EO12866_O3-NAAQS-RIN2060-AP38-NFR-PreambleAndRegText_20150827
 					        			                  6560-50-P

                        ENVIRONMENTAL PROTECTION AGENCY
                       40 CFR Parts 50, 51, 52, 53 and 58
                    [EPA-HQ-OAR-2008-0699; FRL-9913-18-OAR]
                                 RIN 2060-AP38
                National Ambient Air Quality Standards for Ozone
 AGENCY: Environmental Protection Agency (EPA).
 ACTION: Final rule.
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) is revising the primary and secondary NAAQS for O3 to provide requisite protection of public health and welfare, respectively. The EPA is revising both standards to a level of 0.070 parts per million (ppm), and retaining the form and averaging time of the fourth-highest daily maximum 8-hour average O3 concentration. The EPA is making corresponding revisions in data handling conventions for O3 and changes to the Air Quality Index (AQI); revising regulations for the prevention of significant deterioration (PSD) program to add a transition provision for certain applications; and establishing exceptional events schedules and providing information related to implementing the revised standards. The EPA is also revising the O3 monitoring seasons, the Federal Reference Method (FRM) for monitoring O3 in the ambient air, Federal Equivalent Method (FEM) analyzer performance requirements, and the Photochemical Assessment Monitoring Stations (PAMS) network. Along with exceptional events schedules related to implementing the revised O3 standards, the EPA is applying this same schedule approach to other future new or revised NAAQS and removing obsolete regulatory language for expired exceptional events deadlines. The EPA is making minor changes to the procedures and time periods for evaluating potential FRMs and equivalent methods, including making the requirements for nitrogen dioxide (NO2) consistent with the requirements for O3, and removing an obsolete requirement for the annual submission of Product Manufacturing Checklists by manufacturers of FRMs and FEMs for monitors of fine and coarse particulate matter. For a more detailed summary, see the Executive Summary below.
DATES: The final rule is effective on [INSERT 60 DAYS AFTER DATE OF PUBLICATION IN THE FEDERAL REGISTER].
ADDRESSES: EPA has established a docket for this action (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 been incorporated by reference into the rulemaking docket. All documents in the docket are listed on the www.regulations.gov website. Although listed in the docket index, some information is not publicly available, e.g., confidential business information or other information whose disclosure is restricted by statute. Certain other material, such as copyrighted material, is not placed on the Internet and 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, 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<PHONE_NUMBER> 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:<PHONE_NUMBER>; email<EMAIL_ADDRESS>
 SUPPLEMENTARY INFORMATION:
 General Information
Availability of Related Information
A number of the documents that are relevant to this action are available through the EPA's Office of Air Quality Planning and Standards (OAQPS) Technology Transfer Network (TTN) website (http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_index.html). These documents include the Integrated Science Assessment for Ozone (U.S. EPA, 2013), available at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_isa.html; the Health Risk and Exposure Assessment and the Welfare Risk and Exposure Assessment for Ozone, Final Reports (HREA and WREA, respectively; U.S. EPA, 2014a, 2014b), available at
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_rea.html; and the Policy Assessment for the Review of the Ozone National Ambient Air Quality Standards (PA; U.S. EPA, 2014c), available at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pa.html. These and other related documents are also available for inspection and copying in the EPA docket identified above.
Table of Contents
The following topics are discussed in this preamble:
Executive Summary
I. Background
	A. Legislative Requirements
	B. Related Control Programs
	C. Review of Air Quality Criteria and Standards for O3
	D. Ozone Air Quality
	E. Summary of Proposed Revisions to the O3 Standards
	F. Organization and Approach to Decisions in this O3 NAAQS Review
II. Rationale for Decision on the Primary Standard
	A. Introduction
		1. Overview of Health Effects Evidence
		2. Overview of Human Exposure and Health Risk Assessments
	B. Need for Revision of the Primary Standard
		1. Basis for Proposed Decision
		2. Comments on the Need for Revision
		3. Administrator's Conclusions on the Need for Revision
	C. Conclusions on the Elements of a Revised Primary Standard
		1. Indicator
		2. Averaging Time
		3. Form
		4. Level
	 D. Decision on the Primary Standard
III. Communication of Public Health Information
	A. Proposed Revisions to the AQI
	B. Comments on Proposed Revisions to the AQI
	C. Final Revisions to the AQI
IV. Rationale for Decision on the Secondary Standard
	A. Introduction
		1. Overview of Welfare Effects Evidence
		2. Overview of Welfare Exposure and Risk Assessment
		3. Potential Impacts on Public Welfare
	B. Need for Revision of the Secondary Standard
		1. Basis for Proposed Decision
		2. Comments on the Need for Revision
		3. Administrator's Conclusions on the Need for Revision
	C. Conclusions on Revision of the Secondary Standard
		1. Basis for Proposed Revision
		2. Comments on Proposed Revision
		3. Administrator's Conclusions on Revision
	D. 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. Exceptional Events Information Submission Schedule
VI. Ambient Monitoring Related to O3 Standards
      A. Background
      B. Revisions to the Length of the Required O3 Monitoring Seasons
		1. Proposed Changes to the Length of the Required O3 Monitoring Seasons
		2. Comments on the Length of the Required O3 Monitoring Seasons
		3. Final Decisions on the Length of the Required O3 Monitoring Seasons
      C. Revisions to the PAMS Network Requirements
      1. Network Design
      2. Speciated VOC Measurements
      3. Carbonyl Measurements
      4. Nitrogen Oxides Measurements
      5. Meteorology Measurements
      6. PAMS Season
      7. Timing and Other Implementation Issues
      D. Addition of a New FRM for O3
		1. Proposed Changes to the FRM for O3
		2. Comments on the FRM for O3
      E. Revisions to the Analyzer Performance Requirements
		1. Proposed Changes to the Analyzer Performance Requirements
		2. Comments on the Analyzer Performance Requirements
VII.	Grandfathering Provision for Certain PSD Permits
      A. Summary of the Proposed Grandfathering Provision
      B. Comments and Responses
	C. Final Action and Rationale
VIII.	Implementation of the Revised O3 Standards
      A. NAAQS Implementation Plans
      	1. Cooperative Federalism
      	2. Additional New Rules and Guidance
      	3. Background O3
      	4. Section 110 State Implementation Plans
      	5. Nonattainment Area Requirements
      B. O3 Air Quality Designations
      	1. Area Designation Process
      	2. Exceptional Events
      C.	How do the New Source Review (NSR) Requirements apply to the Revised O3 NAAQS?
      	1. NSR Requirements for Major Stationary Sources for the Revised O3 NAAQS
      	2. Prevention of Significant Deterioration (PSD) Program
		3. Nonattainment NSR
      D. Transportation and General Conformity
            1. What are Transportation and General Conformity?
            2. When Would Transportation and General Conformity Apply to Areas Designated Nonattainment for the Revised O3 NAAQS?
            3. Impact of a Revised O3 NAAQS on a State's Existing Transportation and/or General Conformity SIP.
        E. Regional and International Pollution Transport
      1. Interstate Transport
      2. International Transport
IX. 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
      K. Congressional Review Act (CRA)
References

Executive Summary
 This section summarizes information about the purpose of this regulatory action, the major provisions of this action, and provisions related to implementation.
