As discussed at the 
outset in section II.A above, the Administrator strives to balance 
concern about the potential for health effects and their severity with 
the increasing uncertainty associated with our understanding of the 
likelihood of such effects at lower O3 exposure levels.
    The Administrator observes that based on the aggregate exposure 
estimates for the 2002 simulation summarized above in Table 1 (section 
II.B.1) and in the Staff Paper (EPA, 2007b, Table 6-7) for the 12 U.S. 
urban areas included in the exposure analysis, upon just meeting the 
current standard up to about 20 percent of asthmatic or all school age 
children are likely to experience one or more exposures of concern at 
and above the 0.070 ppm benchmark level; the 2004 simulation yielded an 
estimate of about 1 percent of such children. The Administrator notes 
from this comparison that there is substantial year-to-year 
variability, ranging up to an order of magnitude or more in estimates 
of the number of people and the number of occurrences of exposures of 
concern at and above this benchmark level. Moreover, within any given 
year, the exposure assessment indicates that there is substantial city-
to-city variability in the estimates of the children exposed or the 
number of occurrences of exposure at and above this benchmark level. 
For example, city-specific estimates of the percent of asthmatic or all 
school age children likely to experience exposures at and above the 
benchmark level of 0.070 ppm

[[Page 37871]]

ranges from about 1 percent up to about 40 percent across the 12 urban 
areas upon just meeting the current standard based on the 2002 
simulation; the 2004 simulation yielded estimates that range from about 
0 up to about 7 percent. The Administrator judges it is important to 
recognize the substantial year-to-year and city-to-city variability in 
considering these estimates.
    With regard to the results of the risk assessment, as discussed 
above, the Administrator recognizes that a simulation of just meeting 
the current standard in the cities included in the assessment indicate 
that the estimated risk is lower for all of the health endpoints 
evaluated. In considering the adequacy of the current standard, the 
Administrator has focused on the risks estimated to remain upon just 
meeting the current standard. Based on the aggregate risk estimates 
summarized above in Table 2 (section II.B.2 of this notice), the 
Administrator observes that upon just meeting the current standard 
based on the 2002 simulation, approximately 8 percent of asthmatic 
school age children across 5 urban areas (ranging up to about 11 
percent in the city that receives relatively less protection) and 
approximately 3 percent of all school age children across 12 urban 
areas (ranging up to over 5 percent in the city that receives 
relatively less protection) would still be estimated to experience 
moderate or greater lung function decrements one or more times within 
an O3 season. The Administrator recognizes that, as with the 
estimates of exposures of concern, there is substantial year-to-year 
and city-to-city variability in these risk estimates.
    In addition to the percentage of asthmatic or all children 
estimated to experience 1 or more occurrences of an effect, the 
Administrator recognizes that some individuals are estimated to have 
multiple occurrences. For example, across all the cities in the 
assessment, approximately 6 to 7 occurrences of moderate or greater 
lung function decrements per child are estimated to occur in all 
children and approximately 8 to 10 occurrences are estimated to occur 
in asthmatic children in an O3 season, even upon just 
meeting the current standard. In the last review, a general consensus 
view of the adversity of such responses emerged as the frequency of 
occurrences increases, with the judgment that repeated occurrences of 
moderate responses, even in otherwise healthy individuals, may be 
considered adverse since they may well set the stage for more serious 
illness. The Administrator continues to support this view.
    Large lung function decrements (i.e., >=20 percent FEV1 
decrement) would likely interfere with normal activities in many 
healthy individuals, therefore single occurrences would be considered 
to be adverse. In people with asthma, large lung function responses 
(i.e., >= 20 percent FEV1 decrement), would likely interfere 
with normal activities for most individuals and would also increase the 
likelihood that these individuals would use additional medication or 
seek medical treatment. Not only would single occurrences be considered 
to be adverse to asthmatic individuals under the ATS definition, but 
they also would be cause for medical concern for some individuals. Upon 
just meeting the current standard based on the 2002 simulation, close 
to 1 percent of asthmatic and all school age children are estimated to 
experience one or more occurrences of large lung function decrements in 
the aggregate across 5 and 12 urban areas, respectively, with close to 
2 percent of both asthmatic and all school age children estimated to 
experience such effects in the city that receives relatively less 
protection from this standard. These estimates translate into 
approximately 500,000 occurrences of large lung function decrements in 
all children across 12 urban areas, and about 40,000 occurrences in 
asthmatic children across just 5 urban areas upon just meeting the 
current standard based on the 2002 simulation; the 2004 simulation 
yielded estimates that translate into approximately 160,000 and 10,000 
such occurrences in all children and asthmatic children, respectively.
    Upon just meeting the current standard based on the 2002 
simulation, the estimate of the O3-related risk of 
respiratory symptom days in moderate to severe asthmatic children in 
the Boston area is about 8,000 symptom days; the 2004 simulation 
yielded an estimate of about 6,000 such symptoms days. These estimates 
translate into as many as one symptom day in 6, and one symptom day in 
8, respectively, that are attributable to O3 exposure during 
the O3 season of the total number of symptom days associated 
with all causes of respiratory symptoms in asthmatic children during 
those years.
    The estimated O3-related risk of respiratory-related 
hospital admissions upon just meeting the current standard based on the 
2002 simulation is greater than 500 hospital admissions in the New York 
City area alone, or about 1.5 percent of the total incidence of 
respiratory-related admissions associated with all causes; the 2004 
simulation yielded an estimate of approximately 400 such hospital 
admissions. For nonaccidental mortality, just meeting the current 
standard based on the 2002 simulation results in an estimated incidence 
of from 0.3 to 2.4 per 100,000 population; the 2004 simulation resulted 
in an estimated incidence of from 0.3 to 1.2 per 100,000 population. 
Estimates for cardiorespiratory mortality show similar patterns. (Abt 
Associates, 2007, Table 4-26).
    The Administrator recognizes that in considering the estimates of 
the proportion of population affected and the number of occurrences of 
those specific health effects that are included in the risk assessment, 
these limited estimates based on 2002 and 2004 simulations are 
indicative of a much broader array of O3-related health 
endpoints that are part of a ``pyramid of effects'' (discussed above in 
section II.A.4.d) that include various indicators of morbidity that 
could not be included in the risk assessment (e.g., school absences, 
increased medication use, emergency department visits) and which 
primarily affect members of at-risk groups. Moreover, the Administrator 
notes that the CASAC Panel supported a qualitative consideration of the 
much broader array of O3-related health endpoints, and 
specifically referred to respiratory emergency department visits in 
asthmatics and people with other lung diseases, increased medication 
use, and increased respiratory symptoms reported at exposure levels 
well below the current standard.
    The Administrator believes the exposure and risk estimates 
discussed in the Staff Paper and summarized above are important from a 
public health perspective and are indicative of potential exposures and 
risks to at-risk groups. In reaching this proposed judgment, the 
Administrator considered the following factors: (1) The estimates of 
numbers of persons exposed at and above the 0.070 ppm benchmark level; 
(2) the risk estimates of the proportion of the population and number 
of occurrences of various health effects in areas upon just meeting the 
current standard; (3) the year-to-year and city-to-city variability in 
both the exposure and risk estimates; (4) the uncertainties in these 
estimates; and (5) recognition that there is a broader array of 
O3-related adverse health outcomes for which risk estimates 
could not be quantified (that are part of a broader ``pyramid of 
effects'') and that the scope of the assessment was limited to just a 
sample of urban areas and to some but not all at-risk populations, 
leading to an incomplete estimation of public health impacts associated 
with O3 exposures

[[Page 37872]]

across the country. The Administrator also notes that it was the 
unanimous conclusion of the CASAC Panel that there is no scientific 
justification for retaining the current primary O3 standard, 
that the current standard is not sufficiently health-protective with an 
adequate margin of safety, and that the standard needs to be 
substantially reduced to protect human health, particularly in at-risk 
subpopulations.
    Based on all of these considerations, the Administrator proposes 
that the current O3 standard is not requisite to protect 
public health with an adequate margin of safety because it does not 
provide sufficient protection and that revision would result in 
increased public health protection, especially for members of at-risk 
groups.

D. Conclusions on the Elements of the Primary Standard

1. Indicator
    In the last review EPA focused on a standard for O3 as 
the most appropriate surrogate for ambient photochemical oxidants. In 
this review, while the complex atmospheric chemistry in which 
O3 plays a key role has been highlighted, no alternative to 
O3 has been advanced as being a more appropriate surrogate 
for ambient photochemical oxidants.
    The Staff Paper (section 2.2.2) notes that it is generally 
recognized that control of ambient O3 levels provides the 
best means of controlling photochemical oxidants. Among the 
photochemical oxidants, the acute exposure chamber, panel, and field 
epidemiological human health database provides specific evidence for 
O3 at levels commonly reported in the ambient air, in part 
because few other photochemical oxidants are routinely measured. 
However, recent investigations on copollutant interactions have used 
simulated urban photochemical oxidant mixes. These investigations 
suggest the need for similar studies to help in understanding the 
biological basis for effects observed in epidemiological studies that 
are associated with air pollutant mixtures, where O3 is used 
as the surrogate for the mix of photochemical oxidants. Meeting the 
O3 standard can be expected to provide some degree of 
protection against potential health effects that may be independently 
associated with other photochemical oxidants but which are not 
discernable from currently available studies indexed by O3 
alone. Since the precursor emissions that lead to the formation of 
O3 generally also lead to the formation of other 
photochemical oxidants, measures leading to reductions in population 
exposures to O3 can generally be expected to lead to 
reductions in population exposures to other photochemical oxidants.
    The Staff Paper notes that while the new body of time-series 
epidemiological evidence cannot resolve questions about the relative 
contribution of other photochemical oxidant species to the range of 
morbidity and mortality effects associated with O3 in these 
types of studies, control of ambient O3 levels is generally 
understood to provide the best means of controlling photochemical 
oxidants in general, and thus of protecting against effects that may be 
associated with individual species and/or the broader mix of 
photochemical oxidants, independent of effects specifically related to 
O3.
    In its letter to the Administrator, the CASAC O3 Panel 
noted that O3 is ``the key indicator of the extent of 
oxidative chemistry and serves to integrate multiple pollutants.'' 
CASAC also stated that ``although O3 itself has direct 
effects on human health and ecosystems, it can also be considered as an 
indicator of the mixture of photochemical oxidants and of the oxidizing 
potency of the atmosphere'' (Henderson, 2006c, p. 9).
    Based on the available information, and consistent with the views 
of EPA staff and the CASAC, the Administrator proposes to continue to 
use O3 as the indicator for a standard that is intended to 
address effects associated with exposure to O3, alone or in 
combination with related photochemical oxidants. In so doing, the 
Administrator recognizes that measures leading to reductions in 
population exposures to O3 will also reduce exposures to 
other photochemical oxidants.
2. Averaging Time
a. Short-Term and Prolonged (1 to 8 Hours)
    The current 8-hour averaging time for the primary O3 
NAAQS was set in 1997. At that time, the decision to revise the 
averaging time of the primary standard from 1 to 8 hours was supported 
by the following key observations and conclusions:
    (1) The 1-hour averaging time of the previous NAAQS was originally 
selected primarily on the basis of health effects associated with 
short-term (i.e., 1- to 3-hour) exposures.
    (2) Substantial health effects information was available for the 
1997 review that demonstrated associations between a wide range of 
health effects (e.g., moderate to large lung function decrements, 
moderate to severe symptoms and pulmonary inflammation) and prolonged 
(i.e., 6- to 8-hour) exposures below the level of the then current 1-
hour NAAQS.
    (3) Results of the quantitative risk analyses showed that 
reductions in risks from both short-term and prolonged exposures could 
be achieved through a primary standard with an averaging period of 
either 1 or 8 hours. Thus establishing both a 1-hour and an 8-hour 
standard would not be necessary to reduce risks associated with the 
full range of observed health effects.
    (4) The 8-hour averaging time is more directly associated with 
health effects of concern at lower O3 concentrations than 
the 1-hour averaging time. It was thus the consensus of CASAC ``that an 
8-hour standard was more appropriate for a human health-based standard 
than a 1-hour standard.'' (Wolff, 1995)
    (5) An 8-hour averaging results in a significantly more uniformly 
protective national standard than the then current 1-hour standard.
    (6) An 8-hour averaging time effectively limits both 1- and 8-hour 
exposures of concern.
    In looking at the new information that is discussed in section 
7.6.2 of the current Criteria Document, the Staff Paper noted that 
epidemiological studies have used various averaging periods for 
O3 concentrations, most commonly 1-hour, 8-hour and 24-hour 
averages. As described more specifically in sections 3.3 and 3.4 of the 
Staff Paper, in general the results presented from U.S. and Canadian 
studies show no consistent difference for various averaging times in 
different studies. Because the 8-hour averaging time continues to be 
more directly associated with health effects of concern from controlled 
human exposure studies at lower concentrations than do shorter 
averaging periods, the Staff Paper did not evaluate alternative 
averaging times in this review and did not conduct exposure or risk 
assessments for standards with averaging times other than 8 hours.
    The Staff Paper discusses an analysis of a recent three-year period 
of air quality data (2002 to 2004) which was conducted to determine 
whether the comparative 1- and 8-hour air quality patterns that were 
observed in the last review continue to be observed based on more 
recent air quality data. This updated air quality analysis (McCluney, 
2007) is very consistent with the analysis done in the last review in 
that it indicates that only two urban areas of the U.S. have such 
``peaky'' air quality patterns such that the ratio of 1-hour to 8-hour 
design values is greater than 1.5. This suggests that, based on recent 
air quality data, it is reasonable to again conclude that an 8-hour 
average

[[Page 37873]]

standard at or below the current level would generally be expected to 
provide protection equal to or greater than the previous 1-hour 
standard of 0.12 ppm in almost all urban areas. Thus, the Staff Paper 
again concluded that setting a standard with an 8-hour averaging time 
can effectively limit both 1- and 8-hour exposures of concern and is 
appropriate to provide adequate and more uniform protection of public 
health from both short-term and prolonged exposures to O3 in 
the ambient air.
    In its letter to the Administrator, the CASAC O3 Panel 
supported the continued use of an 8-hour averaging time for the primary 
O3 standard (Henderson, 2006c, p. 2), as did many 
commenters. Some other commenters expressed the view that consideration 
should be given to setting or reinstating a 1-hour standard, in 
addition to maintaining the use of an 8-hour averaging time, to protect 
people in those parts of the country with relatively more ``peaky'' 
exposure profiles. These commenters point out that when controlled 
exposure studies using triangular exposure patterns (with relatively 
higher 1-hour peaks) have been compared to constant exposure patterns 
with the same aggregate O3 dose (in terms of concentration x 
time), ``peaky'' exposure patterns are seen to lead to higher risks. 
The California Air Resources Board made particular note of this point, 
expressing the view that a 1-hour standard would more closely represent 
actual exposures, in that many people spend only 1 to 2 hours a day 
outdoors, and that it would be better matched to O3 
concentration profiles along the coasts where O3 levels are 
typically high for shorter averaging periods than 8 hours.
b. Long-term
    During the last review, there was a large animal toxicological 
database for consideration that provided clear evidence of associations 
between long-term (e.g., from several months to years) exposures and 
lung tissue damage, with additional evidence of reduced lung elasticity 
and accelerated loss of lung function. However, there was no 
corresponding evidence for humans, and the state of the science had not 
progressed sufficiently to allow quantitative extrapolation of the 
animal study findings to humans. For these reasons, consideration of a 
separate long-term primary O3 standard was not judged to be 
appropriate at that time, recognizing that the 8-hour standard would 
act to limit long-term exposures as well as short-term and prolonged 
exposures.
    Taking into consideration the currently available evidence on long-
term O3 exposures, discussed above in section II.A.2.a.ii, 
the Staff Paper concludes that a health-based standard with a longer-
term averaging time than 8 hours is not warranted at this time. The 
Staff Paper notes that, while potentially more serious health effects 
have been identified as being associated with longer-term exposure 
studies of laboratory animals and in epidemiology studies, there 
remains substantial uncertainty regarding how these data could be used 
quantitatively to develop a basis for setting a long-term health 
standard. Because long-term air quality patterns would be improved in 
areas coming into attainment with an 8-hour standard, the potential 
risk of health effects associated with long-term exposures would be 
reduced in any area meeting an 8-hour standard. Thus, the Staff Paper 
did not recommend consideration of a long-term, health-based standard 
at this time.
    In its final letter to the Administrator, the CASAC O3 
Panel offered no views on the long-term exposure evidence, nor did it 
suggest that consideration of a primary O3 standard with a 
long-term averaging time was appropriate. In fact, the CASAC 
O3 Panel agreed with the choice of an 8-hour averaging time 
for the primary O3 NAAQS suggested by Agency staff 
(Henderson, 2007). Similarly, no commenters expressed support for 
considering such a long-term standard.
c. Administrator's Conclusions on Averaging Time
    In considering the information discussed above, CASAC views and 
public comments, the Administrator concludes that a standard with an 8-
hour averaging time can effectively limit both 1- and 8-hour exposures 
of concern and that an 8-hour averaging time is appropriate to provide 
adequate and more uniform protection of public health from both short-
term (1- to 3-hour) and prolonged (6- to 8-hour) exposures to 
O3 in the ambient air. This conclusion is based on the 
observations summarized above, particularly: (1) The fact that the 8-
hour averaging time is more directly associated with health effects of 
concern at lower O3 concentrations than are averaging times 
of shorter duration and (2) results from quantitative risk analyses 
showing that attaining an 8-hour standard reduces the risk of 
experiencing health effects associated with both 8-hour and shorter 
duration exposures. Furthermore, the Administrator observes that the 
CASAC O3 Panel agreed with the choice of averaging time 
(Henderson, 2007). Therefore, the Administrator proposes to retain the 
8-hour averaging time and is not proposing a separate 1-hour standard. 
The Administrator also concludes that a standard with a long-term 
averaging time is not warranted at this time.
3. Form
    In 1997, the primary O3 NAAQS was changed from a ``1-
expected-exceedance'' form per year over three years \51\ to a 
concentration-based statistic, specifically the 3-year average of the 
annual fourth-highest daily maximum 8-hour concentrations. The 
principal advantage of the concentration-based form is that it is more 
directly related to the ambient O3 concentrations that are 
associated with the health effects. With a concentration-based form, 
days on which higher O3 concentrations occur would weigh 
proportionally more than days with lower concentrations, since the 
actual concentrations are used in determining whether the standard is 
attained. That is, given that there is a continuum of effects 
associated with exposures to varying levels of O3, the 
extent to which public health is affected by exposure to ambient 
O3 is related to the actual magnitude of the O3 
concentration, not just whether the concentration is above a specified 
level.
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    \51\ The 1-expected-exceedance form essentially requires that 
the fourth-highest air quality value in 3 years, based on 
adjustments for missing data, be less than or equal to the level of 
the standard for the standard to be met at an air quality monitoring 
site.
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    During the 1997 review, consideration was given to a range of 
alternative forms, including the second-, third-, fourth- and fifth-
highest daily maximum 8-hour concentrations in an O3 season, 
recognizing that the public health risks associated with exposure to a 
pollutant without a clear, discernable threshold can be appropriately 
addressed through a standard that allows for multiple exceedances to 
provide increased stability, but that also significantly limits the 
number of days on which the level may be exceeded and the magnitude of 
such exceedances. Consideration was given to setting a standard with a 
form that would provide a margin of safety against possible, but 
uncertain chronic effects, and would also provide greater stability to 
ongoing control programs. The fourth-highest daily maximum was selected 
because it was decided that the differences in the degree of protection 
against potential chronic effects afforded by the alternatives within 
the range were not well enough understood to use any such differences 
as a basis for

[[Page 37874]]

choosing the most restrictive forms. On the other hand, the relatively 
large percentage of sites that would experience O3 peaks 
well above 0.080 ppm and the number of days on which the level of the 
standard may be exceeded, even when attaining a fifth-highest 0.080 ppm 
concentration-based standard, argued against choosing that form.
    As an initial matter, the Staff Paper considered whether it is 
appropriate to continue to specify the level of the O3 
standard to the nearest hundredth (two decimal places) ppm, or whether 
the precision with which ambient O3 concentrations are 
measured supports specifying the standard level to the thousandth ppm 
(i.e., to the part per billion (ppb)). The Staff Paper discusses an 
analysis conducted by EPA staff to determine the impact of ambient 
O3 measurement error on calculated 8-hour average 
O3 design value concentrations, which are compared to the 
level of the standard to determine whether the standard is attained 
(Cox and Camalier, 2006). The results of this analysis suggest that 
instrument measurement error, or possible instrument bias, contribute 
very little to the uncertainty in design values. More specifically, 
measurement imprecision was determined to contribute less than 1 ppb to 
design value uncertainty, and a simulation study indicated that 
randomly occurring instrument bias could contribute approximately 1 
ppb. EPA staff interpreted this analysis as being supportive of 
specifying the level of the standard to the nearest thousandth ppm. If 
the current standard were to be specified to this degree of precision, 
the current standard would effectively be at a level of 0.084 ppm, 
reflecting the data rounding conventions that are part of the 
definition of the current 0.080 ppm 8-hour standard. This information 
was provided to the CASAC O3 Panel and made available to the 
public.
    In evaluating alternative forms for the primary standard in 
conjunction with specific standard levels, the Staff Paper considered 
the adequacy of the public health protection provided by the 
combination of the level and form to be the foremost consideration. In 
addition, the Staff Paper recognized that it is important to have a 
form of the standard that is stable and insulated from the impacts of 
extreme meteorological events that are conducive to O3 
formation. Such instability can have the effect of reducing public 
health protection, because frequent shifting in and out of attainment 
due to meteorological conditions can disrupt an area's ongoing 
implementation plans and associated control programs. Providing more 
stability is one of the reasons that EPA moved to a concentration-based 
form in 1997.
    The Staff Paper considered two concentration-based forms of the 
standard: the nth-highest maximum concentration and a percentile-based 
form. A percentile-based statistic is useful for comparing datasets of 
varying length because it samples approximately the same place in the 
distribution of air quality values, whether the dataset is several 
months or several years long. However, a percentile-based form would 
allow more days with higher air quality values in locations with longer 
O3 seasons relative to places with shorter O3 
seasons. An nth-highest maximum concentration form would more 
effectively ensure that people who live in areas with different length 
O3 seasons receive the same degree of public health 
protection. For this reason, the exposure and risk analyses were based 
on a form specified in terms of an nth-highest concentration, with n 
ranging from 3 to 5.
    The results of some of these analyses are shown in the Staff Paper 
(Figures 6-1 through 6-4) and specifically discussed in chapter 6. 
These figures illustrate the estimated percent change in risk estimates 
for the incidence of moderate or greater decrements in lung function 
(>=15 percent FEV1) in all school age children and moderate 
or greater lung function decrements (>=10 percent FEV1) in 
asthmatic school age children, associated with going from meeting the 
current standard to meeting alternative standards with alternative 
forms based on the 2002 and 2004 simulations. Figures 6-5 and 6-6 
illustrate the estimated percent of change in the estimated incidence 
of non-accidental mortality, associated with going from meeting the 
current standard to meeting alternative standards, based on the 2002 
and 2004 simulations. These results are generally representative of the 
patterns found in all of the analyses. The estimated reductions in risk 
associated with different forms of the standard, ranging from third- to 
fourth-highest daily maximum concentrations at 0.084 ppm, and from 
third- to fifth-highest daily maximum concentrations at 0.074 ppm, are 
generally less than the estimated reductions associated with the 
different levels that were analyzed. As seen in these figures, there is 
much city-to-city variability, particularly in the percent changes 
associated with going from a fourth-highest to third-highest form at 
the current level of 0.084 ppm, and with estimated reductions 
associated with the fifth-highest form at a 0.074 ppm level. In most 
cities, there are generally only small differences in the estimated 
reductions in risks associated with the third- to fifth-highest forms 
at a level of 0.074 ppm simulated using 2002 and 2004 O3 
monitoring data.
    The Staff Paper noted that there is not a clear health-based 
threshold for selecting a particular nth-highest daily maximum form of 
the standard from among the ones analyzed. It also noted that the 
changes in the form considered in the analyses result in only small 
differences in the estimated reductions in risks in most cities, 
although in some cities larger differences are estimated. The Staff 
Paper concluded that a range of concentration-based forms from the 
third- to the fifth-highest daily maximum 8-hour average concentration 
is appropriate for consideration in setting the standard. Given that 
there is a continuum of effects associated with exposures to varying 
levels of O3, the extent to which public health is affected 
by exposure to ambient O3 is related to the actual magnitude 
of the O3 concentration, not just whether the concentration 
is above a specified level. The principal advantage of a concentration-
based form is that it is more directly related to the ambient 
O3 concentrations that are associated with health effects. 
Robust, concentration-based forms, in the range of the third- to fifth-
highest daily maximum 8-hour average concentration, including the 
current 4th-highest daily maximum form, minimize the inherent lack of 
year-to-year stability of exceedance-based forms and provide insulation 
from the impacts of extreme meteorological events. Such instability can 
have the effect of reducing public health protection by disrupting 
ongoing implementation plans and associated control programs.
    With regard to the precision of the standard, in their letter to 
the Administrator, the CASAC concluded that current monitoring 
technology ``allows accurate measurement of O3 
concentrations with a precision of parts per billion'' (Henderson, 
2006c). The CASAC recommended that the specification of the level of 
the O3 standard should reflect this degree of precision 
(Henderson, 2006c). Some public comments supported specifying the 
standard in terms of parts per billion, or to three decimal places if 
specified in terms of parts per million.\52\ Other public commenters 
stated that the

[[Page 37875]]

basis for changing the current rounding procedures is not supported by 
a complete analysis of the O3 compliance monitoring 
procedures, including consideration of uncertainty related to humidity 
effects and interferences from aromatic compounds in the monitoring of 
O3 levels.
---------------------------------------------------------------------------

    \52\ The Staff Paper notes that the 8-hour O3 
standard adopted by the State of California in 2006 is specified to 
the nearest thousandth part per million (at a level of 0.070 ppm) 
(http://www.arb.ca.gov/research/aaqs/ozone-rs/ozone-rs.htm).

---------------------------------------------------------------------------

    With regard to the form of the standard, in their letter to the 
Administrator, CASAC recommended that ``a range of concentration-based 
forms from the third-to the fifth-highest daily maximum 8-hour average 
concentration'' be considered (Henderson, 2006c, p. 5). Some public 
commenters that expressed the view that the current primary 
O3 standard is not adequate also submitted comments that 
supported a more health-protective form of the standard than the 
current form (e.g., a second-or third-highest daily maximum form). 
Commenters who expressed the view that the current standard is adequate 
did not provide any views on alternative forms that would be 
appropriate for consideration should the Administrator consider 
revisions to the standard.
    The Administrator proposes that the level of the standard be 
specified to the nearest thousandth ppm, based on the staff's analysis 
and conclusions discussed in the Staff Paper that current monitoring 
technology allows accurate measurement of O3 to support 
specifying the 8-hour standard to this degree of precision, and on 
CASAC's recommendation with respect to this aspect of the standard. The 
Administrator invites comment on this proposal to specify the standard 
to the thousandth ppm.
    The Administrator recognizes that there is not a clear health-based 
threshold for selecting a particular nth-highest daily maximum form of 
the standard from among the ones analyzed in the Staff Paper, and that 
the current form of the standard provides a stable target for 
implementing programs to improve air quality. The Administrator also 
agrees that the adequacy of the public health protection provided by 
the combination of the level and form is a foremost consideration. 
Based on this, the Administrator proposes to retain the form of the 
current standard, 4th-highest daily maximum 8-hour average 
concentration, recognizing that the public health protection that would 
be provided by the standard is based on combining this form with the 
level discussed below. Mindful of the recommendation of the 
O3 CASAC Panel and the view expressed by commenters, the 
Administrator also invites comment on two alternative forms of the 
standard, the third- and the fifth-highest daily maximum 8-hour average 
concentrations.
4. Level
a. Evidence and Exposure/Risk Based Considerations in the Staff Paper
    The approach used in the Staff Paper as a basis for staff 
recommendations on standard levels builds upon and broadens the general 
approach used by EPA in the last review. This approach reflects the 
more extensive and stronger body of evidence now available on a broader 
range of health effects associated with exposure to O3, 
including: (1) Additional respiratory-related endpoints; (2) new 
information about the mechanisms underlying respiratory morbidity 
effects supporting a judgment that the link between O3 
exposure and these effects is causal; (3) newly identified 
cardiovascular-related health endpoints from animal toxicology, and 
controlled human exposures studies that are highly suggestive that 
O3 can directly or indirectly contribute to cardiovascular 
morbidity, and (4) new U.S. multi-city time series studies, single city 
studies, and several meta-analyses of these studies that provide 
relatively strong evidence for associations between short-term 
O3 exposures and all-cause (nonaccidental) mortality, at 
levels below the current primary standard: as well as (5) evidence of 
increased susceptibility in people with asthma and other lung diseases. 
In evaluating evidence-based and exposure/risk-based considerations, 
the Staff Paper considered: (1) The ranges of levels of alternative 
standards that are supported by the evidence, and the uncertainties and 
limitations in that evidence and (2) the extent to which specific 
levels of alternative standards reduce the estimated exposures of 
concern and risks attributable to O3 and other photochemical 
oxidants, and the uncertainties associated with the estimated exposure 
and risk reductions.
    In taking into account evidence-based considerations, the Staff 
Paper evaluated available evidence from controlled human exposure 
studies and epidemiological studies, as well as the uncertainties and 
limitations in that evidence. In particular, it focused on the extent 
to which controlled human exposure studies provide evidence of lowest-
observed-effects levels and the extent to which epidemiological studies 
provide evidence of associations that extend down to the lower levels 
of O3 concentrations observed in the studies or some 
indication of potential effect thresholds in terms of 8-hour average 
O3 concentrations.
    In considering the available controlled human exposure studies, as 
discussed above in section II.A.2.a.i(a)(i), two new studies are 
notable in that they are the only controlled human exposure studies 
that examined respiratory effects, including lung function decrements 
and respiratory symptoms, in healthy adults at lower exposure levels 
than had previously been examined. EPA's reanalysis of the data from 
the most recent study shows small group mean decrements in lung 
function responses to be statistically significant at the 0.060 ppm 
exposure level, while the author's analysis did not yield statistically 
significant lung function responses (but did yield some statistically 
significant respiratory symptom responses toward the end of the 
exposure period). Notably, these studies report a small percentage of 
subjects experiencing lung function decrements (> 10 percent) at the 
0.060 ppm exposure level. These studies provide very limited evidence 
of O3-related lung function decrements and respiratory 
symptoms at this lower exposure level.
    In considering controlled human exposure studies of pulmonary 
inflammation, airway responsiveness, and impaired host defense 
capabilities, the Staff Paper notes that these studies provide evidence 
of a lowest-observed-effects level for such effects in healthy adults 
at prolonged moderate exertion of 0.080 ppm. As discussed above, these 
physiological effects have been linked to aggravation of asthma and 
increased susceptibility to respiratory infection, potentially leading 
to increased medication use, increased school and work absences, 
increased visits to doctors' offices and emergency departments, and 
increased hospital admissions. Further, pulmonary inflammation is 
related to increased cellular permeability in the lung, which may be a 
mechanism by which O3 exposure can lead to cardiovascular 
system effects, and to potential chronic effects such as chronic 
bronchitis or long-term damage to the lungs that can lead to reduced 
quality of life. These are all indicators of adverse O3-
related morbidity effects, which are consistent with and lend 
plausibility to the adverse morbidity effects and mortality effects 
observed in epidemiological studies.
    In considering epidemiological studies, the Staff Paper first 
recognizes that the available evidence neither supports nor refutes the 
existence of effect thresholds at the population level for morbidity 
and mortality effects and that if a population threshold level does 
exist, it would likely be well below the level of the current 
O3 standard and

