[Federal Register Volume 79, Number 242 (Wednesday, December 17, 2014)]
[Proposed Rules]
[Pages 75233-75411]
[FR Doc No: 2014-28674]

Vol. 79

Wednesday,

No. 242

December 17, 2014

Part II

Environmental Protection Agency

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40 CFR Parts 50, 51, 52, et al.

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National Ambient Air Quality Standards for Ozone; Proposed Rule

Federal Register / Vol. 79 , No. 242 / Wednesday, December 17, 2014 /
Proposed Rules

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 51, 52, 53, and 58

[EPA-HQ-OAR-2008-0699; FRL-9918-43-OAR]
RIN 2060-AP38

National Ambient Air Quality Standards for Ozone

AGENCY: Environmental Protection Agency.

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, the Environmental
Protection Agency (EPA) proposes to make revisions to the primary and
secondary NAAQS for O3 to provide requisite protection of
public health and welfare, respectively. The EPA is proposing to revise
the primary standard to a level within the range of 0.065 to 0.070
parts per million (ppm), and to revise the secondary standard to within
the range of 0.065 to 0.070 ppm, which air quality analyses indicate
would provide air quality, in terms of 3-year average W126 index
values, at or below a range of 13-17 ppm-hours. The EPA proposes to
make corresponding revisions in data handling conventions for
O3 and conforming changes to the Air Quality Index (AQI); to
revise regulations for the prevention of significant deterioration
(PSD) program to add a transition provision for certain applications;
and to propose schedules and convey information related to implementing
any revised standards. The EPA is proposing changes to the
O3 monitoring seasons, the Federal Reference Method (FRM)
for monitoring O3 in the ambient air, Federal Equivalent
Method (FEM) procedures for testing, and the Photochemical Assessment
Monitoring Stations (PAMS) network.
    Along with proposing exceptional event schedules related to
implementing any revised O3 standards, the EPA is proposing
to apply this same schedule approach to other future revised NAAQS and
to remove obsolete regulatory language for expired exceptional event
deadlines. The EPA is proposing to make minor changes to the procedures
and time periods for evaluating potential FRMs and equivalent methods
(including making the requirements for nitrogen dioxide consistent with
the requirements for O3) and to remove an obsolete
requirement for the annual submission of documentation by manufacturers
of certain particulate matter monitors. For additional information, see
the Executive Summary, section I.A.

DATES: Written comments on this proposed rule must be received by March
17, 2015.
    Public Hearings: The EPA intends to hold three public hearings on
this proposed rule in January 2015. These will be announced in a
separate Federal Register notice that provides details, including
specific dates, times, addresses, and contact information for these
hearings.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2008-0699, to the EPA by one of the following methods:
     Federal eRulemaking Portal: http://www.regulations.gov.
Follow the online instructions for submitting comments.
     Email<EMAIL_ADDRESS>Include docket ID No. EPA-
HQ-OAR-2008-0699 in the subject line of the message.
     Fax:<PHONE_NUMBER>.
     Mail: Environmental Protection Agency, EPA Docket Center
(EPA/DC), Mailcode 28221T, Attention Docket ID No. OAR-2008-0699, 1200
Pennsylvania Ave. NW., Washington, DC 20460. Please include a total of
two copies.
     Hand/Courier Delivery: EPA Docket Center, Room 3334, EPA
WJC West Building, 1301 Constitution Ave. NW., Washington, DC. Such
deliveries are only accepted during the Docket's normal hours of
operation, and special arrangements should be made for deliveries of
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2008-0699. The EPA's policy is that all comments received will be
included in the public docket without change and may be made available
online at www.regulations.gov, including any personal information
provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through www.regulations.gov
or email. The www.regulations.gov Web site is an ``anonymous access''
system, which means the EPA will not know your identity or contact
information unless you provide it in the body of your comment. If you
send an email comment directly to the EPA without going through
www.regulations.gov your email 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, the 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 the EPA cannot read your comment due to technical
difficulties and cannot contact you for clarification, the 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: The EPA has established dockets for these actions as
discussed above. All documents in these dockets are listed on the
www.regulations.gov Web site. This includes documents in the rulemaking
docket (Docket ID No. EPA-HQ-OAR-2008-0699) and a separate docket,
established for the Integrated Science Assessment (ISA) (Docket No.
EPA-HQ-ORD-2011-0050) that has have been incorporated by reference into
the rulemaking docket. 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, is not placed on the Internet and may be viewed,
with prior arrangement, at the EPA Docket Center. Publicly available
docket materials are available either electronically in
www.regulations.gov or in hard copy at the Air and Radiation Docket and
Information Center, EPA/DC, EPA WJC West Building, 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<PHONE_NUMBER>. For additional information about
EPA's public docket visit the EPA Docket Center homepage at: http://www.epa.gov/epahome/dockets.htm.

FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Mail code C504-06,
Research Triangle Park, NC 27711; telephone:<PHONE_NUMBER>; fax: (919)
541-0237; email<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

General Information

What should I consider as I prepare my comments for EPA?

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

Availability of Related Information

    A number of documents relevant to this rulemaking are available on
EPA Web sites. The ISA for Ozone and Related Photochemical Oxidants is
available on the EPA's National Center for Environmental Assessment
(NCEA) Web site. To obtain this document, go to http://www.epa.gov/ncea, and click on Ozone in the Quick Finder section. This will open a
page with a link to the February 2013 ISA. The 2014 Policy Assessment
(PA), Health and Welfare Risk and Exposure Assessments (HREA and WREA,
respectively), 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 final 2014 PA is available at:
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pa.html, and the
final 2014 Health and Welfare Risk and Exposure Assessments and other
related technical documents are available at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_rea.html. These and other related
documents are also available for inspection and copying in the EPA
docket identified above.

Environmental Justice

    Analyses evaluating the potential implications of a revised
O3 NAAQS for environmental justice populations are discussed
in appendix 9A of the Regulatory Impact Analysis (RIA) that accompanies
this notice of proposed rulemaking. The RIA is available on the Web,
through the EPA's Technology Transfer Network Web site at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_index.html.

Table of Contents

    The following topics are discussed in this preamble:

I. Background
    A. Executive Summary
    B. Legislative Requirements
    C. Related Control Programs To Implement O3 Standards
    D. Review of Air Quality Criteria and Standards for
O3
    E. Ozone Air Quality
II. Rationale for Proposed Decision on the Primary Standard
    A. Approach
    B. Health Effects Information
    1. Overview of Mechanisms
    2. Nature of Effects
    3. Adversity of O3 Effects
    4. Ozone-Related Impacts on Public Health
    C. Human Exposure and Health Risk Assessments
    1. Air Quality Adjustment
    2. Exposure Assessment
    3. Quantitative Health Risk Assessments
    D. Conclusions on the Adequacy of the Current Primary Standard
    1. Summary of Evidence-Based Considerations in the PA
    2. Summary of Exposure- and Risk-Based Considerations in the PA
    3. Policy Assessment Conclusions on the Current Standard
    4. CASAC Advice
    5. Administrator's Proposed Conclusions Concerning the Adequacy
of the Current Standard
    E. Conclusions on the Elements of the Primary Standard
    1. Indicator
    2. Averaging Time
    3. Form
    4. Level
    F. Proposed Decision on the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
    A. Approach
    B. Welfare Effects Information
    1. Nature of Effects and Biologically Relevant Exposure Metric
    2. Potential Impacts on Public Welfare
    C. Exposure and Risk Assessment Information
    1. Air Quality Analyses
    2. Tree Seedling Growth, Productivity, Carbon Storage and
Associated Ecosystem Services
    3. Crop Yield
    4. Visible Foliar Injury
    D. Conclusions on Adequacy of the Current Secondary Standard
    1. Evidence- and Exposure/Risk-Based Considerations in the
Policy Assessment
    2. CASAC Advice
    3. Administrator's Proposed Conclusions on Adequacy of the
Current Standard
    E. Consideration of Alternative Secondary Standards
    1. Indicator
    2. Consideration of a Cumulative, Seasonal Exposure-based
Standard in the Policy Assessment
    3. CASAC Advice
    4. Air Quality Analyses
    5. Administrator's Proposed Conclusions
    F. Proposed Decision on the Secondary Standard
V. Appendix U: Interpretation of the Primary and Secondary NAAQS for
O3
    A. Background
    B. Data Selection Requirements
    C. Data Reporting and Data Handling Requirements
    D. Considerations for the Possibility of a Distinct Secondary
Standard
    E. Exceptional Events Information Submission Schedule
VI. Ambient Monitoring Related to Proposed O3 Standards
    A. Background
    B. Revisions to the Length of the Required O3
Monitoring Seasons
    C. Revisions to the Photochemical Assessment Monitoring Stations
(PAMS)
    1. Network Design
    2. Speciated VOC Measurements
    3. Carbonyl Sampling
    4. Nitrogen Oxides Sampling
    5. Meteorology Measurements
    6. PAMS Season
    7. Timing and Other Implementation Issues
    D. Addition of a New Federal Reference Method (FRM) for
O3
    E. Revisions to the Procedures for Testing Performance
Characteristics and Determining Comparability Between Candidate
Methods and Reference Methods
VII. Implementation of Proposed O3 Standards
    A. NAAQS Implementation Plans
    1. Background
    2. Timing of Rules and Guidance
    3. Section 110 State Implementation Plans
    4. Nonattainment Area Requirements
    B. Implementing a Distinct Secondary O3 NAAQS, if One
is Established
    C. Designation of Areas

    D. Prevention of Significant Deterioration and Nonattainment New
Source Review Programs for the Proposed Revised Primary and
Secondary O3 NAAQS
    1. Prevention of Significant Deterioration (PSD)
    2. Nonattainment New Source Review
    E. Transportation and General Conformity Programs
    1. What are transportation and general conformity?
    2. Why is the EPA discussing transportation and general
conformity in this proposed rulemaking?
    3. When would transportation and general conformity apply to
areas designated nonattainment for a revised O3 NAAQS, if
one is established?
    4. Will transportation and general conformity apply to a
distinct secondary O3 NAAQS, if one is established?
    5. What impact would the implementation of a revised
O3 NAAQS have on a State's transportation and/or general
conformity SIP?
    F. How Background O3 Is Addressed in CAA
Implementation Provisions
    1. Introduction
    2. Exceptional Events Exclusions
    3. Rural Transport Areas
    4. International Transport
VIII. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review and
Executive Order 13563: Improving Regulation and Regulatory Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children From
Environmental Health & Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution, or Use
    I. National Technology Transfer and Advancement Act
    J. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
References