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 make a final determination by October 1, 2015.
The EPA completed its most recent review of the NAAQS for O3 in 2008. As a result of that review, EPA took four principal actions: (1) revised the level of the 8-hour primary standard to 0.075 ppm; (2) expressed the standard to three decimal places; (3) revised the 8-hour secondary standard by making it identical to the revised primary standard; and (4) made conforming changes to the AQI.
In subsequent litigation, the U.S. Court of Appeals for the District of Columbia Circuit (D.C. Circuit) upheld the EPA's 2008 primary standard but remanded the 2008 secondary standard. 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 finding that the EPA's justification for setting the secondary standard identical to the revised 8-hour primary standard violated the CAA because the EPA had not adequately explained how that standard provided the required public welfare protection. In remanding the 2008 secondary standard, the court did not vacate it. The EPA has addressed the court's remand with this final action.
This final action reflects the Administrator's conclusions based on a review of the O3 NAAQS that began in September 2008, and also concludes the EPA's reconsideration of the 2008 decision that it initiated in 2009 and subsequently consolidated with the current review. In conducting this review, the EPA has carefully evaluated the currently available scientific literature on the health and welfare effects of O3, focusing particularly on the new literature available since the conclusion of the previous review in 2008. 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 subject to 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 pursuant to the CAA and charged with providing advice to the Administrator.
The EPA proposed revisions to the primary and secondary O3 NAAQS on December 17, 2014 (79 FR 75234), and provided a 3-month period for submission of comments from the public. In addition to written comments submitted to EPA, comments were also provided at public hearings held in Washington, DC, and Arlington, Texas, on January 29, 2015, and in Sacramento, California, on February 2, 2015. After consideration of public comments and the advice from the CASAC, the EPA has developed this final rulemaking, which is the final step in the review process.
In this rulemaking, the EPA is revising the suite of standards for O3 to provide requisite protection of public health and welfare. In addition, the EPA is updating the AQI, and making changes in the data handling conventions and ambient air monitoring, reporting, and network design requirements to correspond with the changes to the O3 NAAQS.
Summary of Major Provisions
With regard to the primary standard, the EPA is revising the level of the standard to 0.070 ppm to provide increased public health protection against health effects associated with long- and short-term exposures. The EPA is retaining the indicator (O3), averaging time (8-hour) and form (annual fourth-highest daily maximum, averaged over 3 years) of the existing standard. This action provides increased protection for children, older adults, and people with asthma or other lung diseases, and other at-risk populations against an array of adverse health effects that include reduced lung function, increased respiratory symptoms and pulmonary inflammation; effects that contribute to emergency department visits or hospital admissions; and mortality.
The decisions on the adequacy of the current standard and the appropriate level for the revised standard are based on an integrative assessment of an extensive body of new scientific evidence, which substantially strengthens what was known about O3-related health effects in the last review. The revised standard also reflects consideration of a quantitative risk assessment that estimates public health risks likely to remain upon just meeting the current and various alternative standards. Based on this information, the Administrator concludes that the current primary O3 standard is not requisite to protect public health with an adequate margin of safety, as required by the CAA, and that revision of the level to 0.070 ppm is warranted to provide the appropriate degree of increased public health protection for at-risk populations against an array of adverse health effects. In concluding that a revised primary standard set at a level of 0.070 ppm is requisite to protect public health with an adequate margin of safety, the Administrator relies on several key pieces of information, including: (a) a level of 0.070 ppm is well below the O3 exposure concentration shown to cause the widest range of respiratory effects (i.e., 0.080 ppm) and is below the lowest O3 exposure concentration shown to cause the adverse combination of decreased lung function and increased respiratory symptoms (i.e., 0.072 ppm); (b) a level of 0.070 ppm will eliminate, or nearly eliminate, repeated occurrence of these O3 exposure concentrations (this is important because the potential for adverse effects increases with frequency of occurrence); (c) a level of 0.070 ppm will protect the large majority of the population, including children and people with asthma, from lower exposure concentrations, which can cause lung function decrements and airway inflammation in some people (i.e., 0.060 ppm); and (d) a level of 0.070 ppm will result in important reductions in the risk of O3-induced lung function decrements as well as the risk of O3-associated hospital admissions, emergency department visits, and mortality. In addition, the revised level of the primary standard is within the range that CASAC advised the Agency to consider.
The EPA is also revising the level of the secondary standard to 0.070 ppm to provide increased protection against vegetation-related effects on public welfare. The EPA is retaining the indicator (O3), averaging time (8-hour) and form (annual fourth-highest daily maximum, averaged over 3 years) of the existing secondary standard. This action, reducing the level of the standard, provides increased protection for natural forests in Class I and other similarly protected areas against an array of vegetation-related effects of O3. The Administrator   is making this decision based on judgments regarding the currently available welfare effects evidence, the appropriate degree of public welfare protection for the revised standard, and currently available air quality information on seasonal cumulative exposures that may be allowed by such a standard.
In making this decision on the secondary standard, the Administrator focuses on O3 effects on tree seedling growth as a proxy for the full array of vegetation-related effects of O3, ranging from effects on sensitive species to broader ecosystem-level effects. Using this proxy in judging effects to public welfare, the Administrator has concluded that the requisite protection will be provided by a standard that generally limits cumulative seasonal exposures to 17 ppm-hours (ppm-hrs) or lower, in terms of a 3-year W126 index. Based on air quality analyses which indicate such control of cumulative seasonal exposures will be achieved with a standard set at a level of 0.070 ppm (and the same indicator, averaging time, and form as the current standard), the Administrator concludes that a standard revised in this way will provide the requisite protection. In addition to providing protection of natural forests from growth-related effects, the revised standard is also expected to provide increased protection from other effects, of potential public welfare significance, including crop yield loss and visible foliar injury. Thus, based on all of the information available in this review, the Administrator concludes that the current secondary O3 standard is not requisite to protect public welfare as required by the CAA, and that this revision will provide appropriate protection against known or anticipated adverse effects to the public welfare.
Provisions Related to Implementation
As directed by the CAA, reducing pollution to meet NAAQS 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 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. 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. The EPA also intends to work closely with states to identify locations affected by high background concentrations on high O3 days due to stratospheric intrusions of O3, wildfire O3 plumes, or long-range transport of O3 from sources outside the U.S. and ensure that the appropriate CAA regulatory mechanisms are employed. To this end, the EPA will be proposing revisions to the 2007 Exceptional Events Rule and related draft guidance addressing the effects of wildfires.