[[Page 37876]]

possibly within the range of background levels. As discussed above (and 
more fully in the Staff Paper in chapter 3 and the Criteria Document in 
chapter 7), a number of studies reported some suggestive evidence of 
possible thresholds for morbidity and mortality outcomes in terms of 
24-hour, 8-hour, and 1-hour averaging times. These results, taken 
together, provide some indication of possible 8-hour average threshold 
levels from below about 0.025 to 0.035 ppm up to approximately 0.050 
ppm. Other studies, however, observe linear concentration-response 
functions suggesting no effect threshold. The Staff Paper concludes 
that the statistically significant associations between ambient 
O3 concentrations and lung function decrements, respiratory 
symptoms, indicators of respiratory morbidity including increased 
emergency department visits and hospitals admissions, and possibly 
mortality reported in a large number of studies likely extend down to 
ambient O3 concentrations that are well below the level of 
the current standard (EPA, 2007, p. 6-60). Toward the lower end of the 
range of O3 concentrations observed in such studies, ranging 
down to background levels, however, the Staff paper states that there 
is increasing uncertainty as to whether the observed associations 
remain plausibly related to exposures to ambient O3, rather 
than to the broader mix of air pollutants present in the ambient 
atmosphere.
    The Staff Paper also considered studies that did subset analyses 
that include only days with ambient O3 concentrations below 
the level of the current standard, or below even lower O3 
concentrations, and continue to report statistically significant 
associations. Notably, as discussed above, Bell et al. (2006) conducted 
a subset analysis that continued to show statistically significant 
associations even when only days with a maximum 8-hour average 
O3 concentration below a value of approximately 0.061 ppm 
were included.\53\ Also of note is the large multi-city NCICAS 
(Mortimer et al., 2002) that reported statistically significant 
associations between ambient O3 concentrations and lung 
function decrements even when days with 8-hour average O3 
levels greater than 0.080 ppm were excluded (which consisted of less 
than 5 percent of the days in the eight urban areas in the study).
---------------------------------------------------------------------------

    \53\ Bell et al. (2006) referred to this level as being 
approximately equivalent to 120 [mu]g/m3, daily 8-hour 
maximum, the World Health Organization guideline and European 
Commission target value for O3.
---------------------------------------------------------------------------

    Being mindful of the uncertainties and limitations inherent in 
interpreting the available evidence, the Staff Paper states the view 
that the range of alternative O3 standards for consideration 
should take into account information on lowest-observed-effects levels 
in controlled human exposure studies as well as indications of possible 
effects thresholds reported in some epidemiological studies and 
questions of biological plausibility in attributing associations 
observed down to background levels to O3 exposures alone. 
Based on the evidence and these considerations, it concluded that the 
upper end of the range of consideration should be somewhat below 0.080 
ppm, the lowest-observed-effects level for effects such as pulmonary 
inflammation, increased airway responsiveness and impaired host-defense 
capabilities in healthy adults while at prolonged moderate exertion. 
The Staff Paper also concludes that the lower end to the range of 
alternative O3 standards appropriate for consideration 
should be the lowest-observed-effects level for potentially adverse 
lung function decrements and respiratory symptoms in some healthy 
adults, 0.060 ppm.
    In addition to the evidence-based considerations informing staff 
recommendations on alternative levels, the Staff Paper also evaluated 
quantitative exposures and health risks estimated to occur upon meeting 
the current and alternative standards.\54\ In so doing, it presented 
the important uncertainties and limitations associated with these 
exposure and risk assessments. For example, the Staff Paper noted 
important uncertainties affecting the exposure estimates are related to 
modeling human activity patterns over an O3 season 
(especially repetitive exposures), modeling ambient concentrations near 
roadways and modeling building air exchange rates which impact 
estimates of indoor O3 concentrations. With regard to the 
risk assessment, important uncertainties include, for example, those 
related to exposure estimates for children engaged in moderate or 
greater exertion, as well as those related to estimation of 
concentration-response functions, specification of concentration-
response models, the possible role of copollutants in interpreting 
reported associations with O3, and inferences of a likely 
causal relationship between O3 exposure and nonaccidental 
mortality (for risk estimates based on epidemiological studies).
---------------------------------------------------------------------------

    \54\ As described in the Staff Paper (section 4.5.8) and 
discussed above, recent O3 air quality distributions have 
been statistically adjusted to simulate just meeting the current and 
selected alternative standards. These simulations do not represent 
predictions of when, whether, or how areas might meet the specified 
standards. Modeling that projects whether and how areas might attain 
alternative standards in a future year is presented in the 
Regulatory Impact Analysis being prepared in connection with this 
rulemaking.
---------------------------------------------------------------------------

    Beyond these uncertainties, the Staff Paper also recognized 
important limitations to the exposure and risk analyses. For example, 
the Staff Paper did not have sufficient information to evaluate all 
relevant at-risk groups (e.g., outdoor workers) or all O3-
related health outcomes (e.g., increased medication use, school 
absences, emergency department visits), and the scope of the Staff 
Paper analyses was generally limited to estimating exposures and risks 
in 12 urban areas across the U.S., and to only five or just one area 
for some risk analyses. The Staff Paper notes that it is clear that 
national-scale public health impacts of ambient O3 exposures 
are much larger than the quantitative estimates of O3-
related incidences of adverse health effects and the numbers of 
children likely to experience exposures of concern associated with 
meeting the current or alternative standards. On the other hand, due to 
individual variability in responsiveness, only a subset of individuals 
who are estimated to experience exposures of concern at and above a 
specific benchmark level can be expected to experience certain adverse 
health effects, although susceptible subpopulations such as those with 
asthma are expected to be affected more by such exposures than healthy 
individuals. In taking these limitations into account, the Staff Paper 
reflected CASAC's advice not to rely solely on the results of the 
exposure and risk assessments in considering alternative standards, but 
also to place significant weight on the body of evidence of 
O3-related health effects in drawing conclusions about an 
appropriate range of levels for consideration.
    The Staff Paper focused on alternative standards with the same form 
as the current O3 standard (i.e. the 0.074/4, 0.070/4 and 
0.064/4 scenarios).\55\ Having concluded in the Staff Paper that it was 
appropriate to consider a range of standard levels from somewhat below 
0.080 ppm down to as low as 0.060 ppm, the Staff Paper looked to 
results of the analyses of exposure and risk for the 0.074/4 scenario 
to represent the public health impacts of selecting a standard in

[[Page 37877]]

the upper part of the range, the results of analyses of the 0.070/4 
scenario to represent the impacts in the middle part of the range, and 
the results of the analyses of the 0.064/4 scenario to represent the 
lower part of the range.
---------------------------------------------------------------------------

    \55\ The abbreviated notation used to identify the current and 
alternative standards in this section and in the risk assessment 
section of the Staff Paper is in terms of ppm and the nth highest 
daily maximum 8-hour average. For example, the current standard is 
identified as ``0.084/4.''
---------------------------------------------------------------------------

    As discussed in section II.B.1 of this notice, the exposure 
estimates presented in the Staff Paper are for the number and percent 
of all children and asthmatic children exposed, and the number of 
person-days (occurrences) of exposures, with daily 8-hour maximum 
exposures at or above several benchmark levels while at intermittent 
moderate or greater exertion. For reasons discussed above in section 
II.C.2, the Staff Paper focused on exposures of concern at the 0.070 
and 0.060 ppm benchmark levels for the purpose of evaluating 
alternative standard levels. As shown in the Table 1 in this notice, 
the percent of population exposed at any given level is very similar 
for all and asthmatic school age children. Substantial year-to-year 
variability in exposure estimates is observed, ranging to over an order 
of magnitude at the higher alternative standard levels, in estimates of 
the number of children and the number of occurrences of exposures of 
concern at both of these benchmark levels. The Staff Paper also notes 
that there is substantial city-to-city variability in these estimates, 
and notes that it is appropriate to consider not just the aggregate 
estimates across all cities, but also to consider the public health 
impacts in cities that receive relatively less protection from the 
alternative standards.
    As discussed in the Staff Paper, a standard set at the upper part 
of the range recommended by EPA staff (e.g., the 0.074/4 scenario) 
would result in an aggregate estimate of about 4 percent of all or 
asthmatic school age children likely to experience exposures of concern 
at the >=0.070 ppm benchmark level based on the 2002 simulation, a year 
with relatively high O3 levels, while the estimates range up 
to 12 percent of all or asthmatic school age children in the single 
city with the least degree of protection from this standard. Using the 
2004 simulation, a year with relatively low O3 levels, 
exposures of concern at this level are essentially eliminated. At the 
benchmark level of >=0.060 ppm, in aggregate using the 2002 simulation 
about 22 percent of all or asthmatic school age children are estimated 
to experience exposures of concern; this estimate ranges up to about 46 
percent of all or asthmatic school age children in the single city with 
the least degree of protection from this standard. Using the 2004 
simulation, exposures of concern at this level are estimated to be 
substantially lower. A standard set at this level is estimated to 
reduce the number of all and asthmatic school age children estimated to 
experience one or more moderate lung function decrements by about 30 to 
50 percent relative to the current standard, with city-to-city 
differences accounting for most of the variability in estimates. A 
standard set at this level is estimated to reduce non-accidental 
mortality by about 10 to 40 percent, with most of the variability 
occurring across the 12 city estimates.
    Using the 2002 simulation, a standard set at this level (the 0.074/
4 scenario) is estimated to reduce the incidence of symptom days in 
children with moderate to severe asthma in the Boston area by about 
1,000 days, a 15 percent reduction relative to the current standard. 
With this reduction, it is estimated that about 1 respiratory symptom 
day in 8 during the O3 season would be attributable to 
O3 exposure. Estimated incidence of respiratory-related 
hospital admissions was reduced by 14 to 17 percent by a standard set 
at this level relative to the current standard, in the year with 
relatively high and relatively low O3 air quality levels 
respectively.
    The Staff Paper notes that a standard set at the middle part of the 
staff-recommended range, as indicated by the estimates for the 0.070/4 
scenario, would reduce the exposures of concern at the 0.070 ppm level 
substantially over the current standard, resulting in an aggregate 
estimate of about 1.5 to nearly 2 percent of all or asthmatic school 
age children likely to experience exposures of concern even using the 
2002 simulation, and leaving approximately 5 percent or less of 
children likely to experience exposures of concern in the city with the 
least degree of protection. Using the 2004 simulation, it essentially 
eliminates exposures of concern at this level. It reduces exposures of 
concern at the 0.060 ppm benchmark level less so, leaving larger 
percentages of all school age children unprotected using the 2002 
simulation (about 15 percent in aggregate) or in the city with the 
least protection from this standard (about 33 percent). However, using 
the 2004 simulation, it is estimated to reduce exposures of concern at 
this benchmark level to approximately 5 percent or less of children 
even in the city with the least degree of protection. It provides 
considerable additional protection for members of at-risk groups, over 
the current O3 standard, against respiratory morbidity 
effects such as lung function decrements, respiratory symptom days and 
hospital admissions, as well as non-accidental mortality.
    A standard set at lower part of the staff-recommended range (e.g., 
the 0.064/4 scenario), would result in an aggregate estimate of less 
than 0.5 percent of all and asthmatic school age children likely to 
experience exposures of concern at the 0.070 ppm benchmark level using 
the 2002 simulation and only about 1 percent of all and asthmatic 
school age children in the city with the least degree of protection 
from this standard. At the benchmark level of 0.060 ppm, in aggregate 
using the 2002 simulation about 5 percent of all and asthmatic school 
age children are estimated to experience exposures of concern; this 
number ranges up to 15 percent of all and asthmatic school age children 
in the city with the least degree of protection from this standard. A 
standard set at this level is estimated to reduce the number of all and 
asthmatic school age children estimated to experience one or more 
moderate lung function decrements by about 40 to 75 percent over the 
current standard, and non-accidental mortality by about 25 to 75 
percent, with most of the variability occurring across the 12 city 
estimates.
    A standard set at the 0.064/4 scenario is estimated, based on the 
2002 simulation, to reduce the incidence of symptom days in children 
with moderate to severe asthma in the Boston area by about 1,900 days, 
about a 25 to 30 percent reduction over the current standard. But even 
with this reduction, it is estimated that 1 respiratory symptom day in 
10 during the O3 season is attributable to O3 
exposure. Estimated incidence of respiratory-related hospital 
admissions would be reduced by 30 to 35 percent over the current 
standard, a reduction of 125 to 150 hospital admissions in the New York 
City area alone, using the 2002 and 2004 simulations, respectively.
b. CASAC Views
    As stated in its letter to the Administrator, ``the CASAC 
unanimously recommends that the current primary ozone NAAQS be revised 
and that the level that should be considered for the revised standard 
be from 0.060 to 0.070 ppm'' (Henderson, 2006c, p. 5). This 
recommendation follows from its more general recommendation, discussed 
above, that the current standard of 0.084 ppm needs to be substantially 
reduced to be protective of human health, particularly in at-risk 
subpopulations. The CASAC Panel noted that beneficial reductions in 
some adverse health effects were estimated to occur upon meeting the 
lowest standard level (0.064 ppm)

[[Page 37878]]

considered in the risk assessment (Henderson, 2006c, p. 4). The lower 
end of this range reflects CASAC's views that ``[W]hile data exist that 
adverse health effects may occur at levels lower than 0.060 ppm, these 
data are less certain and achievable gains in protecting human health 
can be accomplished through lowering the ozone NAAQS to a level between 
0.060 and 0.070 ppm.'' (id.). In a subsequent letter to the 
Administrator, the CASAC reiterated that the Panel members ``were 
unanimous in recommending that the level of the current primary ozone 
standard should be lowered from 0.08 ppm to no greater than 0.070 ppm'' 
(Henderson, 2007, p. 2). Further, the CASAC Panel expressed the view 
that the Criteria Document and Staff Paper, together with the 
information in its earlier letter, provide ``overwhelming scientific 
evidence for this recommendation,'' and emphasized the Clean Air Act 
requirement that the primary standard must be set to protect the public 
health with an adequate margin of safety (id.).
c. Administrator's Proposed Conclusions on Level
    For the reasons discussed below, and taking into account 
information and assessments presented in the Criteria Document and 
Staff Paper, the advice and recommendations of CASAC, and the public 
comments to date, the Administrator proposes to revise the existing 8-
hour primary O3 standard. Specifically, the Administrator 
proposes to revise (1) The level of the primary O3 standard 
to within a range from 0.070 to 0.075 ppm and (2) the degree of 
precision to which the level of the standard is specified to the 
thousandth ppm.
    However, in recognition of alternative views of the science, the 
exposure and risk assessments and the uncertainties inherent in these 
assessments, and the appropriate policy responses based on the 
currently available information, the Administrator also solicits 
comments on whether to proceed instead with: (1) Alternative levels of 
the 8-hour primary O3 standard, within ranges of below 0.070 
ppm down to 0.060 ppm and above 0.075 ppm up to and including retaining 
the current standard; (2) alternative forms of the standard, including 
the 3-year average of the annual third- and fifth-highest daily maximum 
8-hour average O3 concentrations; and (3) retaining the 
degree of precision of the current standard (to the nearest hundredth 
ppm). Based on the comments received and the accompanying rationales, 
the Administrator may adopt other standards within the range of the 
alternative levels and forms identified above in lieu of the standards 
he is proposing today.
    The Administrator's consideration of alternative levels of the 
primary O3 standard builds on his proposal, discussed above, 
that the overall body of evidence indicates that the current 8-hour 
O3 standard is not requisite to protect public health with 
an adequate margin of safety because it does not provide sufficient 
protection and that revision would result in increased public health 
protection, especially for members of at-risk groups, notably including 
asthmatic children and other people with lung disease, as well as all 
children and older adults, especially those active outdoors, and 
outdoor workers, against an array of adverse health effects. These 
effects range from health outcomes that could be quantified in the risk 
assessment, including decreased lung function, respiratory symptoms, 
serious indicators of respiratory morbidity such as hospital admissions 
for respiratory causes, and nonaccidental mortality, to health outcomes 
that could not be directly estimated, including pulmonary inflammation, 
increased medication use, emergency department visits, and possibly 
cardiovascular-related morbidity effects. In reaching a proposed 
decision about the level of the O3 primary standard, the 
Administrator has considered: the evidence-based considerations from 
the Criteria Document and the Staff Paper; the results of the exposure 
and risk assessments discussed above and in the Staff Paper, giving 
weight to the exposure and risk assessments as judged appropriate; 
CASAC advice and recommendations, as reflected in discussions of drafts 
of the Criteria Document and Staff Paper at public meetings, in 
separate written comments, and in CASAC's letters to the Administrator; 
EPA staff recommendations; and public comments received during the 
development of these documents, either in connection with CASAC 
meetings or separately. In considering what 8-hour standard is 
requisite to protect public health with an adequate margin of safety, 
the Administrator is mindful that this choice requires judgment based 
on an interpretation of the evidence and other information that neither 
overstates nor understates the strength and limitations of the evidence 
and information nor the appropriate inferences to be drawn.
    The Administrator notes that the most certain evidence of adverse 
health effects from exposure to O3 comes from the clinical 
studies, and that the large bulk of this evidence derives from studies 
of exposures at levels of 0.080 and above. At those levels, there is 
consistent evidence of lung function decrements and respiratory 
symptoms in healthy young adults, as well as evidence of inflammation 
and other medically significant airway responses. Moreover there is no 
evidence that the 0.080 ppm level is a threshold for these effects. 
Although the Administrator takes note of the very limited new evidence 
of lung function decrements and respiratory symptoms in some healthy 
individuals at the 0.060 ppm exposure level, he judges this evidence 
too limited to support a primary focus at this level. The Administrator 
also notes that clinical studies, supported by epidemiological studies, 
provide important new evidence that people with asthma are likely to 
experience larger and more serious effects than healthy people from 
exposure to O3. There are also epidemiological studies that 
provide evidence of statistically significant associations between 
short-term O3 exposures and more serious health effects such 
as emergency department visits and hospital admissions, and premature 
mortality, in areas that likely would have met the current standard. 
There are also many epidemiological studies done in areas that likely 
would not have met the current standard but which nonetheless report 
statistically significant associations that generally extend down to 
ambient O3 concentrations that are below the level of the 
current standard. Further, there are a few studies that have examined 
subsets of data that include only days with ambient O3 
concentrations below the level of the current standard, or below even 
much lower O3 concentrations, and continue to report 
statistically significant associations with respiratory morbidity 
outcomes and mortality. In considering this evidence, the Administrator 
notes that the extent to which these studies provide evidence of causal 
relationships with exposures to O3 alone down to the lowest 
levels observed remains uncertain. To further inform the interpretation 
of this evidence, EPA seeks comment on the degree to which associations 
observed in epidemiological studies reflect causal relationships 
between important health endpoints and exposure to O3 alone 
at ambient O3 levels below the current standard.
    Therefore, the Administrator judges that revising the current 
standard to protect public health with an adequate margin of safety is 
warranted, and

[[Page 37879]]

would reduce risk to public health, based on: (1) The strong body of 
clinical evidence in healthy people at exposure levels of 0.080 and 
above of lung function decrements, respiratory symptoms, pulmonary 
inflammation, and other medically significant airway responses, as well 
as some indication of lung function decrements and respiratory symptoms 
at lower levels; (2) the substantial body of clinical and 
epidemiological evidence indicating that people with asthma are likely 
to experience larger and more serious effects than healthy people; and 
(3) the body of epidemiological evidence indicating associations are 
observed for a wide range of serious health effects, including 
respiratory emergency department visits and hospital admissions, and 
premature mortality, at and below 0.080 ppm. The Administrator also 
judges that the estimates of exposures of concern and risks remaining 
upon just meeting the current standard or a standard at the 0.080 ppm 
level provide additional support for this view. For the same reasons, 
and the reasons discussed above in section II.C on the adequacy of the 
current standard, the Administrator judges that the standard should be 
set below 0.080 ppm, a level at which the evidence provides a high 
degree of certainty about the adverse effects of O3 exposure 
even in healthy people.
    The Administrator next considered what standard level below 0.080 
ppm would be requisite to protect public health with an adequate margin 
of safety, that is sufficient but not more than necessary to achieve 
that result, recognizing that such a standard would result in increased 
public health protection. The assessment of a standard level calls for 
consideration of both the degree of additional protection that 
alternative levels of the standard might be expected to provide as well 
as the certainty that any specific level will in fact provide such 
protection. In the circumstances present in this review, there is no 
evidence-based bright line that indicates a single appropriate level; 
instead there is a combination of scientific evidence and other 
information that needs to be considered holistically in making this 
public health policy judgment, and selecting a standard level from a 
range of reasonable values.
    The Administrator notes that at exposure levels below 0.080 ppm 
there is only a very limited amount of evidence from clinical studies 
indicating effects in some healthy individuals at levels as low as 
0.060 ppm. The great majority of the evidence concerning effects below 
0.080 ppm is from epidemiological studies. The epidemiological studies 
do not identify any bright-line threshold level for effects. At the 
same time, the epidemiological studies are not themselves direct 
evidence of a causal link between exposure to O3 and the 
occurrence of the effects. The Administrator considers these studies in 
the context of all the other available evidence in evaluating the 
degree of certainty that O3-related adverse health effects 
would occur at various ambient levels below 0.080 ppm, including the 
strong human clinical studies and the toxicological studies that 
demonstrate the biological plausibility and mechanisms for the effects 
of O3 on airway inflammation and increased airway 
responsiveness at exposure levels of 0.080 ppm and above.
    Based on consideration of the entire body of evidence and 
information available at this time, as well as the recommendations of 
CASAC, the Administrator proposes that a standard within the range of 
0.070 to 0.075 ppm would be requisite to protect public health with an 
adequate margin of safety. A standard level within this range would 
reduce the risk of a variety of health effects associated with exposure 
to O3, including the respiratory symptoms and lung function 
effects demonstrated in the clinical studies, and the emergency 
department visits, hospital admissions and mortality effects indicated 
in the epidemiological studies. All of these effects are indicative of 
a much broader array of O3-related health endpoints, such as 
school absences and increased medication use, that are plausibly linked 
to these observed effects.
    The Administrator considered the degree of improvements in public 
health that potentially could be achieved by a standard of 0.070 to 
0.075 ppm, giving weight to the exposure and risk assessments as he 
judged appropriate, as discussed below. In considering the results of 
the exposure assessment, as discussed above (section II.C.4), the 
Administrator has primarily focused on exposures at and above the 0.070 
ppm benchmark level as an important surrogate measure for potentially 
more serious health effects for at-risk groups, including people with 
asthma. In so doing, the Administrator particularly notes that although 
the analysis of ``exposures of concern'' was conducted to estimate 
exposures at and above three discrete benchmark levels, the concept is 
appropriately viewed as a continuum. As discussed above, the 
Administrator strives to balance concern about the potential for health 
effects and their severity with the increasing uncertainty associated 
with our understanding of the likelihood of such effects at lower 
O3 exposure levels. In focusing on this benchmark, the 
Administrator notes that upon just meeting a standard within the range 
of 0.070 to 0.075 ppm based on the 2002 simulation, the number of 
school age children likely to experience exposures at and above this 
benchmark level in aggregate (for the 12 cities in the assessment), is 
estimated to be approximately 2 to 4 percent of all and asthmatic 
children, and generally less than 10 percent of children even in cities 
that receive the least degree of protection from such a standard in a 
recent year with relatively high O3 levels. A standard 
within the 0.070 to 0.075 ppm range would thus substantially reduce 
exposures of concern by about 90 to 80 percent, respectively, from 
those estimated to occur upon just meeting the current standard. While 
placing less weight on the results of the risk assessment, in light of 
the important uncertainties inherent in the assessment, the 
Administrator notes that the results indicate that a standard set 
within this range would likely reduce risks to at-risk groups from the 
O3-related health effects considered in the risk assessment, 
and by inference across the much broader array of O3-related 
health effects that can only be considered qualitatively, relative to 
the level of protection afforded by the current standard. This lends 
support to the proposed range.
    The Administrator judges that a standard set within the range of 
0.070 to 0.075 ppm would provide a degree of reduction in risk that is 
important from a public health perspective, and that a standard within 
this range would be requisite to protect public health, including the 
health of at-risk groups, with an adequate margin of safety. EPA's 
evaluation of the body of scientific evidence and quantitative 
estimates of exposures and risks indicates that substantial reductions 
in public health risks would occur throughout this range. Because there 
is no bright line clearly directing the choice of level within this 
reasonable range, the choice of what is appropriate, considering the 
strengths and limitations of the evidence, and the appropriate 
inferences to be drawn from the evidence and the exposure and risk 
assessments, is a public health policy judgment. To further inform this 
judgment, EPA seeks comment on the extent to which the epidemiological 
and clinical evidence provides guidance as to the level of a standard 
that would be requisite to protect public health with

[[Page 37880]]

an adequate margin of safety, especially for at-risk groups.
    In considering the available information, the Administrator also 
judges that a standard level below 0.070 ppm would not be appropriate. 
In reaching this judgment, the Administrator notes that there is only 
quite limited evidence from clinical studies at exposure levels below 
0.080 ppm O3. Moreover, the Administrator recognizes that in 
the body of epidemiological evidence, many studies report positive and 
statistically significant associations, while others report positive 
results that are not statistically significant, and a few do not report 
any positive O3-related associations. In addition, the 
Administrator judges that evidence of a causal relationship between 
adverse health outcomes and O3 exposures becomes 
increasingly uncertain at lower levels of exposure.
    The Administrator also has considered the results of the exposure 
assessments in reaching his judgment that a standard level below 0.070 
ppm would not be appropriate. The Administrator notes that in 
considering the results from the exposure assessment, a standard set at 
the 0.070 ppm level, with the same form as the current standard, is 
estimated to provide substantial reductions in exposures of concern 
(i.e., approximately 90 to 92 percent reductions in the numbers of 
school age children and 94 percent reduction in the total number of 
occurrences) for both all and asthmatic school age children relative to 
just meeting the current standard based on a simulation of a recent 
year with relatively high O3 levels (2002). Thus, a 0.070 
ppm standard would be expected to provide protection from the exposures 
of concern that the Administrator has primarily focused on for over 98 
percent of all and asthmatic school age children even in a year with 
relatively high O3 levels, increasing to over 99.9 percent 
of children in a year with relatively low O3 levels (2004).
    In considering the results of the health risk assessment, as 
discussed in section II.B above, the Administrator notes that there are 
important uncertainties and assumptions inherent in the risk assessment 
and that this assessment is most appropriately used to simulate trends 
and patterns that can be expected as well as providing informed but 
still imprecise estimates of the potential magnitude of risks. The 
Administrator particularly notes that as lower standard levels are 
modeled, including a standard set at a level below 0.070 ppm, the risk 
assessment continues to assume a causal link between O3 
exposures and the occurrence of the health effects examined, such that 
the assessment continues to indicate reductions in O3-
related risks upon meeting a lower standard level. As discussed above, 
however, the Administrator recognizes that evidence of a causal 
relationship between adverse health effects and O3 exposures 
becomes increasingly uncertain at lower levels of exposure. Given all 
of the information available to him at this time, the Administrator 
judges that the increasing uncertainty of the existence and magnitude 
of additional public health protection that standards below 0.070 ppm 
might provide suggests that such lower standard levels would likely be 
below what is necessary to protect public health with an adequate 
margin of safety.
    In addition, the Administrator judges that a standard level higher 
than 0.075 ppm would also not be appropriate. This judgment takes into 
consideration the information discussed above in section II.B, and is 
based on the strong body of clinical evidence in healthy people at 
exposure levels of 0.080 ppm and above, the substantial body of 
clinical and epidemiological evidence indicating that people with 
asthma are likely to experience larger and more serious effects than 
healthy people, the body of epidemiological evidence indicating that 
associations are observed for a wide range of more serious health 
effects at levels below 0.080 ppm, and the estimates of exposure and 
risk remaining upon just meeting a standard set at 0.080 ppm. The much 
greater certainty of the existence and magnitude of additional public 
health protection that such levels would forego provides the basis for 
judging that levels above 0.075 ppm would be higher than what is 
requisite to protect public health, including the health of at-risk 
groups, with an adequate margin of safety.
    For the reasons discussed above, the Administrator proposes to 
revise the level of the primary O3 standard to within the 
range of 0.070 to 0.075 ppm.
    Having reached this decision based on the approach to interpreting 
the evidence described above, the Administrator recognizes that other 
approaches to selecting a standard level have been presented to the 
Agency. As described above, the CASAC has stated in two letters to the 
Administrator (Henderson, 2006c; Henderson, 2007) its unanimous 
recommendation that the current primary O3 NAAQS be revised 
to within the range from 0.060 to 0.070 ppm. The CASAC Panel noted that 
while data exist that adverse health effects may occur at levels lower 
than 0.060 ppm, these data are less certain and that achievable gains 
in protecting human health can be accomplished through lowering the 
O3 NAAQS to a level between 0.060 and 0.070 ppm. In addition 
to the views of CASAC described above, the Agency received the public 
comments described below.
    One group of commenters submitted comments that supported revising 
the level of the primary O3 standard from 0.070 ppm down to 
or even below 0.060 ppm, consistent with or below the range recommended 
by CASAC. In considering the available evidence as a basis for their 
views, these commenters generally noted that the controlled human 
exposure studies, showing statistically significant declines in lung 
function, and increases in respiratory symptoms, airway inflammation 
and airway responsiveness at a 0.080 ppm exposure level, were conducted 
with healthy adults, not members of at-risk groups including people 
with asthma and active children generally. Further, recognizing the 
substantial variability in response between subjects, some of these 
commenters felt that the number of subjects included in these studies 
was too small to ascertain the full range of responses, especially for 
at-risk groups. Such considerations in part were the basis for these 
commenters' view that an O3 standard set at 0.080 ppm is not 
protective of public health and has no margin of safety for at-risk 
groups. In addition, some of these commenters also noted that the World 
Health Organization's guidelines for O3 air quality are in 
the range of 0.061 to 0.051 ppm.
    In considering the results of the human exposure and health risk 
assessment, this group of commenters generally expressed the view that 
these assessments substantially underestimate the public health impacts 
of exposure to O3. For example, several commenters noted 
that the assessments are done for a limited number of cities, they do 
not address risks to important at-risk subpopulations (e.g., outdoor 
workers, active people who spend their summers outdoors, children up to 
5 years of age), and they do not include many health effects that are 
important from a public health perspective (e.g., school absences, 
restricted activity days). Further, some of these commenters expressed 
the view that the primary O3 standard should be set to 
protect the most exposed and most vulnerable groups, and the fact that 
some children are frequently indoors, and thus at lower risk, should 
not weigh against setting a standard to protect those children who are 
active outdoors. To the extent the exposure and risk estimates