I. Background

A. Executive Summary

    This section summarizes information about the purpose of this
regulatory action (I.A.1), the major provisions of this proposal
(I.A.2), and provisions related to implementation (I.A.3).
1. Purpose of This Regulatory Action
    Sections 108 and 109 of the Clean Air Act (CAA) govern the
establishment, review, and revision, as appropriate, of the NAAQS to
protect public health and welfare. The CAA requires the EPA to
periodically review the air quality criteria--the science upon which
the standards are based--and the standards themselves. This rulemaking
is being conducted pursuant to these statutory requirements. The
schedule for completing this review is established by a federal court
order, which requires that the EPA sign a proposal by December 1, 2014,
and make a final determination by October 1, 2015.
    The EPA completed its most recent review of the O3 NAAQS
in 2008. As a result of that review, EPA took four principal actions:
(1) Revised the level of the 8-hour primary O3 standard to
0.075 parts per million (ppm); (2) expressed the standard to three
decimal places; (3) revised the 8-hour secondary O3 standard
by making it identical to the revised primary standard; and (4) made
conforming changes to the AQI for O3.
    In subsequent litigation, the U.S. Court of Appeals for the
District of Columbia Circuit upheld the EPA's 2008 primary
O3 standard, but remanded the 2008 secondary standard. State
of Mississippi v. EPA, 744 F. 3d 1334 (D.C. Cir. 2013). With respect to
the primary standard, the court held that the EPA reasonably determined
that the existing primary standard, set in 1997, did not protect public
health with an adequate margin of safety and required revision. In
upholding the EPA's revised primary standard, the court dismissed
arguments that the EPA should have adopted a more stringent standard.
The court remanded the secondary standard to the EPA after rejecting
the EPA's explanation for setting the secondary standard identical to
the revised 8-hour primary standard. The court held that because the
EPA had failed to identify a level of air quality requisite to protect
public welfare, the EPA's comparison between the primary and secondary
standards for determining if requisite protection for public welfare
was afforded by the primary standard failed to comply with the CAA.
    This proposal reflects the Administrator's proposed conclusions
based on a review of the O3 NAAQS that began in September
2008. In conducting this review, the EPA has carefully evaluated the
currently available scientific literature on the health and welfare
effects of ozone, focusing particularly on the new literature available
since the conclusion of the previous review in 2008. In addition, the
EPA has also addressed the remand of the Agency's 2008 decision on the
secondary standard. Between 2008 and 2014, the EPA prepared draft and
final versions of the Integrated Science Assessment, the Health and
Welfare Risk and Exposure Assessments, and the Policy Assessment.
Multiple drafts of these documents were available for public review and
comment, and as required by the CAA, were peer-reviewed by the Clean
Air Scientific Advisory Committee (CASAC), an independent scientific
advisory committee established by the CAA and charged with providing
advice to the Administrator. The final documents reflect the EPA
staff's consideration of the comments and recommendations made by CASAC
and the public on draft versions of these documents.
2. Summary of Major Provisions
    The EPA is proposing that the current primary O3
standard set at a level of 0.075 ppm is not requisite to protect public
health with an adequate margin of safety, and that it should be revised
to provide increased public health protection. Specifically, the EPA is
proposing to retain the indicator (ozone), averaging time (8-hour) and
form (annual fourth-highest daily maximum, averaged over 3 years) of
the existing primary O3 standard and is proposing to revise
the level of that standard to within the range of 0.065 ppm to 0.070
ppm. The EPA is proposing this revision to increase public health
protection, including for ``at-risk'' populations such as children,
older adults, and people with asthma or other lung diseases, against an
array of O3-related adverse health effects. For short-term
O3 exposures, these effects include decreased lung function,
increased respiratory symptoms and pulmonary inflammation, effects that
result in serious indicators of respiratory morbidity such as emergency
department visits and hospital admissions, and all-cause (total
nonaccidental) mortality. For long-term O3 exposures, these
health effects include a variety of respiratory morbidity effects and
respiratory mortality. Recognizing that the CASAC recommended a range
of levels from 0.060 ppm to 0.070 ppm, and that levels as low as 0.060
ppm could potentially be supported, the Administrator solicits comment
on alternative standard levels below 0.065 ppm, and as low as 0.060
ppm. However, the Administrator notes that setting a standard below
0.065 ppm, down to 0.060 ppm, would inappropriately place very little
weight on the uncertainties in the health effects evidence and
exposure/risk information. Given alternative views of the currently
available evidence and information expressed by some commenters, the
EPA is taking comment on both the Administrator's proposed decision to
revise the current primary O3 standard and the option of
retaining that standard.
    In addition to proposing changes to the level of the standard, the
EPA is

proposing conforming changes to the Air Quality Index (AQI) by
proposing to set an AQI value of 100 equal to the level of the 8-hour
primary O3 standard, and proposing adjustments to the AQI
values of 50, 150, 200 and 300.
    The EPA also proposes to revise the secondary standard to provide
increased protection against vegetation-related effects on public
welfare. As an initial matter, the Administrator proposes to conclude
that air quality in terms of a three-year average seasonal W126 index
value, based on the three consecutive month period within the
O3 season with the maximum index value, with daily exposures
cumulated for the 12-hour period from 8:00 a.m. to 8:00 p.m., within
the range from 13 ppm-hrs to 17 ppm-hrs would provide the requisite
protection against known or anticipated adverse effects to the public
welfare. The EPA solicits comment on this proposed conclusion. In
considering how to achieve that level of air quality, the Administrator
recognizes that air quality data analyses suggest that air quality in
terms of three-year average W126 index values of a range at or below 13
to 17 ppm-hrs would be provided by a secondary standard level within
the range of 0.065 to 0.070 ppm, and that to the extent areas need to
take action to attain a standard in the range of 0.065 to 0.070 ppm,
those actions would also improve air quality as measured by the W126
metric. Thus, the Administrator proposes to revise the level of the
current secondary standard to within the range of 0.065 to 0.070 ppm.
The EPA solicits comments on this proposed revision of the secondary
standard.
    The EPA also solicits comments on the alternative approach of
revising the secondary standard to a W126-based form, averaged over
three years, with a level within the range of 13 ppm-hrs to 17 ppm-hrs.
The EPA additionally solicits comments on such a distinct secondary
standard with a level within the range extending below 13 ppm-hrs down
to 7 ppm-hrs. Further, the EPA solicits comments on retaining the
current secondary standard without revision, along with the alternative
views of the evidence that would support retaining the current
standard.
3. Provisions Related to Implementation
    As directed by the CAA, reducing pollution to meet national air
quality standards always has been a shared task, one involving the
federal government, states, tribes and local air agencies. This
partnership has proved effective since the EPA first issued
O3 standards more than three decades ago, and is evidenced
by significantly lower O3 levels throughout the country. To
provide a foundation that helps air agencies build successful
strategies for attaining new O3 standards, the EPA will
continue to move forward with federal regulatory programs, such as the
proposed Clean Power Plan and the final Tier 3 motor vehicle emissions
standards. To facilitate the development of CAA-compliant
implementation plans and strategies to attain new standards, the EPA
intends to issue timely and appropriate implementation guidance and,
where appropriate and consistent with the law, new rulemakings to
streamline regulatory burdens and provide flexibility in
implementation. In addition, given the regional nature of O3
air pollution, the EPA will continue to work with states to address
interstate transport of O3 and O3 precursors.
    This notice contains several proposed provisions related to
implementation of the proposed standards. In addition to revisions to
the primary and secondary NAAQS, the EPA is proposing to make
corresponding revisions in data handling conventions for O3;
to revise regulations for the Prevention of Significant Deterioration
(PSD) permitting program to add a provision grandfathering certain
pending permits from certain requirements with respect to the proposed
revisions to the O3 NAAQS; and to convey schedules and
information related to implementing any revised standards.
    In conjunction with proposing exceptional event schedules related
to implementing any revised O3 standards, the EPA is also
proposing to extend the new schedule approach to other future revised
NAAQS and to remove obsolete regulatory language associated with
expired exceptional event deadlines for historical standards for both
O3 and other NAAQS pollutants. The EPA is also proposing to
make minor changes to the procedures and time periods for evaluating
potential FRMs and equivalent methods, including making the
requirements for nitrogen dioxide consistent with the requirements for
O3, and removing an obsolete requirement for the annual
submission of documentation by manufacturers of certain particulate
matter monitors.

B. Legislative Requirements

    Two sections of the CAA govern the establishment and revision of
the NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to
identify and list certain air pollutants and then to issue air quality
criteria for those pollutants. The Administrator is to list those air
pollutants that in her ``judgment, cause or contribute to air pollution
which may reasonably be anticipated to endanger public health or
welfare;'' ``the presence of which in the ambient air results from
numerous or diverse mobile or stationary sources;'' and ``for which . .
. [the Administrator] plans to issue air quality criteria . . . .'' Air
quality criteria are intended to ``accurately reflect the latest
scientific knowledge useful in indicating the kind and extent of all
identifiable effects on public health or welfare which may be expected
from the presence of [a] pollutant in the ambient air . . . .'' 42
U.S.C. 7408(b). Section 109 (42 U.S.C. 7409) directs the Administrator
to propose and promulgate ``primary'' and ``secondary'' NAAQS for
pollutants for which air quality criteria are issued. Section 109(b)(1)
defines a primary standard as one ``the attainment and maintenance of
which in the judgment of the Administrator, based on such criteria and
allowing an adequate margin of safety, are requisite to protect the
public health.'' \1\ A secondary standard, as defined in section
109(b)(2), must ``specify a level of air quality the attainment and
maintenance of which, in the judgment of the Administrator, based on
such criteria, is requisite to protect the public welfare from any
known or anticipated adverse effects associated with the presence of
[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 provide an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. See State of Mississippi v. EPA, 744 F. 3d 1334, 1353 (D.C.
Cir. 2013) (``By requiring an `adequate margin of safety', Congress was
directing EPA to build a buffer to protect against uncertain and
unknown dangers to human health''); see also Lead Industries
Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980); American
Petroleum Institute v. Costle,

665 F.2d 1176, 1186 (D.C. Cir. 1981); American Farm Bureau Federation
v. EPA, 559 F. 3d 512, 533 (D.C. Cir. 2009); Association of Battery
Recyclers v. EPA, 604 F. 3d 613, 617-18 (D.C. Cir. 2010). Both kinds of
uncertainties are components of the risk associated with pollution at
levels below those at which human health effects can be said to occur
with reasonable scientific certainty. Thus, in selecting primary
standards that provide an adequate margin of safety, the Administrator
is seeking not only to prevent pollution levels that have been
demonstrated to be harmful but also to prevent lower pollutant levels
that may pose an unacceptable risk of harm, even if the risk is not
precisely identified as to nature or degree. The CAA does not require
the Administrator to establish a primary NAAQS at a zero-risk level or
at background concentrations, see Lead Industries v. EPA, 647 F.2d at
1156 n.51; State of Mississippi v. EPA, 744 F. 3d at 1351, 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, the
EPA considers such factors as the nature and severity of the health
effects, the size of sensitive population(s) \3\ at risk, and the kind
and degree of the uncertainties that must be addressed. The selection
of any particular approach for providing an adequate margin of safety
is a policy choice left specifically to the Administrator's judgment.
See Lead Industries Association v. EPA, 647 F.2d at 1161-62; State of
Mississippi, 744 F. 3d at 1353.
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    \3\ As used here and similarly throughout this document, the
term ``population'' refers to people having a quality or
characteristic in common, including a specific pre-existing illness
or a specific age or life stage.
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    In setting primary and secondary standards that are ``requisite''
to protect public health and welfare, respectively, as provided in
section 109(b), the EPA's task is to establish standards that are
neither more nor less stringent than necessary for these purposes. In
so doing, the EPA may not consider the costs of implementing the
standards. See generally, Whitman v. American Trucking Associations,
531 U.S. 457, 465-472, 475-76 (2001). Likewise, ``[a]ttainability and
technological feasibility are not relevant considerations in the
promulgation of national ambient air quality standards.'' American
Petroleum Institute v. Costle, 665 F. 2d at 1185.
    Section 109(d)(1) 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 . . . .'' Since the early
1980's, the Clean Air Scientific Advisory Committee (CASAC) has
performed this independent review function.\4\
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    \4\ Lists of CASAC members and of members of the CASAC Ozone
Review Panel are available at: http://yosemite.epa.gov/sab/sabpeople.nsf/WebCommitteesSubCommittees/Ozone%20Review%20Panel.
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C. Related Control Programs To Implement O3 Standards