In addition to revisions to the primary and secondary standards, this action is changing the AQI to be consistent with the revised primary standard and also making corresponding revisions in data handling conventions for O3, extending the O3 monitoring season in 33 states, revising the requirements for the PAMS network, and revising regulations for the PSD permitting program to add a provision grandfathering certain pending permits from certain requirements with respect to the revised standards. The preamble also conveys schedules and information related to implementing the revised standards. The rule text also revises schedules associated with exceptional event demonstration submittals for the revised O3 standards and other future revised NAAQS, and makes minor changes related to monitoring for other pollutants.
I. Background
A. Legislative Requirements
Two sections of the CAA govern the establishment and revision of the NAAQS. Section 108 (42 U.S.C. section 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." 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."
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 Mississippi v. EPA, 744 F. 3d 1334, 1353 (D.C. Cir. 2013); 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; 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) 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; Mississippi, 744 F. 3d at 1353.
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 CASAC has performed this independent review function.
B. Related Control Programs
States are primarily responsible for ensuring attainment and maintenance of NAAQS once the EPA has established them. The EPA performs an oversight function, and as necessary takes actions to ensure CAA objectives are achieved. Under section 110 of the CAA, and related provisions, states 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 relevant pollutants. The states, in conjunction with the EPA, also administer the PSD program (CAA sections 160 to 169) which is a pre-construction permit program designed to prevent significant deterioration in air quality. In addition, federal programs provide for nationwide reductions in emissions of O3 precursors and other air pollutants through new source performance standards for stationary sources under section 111 of the CAA and 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. 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 are met. One of the first steps, known as the initial area designations, involves identifying areas of the country that are not meeting the new or revised NAAQS along with the nearby areas that contain emissions sources that contribute to the areas not meeting the NAAQS. For areas designated "nonattainment," the responsible states are required to develop SIPs to attain the standards. In developing their attainment plans, states 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 revised SIPs will be due. Examples of such rules include the Nitrogen Oxides (NOX) SIP Call and Cross-State Air Pollution Rule (CSAPR), regulations controlling on-road and non-road engines and fuels, hazardous air pollutant rules for utility and industrial boilers, and various other programs already adopted by states to reduce emissions from key emissions sources. States will 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 VIII of this preamble includes additional discussion of designation and implementation issues associated with the revised O3 NAAQS.
C. 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 0.08 ppm, as a 1-hour average of 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 (AQCD; U.S. DHEW, 1970). The EPA initiated the first periodic review of the NAAQS for photochemical oxidants in 1977. Based on the 1978 AQCD (U.S. EPA, 1978), the EPA published proposed revisions to the original NAAQS in 1978 (43 FR 26962, June 22, 1978) and final revisions in 1979 (44 FR 8202, February 8, 1979). 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 EPA's 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 AQCD (47 FR 11561; March 17, 1982), and, in 1983, the EPA initiated the second periodic review of the O3 NAAQS (48 FR 38009; August 22, 1983). The EPA subsequently published the 1986 AQCD (U.S. EPA, 1986) and the 1989 Staff Paper (U.S. EPA, 1989). Following publication of the 1986 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). In August of 1992, under the terms of a court order, the EPA proposed to retain the existing primary and secondary standards based on the health and welfare effects information contained in the 1986 AQCD and its 1992 Supplement (57 FR 35542, August 10, 1992). In March 1993, the EPA announced its decision to conclude this review by affirming its proposed decision to retain the standards, without revision (58 FR 13008, March 9, 1993).
In the 1992 notice of its proposed decision in that review, the EPA announced its 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 (57 FR 35542, August 10, 1992). The EPA subsequently published the AQCD and Staff Paper for the review (U.S. EPA, 1996a,b). In December 1996, the EPA proposed revisions to both the primary and secondary standards (61 FR 65716, December 13, 1996). With regard to the primary standard, the EPA proposed to replace the then-existing 1-hour primary standard with an 8-hour standard set at a level of 0.08 ppm (equivalent to 0.084 ppm based on the proposed data handling convention) as a 3-year average of the annual third-highest daily maximum 8-hour concentration. The EPA proposed to revise the secondary standard either by setting it identical to the proposed new primary standard or by setting it as a new seasonal standard using a cumulative form. The EPA completed this review in 1997 by setting the primary standard at a level of 0.08 ppm, based on the annual fourth-highest daily maximum 8-hour average concentration, averaged over three years, and setting the secondary standard identical to the revised primary standard (62 FR 38856, July 18, 1997). In reaching her decision on the primary standard, the Administrator identified several reasons supporting her decision to reject a potential alternate standard set at 0.07 ppm, including first the fact that no CASAC panel member supported a standard level lower than 0.08 ppm and her consideration of the scientific uncertainties with regard to the health effects evidence for exposure concentrations below 0.08 ppm. In addition to those reasons, the Administrator 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. vs. 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 the 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" (283 F. 3d at 378, internal citations omitted). The court also pointed to the significant weight that the EPA properly placed on the advice it received from CASAC (283 F. 3d 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], the EPA could consider that factor when choosing among the three alternative levels" (283 F. 3d at 379).
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 primary standard unchanged (66 FR 57268, Nov. 14, 2001). After considering public comment on the proposed decision, the EPA published its final response to this remand in 2003, re-affirming the 8-hour primary standard set in 1997 (68 FR 614, January 6, 2003).
The EPA initiated the fourth periodic review of the air quality criteria and standards for O3 with a call for information in September 2000 (65 FR 57810, September, 26, 2000). 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 nondiscretionary duty to complete review of the O3 NAAQS within a statutorily mandated deadline. In 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, July 11, 2007). The EPA proposed to revise the secondary standard either by setting it identical to the proposed new primary standard or by setting it as a new seasonal standard using a cumulative form. Documents supporting these proposed decisions included the 2006 AQCD (U.S. EPA, 2006a) and 2007 Staff Paper (U.S EPA, 2007) and related technical support documents. The EPA completed the review in March 2008 by revising the level of the primary standard from 0.08 ppm to 0.075 ppm, and revising the secondary standard to be identical to the revised primary standard (73 FR 16436, March 27, 2008).
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 2010, the EPA issued a notice of proposed rulemaking to reconsider the 2008 final decision (75 FR 2938, January 19, 2010). 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 revise the level of the primary standard from 0.075 ppm to a level within the range of 0.060 to 0.070 ppm, and to revise the secondary standard to one with a cumulative, seasonal form. At the EPA's request, the CASAC reviewed the proposed rule at a public teleconference on January 25, 2010 and provided additional advice in early 2011 (Samet, 2010, 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, 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 decided to consolidate the reconsideration with its statutorily required periodic review.