[[Page 37881]]

are considered, some of these commenters felt that primary 
consideration should be given to the estimates based on 2002 air 
quality, for which most areas had relatively higher O3 
levels than in 2004, so as to ensure public health protection even in 
years with relatively worse O3 air quality levels. Some 
commenters also felt that the exposure analysis should focus on a 
benchmark concentration for exposures of concern at the 0.060 ppm 
level, the lower end of the range of alternative standards advocated by 
the CASAC Panel.
    In sharp contrast to the views discussed above, other public 
commenters supported retaining the current standard. In considering the 
available evidence as a basis for their views, these commenters 
challenged a number of aspects of the interpretation of the evidence 
presented in the Criteria Document. For example, some of these 
commenters asserted that EPA generally overestimates the magnitude and 
consistency of the results of short-term exposure epidemiological 
studies (e.g., for respiratory symptoms, school absences, hospital 
admissions, mortality), mistakenly links statistical significance and 
consistency with strength of associations, and underestimates the 
uncertainties in interpreting the results of such studies. Further, 
these commenters generally express the view that there is significant 
uncertainty related to the reliability of estimates from time-series 
studies, in that ambient monitors do not provide reliable estimates of 
personal exposures, such that the small reported morbidity and 
mortality risks are unlikely to be attributable to people's exposures 
to O3. Rather, these commenters variously attribute the 
reported risks to the inability of time series studies to account for 
key model specification factors such as smoothing for time-varying 
parameters, meteorological factors, and removal of O3 by 
building ventilation systems, and confounding by co-pollutants. In 
particular, these commenters generally asserted that reported 
associations between short-term O3 exposure and mortality 
are not causal, in that the reported relative risks are too small to 
provide a basis for inferring causality and the associations are most 
likely due to confounding, inappropriately specified statistical 
models, or publication bias.
    In considering the results of the human exposure and health risk 
assessment, this group of commenters generally expressed the view that 
these assessments are based on a number of studies that should not be 
used in quantitative risk assessment. For example, some commenters 
asserted that the results of time-series studies should not be used at 
all in quantitative risk assessments, that risk estimates from single 
city time-series studies should not be used since they are highly 
heterogeneous and influenced by publication bias, and that risk 
estimates from multi-city studies should not be used in estimating risk 
for individual cities. This group of commenters also generally 
expressed the view that the assessments generally overestimate the 
public health impacts of exposure to O3. Noting that the 
risk assessment used a nonlinear exposure-response function to estimate 
decreased lung function risks, some commenters expressed the view that 
a nonlinear approach should also be used to assess other acute 
morbidity effects and mortality. This view was in part based on 
judgments that it is not possible to determine if thresholds exist 
using time-series analyses and that the lack of association of 
O3 to mortality in the winter season is highly supportive of 
the likelihood of the existence of an effect threshold. With regard to 
the risk assessment based on controlled human exposure studies of lung 
function decrements, some commenters expressed the view that the 
assessment should not rely on what they characterized as ``outlier'' 
information to define exposure-response relationships, with reference 
to the data in the Adams (2006) study at the 0.060 and 0.040 ppm 
exposure levels, but rather should focus on group central tendency 
response levels. Further, some commenters expressed the view that the 
air quality rollback algorithm used introduces significant uncertainty, 
especially when applied to areas requiring very large reductions in air 
quality to meet the alternative standards examined, and may result in 
overestimates in benefits from emission reductions. Some commenters 
noted that potential beneficial effects of O3 in shielding 
from UV-B radiation are not quantified in the assessment, and that the 
assessment should discuss the evidence for both adverse and beneficial 
effects with the same objectivity. Finally, some of these commenters 
asserted that since estimates of exposures of concern (which they 
defined as the benchmark concentration of 0.080 ppm) and lung function 
decrements are substantially below the estimates available when the 
current O3 standard was set in 1997, retaining the current 
standard is the most appropriate policy alternative.
    Some commenters also have raised concerns about potential 
uncertainties with regard to estimating policy-relevant background 
O3 levels including: (1) Stratospheric O3 
contributions to the mid- and upper troposphere, which are relatively 
long-lived (1 to 2 months), and are transported downward to the surface 
over time; (2) potential trends in stratospheric O3 levels 
due to changes in stratospheric circulation or to reduction of 
O3 depleting chemicals; (3) O3 levels due to 
lightning strikes in estimating policy-relevant background 
concentrations; and (4) potential uncertainty with regard to policy-
relevant background O3 levels having to do with increases in 
O3 precursors elsewhere in the world. EPA asks for comments 
on these issues and on how they may relate to the estimation and 
consideration of policy-relevant background levels in setting the 
O3 standards.
    Several Governors, State Legislators, and other local officials 
have expressed concerns related to a more stringent standard. These 
officials recognize that State and local governments have important 
roles in developing and implementing policy that improve air quality 
while at the same time achieving economic and quality of life 
objectives. In addition, these officials note that States are just 
beginning to implement current air quality standards and raise concern 
with moving forward on revised standards without first realizing the 
results from the last revision.
    As a related concern, a number of areas--including some of the 
cities involved in the risk assessment--will have difficulty in 
complying with the current 8-hour standard within the next decade. As a 
result, the full public health gains in these areas from a more 
stringent 8-hour standard are unlikely to be realized for a number of 
years. In light of the fact that these public health gains may not 
fully materialize within the attainment date structure set forth in the 
Clean Air Act, some commenters question whether the Agency can or 
should consider these projected gains as a health based criterion for 
its decisionmaking. EPA requests comment on this view.
    The Administrator is mindful that the country has important goals 
related to the increased production and use of renewable energy, and 
that these new energy sources can have important public health, 
environmental and other benefits, such as national security benefits. 
In some contexts and situations, however, the use of renewable fuels 
may impact compliance with a lowered ozone NAAQS standard. For example, 
the Agency recently promulgated final regulations pursuant to section 
211(o) of the Clean Air Act,

[[Page 37882]]

which was enacted as part of the Energy Policy Act of 2005. This 
provision requires the use of 7.5 billion gallons of renewable fuel by 
2012, a level which will be greatly exceeded in practice. In the 
Regulatory Impact Analysis which accompanied the renewable fuel 
regulations, the Agency recognized the impact of this program on 
emissions related to ozone, toxics and greenhouse gases and otherwise 
reviewed the impacts on energy security. The Administrator requests 
comment on such factors and any relationship to this rulemaking, 
including the extent of EPA's discretion under the Clean Air Act to 
take such factors into account (see section I.A).
    In general, these commenters' concerns are consistent with the view 
that adopting a more stringent 8-hour standard now, without a better 
understanding of the health effects associated with O3 
exposure at lower levels, would have an uncertain public health 
benefit. The Administrator recognizes that commenters have raised 
numerous concerns regarding various types of uncertainties in the 
available information, including for example uncertainties in (1) The 
assessment of exposures, (2) the estimation of concentration-response 
associations in the epidemiological studies, (3) the potential role of 
co-pollutants in interpreting the reported associations in 
epidemiological studies, and (4) the estimation of background 
concentrations. The Administrator has heard these concerns from 
Governors and other commenters and invites comment on whether it would 
be appropriate to retain the existing standard and delay considering 
modification of the 8-hour standard until the next NAAQS review, when a 
more complete body of information is expected to be available.
    Consistent with the goal of soliciting comment on a wide array of 
views, the Administrator also solicits comments on these alternative 
approaches and views, and on related standard levels, including levels 
down to 0.060 ppm and up to retaining the level of the current 8-hour 
standard (i.e., effectively 0.084 ppm with the current rounding 
convention). The Administrator recognizes that these sharply divergent 
views on the appropriate level of the standard are based on very 
different interpretations of the science itself, including its relative 
strengths and limitations, very different judgments as to how such 
scientific evidence should be used in making policy decisions on 
proposed standards, and very different public health policy judgments.

E. Proposed Decision on the Primary Standard

    For the reasons discussed above, and taking into account 
information and assessments presented in the Criteria Document and 
Staff Paper, the advice and recommendations of CASAC, and the public 
comments to date, the Administrator proposes to revise the existing 8-
hour primary O3 standard. Specifically, the Administrator 
proposes to revise: (1) The level of the primary O3 standard 
to within a range from 0.070 to 0.075 ppm and (2) the degree of 
precision to which the level of the standard is specified to the 
thousandth ppm. The proposed 8-hour primary standard, with a level in 
the range of 0.070 to 0.075 ppm, would be met at an ambient air 
monitoring site when the 3-year average of the annual forth-highest 
daily maximum 8-hour average O3 concentration is less than 
or equal to the level of the standard that is promulgated. Data 
handling conventions are specified in the proposed creation of Appendix 
P, as discussed in section V below.
    However, in recognition of alternative views of the science, the 
exposure and risk assessments and the uncertainties inherent in these 
assessments, and the appropriate policy responses based on the 
currently available information, the Administrator also solicits 
comments on whether to proceed instead with: (1) Alternative levels of 
the 8-hour primary O3 standard, within ranges of below 0.070 
ppm down to 0.060 ppm and above 0.075 ppm up to and including retaining 
the current standard; (2) alternative forms of the standard, including 
the 3-year average of the annual third- and fifth-highest daily maximum 
8-hour average O3 concentrations; and (3) retaining the 
degree of precision of the current standard (to the nearest hundredth 
ppm). Based on the comments received and the accompanying rationales, 
the Administrator may adopt other standards within the range of the 
alternative levels and forms identified above in lieu of the standards 
he is proposing today.

III. Communication of Public Health Information

    Information on the public health implications of ambient 
concentrations of criteria pollutants is currently made available 
primarily through EPA's Air Quality Index (AQI) program. The current 
Air Quality Index has been in use since its inception in 1999 (64 FR 
42530). It provides accurate, timely, and easily understandable 
information about daily levels of pollution (40 CFR 58.50). The AQI 
establishes a nationally uniform system of indexing pollution levels 
for O3, carbon monoxide, nitrogen dioxide, particulate 
matter and sulfur dioxide. The AQI converts pollutant concentrations in 
a community's air to a number on a scale from 0 to 500. Reported AQI 
values enable the public to know whether air pollution levels in a 
particular location are characterized as good (0-50), moderate (51-
100), unhealthy for sensitive groups (101-150), unhealthy (151-200), 
very unhealthy (201-300), or hazardous (300-500). The AQI index value 
of 100 typically corresponds to the level of the short-term NAAQS for 
each pollutant. For the current O3 NAAQS, an 8-hour average 
concentration of 0.084 ppm corresponds to an AQI value of 100. An AQI 
value greater than 100 means that a pollutant is in one of the 
unhealthy categories (i.e., unhealthy for sensitive groups, unhealthy, 
very unhealthy, or hazardous) on a given day; an AQI value at or below 
100 means that a pollutant concentration is in one of the satisfactory 
categories (i.e., moderate or good). Decisions about the pollutant 
concentrations at which to set the various AQI breakpoints, that 
delineate the various AQI categories, draw directly from the underlying 
health information that supports the NAAQS review.
    The Agency recognizes the importance of revising the AQI in a 
timely manner to be consistent with any revisions to the NAAQS. 
Therefore EPA proposes to finalize conforming changes to the AQI, in 
connection with the Agency's final decision on the O3 NAAQS 
if revisions to the primary standard are promulgated. These conforming 
changes would include setting the 100 level of the AQI at the same 
level as the revised primary O3 NAAQS, and also making 
proportional adjustments to AQI breakpoints at the lower end of the 
range (i.e., AQI values of 50, 150 and 200). EPA does not propose to 
change breakpoints at the higher end of the range (from 300 to 500), 
which would apply to state contingency plans or the Significant Harm 
Level (40 CFR 51.16), because the information from this review does not 
inform decisions about breakpoints at those higher levels.

IV. Rationale for Proposed Decision on the Secondary Standard

    This section presents the rationale for the Administrator's 
proposed decision to revise the existing 0.08 ppm, 8-hour O3 
secondary NAAQS. The Administrator proposes to revise the current 
secondary standard by replacing it with one of two standard options. 
One

[[Page 37883]]

option is to adopt a new cumulative, seasonal concentration-weighted 
form, set at an annual level in the range of 7 to 21 ppm-hours. This 
standard would be expressed as a sum of weighted hourly concentrations, 
cumulated over the 12-hour daylight period (8 a.m. to 8 p.m.) during 
the consecutive 3-month period within the O3 monitoring 
season with the maximum index value. This concentration-weighted form 
is commonly called W126, and is defined as the sum of sigmoidally 
weighted hourly O3 concentrations over a specified period, 
where the daily sigmoidal weighting function is defined as:
[GRAPHIC] [TIFF OMITTED] TP11JY07.001

The other option is to revise the current secondary standard by making 
it identical to the proposed 8-hour primary standard, within the 
proposed range of 0.070 to 0.075 ppm. For this option, EPA also 
solicits comment on a wider range of 8-hour secondary standard levels, 
including down to 0.060 ppm and up to and including retaining the 
current 8-hour secondary standard of 0.08 ppm. The Administrator has 
also considered and solicits comment on an alternative approach to 
setting a cumulative, seasonal standard(s).
    As discussed more fully below, the rationale for these proposed 
options is based on a thorough review of the latest scientific 
information on vegetation effects associated with exposure to ambient 
levels of O3, as assessed in the Criteria Document. This 
rationale also takes into account: (1) Staff assessments of the most 
policy-relevant information in the Criteria Document regarding the 
evidence of adverse effects of O3 to vegetation and 
ecosystems, information on biologically-relevant exposure metrics, and 
staff analyses of air quality, vegetation exposure and risks, presented 
in the Staff Paper and described in greater detail in the associated 
Technical Report on Ozone Exposure, Risk, and Impact Assessments for 
Vegetation (Abt, 2007), upon which staff recommendations for revisions 
to the secondary O3 standard are based; (2) CASAC advice and 
recommendations as reflected in discussion of drafts of the Criteria 
Document and Staff Paper at public meetings, in separate written 
comments, and in CASAC's letters to the Administrator (Henderson, 
2006a, b, c; 2007); (3) public comments received during development of 
these documents either in conjunction with CASAC meetings or 
separately; and (4) consideration of the degree of protection to 
vegetation potentially afforded by the proposed 8-hour primary 
standard.
    In developing this rationale, EPA has again focused on direct 
O3 effects on vegetation, specifically drawing upon an 
integrative synthesis of the entire body of evidence, published through 
early 2006, on the broad array of vegetation effects associated with 
exposure to ambient levels of O3 (EPA, 2006a, chapter 9). In 
addition, because O3 can also indirectly affect other 
ecosystem components such as soils, water, and wildlife, and their 
associated ecosystem goods and services, through its effects on 
vegetation, a qualitative discussion of these other indirect impacts is 
also included, though these effects are not quantifiable at this time. 
As was concluded in the 1997 review, and based on the body of 
scientific literature assessed in the current Criteria Document, the 
Administrator believes that it is reasonable to conclude that a 
secondary standard protecting the public welfare from known or 
anticipated adverse effects to trees, native vegetation and crops would 
also afford increased protection from adverse effects to other 
environmental components relevant to the public welfare, including 
ecosystem services and function. The peer-reviewed literature includes 
studies conducted in the U.S., Canada, Europe, and many other countries 
around the world. In its assessment of the evidence judged to be most 
relevant to making decisions on the level of the O3 
secondary standard, however, EPA has placed greater weight on U.S. 
studies, due to the often species-, site- and climate-specific nature 
of O3-related vegetation response.
    As with virtually any policy-relevant vegetation effects research, 
there is uncertainty in the characterization of vegetation effects 
attributable to exposure to ambient O3. As discussed below, 
however, research conducted since the last review provides important 
information coming from field-based exposure studies, including free 
air, gradient and biomonitoring surveys, in addition to the more 
traditional controlled open top chamber (OTC) studies. Moreover, the 
newly available studies evaluated in the Criteria Document have 
undergone intensive scrutiny through multiple layers of peer review and 
many opportunities for public review and comment. While important 
uncertainties remain, the review of the vegetation effects information 
has been extensive and deliberate. In the judgment of the 
Administrator, the intensive evaluation of the scientific evidence that 
has occurred in this review has provided an adequate basis for 
regulatory decision-making at this time. This review also provides 
important input to EPA's research plan for improving our future 
understanding of the effects of ambient O3 at lower levels.

A. Vegetation Effects Information

    This section outlines key information contained in the Criteria 
Document (chapter 9) and in the Staff Paper (chapter 7) on known or 
potential effects on public welfare which may be expected from the 
presence of O3 in ambient air. The information highlighted 
here summarizes: (1) New information available on potential mechanisms 
for vegetation effects associated with exposure to O3; (2) 
the nature of effects on vegetation that have been associated with 
exposure to O3 and consequent potential impacts on 
ecosystems; and (3) considerations in characterizing what constitutes 
an adverse welfare impact of O3.
    Exposures to O3 have been associated quantitatively and 
qualitatively with a wide range of vegetation effects. The decision in 
the last review to set a more protective secondary standard primarily 
reflected consideration of the quantitative information on vegetation 
effects available at that time, particularly growth impairment (e.g., 
biomass loss) in sensitive forest tree species during the seedling 
growth stage and yield loss in important commercial crops. This 
information, derived mainly using the OTC exposure method, found 
cumulative, seasonal O3 exposures were most strongly 
associated with observed vegetation response. The Criteria Document 
prepared for this review discusses a number of additional studies that 
support and strengthen key conclusions regarding O3 effects 
on vegetation and ecosystems found in the previous Criteria Document 
(EPA, 1996a, 2006a), including further clarification of the underlying 
mechanistic and physiological processes at the subcellular, cellular, 
and whole

[[Page 37884]]

system levels within the plant. More importantly, however, in the 
context of this review, new quantitative information is now available 
across a broader array of vegetation effects (e.g., growth impairment 
during seedlings, saplings and mature tree growth stages, visible 
foliar injury, and yield loss in annual crops) and across a more 
diverse set of exposure methods, including chamber, free air, gradient, 
model, and field-based observation. These non-chambered, field-based 
study results begin to address one of the key data gaps cited by the 
Administrator in the last review.
    The following discussion of the policy-relevant science regarding 
vegetation effects associated with cumulative, seasonal exposures to 
ambient levels of O3 integrates information from the 
Criteria Document (chapter 9) and the Staff Paper (chapter 7).
1. Mechanisms Governing Plant Response to Ozone
    The interpretation of predictions of risk associated with 
vegetation response at ambient O3 exposure levels can be 
informed by scientific understanding regarding O3 impacts at 
the genetic, physiological, and mechanistic levels. In most cases, the 
mechanisms of response are similar regardless of the degree of 
sensitivity of the species. The evidence assessed in the 2006 Criteria 
Document (EPA, 2006a) regarding the O3-induced changes in 
physiology continues to support the information discussed in the last 
review (EPA, 1996a, 2006a). In addition, during the last decade 
understanding of the cellular processes within plants has been further 
clarified and enhanced. Therefore, this section reviews the key 
scientific conclusions identified in 1996 Criteria Document (EPA, 
1996a), and incorporates new information from the current Criteria 
Document (EPA, 2006a). This section describes: (1) Plant uptake of 
O3, (2) O3-induced cellular to systemic response, 
(3) plant compensation and detoxification mechanisms, (4) 
O3-induced changes to plant metabolism, and (5) plant 
response to chronic O3 exposures.
a. Plant Uptake of Ozone
    To cause injury, O3 must first enter the plant through 
openings in the leaves called stomata. Leaves exist in a three 
dimensional environment called the plant canopy, where each leaf has a 
unique orientation and receives a different exposure to ambient air, 
microclimatological conditions, and sunlight. In addition, a plant may 
be located within a stand of other plants which further modifies 
ambient air exchange with individual leaves. Not all O3 
entering a plant canopy is absorbed into the leaf stomata, but may be 
adsorbed to other surfaces e.g., leaf cuticles, stems, and soil (termed 
non-stomatal deposition) or scavenged by reactions with intra-canopy 
biogenic VOCs and naturally occurring NOX emissions from 
soils. Because O3 does not penetrate the leaf's cuticle, it 
must reach the stomatal openings in the leaf for absorption to occur. 
The movement of O3 and other gases such as CO2 
into and out of leaves is controlled by stomatal guard cells that 
regulate the size of the stomatal apertures. These guard cells respond 
to a variety of internal species-specific factors as well as external 
site specific environmental factors such as light, temperature, 
humidity, CO2 concentration, soil fertility and water 
status, and in some cases the presence of air pollutants, including 
O3. These modifying factors produce stomatal conductance 
that vary between leaves of the same plant, individuals and genotypes 
within a species and diurnally and seasonally.
b. Cellular to Systemic Response
    Once inside the leaf, O3 can react with a variety of 
biochemical compounds that are exposed to the air spaces within the 
leaf or it can be dissolved into the water lining the cell wall of the 
air spaces. Having entered the aqueous phase, O3 can be 
rapidly altered to form oxidative products that can diffuse more 
readily into and through the cell and react with many biochemical 
compounds. An early step in a series of O3-induced events 
that leads to leaf injury seems to involve alteration in cell membrane 
function, including membrane transport properties (EPA, 2006a). One 
such signaling molecule is hydrogen peroxide 
(H2O2). The presence of higher-than-normal levels 
of H2O2 within the leaf is a potential trigger 
for a set of metabolic reactions that include those typical of the well 
documented ``wounding'' response or pathogen defense pathway generated 
by cutting of the leaf or by pathogen/insect attack. Ethylene is 
another compound produced when plants are subjected to biotic or 
abiotic stressors. Increased ethylene production by plants exposed to 
O3 stress was identified as a consistent marker for 
O3 exposure in studies conducted decades ago (Tingey et al., 
1976).
c. Compensation and Detoxification
    Ozone injury will not occur if (1) the rate and amount of 
O3 uptake is small enough for the plant to detoxify or 
metabolize O3 or its metabolites or (2) the plant is able to 
repair or compensate for the O3 impacts (Tingey and Taylor, 
1982; U.S. EPA, 1996a). A few studies have documented direct stomatal 
closure or restriction in the presence of O3 in some 
species. This response may be initiated ranging from within minutes to 
hours or days of exposure (Moldau et al., 1990; Dann and Pell, 1989; 
Weber et al., 1993). However, exclusion of O3 simultaneously 
restricts the uptake of CO2, which also limits 
photosynthesis and growth. In addition, antioxidants present in plants 
can effectively protect tissue against damage from low levels of 
oxidants by dissipating excess oxidizing power. Since 1996, the role of 
detoxification in providing a level of resistance to O3 has 
been further investigated. A number of antioxidants have been found in 
plants. However, the pattern of changes in the amounts of these 
antioxidants varies greatly among different species and conditions. 
Most recent reports indicate that ascorbate within the cell wall 
provides the first significant opportunity for detoxification to occur. 
In spite of the new research, however, it is still not clear as to what 
extent detoxification protects against O3 injury. 
Specifically, data are needed on potential rates of antioxidant 
production, subcellular location(s) of antioxidants, and whether 
generation of these antioxidants in response to O3-induced 
stress potentially diverts resources and energy away from other vital 
uses. Thus, the Criteria Document concludes that scientific 
understanding of the detoxification mechanisms is not yet complete and 
requires further investigation (EPA, 2006a).
    Once O3 injury has occurred in leaf tissue, some plants 
are able to repair or compensate for the impacts. In general, plants 
have a variety of compensatory mechanisms for low levels of stress 
including reallocation of resources, changes in root/shoot ratio, 
production of new tissue, and/or biochemical shifts, such as increased 
photosynthetic capacity in new foliage and changes in respiration 
rates, indicating possible repair or replacement of damaged membranes 
or enzymes. Since these mechanisms are genetically determined, not all 
plants have the same complement or degree of tolerance, nor are all 
stages of a plant's development equally sensitive to O3. At 
higher levels or over longer periods of O3 stress, some of 
these compensatory mechanisms, such as a reallocation of resources away 
from storage in the roots in favor of leaves or shoots, could occur at 
a cost to the overall health of the plant. However, it is not yet clear 
to what

[[Page 37885]]

degree or how the use of plant resources for repair or compensatory 
processes affects the overall carbohydrate budget or subsequent plant 
response to O3 or other stresses (EPA, 1996a, EPA, 2006a).
d. Changes to Plant Metabolism
    Ozone inhibits photosynthesis, the process by which plants produce 
energy rich compounds (e.g., carbohydrates) in the leaves. This 
impairment can result from direct impact to chloroplast function and/or 
O3-induced stomatal closure resulting in reduced uptake of 
CO2. A large body of literature published since 1996 has 
further elucidated the mechanism of the effect of O3 within 
the chloroplast. Pell et al. (1997) showed that O3 exposure 
results in a loss of the central carboxylating enzyme that plays an 
important role in the production of carbohydrates. Due to its central 
importance, any decrease in this enzyme may have severe consequences 
for the plant's productivity. Several recent studies have found that 
O3 has a greater effect as leaves age, with the greatest 
impact of O3 occurring on the oldest leaves (Fiscus et al., 
1997; Reid and Fiscus, 1998; Noormets et al., 2001; Morgan et al., 
2004). The loss of this key enzyme as a function of increasing 
O3 exposure is also linked to an early senescence or a 
speeding up of normal development leading to senescence. If total plant 
photosynthesis is sufficiently reduced, the plant will respond by 
reallocating the remaining carbohydrate at the level of the whole 
organism (EPA, 1996a, 2006a). This reallocation of carbohydrate away 
from the roots into above ground vegetative components can have serious 
implications for perennial species.
e. Plant Response to Chronic Ozone Exposures
    Though many changes that occur with O3 exposure can be 
observed within hours, or perhaps days, of the exposure, including 
those connected with wounding, other effects take longer to occur and 
tend to become most obvious after chronic exposures to low 
O3 concentrations. These chronic exposures have been linked 
to senescence or some other physiological response very closely linked 
to senescence. In perennial plant species, a reduction in carbohydrate 
storage in one year may result in the limitation of growth the 
following year (Andersen et al., 1997). Such ``carry-over'' effects 
have been documented in the growth of tree seedlings (Hogsett et al., 
1989; Sasek et al., 1991; Temple et al., 1993; EPA, 1996a) and in roots 
(Andersen et al., 1991; EPA, 1996a). Though it is not fully understood 
how chronic O3 affects long-term growth and resistance to 
other biotic and abiotic insults in long-lived trees, accumulation of 
these carry-over effects over time could affect survival and 
reproduction.
2. Nature of Effects
    Ozone injury at the cellular level, when it has accumulated 
sufficiently, will be propagated to the level of the whole leaf or 
plant. These larger scale effects can include: Reduced carbohydrate 
production and/or reallocation; reduced growth and/or reproduction; 
visible foliar injury and/or premature senescence; and reduced plant 
vigor. Much of what is now known about these O3-related 
effects, as summarized below, is based on research that was available 
in the last review. Recent studies continue to support and expand this 
knowledge (EPA, 2006a).
a. Carbohydrate Production and Allocation
    When total plant photosynthesis is sufficiently reduced, the plant 
will respond by reallocating the remaining carbohydrate at the level of 
the whole organism. Many studies have demonstrated that root growth is 
more sensitive to O3 exposure than stem or leaf growth (EPA, 
2006a). When fewer carbohydrates are present in the roots, less energy 
will be available for root-related functions such as acquisition of 
water and nutrients. In addition, by inhibiting photosynthesis and the 
amount of carbohydrates available for transfer to the roots 
O3 can disrupt the association between soil fungi and host 
plants. Fungi in the soil form a symbiotic relationship with many 
terrestrial plants. For host plants, these fungi improve the uptake of 
nutrients, protect the roots against pathogens, produce plant growth 
hormones, and may transport carbohydrates from one plant to another 
(EPA, 1996a). These below-ground effects have recently been documented 
in the field (Grulke et al., 1998; Grulke and Balduman, 1999). Data 
from a long-studied pollution gradient in the San Bernardino Mountains 
of southern California suggest that O3 substantially reduces 
root growth in natural stands of Ponderosa pine (Pinus ponderosa). Root 
growth in mature trees was decreased at least 87 percent in a high-
pollution site as compared to a low-pollution site (Grulke et al., 
1998), and a similar pattern was found in a separate study with whole-
tree harvest along this gradient (Grulke and Balduman, 1999). Though 
effects on other ecosystem components were not examined, a reduction of 
root growth of this magnitude could have significant implications for 
the below-ground communities at those sites. Because effects on leaf 
and needle carbohydrate content under O3 stress can range 
from a reduction (Barnes et al., 1990; Miller et al., 1989), to no 
effect (Alscher et al., 1989), to an increase (Luethy-Krause and 
Landolt, 1990), studies that examine only above-ground vegetative 
components may miss important O3-induced changes below 
ground. These below-ground changes could signal a shift in nutrient 
cycling with significance at the ecosystem level (Young and Sanzone, 
2002).
b. Growth Effects on Trees
    Studies comparing the O3-related growth response of 
different vegetation types (coniferous and deciduous) and growth stages 
(e.g., seedling and mature) have established that on average, 
individual coniferous trees are less sensitive than deciduous trees, 
and deciduous trees are generally less sensitive to O3 than 
most annual plants, with the exception of a few fast growing deciduous 
tree species (e.g., quaking aspen, black cherry, and cottonwood), which 
are highly sensitive and, in some cases, as much or more sensitive to 
O3 than sensitive annual plants. In addition, studies have 
shown that the relationship between O3 sensitivity in 
seedling and mature growth stages of trees can vary widely, with 
seedling growth being more sensitive to O3 exposures in some 
species, while in others, the mature growth stage is the more 
O3 sensitive. In general, mature deciduous trees are likely 
to be more sensitive to O3 than deciduous seedlings, and 
mature evergreen trees are likely to be less sensitive to O3 
than their seedling counterparts. Based on these results, stomatal 
conductance, O3 uptake, and O3 effects cannot be 
assumed to be equivalent in seedlings and mature trees.
    In the last review (EPA, 1996b), analyses of the effects of 
O3 on trees were limited to 11 tree species for which 
concentration-response (C-R) functions for the seedling growth stage 
had been developed from OTC studies conducted by the National Health 
and Environmental Effects Research Lab, Western Ecology Division 
(NHEERL-WED). A number of replicate studies were conducted on these 
species, leading to a total of 49 experimental cases. The Staff Paper 
presented a graph of the composite regression equation that combines 
the results of the C-R functions developed for each of the 49 cases. 
The NHEERL-WED study predicted relative yield loss at various exposure 
levels in terms of a 12-hour W126. For example, 50 percent of the

[[Page 37886]]

tree seedling cases would be protected from greater than 10 percent 
biomass loss at a 3-month, 12-hour W126 of approximately 24 ppm-hrs, 
while 75 percent of cases would be protected from 10 percent biomass 
loss at a 3-month, 12-hour W126 level of approximately 16 ppm-hrs.
    Since the 1996 review, only a few studies have developed C-R 
functions for additional tree seedling species (EPA, 2006a). One such 
study is of particular importance in that it documented growth effects 
from O3 exposure in the field without the use of chambers or 
other fumigation methods that were as great as those seen in OTC 
studies (Gregg et al., 2003). This study placed Eastern cottonwood 
(Populus deltoides) saplings at sites along a continuum of ambient 
O3 exposures that gradually increased from urban to rural 
areas in the New York City area (Gregg et al., 2003). Eastern 
cottonwood was selected because it is fast growing, O3 
sensitive and important ecologically, along stream banks, and 
commercially for pulpwood, furniture manufacturing, and as a possible 
new source for energy biomass (Burns and Hankola, 1990). Gregg et al. 
(2003) found that the cottonwood saplings grown in New York City grew 
faster than saplings grown in downwind rural areas. Because these 
saplings were grown in pots with carefully controlled soil nutrient and 
moisture levels, the authors were able to control for most of the 
differences between sites. After carefully considering these and other 
factors, the authors concluded the primary explanation for the 
difference in growth was the gradient of cumulative O3 
exposures that increased as one moved downwind from urban to less urban 
and more rural sites. It was determined that the lower O3 
exposure within the city center was due to NOX titration 
reactions which removed O3 from the ambient air. The authors 
were able to reproduce the growth responses observed in the field in a 
companion OTC experiment, confirming O3 as the stressor 
inducing the growth loss response (Gregg et al., 2003).
    Another recent set of studies employed a modified Free Air 
CO2 Enrichment (FACE) methodology to expose vegetation to 
elevated O3 without the use of chambers. This exposure 
method was originally developed to expose vegetation to elevated levels 
of CO2, but has been modified to include O3 
exposure in Illinois (SoyFACE) and Wisconsin (AspenFACE) for soybean 
and deciduous trees, respectively (Dickson et al., 2000; Morgan et al., 
2004). The FACE method releases gas (e.g., CO2, 
O3) from a series of orifices placed along the length of the 
vertical pipes surrounding a circular field plot and uses the 
prevailing wind to distribute it. This exposure method has many 
characteristics that differ from those associated with the OTC.
    Most significantly, this exposure method more closely replicates 
conditions in the field than did OTCs. This is because, except for 
O3 levels which are varied across co-located plots, plants 
are exposed to the same ambient growing conditions that occur naturally 
in the field (e.g., location-specific pollutant mixtures; climate 
conditions such as light, temperature and precipitation; insect pests, 
pathogens). By using one of several co-located plots as a control 
(e.g., receives no additional O3), and by exposing the other 
rings to differing levels of elevated O3, the growth 
response signal that is due solely to the change in O3 
exposure can be clearly determined. Furthermore, the FACE system can 
expand vertically with the growth of trees, allowing for exposure 
experiments to span numerous years, an especially useful capability in 
forest research.
    On the other hand, the FACE methodology also has the undesirable 
characteristic of potentially creating hotspots near O3 gas 
release orifices or gradients of exposure in the outer ring of trees 
within the plots, such that averaging results across the entire ring 
potentially overestimates the response. In recognition of this 
possibility, researchers at the AspenFACE experimental site only 
measured trees in the center core of each ring, (e.g., at least 5-6 
meters away from the emission sites of O3) (Dickson et al., 
2000; Karnosky et al. 2005). By taking this precaution, it is unlikely 
that their measurements were influenced by any potential hotspots or 
gradients of exposure within the FACE rings. Taking all of the above 
into account, results from the Wisconsin FACE site on quaking aspen 
appear to demonstrate that the detrimental effects of O3 
exposure seen on tree growth and symptom expression in OTCs can be 
observed in the field using this exposure method (Karnosky et al., 
1999; 2005).
    The Staff Paper thus concluded that the combined evidence from the 
AspenFACE \56\ and Gregg et al. (2003) field studies provide compelling 
and important support for the appropriateness of continued use of the 
C-R functions derived using OTC from the NHEERL-WED studies to estimate 
risk to these tree seedlings under ambient field exposure conditions. 
These studies make a significant contribution to the coherence in the 
weight of evidence available in this review and provide additional 
evidence that O3-induced effects observed in chambers also 
occur in the field.
---------------------------------------------------------------------------