    States are primarily responsible for ensuring attainment and
maintenance of ambient air quality standards once the EPA has
established them. Under section 110 of the CAA, and related provisions,
states are to submit, for the EPA's approval, state implementation
plans (SIPs) that provide for the attainment and maintenance of such
standards through control programs directed to sources of the
pollutants involved. The states, in conjunction with the EPA, also
administer the PSD program (CAA sections 160 to 169). In addition,
federal programs provide for nationwide reductions in emissions of
O3 precursors and other air pollutants through the federal
motor vehicle and motor vehicle fuel control program under title II of
the CAA (sections 202 to 250) which involves controls for emissions
from mobile sources and controls for the fuels used by these sources,
and new source performance standards for stationary sources under
section 111 of the CAA. For some stationary sources, the national
emissions standards for hazardous air pollutants under section 112 of
the CAA may provide ancillary reductions in O3 precursors.
    After the EPA establishes a new or revised NAAQS, the CAA directs
the EPA and the states to take steps to ensure that the new or revised
NAAQS is met. One of the first steps, known as the initial area
designations, involves identifying areas of the country that either are
attaining or not attaining the new or revised NAAQS along with the
nearby areas that contribute to the violations. Upon designation of
nonattainment areas, certain states would then be required to develop
SIPs to attain the standards. In developing their attainment plans,
states would first take into account projected emission reductions from
federal and state rules that have been already adopted at the time of
plan submittal. A number of significant emission reduction programs
that will lead to reductions of O3 precursors are in place
today or are expected to be in place by the time any new SIPs will be
due. Examples of such rules include the Nitrogen Oxides
(NOX) SIP Call, Clean Air Interstate Rule (CAIR), and Cross-
State Air Pollution Rule (CSAPR),\5\ regulations controlling onroad and
nonroad engines and fuels, the utility and industrial boilers hazardous
air pollutant rules, and various other programs already adopted by
states to reduce emissions from key emissions sources. States would
then evaluate the level of additional emission reductions needed for
each nonattainment area to attain the O3 standards ``as
expeditiously as practicable,'' and adopt new state regulations as
appropriate. Section VII of this preamble includes additional
discussion of designation and implementation issues associated with any
revised O3 NAAQS.
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    \5\ The Cross-State Air Pollution Rule was recently upheld by
the Supreme Court in Environmental Protection Agency v. EME Homer
City Generation, U.S. (2014). The DC Circuit has since lifted the
stay of the rule. Order, Document #1518738, EME Homer City
Generation, L.P. v. EPA, Case #11-1302 (D.C. Cir. Oct. 23, 2014).
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D. Review of Air Quality Criteria and Standards for O3
    The EPA first established primary and secondary NAAQS for
photochemical oxidants in 1971 (36 FR 8186, April 30, 1971). The EPA
set both primary and secondary standards at a level of 0.08 parts per
million (ppm), 1-hr average, total photochemical oxidants, not to be
exceeded more than one hour per year. The EPA based the standards on
scientific information contained in the 1970 Air Quality Criteria for
Photochemical Oxidants (U.S. DHEW, 1970). The EPA initiated the first
periodic review of the NAAQS for photochemical oxidants in 1977. Based
on the 1978 Air Quality Criteria for Ozone and Other Photochemical
Oxidants (U.S. EPA, 1978), the EPA published proposed revisions to the
original NAAQS in 1978 (43 FR 16962) and final revisions in 1979 (44 FR
8202). At that time, the EPA revised the level of the primary and
secondary standards from 0.08 to 0.12 ppm and changed the

indicator from photochemical oxidants to O3, and the form of
the standards from a deterministic (i.e., not to be exceeded more than
one hour per year) to a statistical form. This statistical form defined
attainment of the standards as occurring when the expected number of
days per calendar year with maximum hourly average concentration
greater than 0.12 ppm equaled one or less.
    Following the final decision in the 1979 review, the City of
Houston challenged the Administrator's decision arguing that the
standard was arbitrary and capricious because natural O3
concentrations and other physical phenomena in the Houston area made
the standard unattainable in that area. The U.S. Court of Appeals for
the District of Columbia Circuit (D.C. Circuit) rejected this argument,
holding (as noted above) that attainability and technological
feasibility are not relevant considerations in the promulgation of the
NAAQS. The court also noted that the EPA need not tailor the NAAQS to
fit each region or locale, pointing out that Congress was aware of the
difficulty in meeting standards in some locations and had addressed
this difficulty through various compliance related provisions in the
CAA. See API v. Costle, 665 F.2d 1176, 1184-6 (D.C. Cir. 1981).
    In 1982, the EPA announced plans to revise the 1978 Air Quality
Criteria document (47 FR 11561), and in 1983, the EPA initiated the
second periodic review of the O3 NAAQS (48 FR 38009). The
EPA subsequently published the 1986 Air Quality Criteria for Ozone and
Other Photochemical Oxidants (U.S. EPA, 1986) and the 1989 Staff Paper
(U.S. EPA, 1989). Following publication of the 1986 Air Quality
Criteria Document (AQCD), a number of scientific abstracts and articles
were published that appeared to be of sufficient importance concerning
potential health and welfare effects of O3 to warrant
preparation of a Supplement (U.S. EPA, 1992). On August 10, 1992, under
the terms of a court order, the EPA published a proposed decision to
retain the existing primary and secondary standards (57 FR 35542). The
notice explained that the proposed decision would complete the EPA's
review of information on health and welfare effects of O3
assembled over a 7-year period and contained in the 1986 AQCD and its
1992 Supplement. The proposal also announced the EPA's intention to
proceed as rapidly as possible with the next review of the air quality
criteria and standards for O3 in light of emerging evidence
of health effects related to 6- to 8-hour O3 exposures. On
March 9, 1993, the EPA concluded the review by affirming its proposed
decision to retain the existing primary and secondary standards (58 FR
13008).
    In August 1992, the EPA announced plans to initiate the third
periodic review of the air quality criteria and O3 NAAQS (57
FR 35542). In December 1996, the EPA proposed to replace the then-
existing 1-hour primary and secondary standards with 8-hour average
O3 standards set at a level of 0.08 ppm (equivalent to 0.084
ppm using standard rounding conventions) (61 FR 65716). The EPA also
proposed to establish a new distinct secondary standard using a
biologically based cumulative, seasonal form. The EPA completed this
review on July 18, 1997 (62 FR 38856) by setting the primary standard
at a level of 0.08 ppm, based on the annual fourth-highest daily
maximum 8-hr average concentration, averaged over three years, and
setting the secondary standard identical to the revised primary
standard. In reaching this decision, the EPA identified several reasons
supporting its decision to reject a potential alternate standard set at
0.07 ppm. Most importantly, the EPA pointed out the scientific
uncertainty at lower concentrations and placed significant weight on
the fact that no CASAC panel member supported a standard level set
lower than 0.08 ppm (62 FR 38868). In addition to noting the
uncertainties in the health evidence for exposure concentrations below
0.08 ppm and the advice of CASAC, the EPA noted that a standard set at
a level of 0.07 ppm would be closer to peak background concentrations
that infrequently occur in some areas due to nonanthropogenic sources
of O3 precursors (62 FR 38856, 38868; July 18, 1997).
    On May 14, 1999, in response to challenges by industry and others
to the EPA's 1997 decision, the D.C. Circuit remanded the O3
NAAQS to the EPA, finding that section 109 of the CAA, as interpreted
by the EPA, effected an unconstitutional delegation of legislative
authority. American Trucking Assoc. v. EPA, 175 F.3d 1027, 1034-1040
(D.C. Cir. 1999) (``ATA I''). In addition, the court directed that, in
responding to the remand, the EPA should consider the potential
beneficial health effects of O3 pollution in shielding the
public from the effects of solar ultraviolet (UV) radiation, as well as
adverse health effects. Id. at 1051-53. In 1999, the EPA petitioned for
rehearing en banc on several issues related to that decision. The court
granted the request for rehearing in part and denied it in part, but
declined to review its ruling with regard to the potential beneficial
effects of O3 pollution. 195 F.3d 4, 10 (D.C. Cir., 1999)
(``ATA II''). On January 27, 2000, the EPA petitioned the U.S. Supreme
Court for certiorari on the constitutional issue (and two other
issues), but did not request review of the ruling regarding the
potential beneficial health effects of O3. On February 27,
2001, the U.S. Supreme Court unanimously reversed the judgment of the
D.C. Circuit on the constitutional issue. Whitman v. American Trucking
Assoc., 531 U.S. 457, 472-74 (2001) (holding that section 109 of the
CAA does not delegate legislative power to the EPA in contravention of
the Constitution). The Court remanded the case to the D.C. Circuit to
consider challenges to the O3 NAAQS that had not been
addressed by that court's earlier decisions. On March 26, 2002, the
D.C. Circuit issued its final decision on remand, finding the 1997
O3 NAAQS to be ``neither arbitrary nor capricious,'' and so
denying the remaining petitions for review. American Trucking
Associations, Inc. v. EPA, 283 F.3d 355, 379 (D.C. Cir., 2002) (``ATA
III'').
    Specifically, in ATA III, the D.C. Circuit upheld the EPA's
decision on the 1997 O3 standard as the product of reasoned
decision-making. With regard to the primary standard, the court made
clear that the most important support for EPA's decision to revise the
standard was the health evidence of insufficient protection afforded by
the then-existing standard (``the record is replete with references to
studies demonstrating the inadequacies of the old one-hour standard''),
as well as extensive information supporting the change to an 8-hour
averaging time. 283 F.3d at 378. The court further upheld the EPA's
decision not to select a more stringent level for the primary standard
noting ``the absence of any human clinical studies at ozone
concentrations below 0.08 [ppm]'' which supported EPA's conclusion that
``the most serious health effects of ozone are `less certain' at low
concentrations, providing an eminently rational reason to set the
primary standard at a somewhat higher level, at least until additional
studies become available.'' Id. (internal citations omitted). The Court
also pointed to the significant weight that the EPA properly placed on
the advice it received from CASAC. Id. at 379. In addition, the court
noted that ``although relative proximity to peak background
O3 concentrations did not, in itself, necessitate a level of
0.08 [ppm], EPA could consider that factor when choosing among the
three alternative levels.'' Id.
    Independently of the litigation, the EPA responded to the court's
remand to

consider the potential beneficial health effects of O3
pollution in shielding the public from effects of UV radiation. The EPA
provisionally determined that the information linking changes in
patterns of ground-level O3 concentrations to changes in
relevant patterns of exposures to UV radiation of concern to public
health was too uncertain, at that time, to warrant any relaxation in
1997 O3 NAAQS. The EPA also expressed the view that any
plausible changes in UV-B radiation exposures from changes in patterns
of ground-level O3 concentrations would likely be very small
from a public health perspective. In view of these findings, the EPA
proposed to leave the 1997 8-hour NAAQS unchanged (66 FR 57268, Nov.
14, 2001). After considering public comment on the proposed decision,
the EPA published its final response to this remand on January 6, 2003,
re-affirming the 8-hour O3 NAAQS set in 1997 (68 FR 614).
    The EPA initiated the fourth periodic review of the air quality
criteria and O3 standards in September 2000 with a call for
information (65 FR 57810). The schedule for completion of that review
was ultimately governed by a consent decree resolving a lawsuit filed
in March 2003 by plaintiffs representing national environmental and
public health organizations, who maintained that the EPA was in breach
of a mandatory legal duty to complete review of the O3 NAAQS
within a statutorily mandated deadline. On July 11, 2007, the EPA
proposed to revise the level of the primary standard within a range of
0.075 to 0.070 ppm (72 FR 37818). Documents supporting this proposed
decision included the Air Quality Criteria for Ozone and Other
Photochemical Oxidants (U.S. EPA, 2006a) and the Staff Paper (U.S. EPA,
2007) and related technical support documents. The EPA also proposed
two options for revising the secondary standard: (1) Replace the
current standard with a cumulative, seasonal standard, expressed as an
index of the annual sum of weighted hourly concentrations cumulated
over 12 daylight hours 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-hrs, or (2) set the secondary standard
identical to the proposed primary standard. The EPA completed the
review with publication of a final decision on March 27, 2008 (73 FR
16436). In that final rule, the EPA revised the NAAQS by lowering the
level of the 8-hour primary O3 standard from 0.08 ppm to
0.075 ppm, not otherwise revising the primary standard, and adopting a
secondary standard identical to the revised primary standard. In May
2008, state, public health, environmental, and industry petitioners
filed suit challenging the EPA's final decision on the 2008
O3 standards. On September 16, 2009, the EPA announced its
intention to reconsider the 2008 O3 standards, and initiated
a rulemaking to do so. At the EPA's request, the Court held the
consolidated cases in abeyance pending the EPA's reconsideration of the
2008 decision.
    On January 19, 2010 (75 FR 2938), the EPA issued a notice of
proposed rulemaking to reconsider the 2008 final decision. In that
notice, the EPA proposed that further revisions of the primary and
secondary standards were necessary to provide a requisite level of
protection to public health and welfare. The EPA proposed to decrease
the level of the 2008 8-hour primary standard from 0.075 ppm to a level
within the range of 0.060 to 0.070 ppm, and to change the secondary
standard to a new cumulative, seasonal standard expressed as an annual
index of the sum of weighted hourly concentrations, cumulated over 12
hours per day (8 a.m. to 8 p.m.), during the consecutive 3-month period
within the O3 season with a maximum index value, set at a
level within the range of 7 to 15 ppm-hours. The Agency also solicited
CASAC review of the proposed rule on January 25, 2010 and solicited
additional CASAC advice on January 26, 2011. After considering comments
from CASAC and the public, the EPA prepared a draft final rule, which
was submitted for interagency review pursuant to Executive Order 12866.
On September 2, 2011, consistent with the direction of the President,
the Administrator of the Office of Information and Regulatory Affairs
(OIRA), Office of Management and Budget (OMB), returned the draft final
rule to the EPA for further consideration. In view of this return and
the fact that the Agency's next periodic review of the O3
NAAQS required under CAA section 109 had already begun (as announced on
September 29, 2008), the EPA deferred the decisions involved in the
reconsideration until it completed its statutorily required periodic
review.
    In light of EPA's decision to consolidate the reconsideration with
the current review, the D.C. Circuit proceeded with the litigation on
the 2008 final decision. On July 23, 2013, the Court upheld the EPA's
2008 primary O3 standard, but remanded the 2008 secondary
standard to the EPA. State of Mississippi v. EPA, 744 F.3d 1334. With
respect to the primary standard, the court first held that the EPA
reasonably determined that the existing standard was not requisite to
protect public health with an adequate margin of safety, and
consequently required revision. Specifically, the court noted that
there were ``numerous epidemiologic studies linking health effects to
exposure to ozone levels below 0.08 ppm and clinical human exposure
studies finding a causal relationship between health effects and
exposure to ozone levels at and below 0.08 ppm.'' 744 F.3d at 1345. The
court also specifically endorsed the weight of evidence approach
utilized by the EPA in its deliberations. Id. at 1344.
    The court went on to reject arguments that the EPA should have
adopted a more stringent primary standard. Dismissing arguments that a
clinical study (as properly interpreted by the EPA) showing effects at
0.06 ppm necessitated a standard level lower than that selected, the
court noted that this was a single, limited study. Id. at 1350. With
respect to the epidemiologic evidence, the court accepted the EPA's
argument that there could be legitimate uncertainty that a causal
relationship between O3 and 8-hour exposures less than 0.075
ppm exists, so that associations at lower levels reported in
epidemiologic studies did not necessitate a more stringent standard.
Id. at 1351-52.\6\
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    \6\ The court cautioned, however, that ``perhaps more [clinical]
studies like the Adams studies will yet reveal that the 0.060 ppm
level produces significant adverse decrements that simply cannot be
attributed to normal variation in lung function,'' and further
cautioned that ``agencies may not merely recite the terms
`substantial uncertainty' as a justification for their actions.''
Id. at 1350, 1357 (internal citations omitted).
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    The court also rejected arguments that an 8-hour primary standard
of 0.075 ppm failed to provide an adequate margin of safety, noting
that margin of safety considerations involved policy judgments by the
agency, and that by setting a standard ``appreciably below'' the level
of the current standard (0.08 ppm), the agency had made a reasonable
policy choice. Id. Finally, the court rejected arguments that the EPA's
decision was inconsistent with CASAC's scientific recommendations
because CASAC had been insufficiently clear in its recommendations
whether it was providing scientific or policy recommendations, and the
EPA had reasonably addressed CASAC's policy recommendations. Id. at
1357-58.
    With respect to the secondary standard, the court held that because
the EPA had failed to identify a level of air quality requisite to
protect public welfare, the EPA's comparison between