In light of the 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 (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" (Mississippi v. EPA, 744 F. 3d at 1345). The court also specifically endorsed the weight of evidence approach utilized by the EPA in its deliberations (Mississippi v. EPA, 744 F. 3d 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 (Mississippi v. EPA, 744 F. 3d 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 (Mississippi v. EPA, 744 F. 3d at 1351-52).
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 (Mississippi v. EPA, 744 F. 3d at 1351-52). Finally, the court rejected arguments that the EPA's decision was inconsistent with the CASAC's scientific recommendations because the CASAC had been insufficiently clear in its recommendations whether it was providing scientific or policy recommendations, and the EPA had reasonably addressed the CASAC's policy recommendations (Mississippi v. EPA, 744 F. 3d at 1357-58).
With respect to the secondary standard, the court held that the EPA's justification for setting the secondary standard identical to the revised 8-hour primary standard violated the CAA because the EPA had not adequately explained how that standard provided the required public welfare protection. The court thus remanded the secondary standard to the EPA (Mississippi v. EPA, 744 F. 3d 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. This review was formally initiated in 2008 with a call for information in the Federal Register (73 FR 56581, Sept. 29, 2008). On October 28-29, 2008, the EPA held a public workshop to discuss the policy-relevant science, which informed identification of key policy issues and questions to frame the review. 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 and was the subject of a consultation with the CASAC on November 13, 2009 (74 FR 54562; October 22, 2009). After considering the comments received from that consultation and from the public, the EPA completed and released the IRP for the review in 2011 (U.S. EPA, 2011a).
In preparing the first draft ISA, the EPA's National Center for Environmental Assessment (NCEA) considered CASAC and public comments on the IRP, and also comments received from a workshop held on August 6, 2010, to review and discuss preliminary drafts of key ISA sections (75 FR 42085, July 20, 2010). In 2011, the first draft ISA was released for public comment and for review by CASAC at a public meeting on May 19-20, 2011 (U.S. EPA, 2011b; 76 FR 10893, February 28, 2011; 76 FR 23809, April 28, 2011). Based on CASAC and public comments, NCEA prepared a second draft ISA, which was released for public comment and CASAC review (U.S. EPA, 2011c; 76 FR 60820, September 30, 2011). The CASAC reviewed this draft at a January 9-10, 2012, public meeting (76 FR 236, December 8, 2011). Based on CASAC and public comments, NCEA prepared a third draft ISA (U.S. EPA, 2012; 77 FR 36534, June 19, 2012), which was reviewed at a CASAC meeting in September 2012. The EPA released the final ISA in February 2013 (U.S. EPA, 2013).
The EPA presented its plans for conducting Risk and Exposure Assessments (REAs) for health risk and exposure (HREA) and welfare risk and exposure (WREA) in two documents that outlined the scope and approaches for use in conducting quantitative assessments, as well as key issues to be addressed as part of the assessments (U.S. EPA, 2011d, e). 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). The EPA considered CASAC advice and public comments in further planning for the assessments, issuing a memo that described changes to elements of the REA plans and brief explanations regarding them (Samet, 2011; Wegman, 2012).
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; 77 FR 51798, August 27, 2012). The first draft PA was made available for CASAC review and public comment in August 2012 (77 FR 42495, July 19, 2012; 77 FR 51798, August 27, 2012). The first draft REAs and PA were the focus of a CASAC public meeting in September 2012 (Frey and Samet, 2012a, 2012b). The second draft REAs and PA, prepared with consideration of CASAC advice and public comments, were made available for public comment and CASAC review in January 2014 (79 FR 4694, January 29, 2014). These documents were the focus of a CASAC public meeting on March 25-27, 2014 (Frey, 2014a; Frey, 2014b; Frey, 2014c). The final versions of these documents were developed with consideration of the comments and recommendations from CASAC, as well as comments from the public on the draft documents, and were released in August 2014 (U.S. EPA 2014a; U.S. EPA, 2014b; U.S. EPA, 2014c).
The proposed decision (henceforth "proposal") on this review of the O3 NAAQS was signed on November 25, 2014, and published in the Federal Register on December 17, 2014. The EPA held three public hearings to provide direct opportunity for oral testimony by the public on the proposal. The hearings were held on January 29, 2015, in Arlington, Texas, and Washington, DC, and on February 2, 2015, in Sacramento, California.  At these public hearings, the EPA heard testimony from nearly 500 individuals representing themselves or specific interested organizations. Transcripts from these hearings and written testimony provided at the hearings are in the docket for this review. Additionally, approximately 430,000 written comments were received from various commenters during the public comment period on the proposal, approximately 428,000 as part of mass mail campaigns. Significant issues raised in the public comments are discussed in the preamble of this final action. A summary of all other significant comments, along with the EPA's responses, can be found in a separate document (henceforth "Response to Comments") in the docket for this review.
The schedule for completion of this review is governed by a court order resolving a lawsuit filed in January 2014 by a group of plaintiffs who alleged that the EPA had failed to perform its mandatory duty, under section 109(d)(1), to complete a review of the O3 NAAQS within the period provided by statute. The court order that governs this review, entered by the court on April 30, 2014, provides that the EPA will sign for publication a notice of final rulemaking concerning its review of the O3 NAAQS no later than October 1, 2015.
As in prior NAAQS reviews, the EPA is basing its decision in this review on studies and related information included in the ISA, REAs and PA, which have undergone CASAC and public review. The studies assessed in the ISA and PA, and the integration of the scientific evidence presented in them, have undergone extensive critical review by the EPA, the CASAC, and the public. The rigor of that review makes these studies, and their integrative assessment, the most reliable source of scientific information on which to base decisions on the NAAQS, decisions that all parties recognize as of great import. NAAQS decisions can have profound impacts on public health and welfare, and NAAQS decisions should be based on studies that have been rigorously assessed in an integrative manner not only by the EPA but also by the statutorily mandated independent advisory committee, as well as the public review that accompanies this process. Some commenters have referred to and discussed individual scientific studies on the health effects of O3 that were not included in the ISA (USEPA, 2013) ("'new' studies"). In considering and responding to comments for which such "new" studies were cited in support, the EPA has provisionally considered the cited studies in the context of the findings of the ISA. The EPA's provisional consideration of these studies did not and could not provide the kind of in-depth critical review described above.
The decision to rely on studies and related information included in the ISA, REAs and PA, which have undergone CASAC and public review, is consistent with the EPA's practice in prior NAAQS reviews and its interpretation of the requirements of the CAA. Since the 1970 amendments, the EPA has taken the view that NAAQS decisions are to be based on scientific studies and related information that have been assessed as a part of the pertinent air quality criteria, and the EPA has consistently followed this approach. This longstanding interpretation was strengthened by new legislative requirements enacted in 1977, which added section 109(d)(2) of the Act concerning CASAC review of air quality criteria. See 71 FR 61144, 61148 (October 17, 2006) (final decision on review of NAAQS for particulate matter) for a detailed discussion of this issue and the EPA's past practice.