    \56\ Only a few northern forest types in the U.S. have been well 
studied with respect to O3 exposures using the FACE 
method, though these systems are being used to expose numerous other 
ecosystem types to elevated levels of CO2. Additional 
FACE studies with O3 on other U.S. forest types would 
provide a better understanding of whether these results can be 
extrapolated to other forest types and mature forest stands.
---------------------------------------------------------------------------

    Trees and other perennials, in addition to cumulating the effects 
of O3 exposures over the annual growing season, can also 
cumulate effects across multiple years. It has been reported that 
effects can ``carry over'' from one year to another (EPA, 2006a). 
Growth affected by a reduction in carbohydrate storage in one year may 
result in the limitation of growth in the following year (Andersen, et 
al., 1997). Carry-over effects have been documented in the growth of 
some tree seedlings (Hogsett et al. 1989; Simini et al., 1992; Temple 
et al., 1993) and in roots (Andersen et al., 1991; EPA, 1996a). On the 
basis of past and recent OTC and field study data, ambient 
O3 exposures that occur during the growing season in the 
United States are sufficient to potentially affect the annual growth of 
a number of sensitive seedling tree species. However, because most 
studies do not take into account the possibility of carry over effects 
on growth in subsequent years, the true implication of these annual 
biomass losses may be missed. It is likely that under ambient exposure 
conditions, some sensitive trees and perennial plants could experience 
compounded impacts that result from multiple year exposures.
c. Visible Foliar Injury
    Cellular injury can and often does become visible. Acute injury 
usually appears within 24 hours after exposure to O3 and, 
depending on species, can occur under a range of exposures and 
durations from 0.040 ppm for a period of 4 hours to 0.410 ppm for 0.5 
hours for crops and 0.060 ppm for 4 hours to 0.510 ppm for 1 hour for 
trees and shrubs (Jacobson, 1977). Chronic injury may be mild to 
severe. In some cases, cell death or premature leaf senescence may 
occur. The significance of O3 injury at the leaf and whole 
plant levels depends on how much of the total leaf area of the plant 
has been affected, as well as the plant's age, size, developmental 
stage, and degree of functional redundancy among the existing leaf 
area. As a result, it is not presently possible to determine, with 
consistency across species and environments, what degree of injury at

[[Page 37887]]

the leaf level has significance to the vigor of the whole plant.
    The presence of visible symptoms due to O3 exposures 
can, however, by itself, represent an adverse impact to the public 
welfare. Specifically, it can reduce the market value of certain leafy 
crops (such as spinach, lettuce), impact the aesthetic value of 
ornamentals (such as petunia, geranium, and poinsettia) in urban 
landscapes, and affect the aesthetic value of scenic vistas in 
protected natural areas such as national parks and wilderness areas. 
Many businesses rely on healthy looking vegetation for their 
livelihoods (e.g., horticulturalists, landscapers, Christmas tree 
growers, farmers of leafy crops) and a variety of ornamental species 
have been listed as sensitive to O3 (Abt, 1993). Though not 
quantified, there is likely some level of economic impact to businesses 
and homeowners from O3-related injury on sensitive 
ornamental species due to the cost associated with more frequent 
replacement and/or increased maintenance (fertilizer or pesticide 
application). In addition, because O3 not only results in 
discoloration of leaves but can lead to more rapid senescence (early 
shedding of leaves) there potentially could be some lost tourist 
dollars at sites where fall foliage is less available or attractive.
    The use of sensitive plants as biological indicators to detect 
phytotoxic levels of O3 is a longstanding and effective 
methodology (Chappelka and Samuelson, 1998; Manning and Krupa, 1992). 
Each bioindicator exhibits typical O3 injury symptoms when 
exposed under appropriate conditions. These symptoms are considered 
diagnostic as they have been verified in exposure-response studies 
under experimental conditions. In recent years, field surveys of 
visible foliar injury symptoms have become more common, with greater 
attention to the standardization of methods and the use of reliable 
indicator species (Campbell et al., 2000; Smith et al., 2003). 
Specifically, the United States Forest Service (USFS) through the 
Forest Health Monitoring Program (FHM) (1990-2001) and currently the 
Forest Inventory and Analysis (FIA) Program collects data regarding the 
incidence and severity of visible foliar injury on a variety of 
O3 sensitive plant species throughout the U.S. (Coulston et 
al. 2003, 2004; Smith et al. 2003).
    Since the conclusion of the 1996 NAAQS review, the FIA monitoring 
program network and database has continued to expand. This network 
continues to document foliar injury symptoms in the field under ambient 
exposure conditions. Recent survey results show that O3-
induced foliar injury incidence is widespread across the country. The 
visible foliar injury indicator has been identified as a means to track 
O3 exposure stress trends in the nation's natural plant 
communities as highlighted in EPA's most recent Report on the 
Environment (EPA, 2003a; http://www.epa.gov/indicators/roe).

    Previous Criteria Documents have noted the difficulty in relating 
visible foliar injury symptoms to other vegetation effects such as 
individual tree growth, stand growth, or ecosystem characteristics 
(EPA, 1996a) and this difficulty remains to the present day (EPA, 
2006a). It is important to note that direct links between O3 
induced visible foliar injury symptoms and other adverse effects are 
not always found. Therefore, visible foliar injury cannot serve as a 
reliable surrogate measure for other O3-related vegetation 
effects because other effects (e.g., biomass loss) have been reported 
with and without visible injury. In a few cases, visible foliar 
symptoms have been correlated with decreased vegetative growth 
(Karnosky et al., 1996; Peterson et al., 1987; Somers et al., 1998) and 
with impaired reproductive function (Black et al., 2000; Chappelka, 
2002). Therefore, the lack of visible injury should not be construed to 
indicate a lack of phytotoxic concentrations of O3 nor 
absence of other non-visible O3 effects.
d. Reduced Plant Vigor
    Though O3 levels over most of the U.S. are not high 
enough to kill vegetation directly, current levels have been shown to 
reduce the ability of many sensitive species and genotypes within 
species to adapt to or withstand other environmental stresses. These 
may include increased susceptibility to freezing temperatures, pest 
infestations and/or root disease, and compromised ability to compete 
for available resources. For example, when species with differing 
O3-sensitivities occur together, the resulting decrease in 
growth in O3-sensitive species may lead to an increase in 
growth of more O3-tolerant species, which are now able to 
better compete for available resources. The result of such above 
effects can produce a loss in plant vigor in O3-sensitive 
species that over time may lead to premature plant death.
e. Ecosystems
    Ecosystems are comprised of complex assemblages of organisms and 
the physical environment with which they interact. Each level of 
organization within an ecosystem has functional and structural 
characteristics. At the ecosystem level, functional characteristics 
include, but are not limited to, energy flow; nutrient, hydrologic, and 
biogeochemical cycling; and maintenance of food chains. The sum of the 
functions carried out by ecosystem components provides many benefits to 
humankind, as in the case of forest ecosystems (Smith, 1992). Some of 
these benefits, also termed ``ecosystem goods and services'', include 
food, fiber production, aesthetics, genetic diversity, maintenance of 
water quality, air quality, and climate, and energy exchange. A 
conceptual framework for discussing the effects of O3 on 
ecosystems was developed by the EPA Science Advisory Board (Young and 
Sanzone, 2002). In this report, the authors identify six essential 
ecological attributes (EEAs) include landscape condition, biotic 
condition, chemical/physical condition, ecological processes, 
hydrology/geomorphology, and natural disturbance regime. Each EEA is 
depicted as one of six triangles that together build a hexagon. On the 
outside of each triangle is a list of stressors that can act on the 
EEA. Tropospheric O3 is listed as a stressor of both biotic 
condition and the chemical/physical condition of ecosystems. As each 
EEA is linked to all the others, it is clearly envisioned in this 
framework that O3 could either directly or indirectly impact 
all of the EEAs associated with an ecosystem that is being stressed by 
O3.
    Vegetation often plays an influential role in defining the 
structure and function of an ecosystem, as evidenced by the use of 
dominant vegetation forms to classify many types of natural ecosystems, 
e.g., tundra, wetland, deciduous forest, and conifer forest. Plants 
simultaneously inhabit both above- and below-ground environments, 
integrating and influencing key ecosystem cycles of energy, water, and 
nutrients. When a sufficient number of individual plants within a 
community have been affected, O3-related effects can be 
propagated up to ecosystem-level effects. Thus, through its impact on 
vegetation, O3 can be an important ecosystem stressor.
i. Potential Ozone Alteration of Ecosystem Structure and Function
    The Criteria Document (EPA, 2006a) outlines seven case studies 
where O3 effects on ecosystems have either been documented 
or are suspected. The oldest and clearest example involves the San 
Bernardino Mountain forest ecosystem in California. This system 
experienced chronic high O3 exposures over a period of 50 or 
more years. The

[[Page 37888]]

O3-sensitive and co-dominant species of ponderosa and 
Jeffrey pine demonstrated severe levels of foliar injury, premature 
senescence, and needle fall that decreased the photosynthetic capacity 
of stressed pines and reduced the production of carbohydrates resulting 
in a decrease in radial growth and in the height of stressed trees. It 
was also observed that ponderosa and Jeffrey pines with slight to 
severe crown injury lost basal area in relation to competing species 
that are more tolerant to O3. Due to a loss of vigor, these 
trees eventually succumbed to the bark beetle, leading to elevated 
levels of tree death. Increased mortality of susceptible trees shifted 
the community composition towards white fir and incense cedar, 
effectively reversing the development of the normal fire climax mixture 
dominated by ponderosa and Jeffrey pines, and leading to increased fire 
susceptibility. At the same time, numerous other organisms and 
processes were also affected either directly or indirectly, including 
successional patterns of fungal microflora and their relationship to 
the decomposer community. Nutrient availability was influenced by the 
heavy litter and thick needle layer under stands with the most severe 
needle injury and defoliation. The composition of lichens was 
significantly reduced. In this example, O3 appeared to be a 
predisposing factor that led to increased drought stress, windthrow, 
root diseases, and insect infestation (Takemoto et al., 2001). Thus, 
through its effects on tree water balance, cold hardiness, tolerance to 
wind, and susceptibility to insect and disease pests, O3 
potentially impacted the ecosystem-related EEA of natural disturbance 
regime (e.g., fire, erosion). Although the role of O3 was 
extremely difficult to separate from other confounding factors, such as 
high nitrogen deposition, there is evidence that this shift in species 
composition has altered the structure and dynamics of associated food 
webs (Pronos et al., 1999) and carbon (C) and nitrogen (N) cycling 
(Arbaugh et al., 2003). Ongoing and new research in this important 
ecosystem is needed to reveal the extent to which ecosystem services 
have been affected and to what extent strong causal linkages between 
historic and/or current ambient O3 exposures and observed 
ecosystem-level effects can be made.
    Ozone has also been reported to be a selective pressure among 
sensitive tree species (e.g., eastern white pine) in the east. The 
nature of community dynamics in eastern forests is different, however, 
than in the west, consisting of a wider diversity of species and uneven 
aged stands, and the O3 levels are less severe. Therefore, 
lower level chronic O3 stress in the east is more likely to 
produce subtle long-term forest responses such as shifts in species 
composition, rather than wide-spread community degradation.
    One of the best-documented studies of population and community 
response to O3 effects are the long-term studies of common 
plantain (Plantago major) in native plant communities in the United 
Kingdom (Davison and Reiling, 1995; Lyons et al., 1997; Reiling and 
Davison, 1992c). Elevated O3 significantly decreased the 
growth of sensitive populations of common plantain (Pearson et al., 
1996; Reiling and Davison, 1992a, b; Whitfield et al., 1997) and 
reduced its fitness as determined by decreased reproductive success 
(Pearson et al., 1996; Reiling and Davison, 1992a). While spatial 
comparisons of population responses to O3 are complicated by 
other environmental factors, rapid changes in O3 resistance 
were imposed by ambient levels and variations in O3 exposure 
(Davison and Reiling, 1995). Specifically, in this case study, it 
appeared that O3-sensitive individuals are being removed by 
O3 stress and the genetic variation represented in the 
population could be declining. If genetic diversity and variation is 
lost in ecosystems, there may be increased vulnerability of the system 
to other biotic and abiotic stressors, and ultimately a change in the 
EEAs and associated services provided by those ecosystems.
    Recent free-air exposure experiments have also provided new insight 
into how O3 may be altering ecosystem structure and function 
(Karnosky et al., 2005). For example, a field O3 exposure 
experiment at the AspenFACE site in Wisconsin (described in section 
IV.A.2.b. above) was designed to examine the effects of both elevated 
CO2 and O3 on mixed stands of aspen (Populus 
tremuloides), birch (Betula papyrifera), and sugar maple (Acer 
saccharum) that are characteristic of Great Lakes aspen-dominated 
forests (Karnosky et al., 2003; Karnosky et al., 1999). They found 
evidence that the effects on above- and below-ground growth and 
physiological processes have cascaded through the ecosystem, even 
affecting microbial communities (Larson et al., 2002; Phillips et al., 
2002). This study also confirmed earlier observations of O3-
induced changes in trophic interactions involving keystone tree 
species, as well as important insect pests and their natural enemies 
(Awmack et al., 2004; Holton et al., 2003; Percy et al., 2002).
    Collectively these examples suggest that O3 is an 
important stressor in natural ecosystems, but it is difficult to 
quantify the contribution of O3 due to the combination of 
other stresses present in ecosystems. In most cases, because only a few 
components in each of these ecosystems have been examined and 
characterized for O3 effects, the full extent of ecosystem 
changes in these example ecosystems is not fully understood. Clearly, 
there is a need for highly integrated ecosystem studies that 
specifically investigate the effect of O3 on ecosystem 
structure and function in order to fully determine the extent to which 
O3 is altering ecosystem services. Continued research, 
employing new approaches, will be necessary to fully understand the 
extent to which O3 is affecting ecosystem services.
ii. Effects on Ecosystem Services and Carbon Sequestration
    Since it has been established that O3 affects 
photosynthesis and growth of plants, O3 is most likely 
affecting the productivity of forest ecosystems. Therefore, it is 
desirable to link effects on growth and productivity to essential 
ecosystem services. However, it is very difficult to quantify 
ecosystem-level productivity losses because of the amount of complexity 
in scaling from the leaf-level or individual plant to the ecosystem 
level, and because not all organisms in an ecosystem are equally 
affected by O3.
    Terrestrial ecosystems are important in the Earth's carbon (C) 
balance and could help offset emissions of CO2 by humans if 
anthropogenic C is sequestered in vegetation and soils. The annual 
increase in atmospheric CO2 is less than the total inputs 
from fossil fuel burning and land use changes (Prentice et al., 2001) 
and much of this discrepancy is thought to be attributable to 
CO2 uptake by plant photosynthesis (Tans & White, 1998). 
Temperate forests of the northern hemisphere have been estimated to be 
a net sink of C per year (Goodale et al. 2002). Ozone interferes with 
photosynthesis, causes some plants to senesce leaves prematurely and in 
some cases, reduces allocation to stem and root tissue. Thus, 
O3 decreases the potential for C sequestration. For the 
purposes of this discussion, C sequestration is defined as the net 
exchange of carbon by the terrestrial biosphere. However, long-term 
storage in the soil organic matter is considered to be the most stable 
form of C storage in ecosystems.
    In a study including all ecosystem types, Felzer et al. (2004), 
estimated that

[[Page 37889]]

U.S. net primary production (net flux of C into an ecosystem) was 
decreased by 2.6-6.8 percent due to O3 pollution in the late 
1980's to early 1990's. Ozone not only reduces C sequestration in 
existing forests, it can also affect reforestation projects (Beedlow et 
al. 2004). This effect, in turn, has been found to ultimately inhibit C 
sequestration in forest soils which act as long-term C storage (Loya et 
al., 2003; Beedlow et al. 2004). The interaction of rising 
O3 pollution and rising CO2 concentrations in the 
coming decades complicates predictions of future sequestration 
potential. Models generally predict that, in the future, C 
sequestration will increase with increasing CO2, but often 
do not account for the decrease in productivity due to the local 
effects of tropospheric O3. In the presence of high 
O3 levels, the stimulatory effect of rising CO2 
concentrations on forest productivity has been estimated to be reduced 
by more that 20 percent (Tingey et al., 2001; Ollinger et al. 2002; 
Karnosky et al., 2003).
    In summary, it would be anticipated that meeting lower 
O3 standards would increase the amount of CO2 
uptake by many ecosystems in the U.S. However, the amount of this 
improvement would be heavily dependent on the species composition of 
those ecosystems. Many ecosystems in the U.S. do have O3 
sensitive plants. For, example forest ecosystems with dominant species 
such as aspen or ponderosa pine would be expected to increase 
CO2 uptake more with lower O3 than forests with 
more O3 tolerant species.
    A recent critique of the secondary NAAQS review process published 
in the report by the National Academy of Sciences on Air Quality 
Management in the United States (NRC, 2004) stated that ``EPA's current 
practice for setting secondary standards for most criteria pollutants 
does not appear to be sufficiently protective of sensitive crops and 
ecosystems * * *.'' This report made several specific recommendations 
for improving the secondary NAAQS process and concluded that ``There is 
growing evidence that tighter standards to protect sensitive ecosystems 
in the United States are needed * * *.'' An effort has been recently 
initiated within the Agency to identify indicators of ecological 
condition whose responses can be clearly linked to changes in air 
quality that are attributable to Agency environmental programs. Using a 
single indicator to represent the complex linkages and dynamic cycles 
that define ecosystem condition will always have limitations. With 
respect to O3-related impacts on ecosystem condition, only 
two candidate indicators, foliar injury (as described above) and radial 
growth in trees, have been suggested. Thus, while at the present time, 
most O3-related effects on ecosystems must be inferred from 
observed or predicted O3-related effects on individual 
plants, additional research at the ecosystem level could identify new 
indicators and/or establish stronger causal linkages between 
O3-induced plant effects and ecosystem condition.
f. Yield Reductions in Crops
    Ozone can interfere with carbon gain (photosynthesis) and 
allocation of carbon with or without the presence of visible foliar 
injury. As a result of decreased carbohydrate availability, fewer 
carbohydrates are available for plant growth, reproduction, and/or 
yield. Recent studies have further confirmed and demonstrated 
O3 effects on different stages of plant reproduction, 
including pollen germination, pollen tube growth, fertilization, and 
abortion of reproductive structures, as reviewed by Black et al. 
(2000). For seed-bearing plants, these reproductive effects will 
culminate in reduced seed production or yield.
    As described in the last review and again in the current Criteria 
Document and Staff Paper, the National Crop Loss Assessment Network 
(NCLAN) studies undertaken in the early to mid-1980's provide the 
largest, most uniform database on the effects of O3 on 
agricultural crop yields. The NCLAN protocol was designed to produce 
crop exposure-response data representative of the areas in the U.S. 
where the crops were typically grown. In total, 15 species (e.g., corn, 
soybean, winter wheat, tobacco, sorghum, cotton, barley, peanuts, dry 
beans, potato, lettuce, turnip, and hay [alfalfa, clover, and fescue]), 
accounting for greater than 85 percent of U.S. agricultural acreage 
planted at that time, were studied. Of these 15 species, 13 species 
including 38 different cultivars were combined in 54 cases representing 
unique combinations of cultivars, sites, water regimes, and exposure 
conditions. Crops were grown under typical farm conditions and exposed 
in open-top chambers to ambient O3 and increased 
O3 above ambient (i.e., modified ambient). Robust C-R 
functions were developed for each of these crop species. These results 
showed that 50 percent of the studied cases would be protected from 
greater than 10 percent yield loss at a W126 level of 21 ppm-hour, 
while a W126 of 13 ppm-hour would provide protection for 75 percent of 
the cases studied from greater than 10 percent yield loss.
    Recent studies continue to find yield loss levels in crop species 
studied previously under NCLAN that reflect the earlier findings\57\. 
In other words, there has been no evidence that crops are becoming more 
tolerant of O3 (EPA, 2006a). For cotton, some newer 
varieties have been found to have higher yield loss due to 
O3 compared to older varieties (Olszyk et al., 1993, Grantz 
and McCool, 1992). In a meta-analysis of 53 studies, Morgan et al. 
(2003) found consistent deleterious effects of O3 exposures 
on soybean from studies published between 1973 and 2001. Further, early 
results from the field-based exposure experiment SoyFACE in Illinois 
indicate a lack of any apparent difference in the O3 
tolerance of old and recent cultivars of soybean in a study of 22 
soybean varieties (Long et al., 2002). Thus, the Staff Paper concluded 
that the recent scientific literature continues to support the 
conclusions of the 1996 Criteria Document that ambient O3 
concentrations are reducing the yield of major crops in the U.S.
---------------------------------------------------------------------------

    \57\ Given the usefulness of generating robust C-R functions 
such as have been developed under NCLAN, it would be beneficial to 
employ a similar protocol to update and expand this research to 
include more recent and additional crop species and varieties, such 
as fruit and vegetable species, as well as recent O3 air 
quality.
---------------------------------------------------------------------------

    In addition to the effects described on annual crop species, 
several studies published since the last review have focused on 
perennial forage crops (EPA, 2006a). These recent results confirm that 
O3 is also impacting yields and quality of multiple-year 
forage crops at sufficient magnitude to have nutritional and possibly 
economic implications to their use as ruminant animal feed at 
O3 exposures that occur in some years over large areas of 
the U.S.
3. Adversity of Effects
    The Staff Paper recognized that the statute requires that a 
secondary standard be protective against ``adverse'' O3 
effects, not all identifiable effects. In considering what constitutes 
a vegetation effect that is adverse to the public welfare, the Staff 
Paper recognizes that O3 can cause a variety of vegetation 
effects, beginning at the level of the individual cell and accumulating 
up to the level of whole leaves, plants, plant populations, communities 
and whole ecosystems, not all of which have been classified in past 
reviews as ``adverse'' to public welfare.
    Previous reviews have classified O3 vegetation effects 
as either ``injury'' or ``damage'' to help in determining adversity. 
Specifically, ``injury'' is

[[Page 37890]]

defined as encompassing all plant reactions, including reversible 
changes or changes in plant metabolism (e.g., altered photosynthetic 
rate), altered plant quality, or reduced growth, that does not impair 
the intended use or value of the plant (Guderian, 1977). In contrast, 
``damage'' has been defined to include those injury effects that reach 
sufficient magnitude as to also reduce or impair the intended use or 
value of the plant. Examples of effects that are classified as damage 
include reductions in aesthetic values (e.g., foliar injury in 
ornamental species) as well as losses in terms of weight, number, or 
size of the plant part that is harvested (reduced yield or biomass 
production). Yield loss also may include changes in crop quality, i.e., 
physical appearance, chemical composition, or the ability to withstand 
storage, while biomass loss includes slower growth in species harvested 
for timber or other fiber uses. While this construct has proved useful 
in the past, it appears to be most useful in the context of evaluating 
effects on single plants or species grown in monocultures such as 
agricultural crops or managed forests. It is less clear how it might 
apply to potential effects on natural forests or entire ecosystems when 
O3-induced species level impacts lead to shifts in species 
composition and/or associated ecosystem services such as nutrient 
cycling or hydrologic cycles, where the intended use or value of the 
system has not been specifically identified.
    A more recent construct for assessing risks to forests described in 
Hogsett et al. (1997) suggests that ``adverse effects could be 
classified into one or more of the following categories: (1) Economic 
production, (2) ecological structure, (3) genetic resources, and (4) 
cultural values.'' This approach expands the context for evaluating the 
adversity of O3-related effects beyond the species level. 
Another recent publication, A Framework for Assessing and Reporting on 
Ecological Condition: an SAB report (Young and Sanzone, 2002), provides 
additional support for expanding the consideration of adversity beyond 
the species level by making explicit the linkages between stress-
related effects (e.g., O3 exposure) at the species level and 
at higher levels within an ecosystem hierarchy. Taking this recent 
literature into account, the Staff Paper concludes that a determination 
of what constitutes an ``adverse'' welfare effect in the context of the 
secondary NAAQS review can appropriately occur within this broader 
paradigm.

B. Biologically Relevant Exposure Indices

    The Criteria Document concluded that O3 exposure indices 
that cumulate differentially weighted hourly concentrations are the 
best candidates for relating exposure to plant growth responses (EPA, 
2006a). This conclusion follows from the extensive evaluation of the 
relevant studies in the 1996 Criteria Document (EPA, 1996a) and the 
recent evaluation of studies that have been published since that time 
(EPA, 2006a). The following selections, taken from section 5.5 the 1996 
Criteria Document (EPA, 1996a), further elucidate the depth and 
strength of these conclusions. Specifically, with respect to the 
importance of taking into account exposure duration, the 1996 Criteria 
Document stated, ``when O3 effects are the primary cause of 
variation in plant response, plants from replicate studies of varying 
duration showed greater reductions in yield or growth when exposed for 
the longer duration'' and ``the mean exposure index of unspecified 
duration could not account for the year-to-year variation in response'' 
(EPA, 1996a, pg. 5-96). Further, ``because the mean exposure index 
treats all concentrations equally and does not specifically include an 
exposure duration component, the use of a mean exposure index for 
characterizing plant exposures appears inappropriate for relating 
exposure with vegetation effects'' (EPA, 1996a, pg. 5-88). Regarding 
the relative importance of higher concentrations than lower in 
determining plant response, the 1996 Criteria Document concluded that 
``the ultimate impact of long-term exposures to O3 on crops 
and seedling biomass response depends on the integration of repeated 
peak concentrations during the growth of the plant'' (EPA, 1996a, pg. 
5-104). Further, ``at this time, exposure indices that weight the 
hourly O3 concentrations differentially appear to be the 
best candidates for relating exposure with predicted plant response'' 
(EPA, 1996a, pgs. 5-136).
    At the conclusion of the last review, the biological basis for a 
cumulative, seasonal form was not in dispute. There was general 
agreement between the EPA staff, CASAC, and the Administrator, based on 
their review of the air quality criteria, that a cumulative, seasonal 
form was more biologically based than the then current 1-hour and newly 
proposed 8-hour average form. However, in selecting a specific form 
appropriate for a secondary standard, there was less agreement. An 
evaluation of the performance of several seasonal cumulative forms in 
predicting plant response data taken from OTC experiments had found 
that all performed about equally well and was unable to distinguish 
between them (EPA, 1996a). In selecting between two of these cumulative 
forms, the SUM06 \58\ and W126, in the absence of biological evidence 
to distinguish between them, the Administrator based her decision on 
both science and policy considerations. Specifically, these were: (1) 
All cumulative, peak-weighted exposure indices considered, including 
W126 and SUM06, were about equally good as exposure measures to predict 
exposure-response relationships reported in the NCLAN crop studies; and 
(2) the SUM06 form would not be influenced by PRB O3 
concentrations (defined at the time as 0.03 to 0.05 ppm) under many 
typical air quality distributions. On the basis of these 
considerations, the Administrator chose the SUM06 as the most 
appropriate cumulative, seasonal form to consider when proposing an 
alternative secondary standard form (61 FR 65716).
---------------------------------------------------------------------------

    \58\ SUM06: Sum of all hourly O3 concentrations 
greater or equal to 0.06 ppm over a specified time.
---------------------------------------------------------------------------

    Though the scientific justification for a cumulative, seasonal form 
was generally accepted in the last review, an analysis undertaken by 
EPA at that time had shown that there was considerable overlap between 
areas that would be expected not to meet the range of alternative 8-
hour standards being considered for the primary NAAQS and those 
expected not to meet the range of values (expressed in terms of the 
seasonal SUM06 index) of concern for vegetation. This result suggested 
that improvements in national air quality expected to result from 
attaining an 8-hour primary standard within the recommended range of 
levels would also be expected to significantly reduce levels of concern 
for vegetation in those same areas. Thus, in the notice of proposed 
rulemaking, the Administrator proposed two alternatives for 
consideration: one alternative was to make the secondary standard equal 
in every way to the proposed 8-hour, 0.08 ppm primary standard; and the 
second was to establish a cumulative, seasonal secondary standard in 
terms of a SUM06 form as also appropriate to protect public welfare 
from known or anticipated adverse effects given the available 
scientific knowledge and that such a seasonal standard ``* * * is more 
biologically relevant * * *'' (61 FR 65716).
    In the 1997 final rule, the Administrator decided to make the 
secondary standard identical to the primary standard. She acknowledged,

[[Page 37891]]

however, that ``it remained uncertain as to the extent to which air 
quality improvements designed to reduce 8-hr average O3 
concentrations averaged over a 3-year period would reduce O3 
exposures measured by a seasonal SUM06 index.'' (62 FR 38876) In other 
words, it was uncertain as to whether the 8-hour average form would, in 
practice, provide sufficient protection for vegetation from the 
cumulative, seasonal and concentration-weighted exposures described in 
the scientific literature as of concern.
    On the basis of that history, chapter 7 of the current Staff Paper 
revisited the issue of whether the SUM06 was still the most appropriate 
choice of cumulative, seasonal form for a secondary standard to protect 
the public welfare from known and anticipated adverse vegetation 
effects in light of the new information available in this review. 
Specifically, the Staff Paper considered: (1) The continued lack of 
evidence within the vegetation effects literature of a biological 
threshold for vegetation exposures of concern; and (2) new estimates of 
PRB that are lower than in the last review. The W126 form, also 
evaluated in the last review, was again selected for comparison with 
the SUM06 form. Regarding the first consideration, the Staff Paper 
noted that W126 form, by its incorporation of a continuous sigmoidal 
weighting scheme, does not create an artificially imposed concentration 
threshold, yet also gives proportionally more weight to the higher and 
typically more biologically potent concentrations, as supported by the 
scientific evidence. Second, the index value is not significantly 
influenced by O3 concentrations within the range of 
estimated PRB, as the weights assigned to concentrations in this range 
are very small. Thus, it would also provide a more appropriate target 
for air quality management programs designed to reduce emissions from 
anthropogenic sources contributing to O3 formation. On the 
basis of these considerations, the Staff Paper concludes that the W126 
form is the most biologically-relevant cumulative, seasonal form 
appropriate to consider in the context of the secondary standard 
review.