the primary and secondary standards for determining if requisite
protection for public welfare was afforded by the primary standard did
not comply with the CAA. The court thus rejected the EPA's explanation
for setting the secondary standard identical to the revised 8-hour
primary standard, and remanded the secondary standard to the EPA. Id.
at 1360-62.
    At the time of the court's decision, the EPA had already completed
significant portions of its next statutorily required periodic review
of the O3 NAAQS. On September 29, 2008, the EPA announced
the initiation of a new periodic review of the air quality criteria for
O3 and related photochemical oxidants and issued a call for
information in the Federal Register (73 FR 56581, Sept. 29, 2008). A
wide range of external experts, as well as the EPA staff, representing
a variety of areas of expertise (e.g., epidemiology, human and animal
toxicology, statistics, risk/exposure analysis, atmospheric science,
ecology, biology, plant science, ecosystem services) participated in a
workshop. This workshop was held on October 28-29, 2008 in Research
Triangle Park, NC. The workshop provided an opportunity for a public
discussion of the key policy-relevant issues around which the EPA would
structure this O3 NAAQS review and the most meaningful new
science that would be available to inform our understanding of these
issues.
    Based in part on the workshop discussions, the EPA developed a
draft Integrated Review Plan (IRP) outlining the schedule, process, and
key policy-relevant questions that would guide the evaluation of the
air quality criteria for O3 and the review of the primary
and secondary O3 NAAQS. A draft of the IRP was released for
public review and comment in September 2009. This IRP was the subject
of a consultation with the CASAC on November 13, 2009 (74 FR 54562;
October 22, 2009).\7\ The EPA considered comments received from that
consultation and from the public in finalizing the plan and in
beginning the review of the air quality criteria. The EPA's overall
plan and schedule for this review is presented in the Integrated Review
Plan for the Ozone National Ambient Air Quality Standards.\8\
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    \7\ See http://yosemite.epa.gov/sab/sabproduct.nsf/WebProjectsbyTopicCASAC!OpenView for more information on CASAC
activities related to the current O3 NAAQS review.
    \8\ EPA 452/R-11-006; April 2011; Available: http://www.epa.gov/ttn/naaqs/standards/ozone/data/2011_04_OzoneIRP.pdf.
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    As part of the process of preparing the O3 ISA, the
EPA's NCEA hosted a workshop to review and discuss preliminary drafts
of key sections of the ISA on August 6, 2010 (75 FR 42085, July 20,
2010). The CASAC and the public reviewed the first external review
draft ISA (U.S. EPA, 2011a; 76 FR 10893, February 28, 2011) at a
meeting held in May 19-20, 2011 (76 FR 23809; April 28, 2011). Based on
CASAC and public comments, NCEA prepared a second draft ISA (U.S. EPA,
2011b; 76 FR 60820, September 30, 2011). CASAC and the public reviewed
this draft at a January 9-10, 2012 (76 FR 236, December 8, 2011)
meeting. Based on CASAC and public comments, NCEA prepared a third
draft ISA (U.S. EPA 2012a; 77 FR 36534; June 19, 2012), which was
reviewed at a CASAC meeting in September 2012. The EPA released the
final ISA (EPA/600/R-10/076F) in February 2013.
    The EPA presented its plans for conducting the Risk and Exposure
Assessments (REAs) that build on the scientific evidence presented in
the ISA, in two planning documents titled Ozone National Ambient Air
Quality Standards: Scope and Methods Plan for Health Risk and Exposure
Assessment and Ozone National Ambient Air Quality Standards: Scope and
Methods Plan for Welfare Risk and Exposure Assessment (henceforth,
Scope and Methods Plans).\9\ These planning documents outlined the
scope and approaches that staff planned to use in conducting
quantitative assessments, as well as key issues that would be addressed
as part of the assessments. The EPA released these documents for public
comment in April 2011, and consulted with CASAC on May 19-20, 2011 (76
FR 23809; April 28, 2011). In designing and conducting the initial
health risk and welfare risk assessments, the EPA considered CASAC
comments (Samet, 2011) on the Scope and Methods Plans and also
considered public comments. In May 2012, the EPA issued a memo titled
Updates to Information Presented in the Scope and Methods Plans for the
Ozone NAAQS Health and Welfare Risk and Exposure Assessments that
described changes to elements of the scope and methods plans and
provided a brief explanation of each change and the reason for it.
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    \9\ EPA-452/P-11-001 and -002; April 2011; Available: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pd.html.
---------------------------------------------------------------------------

    In July 2012, the EPA made the first drafts of the Health and
Welfare REAs available for CASAC review and public comment (77 FR
42495, July 19, 2012). The first draft PA \10\ was made available for
CASAC review and public comment in August 2012. These documents were
reviewed by the CASAC O3 Panel at a public meeting in
September 2012. The second draft REAs and PA, made available by the EPA
in January 2014 (79 FR 4694, January 29, 2014), were prepared with
consideration of advice from CASAC (Frey and Samet, 2012a, 2012b) and
comments from the public. These drafts were reviewed by the CASAC
O3 Panel at a public meeting on March 25-27, 2014. The CASAC
issued final reports on the second drafts of the HREA on July 1, 2014
(Frey, 2014a), and the WREA on June 18, 2014 (Frey, 2014b),
respectively. The CASAC issued a final report on the second draft PA on
June 26, 2014 (Frey, 2014c). The final versions of the HREA (U.S. EPA
2014a), WREA (U.S. EPA, 2014b), and PA (U.S. EPA, 2014c) were made
available by the EPA in August, 2014. These documents reflect staff's
consideration of the comments and recommendations made by CASAC, as
well as comments made by members of the public, in their review of the
draft versions of these documents.
---------------------------------------------------------------------------

    \10\ The PA is prepared by the staff in the EPA's Office of Air
Quality Planning and Standards (OAQPS). It presents a staff
evaluation of the policy implications of the key scientific and
technical information in the ISA and REAs for the EPA's
consideration. The PA provides a transparent evaluation, and staff
conclusions, regarding policy considerations related to reaching
judgments about the adequacy of the current standards, and if
revision is considered, what revisions may be appropriate to
consider. The PA is intended to help ``bridge the gap'' between the
agency's scientific assessments presented in the ISA and REAs, and
the judgments required of the EPA Administrator in determining
whether it is appropriate to retain or revise the NAAQS.
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E. Ozone Air Quality

    Ozone is formed near the Earth's surface due to chemical
interactions involving solar radiation and precursor pollutants
including volatile organic compounds (VOCs), nitrogen oxides
(NOX), methane (CH4) and carbon monoxide (CO).
The precursor emissions leading to O3 formation can result
from both man-made sources (e.g., motor vehicles and electric power
generation) and natural sources (e.g., vegetation and wildfires).
Occasionally, O3 that is created naturally in the
stratosphere can also contribute to O3 levels near the
surface. Once formed, O3 can be transported by winds before
eventually being removed from the atmosphere via chemical reactions or
deposition to surfaces. In sum, O3 concentrations are
influenced by complex interactions between precursor emissions,
meteorological conditions, and surface characteristics.
    In order to continuously assess O3 air pollution levels,
state and local environmental agencies operate O3 monitors
at various locations and

subsequently submit the data to the EPA. At present, there are
approximately 1,400 monitors across the U.S. reporting hourly
O3 averages during the times of the year when local
O3 pollution can be important. Much of this monitoring is
focused on O3 measurements in urban areas where precursor
emissions tend to be largest, as well as locations directly downwind of
these areas, but there are also over 100 sites in rural areas where
high levels of O3 can periodically exist due to transport
from upwind sources. Based on data from this national network, the EPA
estimates that approximately 133 million Americans live in counties
where O3 concentrations were above the level of the existing
health-based NAAQS of 0.075 ppm at least 4 days in 2012. High
O3 values can occur almost anywhere within the contiguous 48
states, although locations in California, Texas, and the Northeast
Corridor are especially subject to poor O3 air quality. From
a temporal perspective, the highest daily peak O3
concentrations generally tend to occur during the afternoon within the
warmer months due to higher solar radiation and other conducive
meteorological conditions during these times. The exceptions to this
general rule include: (1) Some rural sites where transport of
O3 from upwind areas of regional production can occasionally
result in high nighttime levels of O3, (2) high-elevation
sites periodically influenced by stratospheric intrusions, and (3)
certain locations in the western U.S. where large quantities of
O3 precursors emissions associated with oil and gas
development can be trapped by strong inversions associated with snow
cover during the colder months and efficiently converted to
O3.
    One of the challenging aspects of developing plans to reduce
emissions leading to high O3 concentrations is that the
response of O3 to precursor reductions is nonlinear. In
particular, NOX causes both the formation and destruction of
O3. The net impact of NOX emissions on
O3 concentrations depends on the local quantities of
NOX, VOC, and sunlight which interact in a set of complex
chemical reactions. In some areas, such as urban centers where
NOX emissions typically are high, NOX leads to
the net destruction of O3, making O3 levels lower
in the immediate vicinity. This phenomenon is particularly pronounced
under conditions that lead to low O3 concentrations (i.e.
during cool, cloudy weather and at night when photochemical activity is
limited or nonexistent). However, while NOX can initially
destroy O3 near the emission sources, these same
NOX emissions eventually do react to form more O3
downwind. Photochemical model simulations suggest that the additional
expected reductions in NOX emissions will slightly increase
O3 concentrations on days with lower O3
concentrations in areas in close proximity to NOX sources,
while at the same time decreasing the highest O3
concentrations in outlying areas. See generally, U.S. EPA, 2014a
(section 2.2.1).
    At present, both the primary and secondary NAAQS use the annual
fourth-highest daily maximum 8-hour concentration, averaged over 3
years, as the form of the standard. An additional air quality metric,
referred to as W126, is often used to assess cumulative impact of
O3 exposure on ecosystems and vegetation. W126 is a seasonal
aggregate of weighted hourly O3 values observed between 8
a.m. and 8 p.m. As O3 precursor emissions have decreased
across the U.S., O3 design values \11\ have concurrently
shown a modest downward trend. Ozone design values decreased by
approximately 9% on average between 2000 and 2012. Air quality model
simulations estimate that peak O3 levels will continue to
improve over the next decade as additional reductions in O3
precursors from power plants, motor vehicles, and other sources are
realized.
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    \11\ A design value is a statistic that describes the air
quality status of a given location relative to the level of the
NAAQS.
---------------------------------------------------------------------------