As discussed in the EPA's 1993 decision not to revise the NAAQS for O3, ``new'' studies may sometimes be of such significance that it is appropriate to delay a decision on revision of a NAAQS and to supplement the pertinent air quality criteria so the studies can be taken into account (58 FR at 13013 - 13014, March 9, 1993). In the present case, the EPA's provisional consideration of ``new'' studies concludes that, taken in context, the ``new'' information and findings do not materially change any of the broad scientific conclusions regarding the health and welfare effects and exposure pathways of ambient O3 made in the air quality criteria. For this reason, reopening the air quality criteria review would not be warranted even if there were time to do so under the court order governing the schedule for this rulemaking.
Accordingly, the EPA is basing the final decisions in this review on the studies and related information included in the O3 air quality criteria that have undergone CASAC and public review. The EPA will consider the "new" studies for purposes of decision making in the next periodic review of the O3 NAAQS, which the EPA expects to begin soon after the conclusion of this review and which will provide the opportunity to fully assess these studies through a more rigorous review process involving the EPA, CASAC, and the public. Further discussion of these ``new'' studies can be found in the Response to Comments document, which is in the docket for this rulemaking and also available on the web (http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_index.html).
D. 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) and NOX. Over longer time periods, methane (CH4) and carbon monoxide (CO) can also lead to O3 formation at the global scale. 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 near the surface 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 (U.S. EPA, 2014a).
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 (U.S. EPA, 2014c, Section 2.1). Much of this monitoring is focused on 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 also be measured. Based on data from this national network, the EPA estimates that, in 2013, approximately 99 million Americans lived in counties where O3 design values were above the level of the existing health-based NAAQS of 0.075 ppm. High O3 values can occur almost anywhere within the contiguous 48 states, although the poorest O3 air quality in the U.S. is typically observed in California, Texas, and the Northeast Corridor, locations with some of the most densely populated areas in the country. 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 episodically influenced by stratospheric intrusions which can occur in other months, 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 (U.S. EPA, 2014c, Section 2.3).
One of the challenging aspects of developing plans to address high O3 concentrations is that the response of O3 to precursor reductions is nonlinear. In particular, NOX emissions can lead to both increases and decreases 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 certain urban centers where NOX emissions typically are high compared to local VOC emissions, NOX can suppress O3 locally. This phenomenon is particularly pronounced under conditions associated with low O3 concentrations (i.e., during cool, cloudy weather and at night when photochemical activity is limited or nonexistent). However, while NOX emissions can initially suppress O3 levels near the emission sources, these same NOX emissions ultimately react to form higher O3 levels downwind when conditions are favorable. Photochemical model simulations suggest that, in general, reductions in NOX emissions in the U.S. will slightly increase O3 concentrations on days with lower O3 concentrations in close proximity to NOX sources (e.g., in urban core areas), while at the same time decreasing the highest O3 concentrations in downwind 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 metric, the W126 exposure index, is often used to assess impact of O3 exposure on ecosystems and vegetation. W126 is a cumulative 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., annual fourth-highest 8-hour O3 maxima have concurrently shown a modest downward trend. The national average change in annual fourth-highest daily maximum 8-hour O3 concentrations between 2000 and 2013 was an 18% decrease. The national average change in the annual W126 exposure index over the same period was a 52% decrease. Air quality model simulations estimate that O3 air quality will continue to improve over the next decade as additional reductions in O3 precursors from power plants, motor vehicles, and other sources are realized.
In addition to being affected by changing emissions, future O3 concentrations may also be affected by climate change. Modeling studies in the EPA's Interim Assessment (U.S. EPA, 2009a) that are cited in support of the 2009 Endangerment Finding under CAA section 202(a) (74 FR 66496, Dec. 15, 2009) as well as a recent assessment of potential climate change impacts (Fann et al., 2015) project that climate change may lead to future increases in summer O3 concentrations across the contiguous U.S. While the projected impact is not uniform, climate change has the potential to increase average summertime O3 concentrations by as much as 1-5 ppb by 2030, if greenhouse gas emissions are not mitigated. Increases in temperature are expected to be the principal factor in driving any O3 increases, although increases in stagnation frequency may also contribute (Jacob and Winner, 2009). 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 this air quality issue is the impact from sources of O3 and its precursors beyond those from domestic, anthropogenic sources. Modeling analyses indicate 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. on some days can be substantially influenced by sources that cannot be addressed by domestic control measures. In particular, certain high-elevation sites in the western U.S. are impacted by a combination of non-U.S. sources like international transport, or natural sources such as stratospheric O3, and O3 originating from wildfire emissions. Ambient O3 from these non-U.S. and natural sources is collectively referred to as background O3. See generally section 2.4 of the PA (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.
E. Summary of Proposed Revisions to the O3 Standards
For reasons discussed in the proposal, the Administrator proposed to revise the current primary and secondary standards for O3. With regard to the primary standard, the Administrator proposed to revise the level from 75 ppb to a level within a range from 65 to 70 ppb. The EPA proposed to revise the AQI for O3, consistent with revision to the primary standard.
With regard to the secondary standard, the Administrator proposed to revise the level of the current secondary standard to within the range of 0.065 to 0.070 ppm, which air quality analyses indicate would provide cumulative, seasonal air quality or exposure values, in terms of 3-year average W126 index values, at or below a range of 13-17 ppm-hours.
The EPA also proposed to make corresponding revisions in data handling conventions for O3; to revise regulations for the PSD permitting program to add a provision grandfathering certain pending permits from certain requirements with respect to the proposed revisions to the standards; 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 also proposed to extend the new schedule approach to other future NAAQS revisions and to remove obsolete regulatory language associated with expired exceptional event deadlines for historical standards for both O3 and other pollutants for which NAAQS have been established. The EPA also proposed to make minor changes to the procedures and time periods for evaluating potential FRMs and equivalent methods, including making the requirements for NO2 consistent with the requirements for O3, and removing an obsolete requirement for the annual submission of documentation by manufacturers of certain particulate matter monitors.
F. Organization and Approach to Decisions in this O3 NAAQS Review
This action presents the Administrator's final decisions in the current review of the primary and secondary O3 standards. The final decisions addressing standards for O3 are based on a thorough review in the ISA of scientific information on known and potential human health and welfare effects associated with exposure to O3 at levels typically found in the ambient air. These final decisions also take into account the following: (1) staff assessments in the PA of the most policy-relevant information in the ISA as well as a quantitative health and welfare exposure and risk assessments based on that information; (2) CASAC advice and recommendations, as reflected in its letters to the Administrator and its discussions of drafts of the ISA, REAs, and PA at public meetings; (3) public comments received during the development of these documents, both in connection with CASAC meetings and separately; and (4) extensive public comments received on the proposed rulemaking.