C. Vegetation Exposure and Impact Assessment

    The vegetation exposure and impact assessment conducted for the 
current review and described in the Staff paper, consisted of exposure, 
risk and benefits analyses and improves and builds upon similar 
analyses performed in the last review (EPA 1996b). The vegetation 
exposure assessment was performed using interpolation and included 
information from ambient monitoring networks and results from air 
quality modeling. The vegetation risk assessment included both tree and 
crop analyses. The tree risk analysis includes three distinct lines of 
evidence: (1) Observations of visible foliar injury in the field linked 
to recent monitored O3 air quality for the years 2001-2004; 
(2) estimates of seedling growth loss under current and alternative 
O3 exposure conditions; and (3) simulated mature tree growth 
reductions using the TREGRO model to simulate the effect of meeting 
alternative air quality standards on the predicted annual growth of a 
single western species (ponderosa pine) and two eastern species (red 
maple and tulip poplar). The crop analysis includes estimates of the 
risks to crop yields from current and alternative O3 
exposure conditions and the associated change in economic benefits 
expected to accrue in the agriculture sector upon meeting the levels of 
various alternative standards. Each element of the assessment is 
described below, including discussions of known sources and ranges of 
uncertainties associated with the elements of this assessment.
1. Exposure Characterization
    Though numerous effects of O3 on vegetation have been 
documented as discussed above, it is important in considering risk to 
examine O3 air quality patterns in the U.S. relative to the 
location of O3 sensitive species that have a known 
concentration-response in order to predict whether adverse effects are 
occurring at current levels of air quality, and whether they are likely 
to occur under alternative standard forms and levels.
    The most important information about exposure to vegetation comes 
from the O3 monitoring data that are available from two 
national networks: (1) Air Quality System (AQS; http://www.epa.gov/ttn/airs/airsaqs
) and (2) Clean Air Status and Trends Network (CASTNET; 

http://www.epa.gov/castnet/). The AQS monitoring network currently has 

over 1100 active O3 monitors which are generally sited near 
population centers. However, this network also includes approximately 
36 monitors located in national parks. CASTNET is the nation's primary 
source for data on dry acidic deposition and rural, ground-level 
O3. It consists of over 80 sites across the eastern and 
western U.S. and is cooperatively operated and funded with the National 
Park Service. In the 1997 final O3 rule, it was acknowledged 
that because the national air quality surveillance network for 
O3 was designed principally to monitor O3 
exposure in populated areas, there was limited measured data available 
to characterize O3 air quality in rural and remote sites. 
Since the last review, there has been a small increase in the number of 
CASTNET sites (from approximately 52 sites in 1992 to 84 sites in 
2004), however these monitors are not used for attainment designations.
    National parks represent areas of nationally recognized ecological 
and public welfare significance, which are afforded a higher level of 
protection. Two recent reports presented some discussion of 
O3 trends in a subset of national parks: The Ozone Report: 
Measuring Progress Through 2003 (EPA, 2004), and 2005 Annual 
Performance and Progress Report: Air Quality in National Parks (NPS, 
2005). Unfortunately, much of this information is presented only in 
terms of the current 8-hr average form. The Staff Paper analyzed 
available air quality data in terms of the cumulative 12-hour W126 form 
from 2001 to 2005 for a subset of national parks and other significant 
natural areas representing 4 general regions of the U.S. Many of these 
national parks and natural areas have monitored O3 levels 
above concentrations that have been shown to decrease plant growth and 
above the 12-hour W126 levels analyzed in this review. For example, the 
Great Smokey Mountain, Rocky Mountain, Grand Canyon, Yosemite and 
Sequoia National Parks all had more than one year within the 2001-2005 
period with a 12-hour W126 above 21 ppm-hour. This level of exposure 
has been associated with approximately no more than 10 percent biomass 
loss in 50 percent of the 49 tree seedling cases studied in the NHEERL-
WED experiments (Lee and Hogsett, 1996). Black cherry (Prunus 
serotina), an important O3-sensitive tree species in the 
eastern U.S., occurs in the Great Smoky Mountain National Park and is 
estimated to have O3-related seedling biomass loss of 
approximately 40 percent when exposed to a 3-month, 12-hour W126 
O3 level greater than 21 ppm-hour. Ponderosa pine (Pinus 
ponderosa) which occurs in the Grand Canyon, Yosemite and Sequoia 
National Parks has been reported to have approximately 10 percent 
biomass losses at 3-month, 12-hour W126 O3 levels as low as 
17 ppm-hour (Lee and Hogsett, 1996). Impacts on seedlings may 
potentially affect long-term tree growth and survival, ultimately 
affecting the competitiveness of O3-sensitive tree species 
and genotypes within forest stands.
    In order to characterize exposures to vegetation at the national 
scale,

[[Page 37892]]

however, the Staff Paper concluded that it could not rely solely on 
limited site-specific monitoring data, and that it was necessary to 
select an interpolation method that could be used to characterize 
O3 air quality over broad geographic areas. The Staff Paper 
therefore investigated the appropriateness of using the O3 
outputs from the EPA/NOAA Community Multi-scale Air Quality (CMAQ) \59\ 
model system (http://www.epa.gov/asmdnerl/CMAQ, Byun and Ching, 1999; 

Arnold et al. 2003, Eder and Yu, 2005) to improve spatial 
interpolations based solely on existing monitoring networks. Due to the 
significant resources required to run CMAQ, model outputs were only 
available for a limited number of years. For this review, 2001 outputs 
from CMAQ version 4.5 were the most recent available.
---------------------------------------------------------------------------

    \59\ The CMAQ model is a multi-pollutant, multiscale air quality 
model that contains state-of-the-science techniques for simulating 
all atmospheric and land processes that affect the transport, 
transformation, and deposition of atmospheric pollutants and/or 
their precursors on both regional and urban scales. It is designed 
as a science-based modeling tool for handling many major pollutants 
(including photochemical oxidants/O3, particulate matter, 
and nutrient deposition) holistically. The CMAQ model can generate 
estimates of hourly O3 concentrations for the contiguous 
U.S., making it possible to express model outputs in terms of a 
variety of exposure indices (e.g., W126, 8-hour average).
---------------------------------------------------------------------------

    Based on the significant difference in monitor network density 
between the eastern and western U.S., the Staff Paper concluded that it 
was appropriate to use separate interpolation techniques in these two 
regions. AQS and CASTNET monitoring data were solely used for the 
eastern interpolation since it was determined that enhancing the 
interpolation with CMAQ data did not add much information to the 
eastern U.S. interpolation. In the western U.S., where rural monitoring 
is more sparse, O3 values generated by the CMAQ model were 
used to develop scaling factors to augment the interpolation.
    In order to characterize uncertainty in the interpolation method, 
monitored O3 concentrations were systematically compared to 
interpolated O3 concentrations in areas where monitors were 
located. In general, the interpolation method used in the current 
review performed well in many areas in the U.S., although it under-
predicted higher 12-hour W126 exposures in rural areas. Due to the 
important influence of higher exposures in determining risks to plants, 
this feature of the interpolated surface could result in an under-
estimation of risks to vegetation in some areas. Taking these 
uncertainties into account, and given the absence of more complete 
rural monitoring data, this approach was used in developing national 
vegetation exposure and risk assessments that estimate relative changes 
in risk for the various alternative standards analyzed.
    To evaluate changing vegetation exposures and risks under selected 
air quality scenarios, the Staff Paper utilized adjusted 2001 base year 
O3 air quality distributions with a rollback method (Horst 
and Duff, 1995; Rizzo, 2005 & 2006) to reflect meeting the current and 
alternative secondary standard options. This technique combines both 
linear and quadratic elements to reduce higher O3 
concentrations more than lower ones. In this regard, the rollback 
method attempts to account for reductions in emissions without greatly 
affecting lower concentrations. The following O3 air quality 
scenarios were analyzed: (1) 4th-highest daily maximum 8-hour average: 
0.084 ppm (the effective level of the current standard) and 0.070 ppm 
levels; (2) 3-month, 12-hour. SUM06: 25 ppm-hour (proposed in the 1996 
review) and 15 ppm-hour levels; and (3) 3-month, 12-hour. W126: 21 ppm-
hour and 13 ppm-hour levels.
    The two 8-hour average levels were chosen as possible alternatives 
of the current form for comparison with the cumulative, seasonal 
alternative forms. The SUM06 scenarios were very similar to the W126 
scenarios. Since the W126 was judged to be the more biologically-
relevant cumulative, seasonal form, only the results for the W126 
scenarios are summarized below. For the W126 form, the two levels were 
selected on the basis of the associated levels of tree seedling biomass 
loss and crop yield loss protection identified in the NHEERL-WED and 
NCLAN studies, respectively. Specifically, the upper level of W126 (21 
ppm-hour) was associated with a level of tree and crop protection of 
approximately no more than 10 percent growth or yield loss in 50 
percent of cases studied. Alternatively, the lower level of W126 (13 
ppm-hour) was associated with a level of tree seedling and crop 
protection of approximately no more than 10 percent growth or yield 
loss in 75 percent of studied cases.
    The following discussion highlights key observations drawn from 
comparing predicted changes in interpolated air quality under each 
alternative standard form and level scenario for the base year, 2001:
    (1) Under the base year (2001) ``as is'' air quality, a large 
portion of California had 12-hr W126 O3 levels above 31 ppm-
hour, which has been associated with approximately no more than 14 
percent biomass loss in 50 percent of tree seedling cases studies. 
Broader multi-state regions in the east (NC, TN, KY, IN, OH, PA, NJ, 
NY, DE, MD, VA) and west (CA, NV, AZ, OK, TX) are predicted to have 
levels of air quality above the W126 level of 21 ppm-hour, which is 
approximately equal to the secondary standard proposed in 1996 and is 
associated with approximately no more than 10 percent biomass loss in 
50 percent of tree seedling cases studied. Much of the east and Arizona 
and California have 12-hour W126 O3 levels above 13 ppm-hour 
which has been associated with approximately no more than 10 percent 
biomass loss in 75 percent of tree seedling cases studied. The results 
of the exposure assessment indicate that current air quality levels 
could result in significant impacts to vegetation in some areas.
    (2) When 2001 air quality is rolled back to meet the current 8-hour 
secondary standard, the overall 3-month 12-hour W126 O3 
levels were somewhat improved, but not substantially. Under this 
scenario, there were still many areas in California with 12-hour W126 
O3 levels above 31 ppm-hour. A broad multi-state region in 
the east (NC, TN, KY, IN, OH, PA, MD) and west (CA, NV, AZ, OK, TX) 
were still predicted to have O3 levels above the W126 level 
of 21 ppm-hour.
    (3) Exposures generated for just meeting a 0.070 ppm, 4th-highest 
maximum 8-hour average alternative standard showed substantially 
improved O3 air quality when compared to just meeting the 
current 0.08 ppm, 8-hour standard. Most areas were predicted to have 
O3 levels below the W126 level of 21 ppm-hr, although some 
areas in the east (KY, TN, MI, AR, MO, IL) and west (CA, NV, AZ, UT, 
NM, CO, OK, TX) were still predicted to have O3 levels above 
the W126 level of 13 ppm-hour.
    These results suggest that meeting a proposed 0.070 ppm, 8-hour 
secondary standard would provide substantially improved protection in 
some areas for vegetation from seasonal O3 exposures of 
concern. The Staff Paper recognizes, however, that some areas meeting a 
0.070 ppm 8-hour standard could continue to have elevated seasonal 
exposures, including forested park lands and other natural areas, and 
Class I areas which are federally mandated to preserve certain air 
quality related values. This is especially important in the high 
elevation forests in the Western U.S. where there are few O3 
monitors. This is because the air quality patterns in remote areas can 
result in relatively low 8-hour averages while still experiencing 
relatively high cumulative exposures.

[[Page 37893]]

    To further characterize O3 air quality in terms of 
current and alternative secondary standard forms, an analysis was 
performed in the Staff Paper to evaluate the extent to which county-
level O3 air quality measured in terms of various levels of 
the current 8-hour average form overlapped with that measured in terms 
of various levels of the 12-hour W126 cumulative, seasonal form. The 
Staff Paper presented this analysis using recent (2002-2004) \60\ 
county-level O3 air quality data from AQS sites and the 
subset of CASTNET sites having the highest O3 levels for the 
counties in which they are located. Since the current 8-hour average 
secondary form is a 3-year average, the analysis initially compared the 
3-year averages of both the 8-hour and W126 forms. In addition, 
recognizing that some vegetation effects (e.g. crop yield loss and 
foliar injury) are driven solely by annual O3 exposures and 
are typically evaluated with respect to exposures within the annual 
growing season, the Staff Paper also presented a comparison of the 
current 3-year average 8-hour form to the annual W126 form for the 
individual years, 2002 and 2004.
---------------------------------------------------------------------------

    \60\ This analysis was updated using 2003-2005 air quality as it 
became available, finding similar results.
---------------------------------------------------------------------------

    Results of the 3-year average comparisons showed that of the 
counties with air quality meeting the 3-year average form of the 0.08 
ppm, 8-hour average standard, 7 counties showed 3-year average W126 
values above the 21 ppm-hour level. At the lower W126 level of 13 ppm-
hours, 135 counties with air quality meeting the 3-year average form of 
the 0.08 ppm, 8-hour average standard, would be above this W126 level. 
In addition, when the 3-year average of the 8-hour form was compared to 
annual W126 values, further variability in the degree of overlap 
between the 8-hour form and W126 form became apparent. For example, the 
relatively high 2002 O3 air quality year showed a greater 
degree of overlap between those areas that would meet the levels 
analyzed for the current 8-hour and alternative levels of the W126 form 
than did the relatively low O3 2004 air quality year. This 
lack of a consistent degree of overlap between the two forms in 
different air quality years demonstrates that annual vegetation would 
be expected to receive widely differing degrees of protection from 
cumulative seasonal exposures in some areas from year to year, even 
when the 3-year average of the 8-hour form was consistently met.
    It is clear that this analysis is limited by the lack of monitoring 
in rural areas where important vegetation and ecosystems are located, 
especially at higher elevation sites. This is because O3 air 
quality distributions at high elevation sites often do not reflect the 
typical urban and near-urban pattern of low morning and evening 
O3 concentrations with a high mid-day peak, but instead 
maintain relatively flat patterns with many concentrations in the mid-
range (e.g., 0.05-0.09 ppm) for extended periods. These conditions can 
lead to relatively low daily maximum 8-hour averages concurrently with 
high cumulative values so that there is potentially less overlap 
between an 8-hour average and a cumulative, seasonal form at these 
sites. The Staff Paper concludes that it is reasonable to anticipate 
that additional unmonitored rural high elevation areas important for 
vegetation may not be adequately protected even with a lower level of 
the 8-hour form.
    The Criteria Document (EPA, 2006a), discusses policy relevant 
background (PRB) levels for high elevation sites and makes the 
following observations: (1) PRB concentrations of 0.04 to 0.05 ppm 
occur occasionally at high-elevation sites (e.g., >1.5 km) in the 
spring due to the free-tropospheric influence, including some limited 
contribution from hemispheric pollution (O3 produced from 
anthropogenic emissions outside North America); and (2) stratospheric 
intrusions might occasionally elevate O3 at high-altitude 
sites, however, these events are rare. Therefore, the Staff Paper 
concludes that springtime PRB levels in the range identified above and 
rare stratospheric intrusions of O3 are unlikely to 
influence 3 month cumulative seasonal W126 values significantly.
    It further remains uncertain as to the extent to which air quality 
improvements designed to reduce 8-hour O3 average 
concentrations would reduce O3 exposures measured by a 
seasonal, cumulative W126 index. The Staff Paper indicated this to be 
an important consideration because: (1) The biological database 
stresses the importance of cumulative, seasonal exposures in 
determining plant response; (2) plants have not been specifically 
tested for the importance of daily maximum 8-hour O3 
concentrations in relation to plant response; and (3) the effects of 
attainment of an 8-hour standard in upwind urban areas on rural air 
quality distributions cannot be characterized with confidence due to 
the lack of monitoring data in rural and remote areas. These factors 
are important considerations in determining whether the current 8-hour 
form can appropriately provide requisite protection for vegetation.
2. Assessment of Risk to Vegetation
    The Staff Paper presents results from quantitative and qualitative 
risk assessments of O3 risks to vegetation (EPA, 2007). In 
the last review, crop yield and seedling biomass loss OTC data provided 
the basis for staff analyses, conclusions, and recommendations (EPA, 
1996b). Since then, several additional lines of evidence have 
progressed sufficiently to provide staff with a more complete and 
coherent picture of the scope of O3-related vegetation 
risks, especially those currently faced by seedling, sapling and mature 
tree species growing in field settings, and indirectly, forested 
ecosystems. Specifically, new research reflects an increased emphasis 
on field-based exposure methods (e.g., free air exposure and ambient 
gradient), improved field survey biomonitoring techniques, and 
mechanistic tree process models. Findings from each of these research 
areas are discussed separately below. In conducting these assessments, 
the Staff Paper analyses relied on both measured and modeled air 
quality information. For some effects, like visible foliar injury and 
modeled mature tree growth response, only monitored air quality 
information was used. For other effects categories (e.g., crop yield 
and tree seedling growth), staff relied on interpolated O3 
exposures.
a. Visible Foliar Injury
    As discussed earlier (Section A), recent systematic injury surveys 
continue to document visible foliar injury symptoms diagnostic of 
phytotoxic O3 exposures on sensitive bioindicator plants. 
These surveys produced more expansive evidence than that available at 
the time of the last review that visible foliar injury is occurring in 
many areas of the U.S. under current ambient conditions. The Staff 
Paper presents an assessment combining recent U.S. Forest Service 
Forest Inventory and Analysis (FIA) biomonitoring site data with the 
county level air quality data for those counties containing the FIA 
biomonitoring sites. This assessment showed that incidence of visible 
foliar injury ranged from 21 to 39 percent during the four-year period 
(2001-2004) across all counties with air quality levels at or below 
that of the current 0.08 8-hour standard. Of the counties that met an 
8-hour level of 0.07 ppm in those years, 11 to 30 percent still had 
incidence of visible foliar

[[Page 37894]]

injury. The magnitude of these percentages suggests that phytotoxic 
exposures sufficient to induce visible foliar injury would still occur 
in many areas after meeting the level of the current secondary standard 
or alternative 0.07 ppm 8-hour standard. Additionally, the data show 
that visible foliar injury occurrence is geographically widespread and 
is occurring on a variety of plant species in forested and other 
natural systems. Linking visible foliar injury to other plant effects 
is still problematic. However, its presence indicates that other 
O3-related vegetation effects could also be present.
b. Seedling and Mature Tree Biomass Loss
    In the last review (EPA, 1996b), analyses of the effects of 
O3 on trees were limited to 11 tree species for which C-R 
functions for the seedling growth stage had been developed from OTC 
studies conducted by the NHEERL-WED. Important tree species such as 
quaking aspen, ponderosa pine, black cherry, tulip poplar were found to 
be sensitive to cumulative seasonal O3 exposures. Work done 
since the 1996 review at the AspenFACE site in Wisconsin on quaking 
aspen (Karnosky et al., 2005) and a gradient study performed in the New 
York City area (Gregg et al. 2003) has confirmed the detrimental 
effects of O3 exposure on tree growth in field studies 
without chambers and beyond the seedling stage (King et al., 2005). 
These field studies are discussed above in section IV.A.
    To update the seedling biomass loss analysis, C-R functions for 
biomass loss for available seedling tree species taken from the CD and 
information on tree growing regions derived from the U.S. Department of 
Agriculture's Atlas of United States Trees were combined with 
projections of air quality based on 2001 interpolated exposures, to 
produce estimated biomass loss for each of the seedling tree species 
individually. Maps of these biomass loss projections are presented in 
the Staff Paper. For example, quaking aspen had a wide range of 
O3 exposure across its growing range and therefore, showed 
significant variability in projected seedling biomass loss across its 
range. Quaking aspen seedling biomass loss was projected to be greater 
than 4 percent over much of its geographic range, though it can reach 
above 10 percent in areas of Ohio, Pennsylvania, New York, New Jersey 
and California. Biomass loss for black cherry was projected to be 
greater than 20 percent in approximately half its range. Greater than 
30 percent biomass loss for black cherry was projected in North 
Carolina, Tennessee, Indiana, Ohio, Pennsylvania, Arizona, Michigan, 
New York, New Jersey, Maryland and Delaware. For ponderosa pine, an 
important tree species in the western U.S., biomass loss was projected 
to be above 10 percent in much of its range in California. Biomass loss 
still occurred in many tree species when O3 air quality was 
adjusted to meet the current 8-hour standard. For instance, black 
cherry, ponderosa pine, eastern white pine, and aspen had estimated 
median seedling biomass losses over portions of their growing range as 
high as 24, 11, 6, and 6 percent, respectively, when O3 air 
quality was rolled back to just meet the current 8-hour standard. The 
Staff Paper noted that these results are for tree seedlings and that 
mature trees of the same species may have more or less of a response to 
O3 exposure. Due to the potential for compounding effects 
over multiple years, a consensus workshop on O3 effects 
reported that a biomass loss greater than 2 percent annually can be 
significant (Heck and Cowling, 1997). Decreased seedling root growth 
and survivability could affect overall stand health and composition in 
the long term.
    In addition to the estimation of O3 effects on seedling 
growth, recent work has enhanced our understanding of risks beyond the 
seedling stage. In order to better characterize the potential 
O3 effects on mature tree growth, a tree growth model 
(TREGRO) was used as a tool to evaluate the effect of changing 
O3 air quality scenarios from just meeting alternative 
O3 standards on the growth of mature trees. TREGRO is a 
process-based, individual tree growth simulation model (Weinstein et 
al., 1991) and has been used to evaluate the effects of a variety of 
O3 scenarios and linked with concurrent climate data to 
account for O3 and climate/meteorology interactions on 
several species of trees in different regions of the U.S. (Tingey et 
al., 2001; Weinstein et al., 1991; Retzlaff et al., 2000; Laurence et 
al., 1993; Laurence et al., 2001; Weinstein et al., 2005). The model 
provides an analytical framework that accounts for the nonlinear 
relationship between O3 exposure and response. The 
interactions between O3 exposure, precipitation and 
temperature are integrated as they affect vegetation, thus providing an 
internal consistency for comparing effects in trees under different 
exposure scenarios and climatic conditions. An earlier assessment of 
the effectiveness of national ambient air quality standards in place 
since the early 1970s took advantage of 40 years of air quality and 
climate data for the Crestline site in the San Bernardino Mountains of 
California to simulate ponderosa pine growth over time with the 
improving air quality using TREGRO (Tingey et al., 2004).
    The TREGRO model was used to assess growth of Ponderosa pine in the 
San Bernardino Mountains of California (Crestline) and the growth of 
yellow poplar and red maple in the Appalachian mountains of Virginia 
and North Carolina, Shenandoah National Park (Big Meadows) and Linville 
Gorge Wilderness Area (Cranberry), respectively. Total tree growth 
associated with 'as is' air quality, and air quality adjusted to just 
meet alternative O3 standards was assessed. Ponderosa pine 
is one of the most widely distributed pines in western North America, a 
major source of timber, important as wildlife habitat, and valued for 
aesthetics (Burns and Honkala, 1990). Red maple is one of the most 
abundant species in the eastern U.S. and is important for its brilliant 
fall foliage and highly desirable wildlife browse food (Burns and 
Honkala, 1990). Yellow poplar is an abundant species in the southern 
Appalachian forest. It is 10 percent of the cove hardwood stands in 
southern Appalachians which are widely viewed as some of the country's 
most treasured forests because the protected, rich, moist set of 
conditions permit trees to grow the largest in the eastern U.S. The 
wood has high commercial value because of its versatility and as a 
substitute for increasingly scarce softwoods in furniture and framing 
construction. Yellow poplar is also valued as a honey tree, a source of 
wildlife food, and a shade tree for large areas (Burns and Honkala, 
1990).
    The Staff Paper analyses found that just meeting the current 
standard would likely continue to allow O3-related 
reductions in annual net biomass gain in these species. This is based 
on model outputs that estimate that as O3 levels are reduced 
below those of the current standard, significant improvements in growth 
would occur. For instance, estimated growth in red maple increased by 4 
and 3 percent at Big Meadows and Cranberry sites, respectively, when 
air quality was rolled back to just met a W126 value of 13 ppm-hour. 
Yellow poplar was projected to have a growth increase between 0.6 and 8 
percent under the same scenario at the two eastern sites.
    Though there is uncertainty associated with the above analyses, 
this information should be given careful consideration in light of 
several other pieces of evidence. Specifically, new evidence from 
experimental studies that go beyond the seedling growth stage

[[Page 37895]]

continues to show decreased growth under elevated O3 (King 
et al., 2005). Some mature trees such as red oak have shown an even 
greater sensitivity of photosynthesis to O3 than seedlings 
of the same species (Hanson et al., 1994). As indicated above, smaller 
growth loss increments may be significant for perennial species. The 
potential for cumulative ``carry over'' effects as well as compounding 
must be considered. The accumulation of such ``carry-over'' effects 
over time may affect long-term survival and reproduction of individuals 
and ultimately the abundance of sensitive tree species in forest 
stands.
c. Crops
    As discussed in the Staff Paper, risk of O3 exposure and 
associated monetized benefits were estimated for commodity crops, 
fruits and vegetables. Similar to the tree seedling analysis, this 
analysis combined C-R information on crops, crop growing regions and 
interpolated exposures during each crop growing season. NCLAN crop 
functions were used for commodity crops. According to USDA National 
Agricultural Statistical Survey (NASS) data, the 9 commodity crop 
species (e.g., cotton, field corn, grain sorghum, peanut, soybean, 
winter wheat, lettuce, kidney bean, potato) included in the Staff Paper 
analysis accounted for 69 percent of 2004 principal crop acreage 
planted in the U.S. in 2004.\61\ The C-R functions for six fruit and 
vegetable species (tomatoes-processing, grapes, onions, rice, 
cantaloupes, Valencia oranges) were identified from the California 
fruit and vegetable analysis from the last review (Abt 1995). The Staff 
Paper noted that fruit and vegetable studies were not part of the NCLAN 
program and C-R functions were available only in terms of seasonal 7-
hour or 12-hour mean index. This index form is considered less 
effective in predicting plant response for a given change in air 
quality than the cumulative form used with other crops. Therefore, the 
fruit and vegetable C-R functions were considered more uncertain than 
those for commodity crops.
---------------------------------------------------------------------------

    \61\ Principal crops as defined by the USDA include corn, 
sorghum, oats, barley, winter wheat, rye, Durum wheat, other spring 
wheat, rice, soybeans, peanuts, sunflower, cotton, dry edible beans, 
potatoes, sugar beets, canola, proso millet, hay, tobacco, and 
sugarcane. Acreage data for the principal crops were taken from the 
USDA NASS 2005 Acreage Report (http://usda.mannlib.cornell.edu/reports/nassr/field/pcp-bba/acrg0605.pdf
).

---------------------------------------------------------------------------

    Analyses in the Staff Paper showed that some of the most important 
commodity crops such as soybean, winter wheat and cotton had some 
projected losses under the 2001 base year air quality. Soybean yield 
losses were projected to be 2-4 percent in parts of Pennsylvania, New 
Jersey, Maryland and Texas. Winter wheat was projected to have yield 
losses of 2-6 percent in parts of California. Additionally, cotton was 
projected to have yield losses of above 6 percent in parts of 
California, Texas and North Carolina in 2001. The risk assessment 
estimated that just meeting the current 8-hour standard would still 
allow O3-related yield loss to occur in some commodity crop 
species and fruit and vegetable species currently grown in the U.S. For 
example, based on median C-R function response, in counties with the 
highest O3 levels, potatoes and cotton had estimated yield 
losses of 9-15 percent and 5-10 percent, respectively, when 
O3 air quality just met the level of the current standard. 
Estimated yield improved in these counties when the alternative W126 
standard levels were met. The very important soybean crop had generally 
small yield losses throughout the country under just meeting the 
current standard (0-4 percent).
    The Staff Paper also presented estimates of monetized benefits for 
crops associated with the current and alternative standards. The 
Agriculture Simulation Model (AGSIM) (Taylor, 1994; Taylor, 1993) was 
used to calculate annual average changes in total undiscounted economic 
surplus for commodity crops and fruits and vegetables when current and 
alternative standard levels were met. Meeting the various alternative 
standards did show some significant benefits beyond the current 8-hour 
standard. However, the Staff Paper recognized the AGSIM modeled 
economic benefits had many uncertainties: For example, much of the 
economic benefits were from the fruits and vegetables which had 
uncertain C-R relationships, there was uncertainty in assumptions about 
the treatment and effect of government farm payment programs, and there 
was also uncertainty about near-term changes in agriculture sector due 
to the increased use of crops as biofuels. Although the AGSIM model 
results provided a relative comparison of agricultural benefits between 
alternative standards, the uncertainties limited the utility of the 
absolute numbers.

D. Conclusions on the Adequacy of the Current Standard

1. Background
    The initial issue to be addressed in the current review of the 
secondary O3 standard is whether, in view of the advances in 
scientific knowledge reflected in the Criteria Document and additional 
information on exposure and risk discussed in the Staff Paper, the 
existing standard should be revised. The current secondary standard is 
a 3-year average of the annual 4th-highest maximum 8-hour average 
O3 concentration set at a level of 0.08 ppm. In evaluating 
whether it is appropriate to retain or revise the current secondary 
O3 standard, the Administrator adopts an approach in this 
review that builds upon the general approach used in the last review 
and reflects the broader body of evidence now available.
    In developing proposed conclusions on the adequacy of the current 
secondary O3 standard, the Administrator has considered a 
weight-of-evidence approach that evaluated information across the 
variety of vegetation-related research areas described in the Criteria 
Document (e.g., seedling, sapling and mature forest tree species growth 
stages and commodity, fruit, vegetable and forage crop species), and 
included the assessments of air quality, exposures, and qualitative and 
quantitative risks associated with alternative air quality scenarios. 
Evidence-based considerations included assessment of vegetation effects 
evidence obtained from chamber, free air, gradient, model and field-
based observation studies across an array of vegetation effects 
endpoints. Exposure- and risk-based considerations were drawn from 
exposure and risk assessments that relied upon both monitored and 
interpolated O3 exposures as described in the Staff Paper. 
These assessments reflect the availability of new tools and assessment 
methods, as well as the larger and more diverse body of evidence 
available since the last review. Specifically, estimates of exposures 
and risks associated with recent O3 air quality levels, as 
well as estimates of the relative magnitude of exposure and risk 
reductions potentially associated with meeting the current 8-hour 
secondary O3 NAAQS and alternative standards, have also been 
considered, along with all known associated uncertainties.
    In this review, a series of general questions frames the approach 
to reaching a proposed decision on the adequacy of the current 
standard, beginning with: (1) To what extent does newly available 
information reinforce or call into question evidence of associations of 
O3 exposures with effects identified in the last review?; 
(2) to what extent does newly available information reinforce or call 
into question any of the basic elements of the current standard?;

[[Page 37896]]

and (3) to what extent have important uncertainties identified in the 
last review been reduced and have new uncertainties emerged? To the 
extent the available information suggests that revision of the current 
standard may be appropriate, the question of whether the available 
information supports consideration of a standard that is either more or 
less protective than the current standard is addressed, including: (1) 
Whether there is evidence that vegetation effects extend to ambient 
O3 concentration levels that are as low as or lower than had 
previously been observed, and what are the important uncertainties 
associated with that evidence?; (2) whether vegetation exposures and 
risks of concern estimated to occur in areas upon meeting the current 
standard are considered important from a public welfare perspective; 
and (3) what are the important uncertainties associated with the 
estimated risks?
    The current secondary standard was selected to provide protection 
to the public welfare against a range of O3-induced 
vegetation effects, particularly yield loss in agricultural crops and 
biomass loss in tree seedlings. As an introduction to the discussion in 
this section of the adequacy of the current O3 standard, it 
is useful to summarize the key factors that formed the basis of the 
decision in the last review to revise the averaging time, level and 
form of the then current 1-hour secondary standard.
    In the 1996 proposal notice (61 FR 65716), the Administrator 
proposed to replace the then existing 1-hour O3 secondary 
NAAQS with one of two alternative new standards: a standard identical 
to the proposed and now current 0.08 ppm, 8-hour primary standard 
(described above), or alternatively, a new seasonal standard, SUM06, 
expressed as a sum of hourly concentrations greater than or equal to 
0.06 ppm, cumulated daily over a 12 hour daylight window (8 am to 8 pm) 
during the maximum consecutive 3-month period (e.g., the consecutive 3 
month period with the highest SUM06 index value) during the 
O3 monitoring season, set at a level of 25 ppm-hours. The 
latter form and level were selected to provide protection to vegetation 
on the basis of annual, rather than 3-year average, exposures.
    In the final rule for the O3 NAAQS published in July 
1997 (62 FR 38877), the Administrator decided to replace the then 
current 1-hour, 0.12-ppm secondary NAAQS with a standard that was 
identical in every way to the new revised primary standard of an 0.08 
ppm annual 4th-highest maximum 8-hour average standard averaged over 3 
years. Her decision was based on: (1) Her judgment that the then 
existing secondary standard did not provide adequate protection for 
vegetation against the adverse welfare effects of O3; (2) 
CASAC advice ``that a secondary NAAQS, more stringent than the present 
primary standard, was necessary to protect vegetation from 
O3'' (Wolff, 1996); (3) her judgment that the new 8-hour 
average standard would provide substantially improved protection for 
vegetation from O3-related adverse effects as compared to 
the level of protection provided by the then current 1-hour, 0.12-ppm 
secondary standard; (4) recognition that significant uncertainties 
remained with respect to exposure dynamics, air quality relationships, 
and the exposure, risk, and monetized valuation analyses presented in 
the proposal, resulting in only rough estimates of the increased public 
welfare likely to be afforded by each of the proposed alternative 
standards; (5) her judgment that there was value in allowing more time 
to obtain additional information to better characterize O3-
related vegetation effects under field conditions from additional 
research and to develop a more complete rural monitoring network and 
air quality database from which to evaluate the elements of an 
appropriate seasonal secondary standard; and (6) her judgment that 
there was value in allowing more time to evaluate more specifically the 
improvement in rural air quality and in O3-related 
vegetation effects resulting from measures designed to attain the new 
primary standard (62 FR 38877-78).
    The Administrator further concluded (62 FR 38877-78) that continued 
research on the effects of O3 on vegetation under field 
conditions and on better characterizing the relationship between 
O3 exposure dynamics and plant response would be important 
in the next review because: (1) The available biological database 
highlighted the importance of cumulative, seasonal exposures as a 
primary determinant of plant responses; (2) the association between 
daily maximum 8-hour O3 concentrations and plant responses 
had not been specifically examined in field tests; (3) the impacts of 
attaining an 8-hour, 0.08 ppm primary standard in upwind urban areas on 
rural air quality distributions could not be characterized with 
confidence due to limited monitoring data and air quality modeling in 
rural and remote areas.
2. Evidence- and Exposure/Risk-Based Considerations
    The new evidence available in this review as described in the 
Criteria Document continues to support and strengthen key policy-
relevant conclusions drawn in the previous review (EPA, 2006a). Based 
on this new evidence, the current Criteria Document once more concludes 
that: (1) A plant's response to O3 depends upon the 
cumulative nature of ambient exposure as well as the temporal dynamics 
of those concentrations; (2) current ambient concentrations in many 
areas of the country are sufficient to impair growth of numerous common 
and economically valuable plant and tree species; (3) the entrance of 
O3 into the leaf through the stomata is the critical step in 
O3 effects; (4) effects can occur with only a few hourly 
concentrations above 0.08 ppm; (5) other environmental biotic and 
abiotic factors are also influential to the overall impact of 
O3 on plants and trees; and (6) a high degree of uncertainty 
remains in our ability to assess the impact of O3 on 
ecosystem services.
    In light of the new evidence, as described in the Criteria 
Document, the Staff Paper evaluates the adequacy of the current 
standard based on assessments of both the most policy-relevant 
vegetation effects evidence and exposure and risk-based information, as 
summarized above in sections IV.A and IV.C, respectively. In evaluating 
the strength of this information, the Staff Paper takes into account 
the uncertainties and limitations in the scientific evidence and 
analyses as well as the views of CASAC. The Staff Paper concludes that 
progress has been made since the last review and generally finds 
support in the available effects- and exposure/risk-based information 
for consideration of an O3 standard that is more protective 
than the current standard. The Staff Paper further concludes that there 
is no support for consideration of an O3 standard that is 
less protective than the current standard. This general conclusion is 
consistent with the advice and recommendations of CASAC.
a. Evidence-Based Considerations
    In the last review, crop yield and tree seedling biomass loss data 
obtained in OTC studies provided the basis for the Administrator's 
judgment that the then current 1-hour, 0.12 ppm secondary standard was 
inadequate (EPA, 1996b). Since then, several additional lines of 
evidence have progressed sufficiently to provide a more complete and 
coherent picture of the scope of O3-related