    In addition to being affected by changing emissions, future
O3 concentrations will also be affected by climate change.
Modeling studies in EPA's Interim Assessment (U.S. EPA, 2009b) and
cited in support of the 2009 Endangerment Finding (74 FR 66,496; Dec.
15, 2009) show that, while the impact is not uniform, climate change
has the potential to cause increases in summertime O3
concentrations over substantial regions of the country, with increases
tending to occur during higher peak pollution episodes in the summer,
if offsetting emissions reductions are not made. Increases in
temperature are expected to be the principal factor in driving any
ozone increases, although increases in stagnation frequency may also
contribute (Jacob and Winner, 2009). These increases in O3
pollution over broad areas of the U.S., including in the largest
metropolitan areas with the worst O3 problems, increase the
risk of morbidity and mortality. Children, people with asthma or other
lung diseases, older adults, and people who are active outdoors,
including outdoor workers, are among the most vulnerable to these
O3-related health effects. If unchecked, climate change has
the potential to offset some of the improvements in O3 air
quality, and therefore some of the improvements in public health, that
are expected from reductions in emissions of O3 precursors.
    Another challenging aspect of the O3 issue is the
involvement of sources of O3 and O3 precursors
beyond those from domestic, anthropogenic sources. Modeling analyses
have suggested that nationally the majority of O3
exceedances are predominantly caused by anthropogenic emissions from
within the U.S. However, observational and modeling analyses have
concluded that O3 concentrations in some locations in the
U.S. can be substantially influenced by sources that may not be suited
to domestic control measures. In particular, certain high-elevation
sites in the western U.S. are impacted by a combination of non-local
sources like international transport, stratospheric O3, and
O3 originating from wildfire emissions. Ambient
O3 from these non-local sources is collectively referred to
as background O3. See generally section 2.4 of the Policy
Assessment (U.S. EPA, 2014c). The analyses suggest that, at these
locations, there can be episodic events with substantial background
contributions where O3 concentrations approach or exceed the
level of the current NAAQS (i.e., 75 ppb). These events are relatively
infrequent and the EPA has policies that allow for the exclusion of air
quality monitoring data from design value calculations when they are
substantially affected by certain background influences. Wildfires pose
a direct threat to air quality and public safety--threats that can be
mitigated through management of wildland vegetation. The use of
wildland prescribed fire can influence the occurrence of catastrophic
wildfires which may help manage the contribution of wildfires to
background O3 levels and periodic peak O3 events.
Prescribed fire mimics a natural process necessary to manage and
maintain fire-adapted ecosystems and climate change adaptation, while
reducing risk of uncontrolled emissions from catastrophic wildfires.
Wildfire emissions may make it more challenging to meet the NAAQS.
However, the CAA requires the EPA to set the NAAQS at levels requisite
to protect public health and welfare without regard to the source of
the pollutant. API, 665 F. 2d at 1185-86. The EPA may consider
proximity to background levels as a factor in the decision whether and
how to revise the NAAQS when considering levels within the range of
reasonable values

supported by the air quality criteria and judgments of the
Administrator. ATA III, 283 F. 3d at 379. It is in the implementation
process that states and the EPA can address how to develop effective
public policy in locations in which background sources contribute
substantially to high O3. Section VII.F provides more detail
about how background O3 can be addressed via CAA
implementation provisions.

II. Rationale for Proposed Decision on the Primary Standard

    This section presents the Administrator's rationale for her
proposed decision to revise the existing primary O3 standard
by lowering the level of the standard to within the range of 0.065 to
0.070 ppm. As discussed more fully below, this rationale draws from the
thorough review in the ISA of the available scientific evidence,
published through July 2011, on human health effects associated with
the presence of O3 in the ambient air. This rationale also
takes into account: (1) Analyses of O3 air quality, human
exposures to O3, and O3-associated health risks,
as presented and assessed in the HREA; (2) the EPA staff assessment of
the most policy-relevant scientific evidence and exposure/risk
information in the PA; (3) CASAC advice and recommendations, as
reflected in discussions of drafts of the ISA, REA, and PA at public
meetings, in separate written comments, and in CASAC's letters to the
Administrator; and (4) public input received during the development of
these documents, either in connection with CASAC meetings or
separately.
    Section II.A below provides an overview of the approaches used to
consider the scientific evidence and exposure/risk information as it
relates to the primary O3 standard. This includes summaries
of the approach adopted by the Administrator in the 2008 review of the
O3 NAAQS and of the approach adopted in the PA in the
current review. Section II.B summarizes the body of evidence for health
effects attributable to short- or long-term O3 exposures,
with a focus on effects for which the ISA judges that there is a
``causal'' or a ``likely to be causal'' relationship with O3
exposures. Section II.C summarizes the HREA's quantitative estimates of
O3 exposures and health risks, including key results and
uncertainties. Sections II.D and II.E present the Administrator's
proposed conclusions on the adequacy of the current primary
O3 standard and alternative primary standards, respectively.

A. Approach

    In the 2008 review of the O3 NAAQS, Administrator
Stephen L. Johnson revised the level of the 8-hour primary
O3 standard from 0.08 ppm \12\ to 0.075 ppm (75 parts per
billion (ppb) \13\). This decision was based on his consideration of
the available scientific evidence and exposure/risk information, the
advice and recommendations of CASAC, and comments from the public. The
Administrator placed primary emphasis on the body of available
scientific evidence, while viewing the results of exposure and risk
assessments as providing supporting information. Specifically, he
judged that a standard set at 75 ppb would be appreciably below the
concentration at which adverse effects had been demonstrated in the
controlled human exposure studies available at that time (i.e., 80
ppb), and would provide a significant increase in protection compared
to the then-current standard. The Administrator further concluded that
the body of evidence did not support setting a lower standard level,
given the increasing uncertainty in the evidence at lower O3
concentrations (U.S. EPA, 2014c, Chapter 1).
---------------------------------------------------------------------------

    \12\ Due to rounding convention, the 1997 standard level of 0.08
ppm corresponded to 0.084 ppm (84 ppb).
    \13\ The level of the O3 standard is specified as
0.075 ppm rather than 75 ppb. However, in the PA we refer to ppb,
which is most often used in the scientific literature and in the
ISA, in order to avoid the confusion that could result from
switching units when discussing the evidence in relation to the
standard level. Similarly, in the preamble to this notice we refer
to ppb.
---------------------------------------------------------------------------

    In the current review, the EPA's approach to informing decisions on
the primary O3 standard builds upon the general approach
used in the last review and reflects the broader body of scientific
evidence, updated exposure/risk information, and advances in
O3 air quality modeling now available. This approach,
described in detail in the PA (U.S. EPA, 2014c, section 1.3.1), is
based most fundamentally on using the EPA's assessment of the available
scientific evidence and associated quantitative analyses to inform the
Administrator's judgments regarding a primary standard for
O3 that is ``requisite'' (i.e., neither more nor less
stringent than necessary) to protect public health with an adequate
margin of safety. Specifically, it is based on consideration of the
available body of scientific evidence assessed in the ISA (U.S. EPA,
2013a), exposure and risk analyses presented in the HREA (U.S. EPA,
2014a), advice and recommendations from CASAC (Frey, 2014a, c), and
public comments. Based on the application of this approach, the PA
assesses and integrates the evidence and information, and reaches
conclusions for the Administrator's consideration about the range of
policy options that could be supported. The remainder of this section
describes the PA's approach to reviewing the primary O3
standard, and to informing the Administrator's proposed decisions on
the current and alternative standards.
    As an initial matter, the PA recognizes that the final decision to
retain or revise the current primary O3 standard is a public
health policy judgment to be made by the Administrator and will draw
upon the available scientific evidence for O3-attributable
health effects and on analyses of population exposures and health
risks, including judgments about the appropriate weight to assign the
range of uncertainties inherent in the evidence and analyses. The PA's
general approach to informing these public health policy judgments
recognizes that the available health effects evidence reflects a
continuum from relatively higher O3 concentrations, at which
scientists generally agree that health effects are likely to occur,
through lower concentrations, at which the likelihood and magnitude of
a response become increasingly uncertain. Therefore, the conclusions in
the PA reflect an interpretation of the available scientific evidence
and exposure/risk information that, in the views of the EPA staff,
neither overstates nor understates the strengths and limitations of
that evidence and information.\14\ This approach is consistent with the
requirements of sections 108 and 109 of the CAA, as well as with how
the EPA and the courts have historically interpreted the CAA.
---------------------------------------------------------------------------

    \14\ Draft versions of the PA were subject to review by CASAC
and the final PA reflects consideration of the advice received from
CASAC during the review process. CASAC concluded that ``Overall, we
find the Second Draft PA to be adequate for its intended purpose of
providing a strong scientific basis for findings regarding the
inadequacy of current primary and secondary ozone air quality
standards'' (Frey, 2014c, p. v).
---------------------------------------------------------------------------

    The PA draws upon an integrative synthesis of the entire body of
available scientific evidence for O3-related health effects,
including the evidence newly available in the current review and the
evidence from previous reviews, as presented in the ISA (U.S. EPA,
2013a). Consideration of the scientific evidence is based fundamentally
on information from controlled human exposure and epidemiologic
studies, supplemented by information from animal toxicology studies. In
the PA, such evidence informs the consideration of the health

endpoints and at-risk populations \15\ on which to focus the current
review, and the consideration of the O3 concentrations at
which various health effects can occur.
---------------------------------------------------------------------------

    \15\ In this review, the term ``at-risk population'' is used to
encompass populations or lifestages that have a greater likelihood
of experiencing health effects related to exposure to an air
pollutant due to a variety of factors; other terms used in the
literature include susceptible, vulnerable, and sensitive. These
factors may be intrinsic, such as genetic factors, lifestage, or the
presence of preexisting diseases, or they may be extrinsic, such as
socioeconomic status (SES), activity pattern and exercise level, or
increased pollutant exposures (U.S. EPA 2013, p. lxx, 8-1, 8-2). The
courts and the CAA's legislative history refer to these at-risk
subpopulations as ``susceptible'' or ``sensitive'' populations. See,
e.g., American Lung Ass'n v. EPA, 134 F. 3d 388, 389 (D.C. Cir.
1998) (``NAAQS must protect not only average health individuals, but
also `sensitive citizens'--children, for example, or people with
asthma, emphysema, or other conditions rendering them particularly
vulnerable to air pollution'' (quoting S. Rep. No. 91-1196 at 10).
---------------------------------------------------------------------------

    Since the 2008 review of the O3 NAAQS, the EPA has
developed formal frameworks for characterizing the strength of the
scientific evidence with regard to health effects associated with
exposures to O3 in ambient air and factors that may increase
risk in some populations or lifestages. These frameworks provide the
basis for robust, consistent, and transparent processes for evaluating
the scientific evidence, including uncertainties in the evidence, and
for drawing weight-of-evidence conclusions on air pollution-related
health effects and at-risk populations. These frameworks for
characterizing the strength of the scientific evidence are discussed in
detail in the ISA (U.S. EPA, 2013a, Preamble; Chapter 8).
    With regard to characterization of health effects, the ISA uses a
five-level hierarchy to classify the overall weight of evidence into
one of the following categories: causal relationship, likely to be a
causal relationship, suggestive of a causal relationship, inadequate to
infer a causal relationship, and not likely to be a causal relationship
(U.S. EPA, 2013a, Preamble Table II). In using the 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 the strength, consistency,
and coherence of evidence, increase. Conclusions about biological
plausibility and about the consistency and coherence of O3-
related health effects are drawn from the integration of epidemiologic
studies with mechanistic information from controlled human exposure and
animal toxicological studies, as discussed in the ISA (U.S. EPA, 2013a,
EPA Framework for Causal Determination, p. 1viii). The PA places the
greatest weight on the health effects for which the evidence has been
judged in the ISA to support a ``causal'' or a ``likely to be causal''
relationship with O3 exposures.
    The PA further considers the evidence base assessed in the ISA with
regard to the types and levels of exposure at which health effects are
indicated. This consideration of the evidence, which directly informs
conclusions regarding the adequacy of current or alternative standards,
differs from consideration of the evidence in the ISA with regard to
overarching determinations of causality. Therefore, studies that inform
determinations of causality may or may not be concluded to be
informative with regard to the adequacy of the current or alternative
standards.\16\
---------------------------------------------------------------------------