The primary standard is addressed in section II. Corresponding changes to the AQI are addressed in section III. The secondary standard is addressed in section IV. Related data handling conventions and exceptional events are addressed in section V. Updates to the monitoring regulations are addressed in section VI. Implementation activities, including PSD-related actions, are addressed in sections VII and VIII. Section IX addresses applicable statutory and executive order reviews.
II. Rationale for Decision on the Primary Standard
This section presents the Administrator's final decisions regarding the need to revise the existing primary O3 standard and the appropriate revision to the level of that standard. Based on her consideration of the full body of health effects evidence and exposure/risk analyses, the Administrator concludes that the current primary standard for O3 is not requisite to protect public health with an adequate margin of safety. In order to increase public health protection, she is revising the level of the primary standard to 70 ppb, in conjunction with retaining the current indicator, averaging time and form. The Administrator concludes that such a revised standard will be requisite to protect public health with an adequate margin of safety. As discussed more fully below, the rationale for these final decisions draws from the thorough review in the ISA (U.S. EPA, 2013) of the available scientific evidence, generally 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 (U.S. EPA, 2014a); (2) the EPA staff assessment of the most policy-relevant scientific evidence and exposure/risk information in the PA (U.S. EPA, 2014c); (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; (4) public input received during the development of these documents, either in connection with CASAC meetings or separately; and (5) public comments on the proposal notice.
Section II.A below summarizes the information presented in the proposal regarding O3-associated health effects, O3 exposures, and O3-attributable health risks. Section II.B presents information related to the adequacy of the current primary O3 standard, including a summary of the basis for the Administrator's proposed decision to revise the current standard, public comments received on the adequacy of the current standard, and the Administrator's final conclusions regarding the adequacy of the current standard. Section II.C presents information related to the elements of a revised primary O3 standard, including information related to each of the major elements of the standard (i.e., indicator, averaging time, form, level). Section II.D summarizes the Administrator's final decisions on the primary O3 standard.
A. Introduction
As discussed in section II.A of the proposal (79 FR 75243-75246, December 17, 2014), the EPA's approach to informing decisions on the primary O3 standard in the current review builds upon the general approaches used in previous reviews and reflects the broader body of scientific evidence, updated exposure/risk information, and advances in O3 air quality modeling now available. This approach 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, 2013), exposure and risk analyses presented in the HREA (U.S. EPA, 2014a), evidence- and exposure-/risk-based considerations and conclusions presented in the PA (U.S. EPA, 2014c), advice and recommendations received from CASAC (Frey, 2014a, c), and public comments.
Section II.A.1 below summarizes the information presented in the proposal regarding O3-associated health effects. Section II.A.2 summarizes the information presented in the proposal regarding O3 exposures and O3-attributable health risks.
1. Overview of Health Effects Evidence
The health effects of O3 are described in detail in the ISA (U.S. EPA, 2013). Based on its assessment of the health effects evidence, the ISA determined that a "causal" relationship exists between short-term exposure to O3 in ambient air and effects on the respiratory system and that a "likely to be causal" relationship exists between long-term exposure to O3 in ambient air and respiratory effects (U.S. EPA, 2013, pp. 1-6 to 1-7). The ISA summarizes the longstanding body of evidence for O3 respiratory effects as follows (U.S. EPA, 2013, p. 1-5):
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, 2013, pp. 1-7 to 1-8). The ISA determined that the currently available evidence for additional endpoints is "suggestive" of causal relationships with short-term (central nervous system effects) and long-term exposures (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 determined in the ISA to be caused by, or likely to be caused by, O3 exposures (U.S. EPA, 2013, section 2.5.2). This section summarizes 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 (from section II.B in the proposal, 79 FR 75246-75271).
The information highlighted here is based on the assessment of the evidence in the ISA (U.S. EPA, 2013, Chapters 4 to 8) and consideration of that evidence 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. This section summarizes: (1) information available on potential mechanisms for health effects associated with exposure to O3 (II.A.1.a); (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.A.1.b); (3) considerations related to the adversity of O3-attributable health effects (II.A.1.c); and (4) considerations in characterizing the public health impact of O3, including the identification of "at risk" populations (II.A.1.d).
a. Overview of Mechanisms
This section briefly summarizes the characterization of the key events and pathways that contribute to health effects resulting from O3 exposures, as discussed in the proposal (79 FR 75247, section II.B.1) and in the ISA (U.S. EPA, 2013, section 5.3).
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, 2013, Chapters 6 and 7). Evidence indicates that the initial key event is the formation of secondary oxidation products in the respiratory tract (U.S. EPA, 2013, 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 (U.S. EPA 2014c, at 3-3, 3-9). The resulting secondary oxidation products transmit signals to the epithelium, pain receptive nerve fibers and, if present, immune cells involved in allergic responses. The available evidence indicates that the effects of O3 are mediated by components of ELF and by the multiple cell types in the respiratory tract. Oxidative stress is an implicit part of this initial key event.
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 which leads to lung function decrements; initiation of pulmonary inflammation; alteration of barrier epithelial function; sensitization of bronchial smooth muscle; modification of lung host defenses; airways remodeling; and modulation of autonomic nervous function which may alter cardiac function (U.S. EPA, 2013, section 5.3, Figure 5-8).
Persistent inflammation and injury, which are observed in animal models of chronic and quasi-continuous exposure to O3, are associated with airways remodeling (see section 7.2.3 of the ISA, U.S. EPA, 2013). Chronic quasi-continuous 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 (U.S. EPA, 2013, section 5.3.8). Extrapulmonary effects of O3 occur in numerous organ systems, including the cardiovascular, central nervous, reproductive, and hepatic systems (U.S. EPA, 2013, 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, including airways inflammation. The mechanisms that may underlie the variability in responses seen among individuals are discussed in the ISA (U.S. EPA, 2013, section 5.4.2). Certain functional genetic polymorphisms, pre-existing conditions or diseases, nutritional status, lifestages, and co-exposures can 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, 2013, Chapters 6 and 7).
b. Nature of Effects
This section briefly summarizes the information presented in the proposal on respiratory effects attributable to short-term exposures (II.A.1.b.i), respiratory effects attributable to long-term exposures (II.A.1.b.ii), cardiovascular effects attributable to short-term exposures (II.A.1.b.iii), and premature mortality attributable to short-term exposures (II.A.1.b.iv) (79 FR 75247, section II.B.2).
i. Respiratory Effects  -  Short-term Exposure
Controlled human exposure, animal toxicological, and epidemiologic studies available in the last review provided clear, consistent evidence of a causal relationship between short-term O3 exposure and respiratory effects (U.S. EPA, 2006a). Recent studies evaluated since the completion of the 2006 AQCD support and expand upon the strong body of evidence available in the last review (U.S. EPA, 2013, section 6.2.9).