[[Page 37897]]

vegetation risks, especially those currently faced by sensitive 
seedling, sapling and mature growth stage tree species growing in field 
settings, and their associated forested ecosystems. Specifically, new 
research reflects an increased emphasis on field-based exposure methods 
(e.g., free air, ambient gradient, and biomonitoring surveys). In 
reaching conclusions regarding the adequacy of the current standard, 
the Staff Paper has considered the combined information from all these 
areas together, along with associated uncertainties, in an integrated, 
weight-of-evidence approach.
    Regarding the O3-induced effect of visible foliar 
injury, observations for the years 2001 to 2004 at USDA FIA 
biomonitoring sites showed widespread O3-induced leaf injury 
occurring in the field, including in forested ecosystems, under current 
ambient O3 conditions. For a few studied species, it has 
been shown that the presence of visible foliar injury is further linked 
to the presence of other vegetation effects (e.g., reduced plant growth 
and impaired below ground root development) (EPA, 2006), though for 
most species, this linkage has not been specifically studied or where 
studied, has not been found. Nevertheless, when visible foliar injury 
is present, the possibility that other O3-induced vegetation 
effects could also be present for some species should be considered. 
Likewise, the absence of visible foliar injury should not be construed 
to demonstrate the absence of other O3-induced vegetation 
effects. The Staff Paper concludes that it is not possible at this time 
to quantitatively assess the degree of visible foliar injury that 
should be judged adverse in all settings and across all species, and 
that other environmental factors can mitigate or exacerbate the degree 
of O3-induced visible foliar injury expressed at any given 
concentration of O3. However, the Staff Paper also concludes 
that the presence of visible foliar injury alone can be adverse to the 
public welfare, especially when it occurs in protected areas such as 
national parks and wilderness areas. Thus, on the basis of the 
available information on the widespread distribution of O3-
sensitive species within the U.S. including in areas, such as national 
parks, which are afforded a higher degree of protection, the Staff 
Paper concludes that the current standard continues to allow levels of 
visible foliar injury in some locations that could reasonably be 
considered to be adverse from a public welfare perspective. Additional 
monitoring of both O3 air quality and foliar injury levels 
are needed in these areas of national significance to more fully 
characterize the spatial extent of this public welfare impact.
    With respect to O3-induced biomass loss in trees, the 
Staff Paper concludes that the significant new body of field-based 
research on trees strengthens the conclusions drawn on tree seedling 
biomass loss from earlier OTC work by documenting similar seedling 
responses in the field. For example, recent empirical studies conducted 
on quaking aspen at the AspenFACE site in Wisconsin have confirmed the 
detrimental effects of O3 exposure on tree growth in a field 
setting without chambers (Isebrands et al., 2000, 2001). In addition, 
results from an ambient gradient study (Gregg et al., 2003), which 
evaluated biomass loss in cottonwood along an urban-to-rural gradient 
at several locations, found that conditions in the field were 
sufficient to produce substantial biomass loss in cottonwood, with 
larger impacts observed in downwind rural areas due to the presence of 
higher O3 concentrations. These gradients from low urban to 
higher rural O3 concentrations occur when O3 
precursors generated in urban areas are transported to downwind sites 
and are transformed into O3. In addition,O3 
concentrations typically fall to near 0 ppm at night in urban areas due 
to scavenging of O3 by NOX and other compounds. 
In contrast, rural areas, due to a lack of nighttime scavenging, tend 
to maintain elevated O3 concentrations for longer periods. 
On the basis of such key studies, the Staff Paper concludes that the 
expanded body of field-based evidence, in combination with the 
substantial corroborating evidence from OTC data, provides stronger 
evidence than that available in the last review that ambient levels of 
O3 are sufficient to produce visible foliar injury symptoms 
and biomass loss in sensitive vegetative species growing in natural 
environments. Further, the Staff Paper judges that the consistency in 
response in studied species/genotypes to O3 under a variety 
of exposure conditions and methodologies demonstrates that these 
sensitive genotypes and populations of plants are susceptible to 
adverse impacts from O3 exposures at levels known to occur 
in the ambient air. Due to the potential for compounded risks from 
repeated insults over multiple years in perennial species, the Staff 
Paper concludes that these sensitive subpopulations are not afforded 
adequate protection under the current secondary O3 standard. 
Despite the fact that only a relatively small portion of U.S. plant 
species have been studied with respect to O3 sensitivity, 
those species/genotypes shown to have O3 sensitivity span a 
broad range of vegetation types and public use categories, including 
direct-use categories like food production for human and domestic 
animal consumption; fiber, materials, and medicinal production; urban/
private landscaping. Many of these species also contribute to the 
structure and functioning of natural ecosystems (e.g., the EEAs) and 
thus, to the goods and services those ecosystems provide (Young and 
Sanzone, 2002), including non-use categories such as relevance to 
public welfare based on their aesthetic, existence or wildlife habitat 
value.
    The Staff Paper therefore concludes that the current secondary 
standard is inadequate to protect the public welfare against the 
occurrence of known adverse levels of visible foliar injury and tree 
seedling biomass loss occurring in tree species (e.g., ponderosa pine, 
aspen, black cherry, cottonwood) that are sensitive and clearly 
important to the public welfare.
b. Exposure- and Risk-Based Considerations
    The Staff Paper also presents the results of exposure and risk 
assessments. Due to multiple sources of uncertainty, both known and 
unknown, that continue to be associated with these analyses, the Staff 
Paper put less weight on this information in drawing conclusions on the 
adequacy of the current standard. However, the Staff Paper also 
recognizes that some progress has been made since the last review in 
better characterizing some of these associated uncertainties and, 
therefore concluded that the results of the exposure and risk 
assessments continue to provide information useful to informing 
judgments as to the relative changes in risks predicted to occur under 
exposure scenarios associated with the different standard alternatives 
considered. Importantly, with respect to two key uncertainties, the 
uncertainty associated with continued reliance on C-R functions 
developed from OTC exposure systems to predict plant response in the 
field and the potential for changes in tree seedling and crop 
sensitivities in the intervening period since the C-R functions were 
developed, the Staff Paper concluded that recent research has provided 
information useful in judging how much weight to put on these concerns. 
Specifically, new field-based studies, conducted on a limited number of 
tree seedling and crop species to date, demonstrate plant growth and 
visible foliar injury responses in the field that

[[Page 37898]]

are similar in nature and magnitude to those observed previously under 
OTC exposure conditions, lending qualitative support to the conclusion 
that OTC conditions do not fundamentally alter the nature of the 
O3-plant response. Second, nothing in the recent literature 
suggests that the O3 sensitivity of crop or tree species 
studied in the last review and for which C-R functions were developed 
has changed significantly in the intervening period. Indeed, in the few 
recent studies where this is examined, O3 sensitivities were 
found to be as great as or greater than those observed in the last 
review.
i. Seedling and Mature Tree Biomass Loss
    Biomass loss in sensitive tree seedlings is predicted to occur 
under O3 exposures that meet the level of the current 
secondary standard. For instance, black cherry, ponderosa pine, eastern 
white pine, and aspen had estimated median seedling biomass losses as 
high as 24, 11, 6, and 6 percent, respectively, over some portions of 
their growing ranges when air quality was rolled back to meet the 
current 8-hr standard with the 10 percent downward adjustment for the 
potential O3 gradient between monitor height and short plant 
canopies applied. The Staff Paper notes that these results are for tree 
seedlings and that mature trees of the same species may have more or 
less of a response to O3 exposure. Decreased root growth 
associated with biomass loss has the potential to indirectly affect the 
vigor and survivability of tree seedlings. If such effects occur on a 
sufficient number of seedlings within a stand, overall stand health and 
composition can be affected in the long term. Thus, the Staff Paper 
concludes that these levels of estimated tree seedling growth reduction 
should be considered significant and potentially adverse, given that 
they are well above the 2 percent level of concern identified by the 
1997 consensus workshop (Heck and Cowling, 1997).
    Though there is significant uncertainty associated with this 
analysis, the Staff Paper recommends that this information should be 
given careful consideration in light of several other pieces of 
evidence. Specifically, limited evidence from experimental studies that 
go beyond the seedling growth stage continues to show decreased growth 
under elevated O3 levels (King et al., 2005). Some mature 
trees such as red oak have shown an even greater sensitivity of 
photosynthesis to O3 than seedlings of the same species 
(Hanson et al., 1994). The potential for effects to ``carry over'' to 
the following year or cumulate over multiple years, including the 
potential for compounding, must be considered. The accumulation of such 
``carry-over'' effects over time may affect long-term survival and 
reproduction of individual trees and ultimately the abundance of 
sensitive tree species in forest stands.
ii. Qualitative Ecosystem Risks
    In addition to the quantifiable risk categories discussed above, 
the Staff Paper presents qualitative discussions on a number of other 
public welfare effects categories. In so doing, the Staff Paper 
concludes that the quantified risks to vegetation estimated to be 
occurring under current air quality or upon meeting the current 
secondary standard likely represent only a portion of actual risks that 
may be occurring for a number of reasons.
    First, as mentioned above, out of the over 43,000 plant species 
catalogued as growing within the U.S. (USDA PLANTS database, USDA, 
NRCS, 2006), only a small percentage have been studied with respect to 
O3 sensitivity. Most of the studied species were selected 
because of their commercial importance or observed O3-
induced visible foliar injury in the field. Given that O3 
impacts to vegetation also include less obvious but often more 
significant impacts, such as reduced annual growth rates and below 
ground root loss, the paucity of information on other species means the 
number of O3-sensitive species that exists within U.S., 
could be greater than what is now known. Since no state in the lower 48 
states has less than seven known O3-sensitive plant species, 
with the majority of states having between 11 and 30 (see Appendix 7J-2 
in Staff Paper), protecting O3 sensitive vegetation is 
clearly important to the public welfare at the national scale.
    Second, the Staff Paper also takes into consideration the 
possibility that more subtle and hidden risks to ecosystems are 
potentially occurring in areas where vegetation is being significantly 
impacted. Given the importance of these qualitative and anticipated 
risks to important public welfare effects categories such as ecosystem 
impacts leading to potential losses or shifts in ecosystem goods and 
services (e.g., carbon sequestration, hydrology, and fire disturbance 
regimes), the Staff Paper concludes that any secondary standard set to 
protect against the known and quantifiable adverse effects to 
vegetation should also consider the anticipated, but currently 
unquantifiable, potential effects on natural ecosystems.
iii. Crop Yield Loss
    Exposure and risk assessments in the Staff Paper estimated that 
meeting the current 8-hour standard would still allow O3-
related yield loss to occur in several fruit and vegetable and 
commodity crop species currently grown in the U.S. These estimates of 
crop yield loss are substantially lower than those estimated in the 
last review as a result of several factors, including adjusted exposure 
levels to reflect the presence of a variable O3 gradient 
between monitor height and crop canopies, and use of a different 
econometric agricultural benefits model updated to reflect more recent 
agricultural policies (EPA, 2006b). Though these sources of uncertainty 
associated with the crop risk and benefits assessments were better 
documented in this review, the Staff Paper concludes that the presence 
of these uncertainties make the risk estimates suitable only as a basis 
for understanding potential trends in relative yield loss and economic 
benefits. The Staff Paper further recognizes that actual conditions in 
the field and management practices vary from farm to farm, that 
agricultural systems are heavily managed, and that adverse impacts from 
a variety of other factors (e.g., weather, insects, disease) can be 
orders of magnitude greater than that of yield impacts predicted for a 
given O3 exposure. Thus, the relevance of such estimated 
impacts on crop yields to the public welfare are considered highly 
uncertain and less useful as a basis for assessing the adequacy of the 
current standard. The Staff Paper notes, however, that in some 
experimental cases, exposure to O3 has made plants more 
sensitive or vulnerable to some of these other important stressors, 
including disease, insect pests, and harsh weather (EPA, 2006a). The 
Staff Paper therefore concluded that this remains an important area of 
uncertainty and that additional research to better characterize the 
nature and significance of these interactions between O3 and 
other plant stressors would be useful.
c. Summary
    In summary, the Staff Paper concludes that the current secondary 
O3 standard is inadequate. This conclusion is based on the 
extensive vegetation effects evidence, in particular the recent 
empirical field-based evidence on biomass loss in seedlings, saplings 
and mature trees, and foliar injury incidence that has become available 
in this review, which demonstrates the occurrence of adverse vegetation 
effects at ambient

[[Page 37899]]

levels of recent O3 air quality, as well as evidence and 
exposure- and risk-based analyses indicating that adverse effects would 
be predicted to occur under air quality scenarios that meet the current 
standard.
3. CASAC Views
    In a letter to the Administrator (Henderson, 2006c), the CASAC 
O3 Panel, with full endorsement of the chartered CASAC, 
unanimously concluded that ``despite limited recent research, it has 
become clear since the last review that adverse effects on a wide range 
of vegetation including visible foliar injury are to be expected and 
have been observed in areas that are below the level of the current 8-
hour primary and secondary ozone standards.'' Therefore, ``based on the 
Ozone Panel's review of Chapters 7 and 8 [of the Staff Paper], the 
CASAC unanimously agrees that it is not appropriate to try to protect 
vegetation from the substantial, known or anticipated, direct and/or 
indirect, adverse effects of ambient O3 by continuing to 
promulgate identical primary and secondary standards for O3. 
Moreover, the members of the Committee and a substantial majority of 
the Ozone Panel agree with EPA staff conclusions and encourage the 
Administrator to establish an alternative cumulative secondary standard 
for O3 and related photochemical oxidants that is distinctly 
different in averaging time, form and level from the currently existing 
or potentially revised 8-hour primary standard'' (Henderson, 
2006c).\62\
---------------------------------------------------------------------------

    \62\ One CASAC Panel member reached different conclusions from 
those of the broader Panel regarding certain aspects of the 
vegetation effects information and the appropriate degree of 
emphasis that should be placed on the associated uncertainties. 
These concerns related to how the results of O3/
vegetation exposure experiments carried out in OTC can be 
extrapolated to the ambient environment and how C-R functions 
developed in the 1980's can be used today given that he did not 
expect that current crop species/cultivars in use in 2002 would have 
the same O3 sensitivity as those studied in NCLAN 
(Henderson, 2007, pg. C-18).
---------------------------------------------------------------------------

4. Administrator's Proposed Conclusions Concerning Adequacy of Current 
Standard
    The Administrator recognizes that the secondary standard is to 
protect against ``adverse'' O3 effects, discussed above in 
section IV.A.3. In considering what constitutes a vegetation effect 
that is also adverse to the public welfare, the Administrator took into 
account the Staff Paper conclusions regarding the nature and strength 
of the vegetation effects evidence, the exposure and risk assessment 
results, the degree to which the associated uncertainties should be 
considered in interpreting the results, and the views of CASAC and 
members of the public. On these bases, the Administrator proposes that 
the current secondary standard is inadequate to protect the public 
welfare from known and anticipated adverse O3-related 
effects on vegetation and ecosystems. Ozone levels that would be 
expected to remain after meeting the current secondary standard are 
sufficient to cause visible foliar injury, seedling and mature tree 
biomass loss, and crop yield reductions to degrees that could be 
considered adverse depending on the intended use of the plant and its 
significance to the public welfare, and the current secondary standard 
does not provide adequate protection from such effects. Other 
O3-induced effects described in the literature, including an 
impaired ability of many sensitive species and genotypes within species 
to adapt to or withstand other environmental stresses, such as freezing 
temperatures, pest infestations and/or disease, and to compete for 
available resources, would also be anticipated to occur. In the long 
run, the result of these impairments (e.g., loss in vigor) could lead 
to premature plant death in O3 sensitive species. Though 
effects on other ecosystem components have only been examined in 
isolated cases, effects such as those described above could have 
significant implications for plant community and associated species 
biodiversity and the structure and function of whole ecosystems. These 
considerations also support the proposed conclusion that the current 
secondary standard is not adequate and that revision is needed to 
provide additional public welfare protection.

E. Conclusions on the Elements of the Secondary Standard

    Given his proposed conclusion that the current secondary standard 
is inadequate, the Administrator then considered what revisions to the 
standard are appropriate. In so doing, the Administrator has focused on 
revisions to the key standard elements of indicator, form, averaging 
time, and level. On the basis of the strength and coherence of the 
vegetation effects evidence suggesting that a biologically-based 
standard for vegetation, at a minimum, should cumulate exposures and 
differentially-weight higher O3 concentrations, the 
Administrator judges that it is appropriate to consider revisions to 
the secondary standard that reflect this understanding. In addition, 
the Administrator also judges that the current 8-hour average form, 
though not based on the most biologically relevant and coherent 
vegetation effects literature, can also provide substantially improved 
protection to vegetation when set at an appropriate level. Therefore, 
the Administrator also considered whether revision to the level of the 
current 8-hour secondary standard might provide the requisite level of 
public welfare protection. In light of these considerations, as 
discussed below, the Administrator is proposing two options for 
revising the current secondary standard: one option is a cumulative 
seasonal standard (section IV.E.2) and the other option is an 8-hour 
average standard consistent with the revised 8-hour average standard 
proposed above for the primary standard (section IV.E.3). The 
Administrator has also considered an alternative approach to setting a 
cumulative, seasonal standard(s) as described below in section IV.E.2.
1. Indicator
    In the last review, EPA focused on a standard for O3 as 
the most appropriate surrogate for ambient photochemical oxidants. In 
this review, while the complex atmospheric chemistry in which 
O3 plays a key role has been highlighted, no alternatives to 
O3 have been advanced as being a more appropriate surrogate 
for ambient photochemical oxidants. Thus, as is the case for the 
primary standard, (discussed above in section II.D.1.), the 
Administrator proposes to continue to use O3 as the 
indicator for a standard that is intended to address effects associated 
with exposure to O3, alone and in combination with related 
photochemical oxidants. In so doing, the Administrator recognizes that 
measures leading to reductions in vegetation exposures to O3 
will also reduce exposures to other photochemical oxidants.
2. Cumulative, Seasonal Standard
    The Administrator proposes to replace the current secondary 
standard with a new cumulative, seasonal standard expressed as an index 
of the annual sum of weighted hourly concentrations (using the W126 
form), set at a level in the range of 7 to 21 ppm-hours. The index 
would be cumulated over the 12-hour daylight period (8 a.m. to 8 p.m.) 
during the consecutive 3-month period within the O3 season 
with the maximum index value. In addition, as discussed below, the 
Administrator is considering an alternative approach to setting a 
cumulative, seasonal standard(s) that would afford differing degrees of 
protection for O3-related impacts on different types of 
vegetation with different intended uses.

[[Page 37900]]

a. Form
    The current Criteria Document and Staff Paper concluded that the 
recent vegetation effects literature evaluated in this review 
strengthens and reaffirms conclusions made in the last review that the 
use of a cumulative exposure index that differentially-weights ambient 
concentrations is best able to relate ambient exposures to vegetation 
response at this time (EPA, 2006a, b; see also discussion in IV.B. 
above). The 1996 review focused in particular on two of these 
cumulative forms, the SUM06 and W126. As described in the last review 
(EPA, 1996a, b) it was concluded that, based on statistical reanalysis 
of the NCLAN data, these different cumulative forms performed equally 
well in predicting crop yield loss response to O3 exposure. 
Given that the data available at that time were unable to distinguish 
between these forms, the Administrator, based on the policy 
consideration of not including O3 concentrations considered 
to be within the PRB, concluded that the SUM06 form was the more 
appropriate choice for a secondary standard.
    In this review, the Staff Paper evaluated the continued 
appropriateness of the SUM06 form in light of two key pieces of 
information: new estimates of PRB that are lower than in the last 
review, and continued lack of evidence within the vegetation effects 
literature of a biological threshold for vegetation exposures of 
concern. On the basis of those policy and science-related 
considerations, the Staff Paper concluded that the W126 form was more 
appropriate in the context of this review. Specifically, the W126, by 
its incorporation of a sigmoidal weighting scheme, does not create an 
artificially imposed concentration threshold, gives proportionally more 
weight to the higher and typically more biologically potent 
concentrations, and is not significantly influenced by O3 
concentrations within the range of estimated PRB.
    The CASAC, based on its assessment of the same vegetation effects 
science, agreed with the Criteria Document and Staff Paper and 
unanimously concluded that it is not appropriate to try to protect 
vegetation from the known or anticipated adverse effects of ambient 
O3 by continuing to promulgate identical primary and 
secondary standards for O3. Moreover, the members of CASAC 
and a substantial majority of the CASAC O3 Panel agreed with 
Staff Paper conclusions and encouraged the Administrator to establish 
an alternative cumulative secondary standard for O3 and 
related photochemical oxidants that is distinctly different in 
averaging time, form, and level from the current or potentially revised 
8-hour primary standard. The CASAC also stated that ``the recommended 
metric for the secondary ozone standard is the (sigmoidally-weighted) 
W126 index'' (Henderson, 2007).\63\
---------------------------------------------------------------------------

    \63\ One CASAC Panel member expressed the view that the 
O3 exposure indices, SUM06 and W126, are simply 
mathematical expressions of exposure and, thus, cannot be said to 
have a biological basis (Henderson, 2007, pg. C-18).
---------------------------------------------------------------------------

    The Administrator agrees with the conclusions drawn in the Criteria 
Document, Staff Paper and by CASAC that the scientific evidence 
available in the current review continues to demonstrate the cumulative 
nature of O3-induced plant effects and the need to give 
greater weight to higher concentrations. Thus, the Administrator 
concludes that a cumulative exposure index that differentially-weights 
O3 concentrations represents a reasonable policy choice for 
a seasonal secondary standard to protect against the effects of 
O3 on vegetation. The Administrator further agrees with both 
the Staff Paper and CASAC that the most appropriate cumulative, 
concentration-weighted form to consider in this review is the 
sigmoidally weighted W126 form, due to his recognition that there is no 
evidence in the literature for an exposure threshold that would be 
appropriate across all O3-sensitive vegetation and that this 
form is unlikely to be significantly influenced by O3 air 
quality within the range of PRB levels identified in this review. Thus, 
the Administrator proposes as one option to replace the current 8-hour 
average secondary standard form with the cumulative, seasonal W126 
form.
b. Averaging Times \64\
---------------------------------------------------------------------------

    \64\ While the term ``averaging time'' is used, for the 
cumulative, seasonal standard the time period at issue is one over 
which exposures during a specified period of time are cumulated, not 
averaged.
---------------------------------------------------------------------------

    The Staff Paper, in addition to form, also considers what 
``averaging'' periods or exposure durations are most relevant for 
vegetation, which, unlike people, is exposed to ambient air 
continuously throughout its lifespan. For annual species, this lifespan 
encompasses a period of only one year or less; while for perennials, 
lifespans can range from a few years to decades or centuries. However, 
because O3 levels are not continuously elevated and plants 
are not equally sensitive to O3 over the course of a day, 
season or lifetime, it becomes necessary to identify periods of 
exposure that have the most relevance for plant response. Exposure 
periods are discussed below in terms of a seasonal window, a diurnal 
window, and an annual versus 3-year average standard.
    (1) In considering an appropriate seasonal window, the Staff Paper 
recognizes that, in general, many annual crops are grown for periods of 
a few months before being harvested. In contrast, other annual and 
perennial species may be photosynthetically active longer, and for some 
species and locations, throughout the entire year. In general, the 
period of maximum physiological activity and thus, maximum potential 
O3 uptake for annual crops, herbaceous species, and 
deciduous trees and shrubs coincides with some or all of the intra-
annual period defined as the O3 season, which varies on a 
state-by-state basis. This is because the high temperature and high 
light conditions that promote the formation of tropospheric 
O3 also promote physiological activity in vegetation.
    The Staff Paper notes that the selection of any single seasonal 
exposure period for a national standard would represent a compromise, 
given the significant variability in growth patterns and lengths of 
growing seasons among the wide range of vegetation species occurring 
within the U.S. that may experience adverse effects associated with 
O3 exposures. However, the Staff Paper further concludes 
that the consecutive 3-month period within the O3 season 
with the highest W126 index value (e.g., maximum 3 month period) would, 
in most cases, likely coincide with the period of greatest plant 
sensitivity on an annual basis. Therefore, the Staff Paper again 
concludes, as it did in 1996, that the annual maximum consecutive 3-
month period is a reasonable seasonal time period, when combined with a 
cumulative, concentration weighted form, for protection of sensitive 
vegetation.
    (2) In considering an appropriate diurnal window, the Staff Paper 
recognizes that over the course of the 24-hour diurnal period, plant 
stomatal conductance varies in response to changes in light level, soil 
moisture and other environmentally and genetically controlled factors. 
In general, stomata are most open during daylight hours in order to 
allow sufficient CO2 uptake for use in carbohydrate 
production through the light-driven process of photosynthesis. At most 
locations, O3 concentrations are also highest during the 
daytime, and thus, most likely to coincide with maximum stomatal 
uptake. It is also known however, that in some species, stomata may 
remain

[[Page 37901]]

open sufficiently at night to allow for some nocturnal uptake to occur. 
In addition, at some rural, high elevation sites, the O3 
concentrations remain relatively flat over the course of the day, often 
at levels above estimated PRB. At these sites, nighttime W126 values 
can be of similar magnitude as daytime values, though the significance 
of these exposures is much less certain. This is because O3 
uptake during daylight hours is known to impair the light-driven 
process of photosynthesis, which can then lead to impacts on 
carbohydrate production, plant growth, reproduction (yield) and root 
function. It is less clear at this time to what extent and by what 
mechanisms O3 uptake at night adversely impacts plant 
function. In addition, many species do not take up O3 at 
night or occur in areas with elevated nighttime O3 
concentrations.
    In light of a recent work on this topic conducted by Musselman and 
Minnick (2000), the Staff Paper again revisited the issue of what 
diurnal period is of most relevance in influencing O3-
induced effects on vegetation. This work reports that some species take 
up O3 at night, but that the degree of nocturnal stomatal 
conductance varies widely between species and its relevance to overall 
O3-induced vegetation effects remain unclear. In considering 
this information, the Staff Paper concludes that for the vast majority 
of studied species, daytime exposures represent the majority of diurnal 
plant O3 uptake and are responsible for inducing the plant 
response of most significance to the health and productivity of the 
plant (e.g., reduced carbohydrate production). Until additional 
information is available about the extent to which co-occurrence of 
sensitive species and elevated nocturnal O3 exposures 
exists, and what levels of nighttime uptake are adverse to affected 
species, the Staff Paper concludes that this information continues to 
be preliminary, and does not provide a basis for reaching a different 
conclusion at this time. The Staff Paper further notes that additional 
research is needed to address the degree to which a 12-hour diurnal 
window may be under protective in areas where elevated nighttime levels 
of O3 co-occur with sensitive species with a high degree of 
nocturnal stomatal conductance. Thus, as in the last review, the Staff 
Paper again concludes that based on the available science, the daytime 
12-hour window (8 a.m. to 8 p.m.) is the most appropriate period over 
which to cumulate diurnal O3 exposures, specifically those 
most relevant to plant growth and yield responses.
    (3) In considering whether an annual or 3-year averaging period is 
more appropriate, the Staff Paper recognized that though most 
cumulative seasonal exposure levels of concern for vegetation have been 
expressed in terms of the annual timeframe, it may be appropriate to 
consider a 3-year averaging period for purposes of standard stability. 
However, the Staff Paper notes that for certain welfare effects of 
concern (e.g., foliar injury, yield loss for annual crops, growth 
effects on other annual vegetation and potentially tree seedlings), an 
annual time frame may be a more appropriate period in which to assess 
what level would provide the requisite degree of protection, while for 
other welfare effects (e.g., mature tree biomass loss), a 3-year 
averaging period may also be appropriate. Thus, the Staff Paper 
concludes that it is appropriate to consider both an annual and a 3-
year averaging period. Further, the Staff Paper concludes that should a 
3-year average of the 12-hour W126 form be selected, a potentially 
lower level should be considered to reduce the potential of adverse 
impacts to annual species from a single high O3 year that 
could still occur while attaining a standard on average over 3-years.
    The CASAC, in considering what seasonal and diurnal time periods 
are most appropriate when combined with a cumulative, concentration-
weighted form to protect vegetation from exposures of concern, agreed 
that the Staff Paper conclusion regarding the 3-month seasonal period 
and 12-hour daylight window was appropriate, with the distinction that 
both time designations likely represents the minimum time periods of 
importance. In particular, one O3 Panel member commented 
that for some species, additional O3 exposures of importance 
were occurring outside the 3-month seasonal and 12-hour diurnal 
windows. Further, the CASAC concluded that multi-year averaging to 
promote a ``stable'' secondary standard is less appropriate for a 
cumulative, seasonal secondary standard than for a primary standard 
based on maximum 8-hour concentrations. CASAC further concluded that if 
multi-year averaging is employed to increase the stability of the 
secondary standard, the level of the standard should be revised 
downward to assure that the desired degree of protection is not 
exceeded in individual years.
    The Administrator, in determining which seasonal and diurnal time 
periods are most appropriate to propose, took into account Staff Paper 
and CASAC views. The Administrator, in being careful to consider what 
is needed to provide the requisite degree of protection, no more and no 
less, proposes that the 3-month seasonal period and 12-hour daylight 
period are appropriate. Based on the Staff Paper conclusions discussed 
above, the Administrator is mindful that there is the potential for 
under-protection with a 12-hour diurnal window in areas with 
sufficiently elevated nighttime levels of O3 where sensitive 
species with a high degree of nocturnal stomatal conductance occur. On 
the other hand, the Administrator also recognizes that a longer diurnal 
window (e.g., 24-hour) has the possibility of over-protecting 
vegetation in areas where nighttime O3 levels remain 
relatively high but where no species having significant nocturnal 
uptake exist. In weighing these considerations, the Administrator 
agrees with the Staff Paper conclusion that until additional 
information is available about the extent to which this co-occurrence 
of sensitive species and elevated nocturnal O3 exposures 
exists, and what levels of nighttime uptake are adverse to affected 
species, this information does not provide a basis for reaching a 
different conclusion at this time. The Administrator also considered to 
what extent the 3-month period within the O3 season was 
appropriate, recognizing that many species of vegetation have longer 
growing seasons. The Administrator further proposes that the maximum 3-
month period is sufficient and appropriate to characterize 
O3 exposure levels associated with known levels of plant 
response. Therefore, the Administrator proposes that the most 
appropriate exposure periods for a cumulative, seasonal form is the 
daytime 12-hour window (8 a.m. to 8 p.m.) during the consecutive 3-
month period within the O3 monitoring season with the 
maximum W126 index value.
    The Administrator also proposes an annual rather than a multi-year 
cumulative, seasonal standard. In proposing this alternative, the 
Administrator also believes that it is appropriate to consider the 
benefits to the public welfare that would accrue from establishing a 3-
year average secondary standard, and solicits comment on this 
alternative. In so doing, the Administrator also agrees with Staff 
Paper and CASAC conclusions that should a 3-year standard be finalized, 
the level of the standard should be set so as to provide the requisite 
degree of protection for those vegetation effects judged to be adverse 
to the public welfare within a single annual period.