    \16\ For example, the PA judges that health studies evaluating
exposure concentrations near or below the level of the current
standard and epidemiologic studies conducted in locations meeting
the current standard are particularly informative when considering
the adequacy of the public health protection provided by the current
standard (U.S. EPA, 2014c, Chapters 3 and 4).
---------------------------------------------------------------------------

    As with health endpoints, the ISA's characterization of the weight
of evidence for potential at-risk populations is based on the
evaluation and synthesis of evidence from across scientific
disciplines. The ISA uses the collective evidence to examine the
coherence of effects across disciplines and to determine the biological
plausibility of reported effects. Based on this approach, the ISA
characterizes the evidence for a number of ``factors'' that have the
potential to place populations at increased risk for O3-
related effects. The categories considered in evaluating the evidence
for these potential at-risk factors are ``adequate evidence,''
``suggestive evidence,'' ``inadequate evidence,'' and ``evidence of no
effect.'' For the ``adequate evidence'' category, the ISA concludes
that this category is appropriate when multiple high-quality studies
show ``there is substantial, consistent evidence within a discipline to
conclude that a factor results in a population or lifestage being at
increased risk of air pollutant-related health effect(s) relative to
some reference population or lifestage'' (U.S. EPA, 2013a, p. 8-2). In
addition, where applicable, the ``adequate evidence'' category reflects
a conclusion that there is coherence in the evidence across
disciplines. The other categories reflect greater uncertainty in the
evidence. In this review, the PA focuses on those factors for which the
ISA judges there is adequate evidence of increased risk (U.S. EPA,
2013a, Table 8-5). At-risk populations are discussed in more detail in
section 3.1.5 of the PA (U.S. EPA, 2014c) and these categories are
discussed in more detail in the ISA (U.S. EPA, 2013a, chapter 8, Table
8-1).
    Using the available scientific evidence to inform conclusions on
the current and alternative standards is complicated by the recognition
that a population-level threshold has not been identified below which
it can be concluded with confidence that O3-attributable
effects do not occur (U.S. EPA, 2013a, section <IP_ADDRESS>). In the absence
of a discernible threshold, the PA's general approach to considering
the available O3 health evidence involves characterizing
confidence in the extent to which O3-attributable effects
occur, and the extent to which such effects are adverse, over the
ranges of O3 exposure concentrations evaluated in controlled
human exposure studies and over the distributions of ambient
O3 concentrations in locations where epidemiologic studies
have been conducted. As noted above, the PA recognizes that the
available health effects evidence reflects a continuum from relatively
high O3 concentrations, at which scientists generally agree
that adverse health effects are likely to occur, through lower
concentrations, at which the likelihood and magnitude of a response
become increasingly uncertain. Aspects of the approach used in this
review to evaluate evidence from controlled human exposure and
epidemiologic studies, respectively, are discussed below.
    Controlled human exposure studies provide direct evidence of
relationships between pollutant exposures and human health effects
(U.S. EPA, 2013a, p.lx). 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. Such studies are particularly useful in
defining the specific conditions under which pollutant exposures can
result in health impacts, including the exposure concentrations,
durations, and ventilation rates under which effects can occur. As
discussed in the ISA, controlled human exposure studies provide clear
and compelling evidence for an array of human health effects that are
directly attributable to acute exposures to O3 per se (i.e.,
as opposed to O3 and other photochemical oxidants, for which
O3 is an indicator, or other co-occurring pollutants) (U.S.
EPA, 2013a, Chapter 6). Together with animal toxicological studies,
which can provide

information about more serious health outcomes as well as the effects
of long-term exposures and mode of action, controlled human exposure
studies also help to provide biological plausibility for health effects
observed in epidemiologic studies.
    The PA considers the evidence from controlled human exposure
studies in two ways. First, the PA considers the extent to which
controlled human exposure studies provide evidence for health effects
following exposures to different O3 concentrations, down to
the lowest-observed-effects levels in those studies. Second, the PA
uses these studies to help evaluate the extent to which there is
confidence in health effect associations reported in epidemiologic
studies down through lower ambient O3 concentrations, where
the likelihood and magnitude of O3-attributable effects
become increasingly uncertain.
    The PA considers the range of O3 exposure concentrations
evaluated in controlled human exposure studies, including
concentrations near or below the level of the current standard. The PA
considers both group mean responses, which provide insight into the
extent to which observed changes are due to O3 exposures
rather than to chance alone, and interindividual variability in
responses, which provides insight into the fraction of the population
that might be affected by such O3 exposures (U.S. EPA,
2013a, section <IP_ADDRESS>). When considering the relative weight to place
on various controlled human exposure studies, the discussion in the PA
focuses on the exposure conditions evaluated (e.g., exercising versus
resting, exposure duration); the nature, magnitude, and likely
adversity of effects over the range of reported O3 exposure
concentrations; the statistical precision of reported effects; and the
consistency of results across studies for a given health endpoint and
exposure concentration. In addition, because controlled human exposure
studies typically involve healthy individuals and do not evaluate the
most sensitive individuals in the population (U.S. EPA, 2013a, Preamble
p. lx), when considering the implications of these studies for
evaluation of the current and alternative standards, the PA also
considers the extent to which reported effects are likely to reflect
the magnitude and/or severity of effects in at-risk groups.
    The PA also considers epidemiologic studies of short- and long-term
O3 concentrations in ambient air. Epidemiologic studies
provide information on associations between variability in ambient
O3 concentrations and variability in various health
outcomes, including lung function decrements, respiratory symptoms,
school absences, hospital admissions, emergency department visits, and
premature mortality (U.S. EPA, 2013a, Chapters 6 and 7). Epidemiologic
studies can inform understanding of the effects in the study population
(which may include at-risk groups) of real-world exposures to the range
of O3 concentrations in ambient air, as well as provide
evidence of associations between ambient O3 levels and more
serious acute and chronic health effects 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 (e.g., effects modifiers
such as averting behavior) affects the level of confidence that the
health effects being investigated are attributable to O3
exposures, alone and in combination with copollutants.
    Available epidemiologic studies have generally not indicated a
discernible population threshold below which O3 is no longer
associated with health effects (U.S. EPA, 2013a, section <IP_ADDRESS>).
However, the currently available epidemiologic evidence indicates
decreased confidence in reported concentration-response relationships
for O3 concentrations at the lower ends of ambient
distributions due to the low density of data in this range (U.S. EPA,
2013a, section <IP_ADDRESS>). As discussed more fully in Chapter 1 of the PA
(U.S. EPA, 2014c), the general approach to considering the results of
epidemiologic studies within the context of the current and alternative
standards focuses on characterizing the range of ambient O3
concentrations over which studies indicate the most confidence in
O3-associated health effects, and the concentrations below
which confidence in such health effect associations becomes appreciably
lower.
    In placing emphasis on specific epidemiologic studies, as in past
reviews, the discussion in the PA focuses on the epidemiologic studies
conducted in the U.S. and Canada. Such studies reflect air quality and
exposure patterns that are likely more typical of the U.S. population,
since studies conducted outside the U.S. and Canada may well reflect
different demographic and air pollution characteristics.\17\ The PA
also focuses on studies reporting associations with effects judged in
the ISA (U.S. EPA, 2013a) to be robust to confounding by other factors,
including co-occurring air pollutants.
---------------------------------------------------------------------------

    \17\ Though the PA recognizes that a broader body of studies,
including international studies, informs the causal determinations
in the ISA.
---------------------------------------------------------------------------

    To put staff conclusions about O3-related health effects
into a broader public health context, the PA also considers exposure
and risk estimates from the HREA, which develops and applies models to
estimate human exposures to O3 and O3-related
health risks in urban study areas across the United States (U.S. EPA,
2014a). The HREA estimates exposures of concern, based on interpreting
quantitative exposure estimates within the context of controlled human
exposure study results; lung function risks, based on applying
exposure-response relationships from controlled human exposure studies
to quantitative estimates of exposures; and epidemiologic-based risk
estimates, based on applying concentration-response relationships drawn
from epidemiologic studies to adjusted air quality. Each of these types
of assessments is discussed briefly below.
    As in the 2008 review, the HREA estimates exposures at or above
benchmark concentrations of 60, 70, and 80 ppb, reflecting exposure
concentrations of concern based on the available health evidence.\18\
Estimates of exposures of concern, defined as personal exposures while
at moderate or greater exertion to 8-hour average ambient O3
levels, at or above these discrete benchmark concentrations provide
perspective on the public health risks of O3-related health
effects that have been demonstrated in controlled human exposure and
toxicological studies. However, because of a lack of exposure-response
information across a range of exposure concentrations in these studies,
these risks cannot be assessed using a quantitative risk assessment.
Though this analysis is conducted using discrete benchmark
concentrations, information from the broad body of evidence indicates
that health-relevant exposures are more appropriately viewed as a
continuum with greater confidence and certainty about the existence of
health effects at higher O3 exposure concentrations and less
confidence and certainty at lower exposure concentrations. This
approach recognizes that there is no sharp breakpoint within the
exposure-response relationship for exposure concentrations at and above
80 ppb down to 60 ppb.
---------------------------------------------------------------------------

    \18\ For example, see 75 FR 2945-2946 (January 19, 2010) and 73
FR 16441-16442 (March 27, 2008) discussing ``exposures of concern.''
---------------------------------------------------------------------------

    Within the context of this continuum, estimates of exposures of
concern at these discrete benchmark

concentrations provide some perspective on the public health impacts of
O3-related health effects, such as pulmonary inflammation,
that are plausibly linked to the more serious effects seen in
epidemiologic studies but cannot be evaluated in quantitative risk
assessments. They also help elucidate the extent to which such impacts
may be reduced by meeting the current and alternative standards.
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 due
to individual variability in responsiveness. Only a subset of
individuals can be expected to experience such adverse health effects,
and at-risk populations or lifestages, such as people with asthma or
children, are expected to be affected more by such exposures than
healthy adults.
    The HREA also generates quantitative estimates of O3
health risks for air quality adjusted to just meet the current \19\ and
alternative standards. One approach to estimating O3 health
risks is to combine modeled exposure estimates with exposure-response
relationships derived from controlled human exposure studies of
O3-induced health effects. The HREA uses this approach to
estimate the occurrence of O3-induced lung function
decrements in at-risk populations, including school-age children,
school-age children with asthma, adults with asthma, and older adults.
The available exposure-response information does not support this
approach for other endpoints evaluated in controlled human exposure
studies (U.S. EPA, 2014a, section 2.3).
---------------------------------------------------------------------------

    \19\ For purposes of the exposure and risk estimates with
adjusted air quality, the REA considered any value <76 ppb to be
``just meeting'' the current 75 ppb standard (U.S. EPA, 2014a).
---------------------------------------------------------------------------

    The other approach used in this review to estimate O3-
associated health risks is to apply concentration-response
relationships derived from short- and/or long-term epidemiologic
studies to air quality adjusted to just meet current and alternative
standards. The concentration-response relationships drawn from
epidemiologic studies are based on population exposure surrogates, such
as 8-hour concentrations averaged across monitors and over more than
one day (U.S. EPA, 2013a, Chapter 6). The HREA presents epidemiologic-
based risk estimates for O3-associated mortality, hospital
admissions, emergency department visits, and respiratory symptoms (U.S.
EPA, 2014a, section 2.3). These estimates are derived from the full
distributions of ambient O3 concentrations estimated for the
study locations.\20\ In addition, the HREA estimates mortality risks
associated with various portions of distributions of short-term
O3 concentrations (U.S. EPA, 2014a). The PA considers risk
estimates based on the full distributions of ambient O3
concentrations and, when available, estimates of the risk associated
with various portions of those ambient distributions.\21\ In doing so,
the PA takes note of the ISA conclusions regarding confidence in linear
concentration-response relationships over distributions of ambient
concentrations (see above), and of the extent to which health effect
associations at various ambient O3 concentrations are
supported by the evidence from experimental studies for effects
following specific O3 exposures.
---------------------------------------------------------------------------