Key aspects of this evidence are discussed below with regard to (1) lung function decrements; (2) pulmonary inflammation, injury, and oxidative stress; (3) airway hyperresponsiveness; (4) respiratory symptoms and medication use; (5) lung host defense; (6) allergic and asthma-related responses; (7) hospital admissions and emergency department visits; and (8) respiratory mortality.
Lung Function Decrements
Lung function decrements are typically measured by spirometry and refer to reductions in the maximal amount of air that can be forcefully exhaled. Forced expiratory volume in 1 second (FEV1) is a common index used to assess the effect of O3 on lung function. The ISA summarizes the currently available evidence from multiple controlled human exposure studies evaluating changes in FEV1 following 6.6-hour O3 exposures in young, healthy adults engaged in moderate levels of physical activity (U.S. EPA, 2013, section <IP_ADDRESS>, Figure 6-1). Exposures to an average O3 concentration of 60 ppb results in group mean decrements in FEV1 ranging from 1.8% to 3.6% (Adams, 2002; Adams, 2006; Schelegle et al., 2009; Kim et al., 2011). The weighted average group mean decrement was 2.7% from these studies. 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). Prolonged exposure to an average O3 concentration of 72 ppb results in a statistically significant group mean decrement in FEV1 of about 6% (Schelegle et al., 2009). There is a smooth dose-response curve without evidence of a threshold for exposures between 40 and 120 ppb O3 (U.S. EPA, 2013, Figure 6-1). When these data are taken together, the ISA concludes that "mean FEV1 is clearly decreased by 6.6-hour exposures to 60 ppb O3 and higher concentrations in [healthy, young adult] subjects performing moderate exercise" (U.S. EPA, 2013, p. 6-9).
As described in the proposal (79 FR 75250), the ISA focuses on individuals with >10% decrements in FEV1 because (1) it is accepted by the American Thoracic Society (ATS) as an abnormal response and a reasonable criterion for assessing exercise-induced bronchoconstriction, and (2) some individuals in the Schelegle et al. (2009) study experienced 5-10% FEV1 decrements following exposure to filtered air. The proportion of healthy adults experiencing FEV1 decrements > 10% following prolonged exposures to 80 ppb O3 while at moderate exertion ranged from 17% to 29% and following exposures to 60 ppb O3 ranged from 3% to 20%.  The weighted average proportion (i.e., based on numbers of subjects in each study) of young, healthy adults with >10% FEV1 decrements is 25% following exposure to 80 ppb O3 and 10% following exposure to 60 ppb O3, for 6.6 hours at moderate exertion (U.S. EPA, 2013, page 6-18 and 6-19). Responses within an individual tend to be reproducible over a period of several months, reflecting differences in intrinsic responsiveness. Given this, the ISA concludes that "[t]hough group mean decrements are biologically small and generally do not attain statistical significance, a considerable fraction of exposed individuals [in the clinical studies] experience clinically meaningful decrements in lung function" when exposed for 6.6 hours to 60 ppb O3 during quasi-continuous, moderate exertion (U.S. EPA, 2013, section <IP_ADDRESS>, p. 6-20).
This review has marked an advance in the ability to make reliable quantitative predictions of the potential lung function response to O3 exposure, and, thus, to reasonably predict the degree of interindividual response of lung function to that exposure. McDonnell et al. (2012) and Schelegle et al. (2012) developed models, described in more detail in the proposal (79 FR 75250), that included mathematical approaches to simulate the potential protective effect of antioxidants in the ELF at lower ambient O3 concentrations, and that included a dose threshold below which changes in lung function do not occur. The resulting empirical models can estimate the frequency distribution of individual responses and summary measures of the distribution such as the mean or median response and the proportions of individuals with FEV1 decrements > 10%, 15%, and 20%. The predictions of the models are consistent with the observed results from the individual controlled human exposure studies of O3-induced FEV1 decrements (79 FR 75250-51). CASAC agreed that these models mark a significant technical advance over the exposure-response modeling approach used for the lung function risk assessment in the last review and explicitly found that "[t]he MSS model to be scientifically and biologically defensible" (Frey, 2014a, pp. 8, 2). CASAC also stated that "the comparison of the MSS model results to those obtained with the exposure-response model is of tremendous importance. Typically, the MSS model gives a result about a factor of three higher ... for school-age children, which is expected because the MSS model includes responses for a wider range of exposure protocols" (Frey, 2014a, pp. 8, 2).
Epidemiologic studies have consistently linked short-term increases in ambient O3 concentrations with lung function decrements in diverse populations and lifestages, including children attending summer camps, adults exercising or working outdoors, and groups with pre-existing respiratory diseases such as asthmatic children (U.S. EPA, 2013, section <IP_ADDRESS>). Some of these studies reported O3-associated lung function decrements accompanied by respiratory symptoms in asthmatic children. In contrast, studies of children in the general population have reported similar O3-associated lung function decrements but without accompanying respiratory symptoms (79 FR 75251; U.S. EPA, 2013, section <IP_ADDRESS>). As noted in the PA (EPA, 2014c, p. 4-70), additional research is need to evaluate responses of people with asthma and healthy people in the 40 to 70 ppb range. Further epidemiologic studies and meta-analyses of the effects of O3 exposure on children will help elucidate the concentration-response functions for lung function and respiratory symptom effects at lower O3 concentrations.
Several epidemiologic panel studies reported statistically significant associations with lung function decrements at relatively low ambient O3 concentrations. For outdoor recreation or exercise, associations were reported in analyses restricted to 1-hour average O3 concentrations less than 80 ppb, down to less than 50 ppb. Among outdoor workers, Brauer et al. (1996) found a robust association with daily 1-hour max O3 concentrations less than 40 ppb. Ulmer et al. (1997) found a robust association in schoolchildren with 30-minute maximum O3 concentrations less than 60 ppb. For 8-hour average O3 concentrations, associations with lung function decrements in children with asthma were found to persist at concentrations less than 80 ppb in a U.S. multicity study (Mortimer et al., 2002) and less than 51 ppb in a study conducted in the Netherlands (Gielen et al., 1997).
As described in the proposal (79 FR 75251), several epidemiologic panel studies provided information on potential confounding by copollutants and most O3 effect estimates for lung function were robust to adjustment for temperature, humidity, and copollutants such as particulate matter with mass median aerodynamic diameter less than or equal to 2.5 micrometers (PM2.5), particulate matter with mass median aerodynamic diameter less than or equal to 10 micrometers (PM10), NO2, or sulfur dioxide (SO2) (Hoppe et al., 2003; Brunekreef et al., 1994; Hoek et al. 1993; U.S. EPA, 2013, pp. 6-67 to 6-69). Although examined in only a few epidemiologic studies, O3 also remained associated with decreases in lung function with adjustment for pollen or acid aerosols (79 F 75251; U.S. EPA, 2013, section <IP_ADDRESS>).