[[Page 37902]]

c. Level
    The Staff Paper, in identifying a range of levels for a 3-month, 
12-hour W126 annual form appropriate to protect the public welfare from 
adverse impacts to vegetation from O3 exposures, considers 
what information from the array of vegetation effects evidence and 
exposure and risk assessment results was most useful. In regards to the 
vegetation effects evidence, the Staff Paper finds stronger support 
than what was available at the time of the last review for an increased 
level of protection for trees and ecosystems. Specifically, this 
expanded body of support includes: (1) Additional field based data from 
free air, gradient and biomonitoring surveys demonstrating adverse 
levels of O3-induced above and/or below-ground growth 
reductions on trees at the seedling, sapling and mature growth stages 
and incidence of visible foliar injury occurring at biomonitoring sites 
in the field at ambient levels of exposure; (2) qualitative support 
from free air (e.g., AspenFACE) and gradient studies on a limited 
number of tree species for the continued appropriateness of using OTC-
derived C-R functions to predict tree seedling response in the field; 
(3) studies that continue to document below-ground effects on root 
growth and ``carry-over'' effects occurring in subsequent years from 
O3 exposures; and (4) increased recognition and 
understanding of the structure and function of ecosystems and the 
complex linkages through which O3, and other stressors, 
acting at the organism and species level can influence higher levels 
within the ecosystem hierarchy and disrupt essential ecological 
attributes critical to the maintenance of ecosystem goods and services 
important to the public welfare.
    Based on the above observations and on the vegetation effects and 
the results of the exposure and impact assessment summarized above, the 
Staff Paper concludes that just meeting the current standard would 
still allow adverse levels of tree seedling biomass loss in sensitive 
commercially and ecologically important tree species in many regions of 
the country. Seedling risk assessment results showed that some tree 
seedling species are extremely sensitive (e.g., cottonwood, black 
cherry and aspen), with annual biomass losses occurring in the field of 
the same or greater magnitude that that of annual crops. Such 
information from the tree seedling risk assessment suggests that air 
quality levels would need to be substantially reduced to protect 
sensitive tree seedlings like black cherry from growth and foliar 
injury effects.
    In addition to the currently quantifiable risks to trees from 
ambient exposures, the Staff Paper also considers the more subtle 
impacts of O3 acting in synergy with other natural and man-
made stressors to adversely affect individual plants, populations and 
whole systems. By disrupting the photosynthetic process, decreasing 
carbon storage in the roots, increasing early senescence of leaves and 
affecting water use efficiency in trees, O3 exposures could 
potentially disrupt or change the nutrient and water flow of an entire 
system. Weakened trees can become more susceptible to other 
environmental stresses such as pest and pathogen outbreaks or harsh 
weather conditions. Though it is not possible to quantify all the 
ecological and societal benefits associated with varying levels of 
alternative secondary standards, the Staff Paper concludes that this 
information should be weighed in considering the extent to which a 
secondary standard should be set so as to provide potential protection 
against effects that are anticipated to occur.
    In addition, the Staff Paper also recognizes that in the last 
review, the Administrator took into account the results of a 1996 
consensus-building workshop as described in a January 1997 report (Heck 
and Cowling, 1997). At this workshop, a group of independent scientists 
expressed their judgments on what standard form(s) and level(s) would 
provide vegetation with adequate protection from O3-related 
adverse effects. Consensus was reached with respect to selecting 
appropriate ranges of levels in terms of a cumulative, seasonal 3-
month, 12-hr SUM06 standard for a number of vegetation effects 
endpoints. These ranges are identified below, with the estimated 
approximate equivalent W126 standard values shown in parentheses. For 
growth effects to tree seedlings in natural forest stands, a consensus 
was reached that a range of 10 to 15 (7 to 13) ppm-hours would be 
protective. For growth effects to tree seedlings and saplings in 
plantations, the consensus range was 12 to 16 (9 to 14) ppm-hours. For 
visible foliar injury to natural ecosystems, the consensus range was 8 
to 12 (5 to 9) ppm-hours (Heck and Cowling, 1997).
    Taking these consensus statements into account, the Administrator 
stated in the final rule (62 FR 38856) that ``the report lends 
important support to the view that the current secondary standard is 
not adequately protective of vegetation * * * [and] * * * foreshadows 
the direction of future scientific research in this area, the results 
of which could be important in future reviews of the O3 
secondary standard'' (62 FR 38856).
    Given the importance the Administrator put on the consensus report 
in the last review, the Staff Paper considered to what extent new 
research provided empirical support for the ranges of levels identified 
by the experts as protective of different types of O3-
induced effects. On the basis of new field-based tree seedling growth 
loss and foliar injury data, and including both the above quantitative 
and qualitative information regarding O3-induced effects on 
sensitive trees and forested ecosystems, the Staff Paper concludes that 
it is appropriate to consider a range for a 3-month, 12-hour, W126 
standard that includes the consensus recommendations for growth effects 
in tree seedlings in natural forest stands.
    In considering the newly available information on O3-
related effects on crops in this review, the Staff Paper observes the 
following regarding the strength of the underlying crop science: (1) 
Nothing in the recent literature points to a change in the relationship 
between O3 exposure and crop response across the range of 
species and/or cultivars of commodity crops currently grown in the U.S. 
that could be construed to make less appropriate the use of commodity 
crop C-R functions developed in the NCLAN program; (2) new field-based 
studies (e.g., SoyFACE) provide qualitative support in a few limited 
cases for the appropriateness of using OTC-derived C-R functions to 
predict crop response in the field; and (3) refinements in the 
exposure, risk and benefits assessments in this review reduce some of 
the uncertainties present in 1996. On the basis of these observations, 
the Staff Paper concludes that nothing in the newly assessed 
information calls into question the strength of the underlying science 
upon which the Administrator based her proposed decision in the last 
review to select a level of a cumulative, seasonal form associated with 
protecting 50 percent of crop cases from no more than 10 percent yield 
loss as providing the requisite degree of protection for commodity 
crops.
    The Staff Paper then considered whether any additional information 
is available to inform judgments as to the adversity of various 
O3-induced levels of crop yield loss to the public welfare. 
As noted above, the Staff Paper observes that agricultural systems are 
heavily managed, and that in addition to stress from O3, the 
annual productivity of agricultural systems is vulnerable to

[[Page 37903]]

disruption from many other stressors (e.g., weather, insects, disease), 
whose impact in any given year can greatly outweigh the direct 
reduction in annual productivity resulting from elevated O3 
exposures. On the other hand, O3 can also more subtly impact 
crop and forage nutritive quality and indirectly exacerbate the 
severity of the impact from other stressors. Though these latter 
effects currently cannot be quantified, they should be considered in 
judging to what extent a level of protection selected to protect 
commodity crops should be precautionary.
    Based on the above considerations, the Staff Paper concludes that 
the level of protection judged requisite in the last review to protect 
the public welfare from adverse levels of O3-induced 
reductions in crop yields, as provided by a W126 level of 21 ppm-hours, 
remains appropriate for consideration as an upper bound of a range of 
appropriate levels.
    Thus, the Staff Paper concludes, based on all the above 
considerations, that an appropriate range of 3-month, 12-hour W126 
levels is 7 to 21 ppm-hours, recognizing that the level selected is 
largely a policy judgment as to the requisite level of protection 
needed. In determining the requisite level of protection for crops and 
trees, the Staff Paper recognizes that it is appropriate to weigh the 
importance of the predicted risks of these effects in the overall 
context of public welfare protection, along with a determination as to 
the appropriate weight to place on the associated uncertainties and 
limitations of this information.
    The CASAC, in its final letter to the Administrator (Henderson, 
2007), agreed with the Staff Paper recommendations that the lower bound 
of the range within which a seasonal W126 welfare-based (secondary) 
O3 standard should be considered is approximately 7 ppm-
hours; however, it did not agree with Staff's recommendation that the 
upper bound of the range should be as high as 21 ppm-hours. Rather, 
CASAC recommended that the upper bound of the range considered should 
be no higher than 15 ppm-hours, which the Panel estimates is 
approximately equivalent to a seasonal 12-hour SUM06 level of 20 ppm-
hours. The lower end of this range (7 ppm-hours) is the same as the 
lower end of the range identified in the 1997 Consensus Workshop as 
protective of tree seedlings in natural forest stands from growth 
effects (Heck and Cowling, 1997).
    The Administrator, taking Staff Paper and CASAC views into account, 
proposes a range of levels for a cumulative, seasonal secondary 
standard as expressed in terms of the maximum 3 month, 12-hour W126 
form, in the range of 7 to 21 ppm-hours. This range encompasses the 
range of levels recommended by CASAC, and also includes a higher level 
as recommended in the Staff Paper. Given the uncertainty in determining 
the risk attributable to various levels of exposure to O3, 
the Administrator believes as a public welfare policy judgment that 
this is a reasonable range to propose.
    In taking into account the uncertainty associated with the above, 
the Administrator has also considered an alternative approach to 
establishing a secondary standard(s). This alternative approach would 
establish a cumulative, seasonal standard(s) that would afford 
differing degrees of protection for O3-related impacts on 
different types of vegetation with different intended uses.
    The Administrator recognizes that known O3-sensitive 
plant species growing within the U.S experience a variety of 
O3-induced effects, including visible foliar injury, biomass 
loss and yield loss, and that the public welfare significance of each 
of these effects can vary significantly, depending on the nature of the 
effect, the intended use of the plant, and/or the type of environment 
or location in which the plant grows. Any given O3-related 
effect on vegetation (e.g., biomass loss, or foliar injury) may be 
judged to have a different degree of impact on public welfare 
depending, for example, on whether that effect occurs in a Class I 
area, commercial cropland, or a city park. This variation in the 
significance of O3-related vegetation effects from a public 
welfare perspective across type of effect, intended plant use, and area 
grown means that the level of ambient O3 that is requisite 
to protect the public welfare may also vary. The level of ambient 
O3 that is requisite in a federally designated Class I area 
may be lower than the level that is requisite in a cropland area. EPA 
is therefore considering and soliciting comment on an alternative 
approach for the secondary O3 standard, with the aim of 
reasonably reflecting these variations.
    Specifically, the Administrator seeks comment on an alternative 
approach that would establish a suite of secondary standards. The suite 
of standards would contain different ambient levels, with each standard 
at a level that is requisite to protect public welfare for that 
variation in plant effect, use, and/or location. For example, a 
secondary standard intended to provide protection to natural systems 
valued for their aesthetic beauty and/or important ecological functions 
they might serve could be set at a lower, more protective level to 
provide the requisite degree of protection against a broad array of 
O3-related effects on important sensitive species in such 
areas. In contrast, while negative impacts on yield production in 
sensitive agricultural crops is also an important public welfare 
effect, O3-related reductions in yield may be considered 
less significant or adverse to the public welfare, depending on the 
degree of impact, since the intended use of such land is to produce 
optimum yields and croplands are already heavily managed to achieve 
that goal. Thus, a secondary standard set to provide the requisite 
degree of crop protection for such an area could be set at a higher 
level.
    The Administrator recognizes that variation in vegetation type and 
location, intended use, and impacts related to O3 exposure 
can be diverse, and believes that it is appropriate to consider whether 
it is appropriate and feasible to establish a suite of standards that 
accounts more broadly for such variation. EPA recognizes that this 
approach is unique with regard to secondary standards and will pose 
unique challenges, including how to classify areas according to 
intended use. Some geographic areas have already been identified for 
specific uses, such as Federal Class I areas,\65\ which are intended to 
conserve unimpaired natural ecosystems and their associated species for 
the enjoyment of future generations. Likewise, the USDA has classified 
cultivated areas in the U.S. into certain categories of intended use 
(such as cropland, rangeland, timberland) that could help inform the 
setting of a suite of standards.
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    \65\ The Clean Air Act defines Class I areas as national parks 
over 6,000 acres, national wilderness areas and national memorial 
parks over 5,000 acres, and international parks. The National Park 
Service was created in 1916 by Congress through the National Park 
Service Organic Act in order to ``conserve the scenery and the 
natural and historic objects and the wild life therein and to 
provide for the enjoyment of the same in such manner and by such 
means as will leave them unimpaired for the enjoyment of future 
generations.''
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    EPA is taking comment on all aspects of this alternative approach, 
including whether it is appropriate to set a suite of secondary 
standards that varies depending on use, location, and type of effect on 
vegetation. EPA invites comment on the appropriateness of this 
approach, from the scientific, legal, and policy perspectives, and on 
other factors that should be considered in determining the 
applicability of any one level within a suite of standards.

[[Page 37904]]

3. 8-Hour Average Standard
    The Administrator is also proposing to revise the current secondary 
standard by making it identical to the proposed 8-hour primary 
standard, which is proposed to be within the range of 0.070 to 0.075 
ppm. For this option, EPA also solicits comment on a wider range of 8-
hour standard levels, including levels down to 0.060 ppm and up to the 
current standard (i.e., effectively 0.084 ppm with the current rounding 
convention).
    In the last review, the Staff Paper included an analysis to compare 
the degree of overlap between areas that would be expected not to meet 
the range of alternative 8-hour standards being considered for the 
primary NAAQS and those expected not to meet the range of values 
(expressed in terms of the seasonal SUM06 index) of concern for 
vegetation. This result suggested that improvements in national air 
quality expected to result from attaining an 8-hour primary standard 
within the recommended range of levels would also be expected to reduce 
levels of concern for vegetation in those same areas. In the 1997 final 
rule, the decision was made, on the basis of both science and policy 
considerations, to make the secondary identical to the primary 
standard. It acknowledged, however, that uncertainties remained ``as to 
the extent to which air quality improvements designed to reduce 8-hour 
average O3 concentrations averaged over a 3-year period 
would reduce O3 exposures measured by a seasonal SUM06 
index'' (62 FR 38876).
    On the basis of that history, the current Staff Paper analyzed the 
degree of overlap expected between alternative 8-hour and cumulative 
seasonal secondary standards (as discussed above in section IV.C.1) 
using recent air quality. Based on the results, the Staff Paper 
concluded that the degree to which the current 8-hour standard form and 
level would overlap with areas of concern for vegetation expressed in 
terms of the 12-hour W126 standard is inconsistent from year to year 
and would depend greatly on the level of the 12-hour W126 and 8-hour 
standards selected and the distribution of hourly O3 
concentrations within the annual and/or 3-year average period.
    Thus, though the Staff Paper recognized again that meeting the 
current or alternative levels of the 8-hour average standard could 
result in air quality improvements that would potentially benefit 
vegetation in some areas, it urges caution be used in evaluating the 
likely vegetation impacts associated with a given level of air quality 
expressed in terms of the 8-hour average form in the absence of 
parallel W126 information. This caution is due to the concern that the 
analysis in the Staff Paper may not be an accurate reflection of the 
true situation in non-monitored, rural counties due to the lack of more 
complete monitor coverage in many rural areas. Further, of the counties 
that did not show overlap between the two standard forms, most were 
located in rural/remote high elevation areas which have O3 
air quality patterns that are typically different from those associated 
with urban and near urban sites at lower elevations. Because the 
majority of such areas are currently not monitored, it is believed 
there are likely to be additional areas that have similar air quality 
distributions that would lead to the same disconnect between forms. 
Thus, the Staff Paper concluded that it remains problematic to 
determine the appropriate level of protection for vegetation using an 
8-hour average form.
    The CASAC recognized that an important difference between the 
effects of acute exposures to O3 on human health and the 
effects of O3 exposures on welfare is that vegetation 
effects are more dependent on the cumulative exposure to, and uptake 
of, O3 over the course of the entire growing season 
(Henderson, 2006c). The CASAC O3 Panel members were 
unanimous in concluding the protection of natural terrestrial 
ecosystems and managed agricultural crops requires a secondary 
O3 standard that is substantially different from the primary 
O3 standard in averaging time, level, and form (Henderson, 
2007).
    A number of public commenters also presented views for the 
Administrator's consideration regarding the adequacy of the current 
standard and whether or not revisions to that standard were warranted. 
These commenters did not support adopting an alternative, cumulative 
form for the secondary standard. These commenters stated that ``though 
directionally a cumulative form of the standard may better match the 
underlying data,'' they believed further work is needed to determine 
whether a cumulative exposure index for the form of the secondary 
standard is necessary. These commenters identified a number of key 
concerns regarding the available evidence that, in their view, make it 
inappropriate to revise the secondary standard at this time. In 
particular they assert that (1) The key uncertainties, cited by the 
Administrator in the 1997 review as reasons for deciding it was not 
appropriate to move forward with a seasonal secondary, have not been 
materially reduced in the current review; and (2) the exposure 
assessment is inaccurate and too uncertain due to the use of low 
estimates of PRB, an arbitrary rollback method that is uninformed by 
atmospheric chemistry from photochemical models, and the use of the 
CMAQ model in the west, whose biases and uncertainties are 
insufficiently characterized and evaluated.
    In considering the appropriateness of proposing a revised secondary 
standard that would be identical to the proposed primary standard, the 
Administrator took into account the approach used by the Agency in the 
last review, the conclusions of the Staff Paper, CASAC advice, and the 
views of public commenters. The Administrator first considered the 
Staff Paper analysis of the projected degree of overlap between 
counties with air quality expected to meet various alternative levels 
of an 8-hour standard and alternative levels of a W126 standard based 
on monitored air quality data. This analysis showed significant overlap 
within the proposed range of the primary 8-hour form and selected 
levels of the W126 standard form being considered, with the degree of 
overlap between these two forms depending greatly on the levels 
selected and the distribution of hourly O3 concentrations 
within the annual and/or 3-year average period. On this basis, the 
Administrator recognizes that a secondary standard set identical to the 
proposed primary standard would provide a significant degree of 
additional protection for vegetation as compared to that provided by 
the current secondary standard. The Administrator also recognizes that 
lack of rural monitoring data makes uncertain the degree to which the 
proposed 8-hour or W126 alternatives would be protective, and that 
there would be the potential for not providing the appropriate degree 
of protection for vegetation in areas with air quality distributions 
that result in a high cumulative, seasonal exposure but do not result 
in high 8-hour average exposures. While this potential for under-
protection is clear, the number and size of areas at issue and the 
degree of risk is hard to determine. However, such a standard would 
also tend to avoid the potential for providing more protection than is 
necessary, a risk that would arise from moving to a new form for the 
secondary standard despite significant uncertainty in determining the 
degree of risk for any exposure level and the appropriate level of 
protection, as well as uncertainty in predicting exposure and risk 
patterns.
    The Administrator also considered the views and recommendations of

[[Page 37905]]

CASAC, and agrees that a cumulative, seasonal standard is the most 
biologically relevant way to relate exposure to plant growth response. 
However, as reflected in the public comments, the Administrator also 
recognizes that there remain significant uncertainties in determining 
or quantifying the degree of risk attributable to varying levels of 
O3 exposure, the degree of protection that any specific 
cumulative, seasonal standard would produce, and the associated 
potential for error in determining the standard that will provide a 
requisite degree of protection--i.e. sufficient but not more than what 
is necessary. Given this uncertainty, the Administrator also believes 
it is appropriate to consider the degree of protection that would be 
afforded by a secondary standard that is identical to the proposed 
primary standard. Based on his consideration of the full range of views 
as described above, the Administrator proposes as a second option to 
revise the secondary standard to be identical in every way to the 
proposed primary standard.

F. Proposed Decision on the Secondary Standard

    The Administrator proposes to replace the current secondary 
standard with one of two options. One option is a new cumulative, 
seasonal standard expressed as an index of the annual sum of weighted 
hourly concentrations (using the W126 form), set at a level in the 
range of 7 to 21 ppm-hours. The index would be cumulated over the 12-
hour daylight period (8 a.m. to 8 p.m.) during the consecutive 3-month 
period within the O3 season with the maximum index value. 
The other option is to revise the current secondary standard by making 
it identical to the proposed 8-hour primary standard, which is proposed 
to be within the range of 0.070 to 0.075 ppm. For this option, EPA also 
solicits comment on a wider range of 8-hour standard levels, including 
levels down to 0.060 ppm and up to the current standard (i.e., 
effectively 0.084 ppm with the current rounding convention. The 
Administrator is also soliciting comment on an alternative approach for 
a setting cumulative, seasonal standard(s) that would afford differing 
degrees of protection for O3-related impacts on different 
types of vegetation with different intended uses.

V. Creation of Appendix P--Interpretation of the NAAQS for Ozone

    The EPA is proposing to create Appendix P to 40 CFR part 50 to 
reflect the proposed revisions to the primary and secondary standards 
discussed above. This Appendix would explain the computations necessary 
for determining when the proposed primary and secondary standards are 
met. More specifically, Appendix P addresses data completeness 
requirements, data reporting, handling, and rounding conventions, and 
example calculations. Although EPA is proposing two alternative 
secondary standards, the proposed Appendix has been written to address 
a seasonal secondary standard expressed in the W126 form. If EPA adopts 
a secondary standard identical to the primary standard, Appendix P will 
be modified accordingly. The proposed Appendix also reflects the final 
rule promulgated on March 22, 2007 for the treatment of data influenced 
by exceptional events (72 FR 13560).
Key elements of the proposed revisions to Appendix P are outlined 
below.

A. Data Completeness

    The data completeness requirements in Appendix P proposed here for 
the proposed 8-hr primary standard secondary standards are the same as 
those in Appendix I to 40 CFR part 50 required for the current 
standard. To satisfy the date completeness requirement, Appendix P 
would require 90% data completeness, on average, for the 3-year period 
at a monitoring site, with no single year within the period having less 
than 75% data completeness. This data completeness requirement would 
have to be satisfied in order to determine that the standard(s) have 
been met at a monitoring site. A site could be found not to have met 
the standard(s) with less than complete data. EPA concluded in adopting 
these same data completeness requirements in Appendix I in 1997 that 
these proposed requirements are reasonable based on its earlier 
analysis of available air quality data that showed that 90% of all 
monitoring sites that are operated on a continuous basis routinely meet 
this objective. The EPA is seeking comment, however, on whether 
meteorological data would provide an objective basis for determining, 
on a day for which there is missing data, that the meteorological 
conditions were not conducive to high O3 concentrations, and 
therefore, that the day could be assumed to have an O3 
concentration less than 0.070 to 0.075 ppm.
    We are proposing separate data completeness requirements for the 
proposed seasonal secondary standard expressed in the W126 form. For 
such a standard, Appendix P would require a site to have 75% data 
completeness in a given month. Appendix P would also provide a 
mechanism for adjusting for missing data. Because this alternative is a 
seasonal cumulative index, representing a distribution of O3 
values under a range of meteorological conditions, rather than a peak 
statistic, the EPA is proposing a missing data procedure that would 
require the monthly total index to be adjusted for incomplete data by 
multiplying the unadjusted W126 value by the ratio of the number of 
possible daylight hours (8:00 a.m. to 8:00 p.m.) to the number of hours 
with valid ambient hourly concentrations. This adjustment is analogous 
to calculating an estimated number of exceedances contained within part 
50 Appendix I for the one hour O3 standard.

B. Data Handling and Rounding Conventions

    Almost all State agencies now report hourly O3 
concentrations to three decimal places, in ppm, since the typical 
incremental sensitivity of currently used O3 monitors is 
0.001 ppm. Consistent with the current approach for computing 8-hr 
averages, in calculating 8-hr average O3 concentrations from 
such hourly data, any calculated digits past the third decimal place 
would be truncated to preserve the number of significant digits in the 
reported data. In calculating 3-year averages of the fourth highest 
maximum 8-hr average concentrations, EPA is proposing to require the 
result to be reported to the third decimal place with digits to the 
right of the third decimal place truncated to preserve the number of 
significant digits in the reported data, as prescribed by the current 
standard. Analyses discussed in the Staff Paper demonstrated that 
taking into account the precision and bias in 1-hour O3 
measurements, the 8-hour design value had an uncertainty of 
approximately 0.001 ppm. Thus, EPA considers any value less than 0.001 
ppm to be highly uncertain and, therefore, proposes truncating both the 
individual 8-hour averages used to determine the annual fourth maximum 
as well as the 3-year average of the fourth maxima to the third decimal 
place. Nevertheless, EPA solicits comment on the appropriateness of 
rounding to the third decimal place as well as the policy reasons 
behind either truncating or rounding the 3-year average to the third 
decimal place (with 0.0005 and greater rounding up). EPA is also 
seeking comment on the scientific validity of truncating the three year 
average as opposed to rounding it as well as the policy reasons behind 
either truncating or rounding the average to the third decimal place.

[[Page 37906]]

    To determine whether the proposed standard is met, the calculated 
value of the fourth highest maximum 8-hour average concentrations, 
averaged over three years, would be compared to the level of the 
standard. As discussed in section II, the EPA is proposing to issue an 
8-hr standard extending to three decimal places, based on the staff's 
analysis and conclusions discussed in the Staff paper that expressing 
the proposed standard to the third decimal place is consistent with the 
precision requirements of the current O3 monitoring 
technology. Given that both the proposed standard and the calculated 
value of the 3-year average of the fourth highest maximum 8-hr 
O3 concentration are expressed to three decimal places, the 
two values can be compared directly. This is different than the 
approach for determining compliance with the current standard 
O3 standard. In comparing the calculated 3-year average 
(which is expressed to three decimal places) to the current standard 
O3 standard (which is expressed to only two decimal places), 
Appendix I requires the calculated 3-year average to be rounded to two 
decimal places. This additional step would not be necessary for the 
proposed standard given that the standard and the 3-year average are 
each expressed to three decimal places.
    For the proposed seasonal secondary standard, the annual maximum 3-
month W126 value computed on a calendar year basis using the three 
highest, consecutive monthly W126 values would be used as the summary 
statistic. The resulting value would then be compared to the level of 
the secondary O3 standard. The Agency is also interested in 
receiving comments regarding a 3-year average form summary statistic.

VI. Ambient Monitoring Related to Proposed Revised O3 
Standards

    The EPA is not proposing any specific changes to existing 
requirements for monitoring of O3 in the ambient air. 
However, we invite comment on a number of issues which naturally arise 
in connection with the proposed revision of the O3 NAAQS. 
The EPA may propose changes to some of the existing requirements at a 
later date.
    Current requirements regarding EPA-approved measurement methods for 
ambient O3 are stated in 40 CFR part 50 Appendix D, 
Measurement Principle and Calibration Procedure for the Measurement of 
Ozone in the Atmosphere, and in 40 CFR part 53, Ambient Air Monitoring 
Reference and Equivalent Methods. The EPA does not intend to propose 
any changes to these requirements, because we believe these 
requirements would continue to be appropriate to support implementation 
of a revised O3 NAAQS.
    Presently, States (including the District of Columbia, Puerto Rico, 
and the Virgin Islands, and including local agencies when so delegated 
by the State) are required to operate minimum numbers of EPA-approved 
O3 monitors based on the population of each of their 
Metropolitan Statistical Areas (MSA) and the most recently measured 
O3 levels in each area. Each State (or in some cases 
portions of a State) also has a required O3 monitoring 
season based on historical experience on when O3 levels are 
high enough to be of regulatory or public health concern. These 
requirements are contained in 40 CFR part 58 Appendix D, Network Design 
Criteria for Ambient Air Quality Monitoring. See section 4.1, 
especially Tables D-2 and D-3. These requirements were last revised on 
October 17, 2006 as part of a comprehensive review of ambient 
monitoring requirements for all criteria pollutants. (71 FR 61236) 
Certain deviations including minimum monitoring requirements and/or 
monitoring season requirements may be approved by the EPA Regional 
Administrator on a case-by-case basis.
    Required O3 monitoring seasons range from four to 12 
months. The minimum number of monitors in an MSA ranges from zero (for 
an area with population under 350,000 and no recent history of an 
O3 design value greater than 85 percent of the NAAQS) to 
four (for an area with population greater than 10 million and an 
O3 design value greater than 85 percent of the NAAQS). 
Because these requirements apply at the MSA level, large urban areas 
consisting of multiple MSAs can require more than four monitors. For 
example, the New York-Newark-Bristol NY-NJ-CT-PA combined statistical 
area requires about 14 monitors. In total, about 400 monitors are 
required in MSAs, but about 1100 are actually operating in MSAs because 
most States operate more than the minimum required number of monitors.
    There are no EPA requirements for O3 monitoring in less 
populated areas outside of MSA boundaries (e.g., Metropolitan 
Statistical Areas) or in rural areas. However, there are about 250 
O3 monitors in counties that are not part of MSAs. Some 
required State monitors are placed downwind of the urban center of the 
MSA of interest in locations that are in some cases in a county outside 
the MSA itself; some States also operate a few rural monitors for 
research purposes. The EPA operates a network of about 56 O3 
monitors as part of its Clean Air Status and Trends Network (CASTNET). 
The National Park Service (NPS) operates about 27 monitors at other 
CASTNET sites. The NPS also has O3 monitoring stations in 
parks that are not part of the CASTNET dry deposition monitoring effort 
including multiple O3 stations in Great Smoky Mountains, 
Sequoia, Yosemite, and Joshua Tree National Parks.
    Required quality assurance procedures for O3 monitoring 
are given in 40 CFR Part 58 Appendix A, Quality Assurance Requirements 
for State and local air monitoring stations (SLAMS), special purpose 
monitors (SPM), and prevention of significant deterioration (PSD) Air 
Monitoring. The EPA does not intend to propose any changes to these 
quality assurance requirements, because we believe that the current 
measurement uncertainty goals and related procedures for assessing 
precision and bias as documented in paragraph 2.3.1.2 of Appendix A are 
appropriate to support the implementation of a revised O3 
NAAQS.
    States are required to report O3 data quarterly to EPA's 
Air Quality System (AQS), and most also voluntarily report their pre-
validated O3 data on an hourly basis to EPA's real time 
AirNow data system, where the data are used to forecast O3 
concentrations and to provide public advisories. The National Park 
Service and many other organizations also report their O3 
data to AQS and/or AirNow. The locations of currently operating 
O3 monitors which report data to EPA's Air Quality System 
are available through the EPA AirData Web site http://www.epa.gov/air/data/index.html
.