    \20\ In previous reviews, including the 2008 review and
reconsideration, such risks were separately estimated for
O3 concentrations characterized as above policy-relevant
background concentrations. Policy-relevant background concentrations
were defined as the distribution of O3 concentrations
attributable to sources other than anthropogenic emissions of
O3 precursor emissions (e.g., VOC, CO, NOX) in
the U.S., Canada, and Mexico. The decision in this review to
estimate total risk across the full range of O3
concentrations reflects consideration of advice from CASAC (Frey and
Samet, 2012b).
    \21\ In a series of sensitivity analyses, the HREA also
evaluates a series of threshold models for respiratory mortality
associated with long-term O3 concentrations. The PA
considers these risk estimates based on threshold models, in
addition to HREA core estimates based on the linear model (U.S. EPA,
2014a, sections <IP_ADDRESS>, <IP_ADDRESS>).
---------------------------------------------------------------------------

B. Health Effects Information

    This section outlines key information contained in the ISA (U.S.
EPA, 2013a, Chapters 4 to 8) and in the PA (U.S. EPA, 2014c, Chapters 3
and 4) on the known or potential effects on public health which may be
expected from the presence of O3 in the ambient air. The
information highlighted here summarizes: (1) New information available
on potential mechanisms for health effects associated with exposure to
O3 (II.B.1); (2) the nature of effects that have been
associated directly with both short- and long-term exposure to
O3 and indirectly with the presence of O3 in
ambient air (II.B.2); (3) considerations related to the adversity of
O3-attributable health effects (II.B.3); and (4)
considerations in characterizing the public health impact of
O3, including the identification of ``at risk'' populations
(II.B.4).
    The decision in the 2008 rulemaking emphasized the large number of
epidemiologic studies published since the 1997 review that continued to
report associations with respiratory hospital admissions and emergency
department visits, as well as additional health endpoints, including
the effects of acute (short-term and prolonged) and chronic exposures
to O3 on lung function decrements and enhanced respiratory
symptoms in asthmatic individuals, school absences, and premature
mortality. It also emphasized controlled human exposure studies showing
respiratory effects with prolonged O3 exposures at levels
below 80 ppb, changes in lung host defenses, and increased airway
responsiveness, and animal toxicology studies that provided information
about mechanisms of action.
    The ISA (U.S. EPA, 2013a) prepared for this review emphasizes a
large number of new epidemiologic studies published since the last
review on effects associated with both short- and long-term exposures,
including new epidemiologic studies about risk factors. It also
emphasizes important new information from controlled human exposure,
dosimetry and toxicology studies. Highlights of the new evidence
included:

    (1) Two controlled human exposure studies new since the 2008
review are now available that examine respiratory effects associated
with prolonged, 6.6-hour, O3 exposures to levels of 72
ppb \22\ and 60 ppb. These studies observed effects in healthy
adults, including lung function decrements combined with respiratory
symptoms at 72 ppb, and lung function decrements and pulmonary
inflammation at 60 ppb. These studies expand on evidence of lung
function decrements with O3 exposure at 60 ppb available
in the last review, and provide new evidence of airway inflammation,
a mechanism by which O3 may cause other more serious
respiratory effects (e.g., asthma exacerbations).
---------------------------------------------------------------------------

    \22\ As noted below, for the 70 ppb exposure concentration,
Schelegle et al. (2009) reported that the actual mean exposure
concentration was 72 ppb.
---------------------------------------------------------------------------

    (2) Recent multicity and single city epidemiologic studies
continue to report associations between short-term O3
exposures and respiratory hospital admissions and respiratory
emergency department visits. Recent multicity studies and a multi-
continent study have reported consistent positive associations
between short-term O3 exposure and total (nonaccidental)
mortality, expanding upon evidence available in the last review.
They also observed associations between O3 exposure and
cardiovascular and respiratory mortality.\23\
---------------------------------------------------------------------------

    \23\ The consideration of ambient O3 concentrations
in the locations of these epidemiologic studies are discussed in
sections II.D.1.b and II.E.4.a below, for the current standard and
alternative standards, respectively.
---------------------------------------------------------------------------

    (3) Recent controlled human exposure studies reporting systemic
inflammation and cardiac changes provide support for the expanded
body of epidemiologic evidence for

cardiovascular mortality, although lack of coherence with
epidemiologic studies of cardiovascular morbidity remains an
important uncertainty.
    (4) New epidemiologic studies provide expanded evidence for
respiratory effects associated with long-term or repeated
O3 concentrations (e.g., seasonal average of 1- or 8-hour
daily max concentrations). Recent studies report interactions
between exercise or different genetic variants and both new-onset
asthma in children and increased respiratory symptom effects in
individuals with asthma; additional studies of respiratory morbidity
and mortality support the association between long-term exposure to
O3 and a range of respiratory health effects.
    (5) New evidence of risk factors (i.e., people with certain
genetic variants related to antioxidant status or inflammation, and
people with reduced intake of antioxidant nutrients) strengthens our
understanding of the potential modes of action from O3-
induced effects.
1. Overview of Mechanisms
    The purpose of this section is to describe the ISA's
characterization of the key events and pathways that contribute to
health effects resulting from both short-term and long-term exposures
to O3. The information in this section draws from section
5.3 of the ISA (U.S. EPA, 2013a). Mode of action refers to a sequence
of key events and processes that result in a given toxic effect.
Elucidation of mechanisms provides a more detailed understanding of
these key events and processes. Experimental evidence elucidating modes
of action and/or mechanisms contributes to our understanding of the
biological plausibility of adverse O3-related health
effects, including respiratory effects and effects outside the
respiratory system (U.S. EPA, 2013a, Chapters 6 and 7).
    Figure 3.1 in the PA (U.S. EPA, 2014c) shows the current
understanding of key events in the toxicity pathway of O3,
based on the available evidence. These key events are described briefly
here and in more detail in section 3.1.1 of the PA. The initial key
event is the formation of secondary oxidation products in the
respiratory tract (U.S. EPA, 2013a, section 5.3). This mainly involves
direct reactions with components of the extracellular lining fluid
(ELF). Although the ELF has inherent capacity to quench (based on
individual antioxidant capacity), this capacity can be overwhelmed,
especially with exposure to elevated concentrations of O3.
The resulting secondary oxidation products transmit signals to the
epithelium, pain receptive nerve fibers and, if present, immune cells
(i.e., eosinophils, dendritic cells and mast cells) involved in
allergic responses. Thus, the available evidence indicates that the
effects of O3 are mediated by components of ELF and by the
multiple cell types found in the respiratory tract. Further, oxidative
stress is an implicit part of this initial key event.
    It is well understood that secondary oxidation products initiate
numerous responses at the cellular, tissue, and whole organ level of
the respiratory system. These responses include the activation of
neural reflexes leading to lung function decrements, airway
obstruction, and extrapulmonary effects such as slow resting heart
rate; initiation of inflammation; alteration of barrier epithelial
function; sensitization of bronchial smooth muscle; modification of
lung host defenses; and airways remodeling (U.S. EPA, 2013a, section
5.3.10, Figure 5-8). Each of these effects is discussed in more detail
in section 3.1.1 of the PA (U.S. EPA, 2014c).
    Persistent inflammation and injury, which are observed in animal
models of chronic and intermittent exposure to O3, are
associated with airways remodeling (see Section 7.2.3 of the ISA, U.S.
EPA 2013). Chronic intermittent exposure to O3 has also been
shown to result in effects on the developing lung and immune system.
Systemic inflammation and vascular oxidative/nitrosative stress are
also key events in the toxicity pathway of O3.
Extrapulmonary effects of O3 occur in numerous organ
systems, including the cardiovascular, central nervous, reproductive,
and hepatic systems (U.S. EPA, 2013a, sections 6.3 to 6.5 and sections
7.3 to 7.5).
    Responses to O3 exposure are variable within the
population. Studies have shown a large range of pulmonary function
(i.e., spirometric) responses to O3 among healthy young
adults, while responses within an individual are relatively consistent
over time. Other responses to O3 have also been
characterized by a large degree of interindividual variability. For
example, a 3- to 20-fold difference among subjects in their studies in
airways inflammation (i.e., neutrophilia influx) following
O3 exposure has been reported (Schelegle et al., 1991 and
Devlin et al., 1991, respectively). Reproducibility of an individual's
inflammatory response to O3 exposure in humans, measured as
sputum neutrophilia, was demonstrated by Holz et al (1999). Since
individual inflammatory responses were relatively consistent across
time, it was thought that inflammatory responsiveness reflected an
intrinsic characteristic of the subject (Mudway and Kelly, 2000). While
the basis for the observed interindividual variability in
responsiveness to O3 is not clear, section 5.4.2 of the ISA
discusses mechanisms that may underlie the variability in responses
seen among individuals. Certain functional genetic polymorphisms, pre-
existing conditions or diseases, nutritional status, lifestages, and
co-exposures contribute to altered risk of O3-induced
effects. Experimental evidence for such O3-induced changes
contributes to our understanding of the biological plausibility of
adverse O3-related health effects, including a range of
respiratory effects as well as effects outside the respiratory system
(e.g., cardiovascular effects) (U.S. EPA, 2013a, Chapters 6 and 7).
2. Nature of Effects
    The health effects of O3 are described in detail and
assessed in the ISA (U.S. EPA, 2013a). Based on this assessment, the
ISA determined that a ``causal'' relationship exists between short-term
exposure to O3 in ambient air \24\ and effects on the
respiratory system and that a ``likely to be causal'' relationship \25\
exists between long-term exposure to O3 in ambient air and
respiratory effects (U.S. EPA 2013a, pp. 1-6 to 1-7). As stated in the
ISA, ``[c]ollectively, a very large amount of evidence spanning several
decades supports a relationship between exposure to O3 and a
broad range of respiratory effects'' (US. EPA, 2013a, p. 1-6). The ISA
summarizes the longstanding body of evidence for O3
respiratory effects as follows (U.S. EPA, 2013a, p. 1-5):
---------------------------------------------------------------------------

    \24\ In determining that a causal relationship exists for
O3 with specific health effects, the EPA has concluded
that ``[e]vidence is sufficient to conclude that there is a causal
relationship with relevant pollutant exposures'' (U.S. EPA, 2013a,
p. lxiv).
    \25\ In determining a ``likely to be a causal'' relationship
exists for O3 with specific health effects, the EPA has
concluded that ``[e]vidence is sufficient to conclude that a causal
relationship is likely to exist with relevant pollutant exposures,
but important uncertainties remain'' (U.S. EPA, 2013a, p. lxiv).

    The clearest evidence for health effects associated with
exposure to O3 is provided by studies of respiratory
effects. Collectively, a very large amount of evidence spanning
several decades supports a relationship between exposure to
O3 and a broad range of respiratory effects (see Section
6.2.9 and Section 7.2.8). The majority of this evidence is derived
from studies investigating short-term exposures (i.e., hours to
weeks) to O3, although animal toxicological studies and
recent epidemiologic evidence demonstrate that long-term exposure
---------------------------------------------------------------------------
(i.e., months to years) may also harm the respiratory system.