    Data from O3 monitors at CASTNET stations are currently 
kept in a separate national data base.\66\
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    \66\ At present, not all ozone monitors at CASTNET sites are 
operated in full compliance with the quality assurance requirements 
of 40 CFR Part 58 Appendix D, as they have not been primarily 
intended for regulatory use. The EPA is working towards such 
compliance in the near future and towards making CASTNET ozone data 
available through AQS.
---------------------------------------------------------------------------

    The EPA invites comments on O3 monitoring issues (other 
than O3 monitoring methods and quality assurance 
requirements), including the following:
    (1) Ozone monitoring network requirements in urban areas. Table D-2 
of 40 CFR Part 58 Appendix D is based on the percentage of the 
O3 NAAQS, with a break point at 85 percent of the NAAQS. 
Therefore, a revision of the NAAQS would automatically increase the 
required number of O3 monitors. For example, assuming a 
final NAAQS of

[[Page 37907]]

0.070 ppm for purposes of illustration only, about 70 MSAs with current 
O3 design values in the range of about 0.060 ppm (about 85 
percent of the current NAAQS) to 0.070 ppm (about 85 percent of 0.070 
ppm) would be affected, with most changing from no required monitors to 
one, or from one required monitor to two. Because most of these areas 
already are operating at least as many monitors as the possible new 
requirement, the number of monitors which would need to be initiated 
(or moved from a location of excess monitors) would be only about five 
monitors. About 100 MSAs with populations less than 350,000 presently 
are without any O3 monitors, and hence they do not have an 
O3 design value for use with Table D-2. If for the purpose 
of applying Table D-2, these areas are treated as if they have 
O3 concentrations below 85 percent of the revised NAAQS, 
then a NAAQS revision would not automatically result in a requirement 
for O3 monitoring in these MSAs.\67\ EPA invites comments on 
the appropriateness of the existing minimum monitoring requirements for 
purposes of implementing the proposed revised NAAQS, including the 
automatic changes to minimum monitoring requirements that would be 
triggered by a NAAQS revision.
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    \67\ EPA might instead treat one or more of these counties as 
having a design value based on a monitor in a nearby monitored 
county, in which case ozone monitoring might become required in 
certain currently unmonitored MSAs and the number of new required 
monitors would increase in the illustrative NAAQS example stated 
above.
---------------------------------------------------------------------------

    (2) Ozone monitoring seasons. As mentioned, the currently required 
O3 monitoring seasons range from four to 12 months of the 
year. In some cases, O3 monitoring may start a couple of 
weeks before and may end a couple of weeks after the required season. 
With a lower O3 NAAQS, the issue arises of whether in some 
areas the required O3 monitoring season should be made 
longer. The EPA notes that under the existing regulations, the Regional 
Administrator may approve State-requested deviations from the 
established O3 monitoring season but EPA may not increase 
the length of the season for an area at EPA's own initiative other than 
by notice and comment rulemaking.
    (3) Monitoring to support implementation of a secondary 
O3 NAAQS. It is fair to say that the existing O3 
monitoring requirements and current State monitoring practices are 
primarily oriented towards protecting against health effects in people, 
i.e., towards implementation of the primary NAAQS. This accounts for 
the focus on urban areas, which can combine large populations, large 
emissions of O3-forming precursors, and O3 
concentrations of concern. The purpose of the secondary NAAQS is to 
protect against vegetation damage and other welfare effects, which can 
occur in both urban and rural areas. States have largely been given 
discretion on whether to add additional monitors aimed specifically at 
achieving the objectives of the previous and current secondary NAAQS. 
In urban areas, EPA in general believes that an O3 
monitoring network (and monitoring season) appropriate to support 
implementation of the primary NAAQS will also be appropriate for 
implementing the secondary NAAQS. However, rural areas are presently 
only sparsely monitored for O3 so violations of the 
secondary NAAQS in areas with sensitive vegetation may occur 
undetected, as a result of transport from urban areas with high 
precursor emissions and/or O3 concentrations or from 
formation of additional O3 from precursors emitted from 
sources outside urban areas. It is conceivable that rural violations of 
a secondary NAAQS could occur in areas with sensitive vegetation even 
though urban monitoring networks are showing compliance with the 
primary NAAQS, whether the forms and levels of the two standards are 
the same or different. The EPA invites comment on the likelihood of 
this occurring under the possible combinations of primary and secondary 
standards proposed in this notice, and on whether, where, and how EPA 
should require monitoring in rural areas specifically aimed at 
implementation of the secondary NAAQS (and/or promote more voluntary 
monitoring or conduct monitoring itself in rural areas).

VII. Statutory and Executive Order Reviews

A. Executive Order 12866: Regulatory Planning and Review

    Under section 3(f)(1) of Executive Order (EO) 12866 (58 FR 51735, 
October 4, 1993), the O3 NAAQS action is an ``economically 
significant regulatory action'' because it is likely to have an annual 
effect on the economy of $100 million or more. Accordingly, EPA 
prepared this regulatory impact analysis (RIA) of the potential costs 
and benefits associated with this action. The RIA estimates the costs 
and monetized human health and welfare benefits of attaining three 
alternative O3 NAAQS nationwide. Specifically, the RIA 
examines the alternatives of 0.075 ppm, 0.070 ppm, and 0.065 ppm. The 
RIA contains illustrative analyses that consider a limited number of 
emissions control scenarios that States and Regional Planning 
Organizations might implement to achieve these alternative 
O3 NAAQS. However, the Clean Air Act (CAA) and judicial 
decisions make clear that the economic and technical feasibility of 
attaining ambient standards are not to be considered in setting or 
revising NAAQS, although such factors may be considered in the 
development of State plans to implement the standards. Accordingly, 
although an RIA has been prepared, the results of the RIA have not been 
considered in issuing this final rule.

B. Paperwork Reduction Act

    This action does not impose an information collection burden under 
the provisions of the Paperwork Reduction Act, 44 U.S.C. 3501 et seq. 
There are no information collection requirements directly associated 
with the establishment of a NAAQS under section 109 of the CAA.
    Burden means the total time, effort, or financial resources 
expended by persons to generate, maintain, retain, or disclose or 
provide information to or for a Federal agency. This includes the time 
needed to review instructions; develop, acquire, install, and utilize 
technology and systems for the purposes of collecting, validating, and 
verifying information, processing and maintaining information, and 
disclosing and providing information; adjust the existing ways to 
comply with any previously applicable instructions and requirements; 
train personnel to be able to respond to a collection of information; 
search data sources; complete and review the collection of information; 
and transmit or otherwise disclose the information.
    An agency may not conduct or sponsor, and a person is not required 
to respond to a collection of information unless it displays a 
currently valid OMB control number. The OMB control numbers for EPA's 
regulations in 40 CFR are listed in 40 CFR part 9.

C. Regulatory Flexibility Act

    The Regulatory Flexibility Act (RFA) generally requires an agency 
to prepare a regulatory flexibility analysis of any rule subject to 
notice and comment rulemaking requirements under the Administrative 
Procedure Act or any other statute unless the agency certifies that the 
rule will not have a significant economic impact on a substantial 
number of small entities. Small entities include small businesses, 
small organizations, and small governmental jurisdictions.

[[Page 37908]]

    For purposes of assessing the impacts of today's rule on small 
entities, small entity is defined as: (1) A small business that is a 
small industrial entity as defined by the Small Business 
Administration's (SBA) regulations at 13 CFR 121.201; (2) a small 
governmental jurisdiction that is a government of a city, county, town, 
school district or special district with a population of less than 
50,000; and (3) a small organization that is any not-for-profit 
enterprise which is independently owned and operated and is not 
dominant in its field.
    After considering the economic impacts of today's proposed rule on 
small entities, I certify that this action will not have a significant 
economic impact on a substantial number of small entities. This 
proposed rule will not impose any requirements on small entities. 
Rather, this rule establishes national standards for allowable 
concentrations of O3 in ambient air as required by section 
109 of the CAA. See also American Trucking Associations v. EPA. 175 F. 
3d at 1044-45 (NAAQS do not have significant impacts upon small 
entities because NAAQS themselves impose no regulations upon small 
entities). We continue to be interested in the potential impacts of the 
proposed rule on small entities and welcome comments on issues related 
to such impacts.

D. Unfunded Mandates Reform Act

    Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public 
Law 104-4, establishes requirements for Federal agencies to assess the 
effects of their regulatory actions on State, local, and Tribal 
governments and the private sector. Under section 202 of the UMRA, EPA 
generally must prepare a written statement, including a cost-benefit 
analysis, for proposed and final rules with ``Federal mandates'' that 
may result in expenditures to State, local, and Tribal governments, in 
the aggregate, or to the private sector, of $100 million or more in any 
1 year. Before promulgating an EPA rule for which a written statement 
is needed, section 205 of the UMRA generally requires EPA to identify 
and consider a reasonable number of regulatory alternatives and to 
adopt the least costly, most cost-effective or least burdensome 
alternative that achieves the objectives of the rule. The provisions of 
section 205 do not apply when they are inconsistent with applicable 
law. Moreover, section 205 allows EPA to adopt an alternative other 
than the least costly, most cost-effective or least burdensome 
alternative if the Administrator publishes with the final rule an 
explanation why that alternative was not adopted. Before EPA 
establishes any regulatory requirements that may significantly or 
uniquely affect small governments, including Tribal governments, it 
must have developed under section 203 of the UMRA a small government 
agency plan. The plan must provide for notifying potentially affected 
small governments, enabling officials of affected small governments to 
have meaningful and timely input in the development of EPA regulatory 
proposals with significant Federal intergovernmental mandates, and 
informing, educating, and advising small governments on compliance with 
the regulatory requirements.
    Today's rule contains no Federal mandates (under the regulatory 
provisions of Title II of the UMRA) for State, local, or Tribal 
governments or the private sector. The rule imposes no new expenditure 
or enforceable duty on any State, local or Tribal governments or the 
private sector, and EPA has determined that this rule contains no 
regulatory requirements that might significantly or uniquely affect 
small governments. Furthermore, as indicated previously, in setting a 
NAAQS EPA cannot consider the economic or technological feasibility of 
attaining ambient air quality standards, although such factors may be 
considered to a degree in the development of State plans to implement 
the standards. See also American Trucking Associations v. EPA, 175 F. 
3d at 1043 (noting that because EPA is precluded from considering costs 
of implementation in establishing NAAQS, preparation of a Regulatory 
Impact Analysis pursuant to the Unfunded Mandates Reform Act would not 
furnish any information which the court could consider in reviewing the 
NAAQS). Accordingly, EPA has determined that the provisions of sections 
202, 203, and 205 of the UMRA do not apply to this proposed decision. 
The EPA acknowledges, however, that any corresponding revisions to 
associated SIP requirements and air quality surveillance requirements, 
40 CFR part 51 and 40 CFR part 58, respectively, might result in such 
effects. Accordingly, EPA will address, as appropriate, unfunded 
mandates if and when it proposes any revisions to 40 CFR parts 51 or 
58.

E. Executive Order 13132: Federalism

    Executive Order 13132, entitled ``Federalism'' (64 FR 43255, August 
10, 1999), requires EPA to develop an accountable process to ensure 
``meaningful and timely input by State and local officials in the 
development of regulatory policies that have federalism implications.'' 
``Policies that have federalism implications'' is defined in the 
Executive Order to include regulations that have ``substantial direct 
effects on the States, on the relationship between the national 
government and the States, or on the distribution of power and 
responsibilities among the various levels of government.''
    This proposed rule does not have federalism implications. It will 
not have substantial direct effects on the States, on the relationship 
between the national government and the States, or on the distribution 
of power and responsibilities among the various levels of government, 
as specified in Executive Order 13132. The rule does not alter the 
relationship between the Federal government and the States regarding 
the establishment and implementation of air quality improvement 
programs as codified in the CAA. Under section 109 of the CAA, EPA is 
mandated to establish NAAQS; however, CAA section 116 preserves the 
rights of States to establish more stringent requirements if deemed 
necessary by a State. Furthermore, this rule does not impact CAA 
section 107 which establishes that the States have primary 
responsibility for implementation of the NAAQS. Finally, as noted in 
section E (above) on UMRA, this rule does not impose significant costs 
on State, local, or Tribal governments or the private sector. Thus, 
Executive Order 13132 does not apply to this rule.
    However, as also noted in section E (above) on UMRA, EPA recognizes 
that States will have a substantial interest in this rule and any 
corresponding revisions to associated SIP requirements and air quality 
surveillance requirements, 40 CFR part 51 and 40 CFR part 58, 
respectively. Therefore, in the spirit of Executive Order 13132, and 
consistent with EPA policy to promote communications between EPA and 
State and local governments, EPA specifically solicits comment on this 
proposed rule from State and local officials.

F. Executive Order 13175: Consultation and Coordination With Indian 
Tribal Governments

    Executive Order 13175, entitled ``Consultation and Coordination 
with Indian Tribal Governments'' (65 FR 67249, November 9, 2000), 
requires EPA to develop an accountable process to ensure ``meaningful 
and timely input by tribal officials in the development of regulatory 
policies that have tribal implications.'' This rule concerns the 
establishment of O3 NAAQS. The Tribal Authority Rule gives 
Tribes the opportunity to develop and implement

[[Page 37909]]

CAA programs such as the O3 NAAQS, but it leaves to the 
discretion of the Tribe whether to develop these programs and which 
programs, or appropriate elements of a program, they will adopt.
    This proposed rule does not have Tribal implications, as specified 
in Executive Order 13175. It does not have a substantial direct effect 
on one or more Indian Tribes, since Tribes are not obligated to adopt 
or implement any NAAQS. Thus, Executive Order 13175 does not apply to 
this rule.
    Although Executive Order 13175 does not apply to this rule, EPA 
contacted tribal environmental professionals during the development of 
this rule. The EPA staff participated in the regularly scheduled Tribal 
Air call sponsored by the National Tribal Air Association during the 
spring of 2007 as this proposal was under development. EPA specifically 
solicits additional comment on this proposed rule from Tribal 
officials.

G. Executive Order 13045: Protection of Children From Environmental 
Health & Safety Risks

    Executive Order 13045, ``Protection of Children from Environmental 
Health Risks and Safety Risks'' (62 FR 19885, April 23, 1997) applies 
to any rule that: (1) Is determined to be ``economically significant'' 
as defined under Executive Order 12866, and (2) concerns an 
environmental health or safety risk that EPA has reason to believe may 
have a disproportionate effect on children. If the regulatory action 
meets both criteria, the Agency must evaluate the environmental health 
or safety effects of the planned rule on children, and explain why the 
planned regulation is preferable to other potentially effective and 
reasonably feasible alternatives considered by the Agency.
    This proposed rule is subject to Executive Order 13045 because it 
is an economically significant regulatory action as defined by 
Executive Order 12866, and we believe that the environmental health 
risk addressed by this action may have a disproportionate effect on 
children. The proposed rule will establish uniform national ambient air 
quality standards for O3; these standards are designed to 
protect public health with an adequate margin of safety, as required by 
CAA section 109. However, the protection offered by these standards may 
be especially important for children because children, especially 
children with asthma, along with other sensitive population subgroups 
such as all people with lung disease and people active outdoors, are 
potentially susceptible to health effects resulting from O3 
exposure. Because children are considered a potentially susceptible 
population, we have carefully evaluated the environmental health 
effects of exposure to O3 pollution among children. These 
effects and the size of the population affected are summarized in 
section 8.7 of the Criteria Document and section 3.6 of the Staff 
Paper, and the results of our evaluation of the effects of 
O3 pollution on children are discussed in sections II.A-C of 
this preamble.

H. Executive Order 13211: Actions That Significantly Affect Energy 
Supply, Distribution or Use

    This proposed rule is not a ``significant energy action'' as 
defined in Executive Order 13211, ``Actions Concerning Regulations That 
Significantly Affect Energy Supply, Distribution, or Use'' (66 FR 28355 
(May 22, 2001)) because in the Agency's judgment it is not likely to 
have a significant adverse effect on the supply, distribution, or use 
of energy. The purpose of this rule is to establish revised NAAQS for 
O3. The rule does not prescribe specific pollution control 
strategies by which these ambient standards will be met. Such 
strategies will be developed by States on a case-by-case basis, and EPA 
cannot predict whether the control options selected by States will 
include regulations on energy suppliers, distributors, or users. Thus, 
EPA concludes that this rule is not likely to have any adverse energy 
effects and does not constitute a significant energy action as defined 
in Executive Order 13211.

I. National Technology Transfer and Advancement Act

    Section 12(d) of the National Technology Transfer and Advancement 
Act of 1995 (NTTAA), Public Law No. 104-113, Sec.  12(d) (15 U.S.C. 272 
note) directs EPA to use voluntary consensus standards in its 
regulatory activities unless to do so would be inconsistent with 
applicable law or otherwise impractical. Voluntary consensus standards 
are technical standards (e.g., materials specifications, test methods, 
sampling procedures, and business practices) that are developed or 
adopted by voluntary consensus standards bodies. The NTTAA directs EPA 
to provide Congress, through OMB, explanations when the Agency decides 
not to use available and applicable voluntary consensus standards.
    This proposed rulemaking does not involve technical standards. 
Therefore, EPA is not considering the use of any voluntary consensus 
standards.

J. Executive Order 12898: Federal Actions To Address Environmental 
Justice in Minority Populations and Low-Income Populations

    Executive Order 12898 (59 FR 7629 (Feb. 16, 1994)) establishes 
federal executive policy on environmental justice. Its main provision 
directs federal agencies, to the greatest extent practicable and 
permitted by law, to make environmental justice part of their mission 
by identifying and addressing, as appropriate, disproportionately high 
and adverse human health or environmental effects of their programs, 
policies, and activities on minority populations and low-income 
populations in the United States.
    EPA has determined that this proposed rule will not have 
disproportionately high and adverse human health or environmental 
effects on minority or low-income populations because it increases the 
level of environmental protection for all affected populations without 
having any disproportionately high and adverse human health or 
environmental effects on any population, including any minority or low-
income population. The proposed rule will establish uniform national 
standards for O3 air pollution.

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List of Subjects in 40 CFR Part 50

    Environmental protection, Air pollution control, Carbon monoxide, 
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.

    Dated: June 20, 2007.
Stephen L. Johnson,
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. Section 50.15 is added to read as follows:


Sec.  50.15  National primary and secondary ambient air quality 
standards for ozone.

    (a) The level of the national 8-hour primary ambient air quality 
standard for O3 is (0.070-0.075) parts per million (ppm), 
daily maximum 8-hour average, measured by a reference method based on 
Appendix D to this part and designated in accordance with part 53 of 
this chapter.
    (b) The 8-hour primary O3 ambient air quality standard 
is met at an ambient air quality monitoring site when the average of 
the annual fourth-highest daily maximum 8-hour average O3 
concentration is less than or equal to (0.070-0.075) ppm, as determined 
in accordance with appendix P to this part.
    (c) The level of the national secondary ambient air quality 
standard for O3 is a cumulative index value of (7-21) ppm-
hours, measured by a reference method based on Appendix D to this part 
and designated in accordance with part 53 of this chapter.
    (d) The secondary O3 ambient air quality standard is a 
seasonal standard expressed as a sum of weighted hourly concentrations, 
cumulated over the 12 hour daylight period from 8 a.m. to 8 p.m. local 
standard time, during the consecutive 3-month period within the 
O3 monitoring season with the maximum index value. The 
secondary O3 standard is met at an ambient air quality 
monitoring site when the annual maximum consecutive 3-month cumulative 
index value (W126) is less than or equal to (7-21) ppm-hours, as


[[Continued on page 37917]]


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]                         
 
[[pp. 37917-37919]] National Ambient Air Quality Standards for Ozone

[[Continued from page 37916]]

[[Page 37917]]

determined in accordance with appendix P to this part.
    3. Appendix P is added to read as follows:

Appendix P to Part 50--Interpretation of the Primary and Secondary 
National Ambient Air Quality Standards for Ozone

1. General

    (a) This appendix explains the data handling conventions and 
computations necessary for determining whether the national 8-hour 
primary and secondary ambient air quality standards for 
O3 specified in Sec.  50.14 are met at an ambient 
O3 air quality monitoring site. Ozone is measured in the 
ambient air by a Federal reference method (FRM) based on appendix D 
of this part, as applicable, and designated in accordance with part 
53 of this chapter, or by a Federal equivalent method (FEM) 
designated in accordance with part 53 of this chapter, or by an 
Approved Regional Method (ARM) designated in accordance with part 58 
of this chapter. Data reporting, data handling, and computation 
procedures to be used in making comparisons between reported 
O3 concentrations and the level of the O3 
standard are specified in the following sections. Whether to 
exclude, retain, or make adjustments to the data affected by 
exceptional events, including stratospheric O3 intrusion 
and other natural events, is subject to the requirements under Sec.  
50.1, Sec.  50.14 and Sec.  51.930.
    (b) The terms used in this appendix are defined as follows:
    8-hour average is the rolling average of hourly O3 
concentrations as explained in section 2 of this appendix.
    Annual fourth highest daily maximum refers to the fourth highest 
value measured at a monitoring location during the O3 
season for a particular year.
    Daily maximum 8-hour average concentration refers to the maximum 
calculated 8 hour average for a particular day as explained in 
section 2 of this appendix.
    Design values are the metrics (i.e., statistics) that are 
compared to the NAAQS levels to determine compliance, calculated as 
shown in sections 3 and 4 of this appendix.
    Ozone monitoring season refers to the span of time within a 
calendar year when individual States are required to measure ambient 
O3 concentrations as listed in part 58 appendix D to this 
chapter.
    W126 is the weighted hourly O3 concentrations based 
on seasonal measurements as explained in section 4 of this appendix.
    Year refers to calendar year.

2. Primary Ambient Air Quality Standard for Ozone

2.1 Data Reporting and Handling Conventions

    Computing 8-hour averages. Hourly average concentrations shall 
be reported in parts per million (ppm) to the third decimal place, 
with additional digits to the right being truncated. Running 8-hour 
averages shall be computed from the hourly O3 
concentration data for each hour of the year and the result shall be 
stored in the first, or start, hour of the 8-hour period. An 8-hour 
average shall be considered valid if at least 75% of the hourly 
averages for the 8-hour period are available. In the event that only 
6 (or 7) hourly averages are available, the 8-hour average shall be 
computed on the basis of the hours available using 6 (or 7) as the 
divisor (8-hour periods with three or more missing hours shall not 
be ignored if, after substituting one-half the minimum detectable 
limit for the missing hourly concentrations, the 8-hour average 
concentration is greater than the level of the standard). The 
computed 8-hour average O3 concentrations shall be 
reported to three decimal places (the insignificant digits to the 
right of the third decimal place are truncated, consistent with the 
data handling procedures for the reported data).
    Daily maximum 8-hour average concentrations. (a) There are 24 
possible running 8-hour average O3 concentrations for 
each calendar day during the O3 monitoring season. The 
daily maximum 8-hour concentration for a given calendar day is the 
highest of the 24 possible 8-hour average concentrations computed 
for that day. This process is repeated, yielding a daily maximum 8-
hour average O3 concentration for each calendar day with 
ambient O3 monitoring data. Because the 8-hour averages 
are recorded in the start hour, the daily maximum 8-hour 
concentrations from two consecutive days may have some hourly 
concentrations in common. Generally, overlapping daily maximum 8-
hour averages are not likely, except in those non-urban monitoring 
locations with less pronounced diurnal variation in hourly 
concentrations.
    (b) An O3 monitoring day shall be counted as a valid 
day if valid 8-hour averages are available for at least 75% of 
possible hours in the day (i.e., at least 18 of the 24 averages). In 
the event that less than 75% of the 8-hour averages are available, a 
day shall also be counted as a valid day if the daily maximum 8-hour 
average concentration for that day is greater than the level of the 
ambient standard.

2.2 Primary Standard-Related Summary Statistic

    The standard-related summary statistic is the annual fourth-
highest daily maximum 8-hour O3 concentration, expressed 
in parts per million, averaged over three years. The 3-year average 
shall be computed using the three most recent, consecutive calendar 
years of monitoring data meeting the data completeness requirements 
described in this appendix. The computed 3-year average of the 
annual fourth-highest daily maximum 8-hour average O3 
concentrations shall be reported to three decimal places (the 
insignificant digits to the right of the third decimal place are 
truncated, consistent with the data handling procedures for the 
reported data).

2.3 Comparisons With the Primary Ozone Standard

    (a) The primary O3 ambient air quality standard is 
met at an ambient air quality monitoring site when the 3-year 
average of the annual fourth-highest daily maximum 8-hour average 
O3 concentration is less than or equal to [0.070 to 
0.075] ppm.
    (b) This comparison shall be based on three consecutive, 
complete calendar years of air quality monitoring data. This 
requirement is met for the three year period at a monitoring site if 
daily maximum 8-hour average concentrations are available for at 
least 90%, on average, of the days during the designated 
O3 monitoring season, with a minimum data completeness in 
any one year of at least 75% of the designated sampling days. When 
computing whether the minimum data completeness requirements have 
been met, meteorological or ambient data may be sufficient to 
demonstrate that meteorological conditions on missing days were not 
conducive to concentrations above the level of the standard. Missing 
days assumed less than the level of the standard are counted for the 
purpose of meeting the data completeness requirement, subject to the 
approval of the appropriate Regional Administrator.
    (c) Years with concentrations greater than the level of the 
standard shall not be ignored on the ground that they have less than 
complete data. Thus, in computing the 3-year average fourth maximum 
concentration, calendar years with less than 75% data completeness 
shall be included in the computation if the average annual fourth 
maximum 8-hour concentration is greater than the level of the 
standard.
    (d) Comparisons with the primary O3 standard is 
demonstrated by examples 1 and 2 in paragraphs (d)(1) and (d)(2) 
respectively as follows:

                                          Example 1.--Ambient Monitoring Site Attaining the Primary O3 Standard
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                            1st Highest     2nd Highest     3rd Highest     4th Highest     5th Highest
                                                           Percent valid   daily max  8-   daily max  8-   daily max  8-   daily max  8-   daily max  8-
                          Year                                 days         hour Conc.      hour Conc.      hour Conc.      hour Conc.      hour Conc.
                                                             (percent)         (ppm)           (ppm)           (ppm)           (ppm)           (ppm)
--------------------------------------------------------------------------------------------------------------------------------------------------------
2004....................................................             100           0.092           0.090           0.085           0.079           0.078
2005....................................................              96           0.084           0.083           0.075           0.072           0.070
2006....................................................              98           0.080           0.079           0.073           0.061           0.060
                                                         -----------------------------------------------------------------------------------------------

[[Page 37918]]


    Average.............................................              98  ..............  ..............  ..............           0.070  ..............
--------------------------------------------------------------------------------------------------------------------------------------------------------

    (1) As shown in example 1, the primary standard is met at this 
monitoring site because the 3-year average of the annual fourth-
highest daily maximum 8-hour average O3 concentrations 
(i.e., 0.0707 ppm, truncated to 0.070 ppm) is less than or equal to 
[0.070 to 0.75] ppm. The data completeness requirement is also met 
because the average percent of days with valid ambient monitoring 
data is greater than 90%, and no single year has less than 75% data 
completeness. In Example 1, the individual 8-hour averages used to 
determine the annual fourth maximum are truncated to the third 
decimal place.

                                       Example 2.--Ambient Monitoring Site Failing To Meet the Primary O3 Standard
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                            1st Highest     2nd Highest     3rd Highest     4th Highest     5th Highest
                                                           Percent valid   daily max  8-   daily max  8-   daily max  8-   daily max  8-   daily max  8-
                          Year                                 days         hour Conc.      hour Conc.      hour Conc.      hour Conc.      hour Conc.
                                                             (percent)         (ppm)           (ppm)           (ppm)           (ppm)           (ppm)
--------------------------------------------------------------------------------------------------------------------------------------------------------
2004....................................................              96           0.105           0.103           0.103           0.102           0.102
2005....................................................              74           0.104           0.103           0.092           0.091           0.088
2006....................................................              98           0.103           0.101           0.101           0.095           0.094
                                                         -----------------------------------------------------------------------------------------------
    Average.............................................              89  ..............  ..............  ..............           0.096  ..............
--------------------------------------------------------------------------------------------------------------------------------------------------------

    As shown in example 2, the primary standard is not met at this 
monitoring site because the 3-year average of the fourth-highest 
daily maximum 8-hour average O3 concentrations (i.e., 
0.0960 ppm, truncated to 0.096 ppm) is greater than [0.070 to 0.075] 
ppm. Note that the O3 concentration data for 2005 is used 
in these computations, even though the data capture is less than 
75%, because the average fourth-highest daily maximum 8-hour average 
concentration is greater than [0.070 to 0.075] ppm. In Example 2, 
the individual 8-hour averages used to determine the annual fourth 
maximum are truncated to the third decimal place.

3. Design Values for Primary Ambient Air Quality Standards for Ozone

    The air quality design value at a monitoring site is defined as 
that concentration that when reduced to the level of the standard 
ensures that the site meets the standard. For a concentration-based 
standard, the air quality design value is simply the standard-
related test statistic. Thus, for the primary standard, the 3-year 
average annual fourth-highest daily maximum 8-hour average 
O3 concentration is also the air quality design value for 
the site.

4. Secondary Ambient Air Quality Standard for Ozone

4.1 Data Reporting and Handling Conventions

    Computing the daily index value (D.I.). The secondary 
O3 standard is a seasonal standard expressed as the sum 
of weighted hourly concentrations, cumulated over the 12 hour 
daylight period, 8 a.m. to 8 p.m. local standard time (LST), during 
the maximum consecutive 3-month period within the O3 
monitoring season. Hourly average concentrations for each hour from 
8 a.m. to 8 p.m. LST shall be reported in parts per million (ppm) to 
the third decimal place, with additional digits to the right being 
truncated. The first step in computing the daily index value, D.I., 
for the daylight hours is to apply a sigmoidal weighting function in 
the form of Equation 1 in this appendix:
[GRAPHIC] [TIFF OMITTED] TP11JY07.002

to each measurement of hourly average concentration, where 
O3 is the average hourly O3 concentration 
expressed in ppm. The computed value of the sigmoidally weighted 
hourly concentration shall be expressed to three decimal places (the 
remaining digits to the right are truncated). An illustration of 
computing a daily index value is below:

 Example 3.--Daily Index Value Calculation for an Ambient O3 Monitoring
                                  Site
------------------------------------------------------------------------
                                                             Weighted
               Start hour                  Concentration   concentration
                                               (ppm)           (ppm)
------------------------------------------------------------------------
8:00 AM.................................           0.045           0.002
9:00 AM.................................           0.060           0.018
10:00 AM................................           0.075           0.055
11:00 AM................................           0.080           0.067
12:00 PM................................           0.079           0.065
1:00 PM.................................           0.082           0.071
2:00 PM.................................           0.085           0.077
3:00 PM.................................           0.088           0.082
4:00 PM.................................           0.083           0.073
5:00 PM.................................           0.081           0.069
6:00 PM.................................           0.065           0.029
7:00 PM.................................           0.056           0.011
------------------------------------------------------------------------


[[Page 37919]]

Daily index value (D.I.) = 0.002 + 0.018 + 0.055 + 0.067 + 0.065 + 
0.071 + 0.077 + 0.082 + 0.073 + 0.069 + 0.029 + 0.011 = 0.619 ppm-
hours
    Computing the monthly cumulative index (W126). The daily index 
value is computed at each monitoring site for each calendar day in 
each month during the O3 monitoring. At an individual 
monitoring site, a month is counted as a valid O3 
monitoring month if hourly average O3 concentrations are 
available for at least 75% of the possible index hours in the month. 
For months with less than 75% data completeness, the monthly 
cumulative index value shall be adjusted for incomplete sampling by 
multiplying the unadjusted W126 cumulative index value by the ratio 
of the number of possible daylight hours to the number of hours with 
valid ambient hourly concentrations using Equation 2 in this 
appendix:
[GRAPHIC] [TIFF OMITTED] TP11JY07.003

Where,

M.I. = the monthly sum of the weighted daylight hours,
D.I. = the daily sum of the weighted daylight hours,
n = the number of days in the calendar month,
v = the number of daylight hours (8:00 a.m.--8:00 p.m. LST) with 
valid hourly O3 concentrations.

4.2 Secondary Standard-related Summary Statistic

    The standard-related summary statistic is the annual maximum 
consecutive 3-month W126 value expressed in ppm-hours. Specifically, 
the annual W126 value is computed on a calendar year basis using the 
three highest, consecutive monthly W126 values.

4.3 Comparisons with the Secondary Ozone Standard

    The secondary ambient O3 air quality standard is met 
when the annual maximum W126 value based on a consecutive 3-month 
period at an O3 air quality monitoring site is less than 
or equal to [7 to 21] ppm-hours. The number of significant figures 
in the level of the standard dictates the rounding convention for 
comparing the computed W126 value with the level of the standard. 
The first decimal place of the computed W126 value is rounded, with 
values equal to or greater than of 0.5 rounding up.

      Example 4.--Calculation of the Maximum 3-Month W126 Value at an Ambient Air Quality Monitoring Site Failing To Meet the Secondary O3 Standard
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                  April         May          June         July        August     September     October
--------------------------------------------------------------------------------------------------------------------------------------------------------
Monthly W126.................................................        4.442        9.124       12.983       16.153       13.555        4.364        1.302
3-Month Total................................................           na           na       26.549       38.260       42.691       34.072       19.221
--------------------------------------------------------------------------------------------------------------------------------------------------------

    As shown in example 4, the maximum consecutive 3-month W126 
value for this site is 43 ppm-hours. Because 43 ppm-hours is greater 
than [7 to 21] ppm-hours, the secondary standard is not met at this 
ambient air quality monitoring site.

[FR Doc. E7-12416 Filed 7-10-07; 8:45 am]

BILLING CODE 6560-50-P