Additionally, the ISA determined that the relationships between short-
term exposures to O3 in ambient air and both total mortality
and cardiovascular effects are likely to be causal, based on expanded
evidence bases in the current review (U.S. EPA, 2013a, pp. 1-7 to 1-

8). In the ISA, the EPA additionally determined that the currently
available evidence for additional endpoints is ``suggestive'' of causal
relationships between short-term (central nervous system effects) and
long-term exposure (cardiovascular effects, reproductive and
developmental effects, central nervous system effects and total
mortality) to ambient O3.
    Consistent with emphasis in past reviews on O3 health
effects for which the evidence is strongest, in this review the EPA
places the greatest emphasis on studies of health effects that have
been judged in the ISA to be caused by, or likely to be caused by,
O3 exposures (U.S. EPA, 2013a, section 2.5.2). This section
discusses the evidence for health effects attributable to O3
exposures, with a focus on respiratory morbidity and mortality effects
attributable to short- and long-term exposures, and cardiovascular
system effects (including mortality) and total mortality attributable
to short-term exposures. This section focuses particularly on
considering the extent to which the scientific evidence available in
the current review has been strengthened since the last review, and the
extent to which important uncertainties and limitations in the evidence
from the last review have been addressed.
    a. Respiratory Effects--Short-Term
    The 2006 O3 AQCD concluded that there was clear,
consistent evidence of a causal relationship between short-term
O3 exposure and respiratory effects (U.S. EPA, 2006a). This
conclusion was substantiated by evidence from controlled human exposure
and toxicological studies indicating a range of respiratory effects in
response to short-term O3 exposures, including pulmonary
function decrements and increases in respiratory symptoms, lung
inflammation, lung permeability, and airway hyperresponsiveness.
Toxicological studies provided additional evidence for O3-
induced impairment of host defenses. Combined, these findings from
experimental studies provided support for epidemiologic evidence, in
which short-term increases in ambient O3 concentration were
consistently associated with decreases in lung function in populations
with increased outdoor exposures, especially children with asthma and
healthy children; increases in respiratory symptoms and asthma
medication use in children with asthma; and increases in respiratory-
related hospital admissions and asthma-related emergency department
visits (U.S. EPA, 2013a, pp. 6-1 to 6-2).
    As discussed in detail in the ISA (U.S. EPA, 2013a, section 6.2.9),
studies evaluated since the completion of the 2006 O3 AQCD
support and expand upon the strong body of evidence that, in the last
review, indicated a causal relationship between short-term
O3 exposures and respiratory health effects. Recent
controlled human exposure studies conducted in young, healthy adults
with moderate exertion have reported forced expiratory volume in 1
second (FEV1) decrements and pulmonary inflammation
following prolonged exposures to O3 concentrations as low as
60 ppb, and respiratory symptoms following exposures to concentrations
as low as 72 ppb (based on group mean responses).\26\ Epidemiologic
studies provide evidence that increases in ambient O3
exposures are associated with lung function decrements, increases in
respiratory symptoms, and pulmonary inflammation in children with
asthma; increases in respiratory-related hospital admissions and
emergency department visits; and increases in respiratory mortality.
Some of these studies report such associations even for O3
concentrations at the low end of the distribution of daily
concentrations. Recent epidemiologic studies report that associations
with respiratory morbidity and mortality are stronger during the warm/
summer months and remain robust after adjustment for copollutants.
Recent toxicological studies reporting O3-induced
inflammation, airway hyperresponsiveness, and impaired lung host
defense continue to support the biological plausibility and modes of
action for the O3-induced respiratory effects observed in
the controlled human exposure and epidemiologic studies. Further
support is provided by recent studies that found O3-
associated increases in indicators of airway inflammation and oxidative
stress in children with asthma (U.S. EPA, 2013a, section 6.2.9).
Together, epidemiologic and experimental studies support a continuum of
respiratory effects associated with O3 exposure that can
result in respiratory-related emergency department visits, hospital
admissions, and/or mortality (U.S. EPA, 2013a, section 6.2.9).
---------------------------------------------------------------------------

    \26\ Schelegle et al. (2009) reported a statistically
significant increase in respiratory symptoms in healthy adults at a
target O3 exposure concentration of 70 ppb, averaged over
the study period. For this 70 ppb target exposure concentration,
Schelegle et al. (2009) reported that the actual mean exposure
concentration was 72 ppb.
---------------------------------------------------------------------------

    Across respiratory endpoints, evidence indicates antioxidant
capacity may modify the risk of respiratory morbidity associated with
O3 exposure (U.S. EPA, 2013a, section 6.2.9, p. 6-161). The
potentially elevated risk of populations with diminished antioxidant
capacity and the reduced risk of populations with sufficient
antioxidant capacity is supported by epidemiologic studies and from
controlled human exposure studies. Additional evidence characterizes
O3-induced decreases in antioxidant levels as a key event in
the mode of action for downstream effects.
    Key aspects of this evidence are discussed below with regard to
lung function decrements; pulmonary inflammation, injury, and oxidative
stress; airway hyperresponsiveness; respiratory symptoms and medication
use; lung host defense; allergic and asthma-related responses; hospital
admissions and emergency department visits; and respiratory
mortality.\27\
---------------------------------------------------------------------------

    \27\ CASAC concurred that these were ``the kinds of identifiable
effects on public health that are expected from the presence of
ozone in the ambient air'' (Frey 2014c, p. 3).
---------------------------------------------------------------------------

i. Lung Function Decrements
    In the 2008 review, a large number of controlled human exposure
studies\28\ reported O3-induced lung function decrements in
young, healthy adults engaged in intermittent, moderate exertion
following 6.6 hour exposures to O3 concentrations at or
above 80 ppb. Although two studies also reported effects following
exposures to lower concentrations, an important uncertainty in the last
review was the extent to which exposures to O3
concentrations below 80 ppb result in lung function decrements. In
addition, in the last review epidemiologic panel studies had reported
O3-associated lung function decrements in a variety of
different populations (e.g., children, outdoor workers) likely to
experience increased exposures. In the current review, additional
controlled human exposure studies are available that have evaluated
exposures to O3 concentrations of 60 or 72 ppb. The
available evidence from controlled human exposure and panel studies is

assessed in detail in the ISA (U.S. EPA, section 6.2.1) and is
summarized below.
---------------------------------------------------------------------------

    \28\ The controlled human exposure studies emphasized in the PA
utilize only healthy adult subjects. In the near absence of
controlled human exposure data for children, HREA estimates of lung
function decrements are based on the assumption that children
exhibit the same lung function responses following O3
exposures as healthy 18 year olds (U.S. EPA, 2014a, section 6.2.4
and 6.5). This assumption is justified in part by the findings of
McDonnell et al. (1985), who reported that children (8-11 years old)
experienced FEV1 responses similar to those observed in
adults (18-35 years old). Thus, the conclusions about the occurrence
of lung function decrements that follow generally apply to children
as well as to adults.
---------------------------------------------------------------------------

    Controlled exposures to O3 concentrations that can be
found in the ambient air can result in a number of lung function
effects, including decreased inspiratory capacity, mild
bronchoconstriction, and rapid, shallow breathing patterns during
exercise. Reflex inhibition of inspiration results in a decrease in
forced vital capacity (FVC) and total lung capacity (TLC) and, in
combination with mild bronchoconstriction, contributes to a decrease in
FEV1 (U.S. EPA, 2013a, section <IP_ADDRESS>). Accumulating
evidence indicates that such effects are mediated by activation of
sensory nerves, resulting in the involuntary truncation of inspiration
and a mild increase in airway obstruction due to bronchoconstriction
(U.S. EPA, 2013a, section 5.3.10).
    Data from controlled human exposure studies show that increasing
the duration of O3 exposures and increasing ventilation
rates decreases the O3 exposure concentrations required to
impair lung function. Ozone exposure concentrations well above those
typically found in ambient air are required to impair lung function in
healthy resting adults, while exposure to O3 concentrations
at or below those in the ambient air have been reported to impair lung
function in healthy adults exposed for longer durations while
undergoing intermittent, moderate exertion (U.S. EPA, 2013a, section
<IP_ADDRESS>). With repeated O3 exposures over several days,
FEV1 responses become attenuated in both healthy adults and
adults with mild asthma, though this attenuation of response is lost
after about a week without exposure (U.S. EPA, 2013a, section <IP_ADDRESS>;
p. 6-27).
    When considering controlled human exposure studies of
O3-induced lung function decrements, the ISA and PA evaluate
both group mean changes in lung function and the interindividual
variability in the magnitude of responses. An advantage of
O3 controlled human exposure studies (i.e., compared to the
epidemiologic panel studies discussed below) is that reported effects
necessarily result from exposures to O3 itself.\29\ To the
extent studies report statistically significant decrements in mean lung
function following O3 exposures after controlling for other
factors, these studies provide greater confidence that measured
decrements are due to the O3 exposure itself, rather than to
chance alone. As discussed below, group mean changes in lung function
are often small, especially following exposures to relatively low
O3 concentrations (e.g., 60 ppb). However, even when group
mean decrements in lung function are small, some individuals could
experience decrements that are ``clinically meaningful'' (Pellegrino et
al., 2005; ATS, 1991) with respect to criteria for spirometric testing,
and/or that could be considered adverse with respect to public health
policy decisions (see section II.B.3, below).
---------------------------------------------------------------------------

    \29\ The ISA notes that the use of filtered air responses as a
control for the assessment of responses following O3
exposure in controlled human exposure studies serves to eliminate
alternative explanations other than O3 itself in causing
the measured responses (U.S. EPA, 2013a, section <IP_ADDRESS>).
---------------------------------------------------------------------------

    At the time of the last review, a number of controlled human
exposure studies had reported lung function decrements in young,
healthy adults following prolonged (6.6-hour) exposures while at
moderate exertion to O3 concentrations at and above 80 ppb.
In addition, there were two controlled human exposure studies by Adams
(2002, 2006) that examined lung function effects following exposures to
60 ppb O3. The EPA's analysis of the data from the Adams
(2006) study reported a small but statistically significant
O3-induced decrement in group mean FEV1 following
exposures of young, healthy adults to 60 ppb O3 while at
moderate exertion, when compared with filtered air controls (Brown et
al., 2008).\30\ Further examination of the post-exposure
FEV1 data, and mean data for other time points and other
concentrations, indicated that the temporal pattern of the response to
60 ppb O3 was generally consistent with the temporal
patterns of responses to higher O3 concentrations in this
and other studies (75 FR 2950, January 19, 2010). This suggested a
pattern of response following exposures to 60 ppb O3 that
was consistent with a dose-response relationship, rather than random
variability. See also State of Mississippi v. EPA, F. 3d at 1347
(upholding EPA's interpretation of the Adams studies).
---------------------------------------------------------------------------

    \30\ Adams (2006) did not find effects on FEV1 at 60
ppb to be statistically significant. In an analysis of the Adams
(2006) data, Brown et al. (2008) showed that even after removal of
potential outliers, the average effect on FEV1 at 60 ppb
was small, but highly statistically significant (p <0.002) using
several common statistical tests.
---------------------------------------------------------------------------

    Figure 6-1 in the ISA summarizes the currently available evidence
from multiple controlled human exposure studies evaluating group mean
changes in FEV1 following prolonged O3 exposures
(i.e., 6.6 hours) in young, healthy adults engaged in moderate levels
of physical activity (U.S. EPA, 2013a, section <IP_ADDRESS>). With regard to
the group mean changes reported in these studies, the ISA specifically
notes the following (U.S. EPA, 2013a, section <IP_ADDRESS>, Figure 6-1):
    1. Prolonged exposure to 40 ppb O3 results in a small
decrease in group mean FEV1 that is not statistically
different from responses following exposure to filtered air (Adams,
2002; Adams, 2006).
    2. Prolonged exposure to an average O3 concentration of
60 ppb results in group mean FEV1 decrements ranging from
1.8% to 3.6% (Adams 2002; Adams, 2006; \31\ Schelegle et al., 2009;
\32\ Kim et al., 2011). Based on data from multiple studies, the
weighted average group mean decrement was 2.7%. In some analyses, these
group mean decrements in lung function were statistically significant
(Brown et al., 2008; Kim et al., 2011), while in other analyses they
were not (Adams, 2006; Schelegle et al., 2009).\33\
---------------------------------------------------------------------------

    \31\ Adams (2006); (2002) both provide data for an additional
group of 30 healthy subjects that were exposed via facemask to 60
ppb (square-wave) O3 for 6.6 hours with moderate exercise
(VE = 23 L/min per m\2\ BSA). These subjects are
described on page 133 of Adams (2006) and pages 747 and 761 of Adams
(2002). The FEV1 decrement may be somewhat increased due
to a target VE of 23 L/min per m\2\ BSA relative to other
studies having the target VE of 20 L/min per m\2\ BSA.
The facemask exposure is not expected to affect the FEV1
responses relative to a chamber exposure.
    \32\ For the 60 ppb target exposure concentration, Schelegle et
al. (2009) reported that the actual mean exposure concentration was
63 ppb.
    \33\ Adams (2006) did not find effects on FEV1 at 60
ppb to be statistically significant. In an analysis of the Adams
(2006) data, Brown et al. (2008) addressed the more fundamental
question of whether there were statistically significant differences
in responses before and after the 6.6 hour exposure period and found
the average effect on FEV1 at 60 ppb to be small, but