Pulmonary Inflammation, Injury and Oxidative Stress
As described in detail in section II.B.2.a.ii of the proposal (79 FR 75252), O3 exposures can result in increased respiratory tract inflammation and epithelial permeability. Inflammation is a host response to injury, and the induction of inflammation is evidence that injury has occurred. Oxidative stress has been shown to play a key role in initiating and sustaining O3-induced inflammation. As noted in the ISA (U.S. EPA, 2013, section 6.2.3), O3 exposures can initiate an acute inflammatory response throughout the respiratory tract that has been reported to persist for at least 18-24 hours after exposure.
Inflammation induced by exposure of humans to O3 can have several potential outcomes, ranging from resolving entirely following a single exposure to becoming a chronic inflammatory state, as described in detail in section II.B.2.a.ii of the proposal (79 FR 75252) and in the ISA (U.S. EPA, 2013, section 6.2.3). Lung injury and the resulting inflammation provide a mechanism by which O3 may cause other more serious morbidity effects (e.g., asthma exacerbations) (U.S. EPA, 2013, section 6.2.3).
Building on the last review, recent studies continue to support the evidence for airway inflammation and injury with new evidence for such effects following exposures to lower concentrations than had been evaluated previously. These studies include recent controlled human exposure and epidemiologic studies and are discussed more below.
An extensive body of evidence from controlled human exposure studies, described in section II.B.2.a.ii of the proposal, indicates that short-term exposures to O3 can cause pulmonary inflammation and increases in polymorphonuclear leukocyte (PMN) influx and permeability following 80-600 O3 ppb exposures, eosinophilic inflammation following exposures at or above 160 ppb, and O3-induced PMN influx following exposures of healthy adults to 60 ppb O3, the lowest concentration that has been evaluated for inflammation. A meta-analysis of 21 controlled human exposure studies (Mudway and Kelly, 2004) using varied experimental protocols (80-600 ppb O3 exposures; 1-6.6 hours exposure duration; light to heavy exercise; bronchoscopy at 0-24 hours post- O3 exposure) reported that PMN influx in healthy subjects is linearly associated with total O3 dose.
As with FEV1 responses to O3, inflammatory responses to O3 are generally reproducible within individuals, with some individuals experiencing more severe O3-induced airway inflammation than indicated by group averages. Unlike O3-induced decrements in lung function, which are attenuated following repeated exposures over several days, some markers of O3-induced inflammation and tissue damage remain elevated during repeated exposures, indicating ongoing damage to the respiratory system (79 FR 75252). Most controlled human exposure studies have reported that asthmatics experience larger O3-induced inflammatory responses than non-asthmatics.
      In the previous review (U.S. EPA, 2006a), the epidemiologic evidence of O3-associated changes in airway inflammation and oxidative stress was limited (79 FR 75253). Since then, as a result of the development of less invasive test methods, there has been a large increase in the number of studies assessing ambient O3-associated changes in airway inflammation and oxidative stress, the types of biological samples collected, and the types of indicators. Most of these recent studies have evaluated biomarkers of inflammation or oxidative stress in exhaled breath, nasal lavage fluid, or induced sputum (U.S. EPA, 2013, section <IP_ADDRESS>). These recent studies form a larger database to establish coherence with findings from controlled human exposure and animal studies that have measured the same or related biological markers. Additionally, results from these studies provide further biological plausibility for the associations observed between ambient O3 concentrations and respiratory symptoms and asthma exacerbations.
Airway Hyperresponsiveness (AHR)
A strong body of controlled human exposure and animal toxicological studies, most of which were available in the last review of the O3 NAAQS, report O3-induced AHR after either acute or repeated exposures (U.S. EPA, 2013, section <IP_ADDRESS>). People with asthma often exhibit increased airway responsiveness at baseline relative to healthy control subjects, and asthmatics can experience further increases in responsiveness following exposures to O3. Studies reporting increased airway responsiveness after O3 exposure contribute to a plausible link between ambient O3 exposures and increased respiratory symptoms in asthmatics, and increased hospital admissions and emergency department visits for asthma (section II.B.2.a.iii, 79 FR 75254; U.S. EPA, 2013, section <IP_ADDRESS>).
Respiratory Symptoms and Medication Use
Respiratory symptoms are associated with adverse outcomes such as limitations in activity, and are the primary reason for people with asthma to use quick relief medication and to seek medical care. Studies evaluating the link between O3 exposures and such symptoms allow a direct characterization of the clinical and public health significance of ambient O3 exposure. Controlled human exposure and toxicological studies have described modes of action through which short-term O3 exposures may increase respiratory symptoms by demonstrating O3-induced AHR (U.S. EPA, 2013, section 6.2.2) and pulmonary inflammation (U.S. EPA, 2013, section 6.2.3).
The link between subjective respiratory symptoms and O3 exposures has been evaluated in both controlled human exposure and epidemiologic studies, and the link with medication use has been evaluated in epidemiologic studies. In the last review, several controlled human exposure studies reported respiratory symptoms following exposures to O3 concentrations at or above 80 ppb. In addition, one study reported such symptoms following exposures to 60 ppb O3, though the increase was not statistically different from filtered air controls. Epidemiologic studies reported associations between ambient O3 and respiratory symptoms and medication use in a variety of locations and populations, including asthmatic children living in U.S. cities (U.S. EPA, 2013, pp. 6-1 to 6-2). In the current review, additional controlled human exposure studies have evaluated respiratory symptoms following exposures to O3 concentrations below 80 ppb and recent epidemiologic studies have evaluated associations with respiratory symptoms and medication use (U.S. EPA, 2013, sections 6.2.1, 6.2.4).
	As noted in section II.B.2.a.iv in the proposal (79 FR 75255), the findings for O3-induced respiratory symptoms in controlled human exposure studies, and the evidence integrated across disciplines describing underlying modes of action, provide biological plausibility for epidemiologic associations observed between short-term increases in ambient O3 concentration and increases in respiratory symptoms (U.S. EPA, 2013, section 6.2.4).
Most epidemiologic studies of O3 and respiratory symptoms and medication use have been conducted in children and/or adults with asthma, with fewer studies, and less consistent results, in non-asthmatic populations (U.S. EPA, 2013, section 6.2.4). The 2006 AQCD (U.S. EPA, 2006a; U.S. EPA, 2013, section 6.2.4) concluded that the collective body of epidemiologic evidence indicated that short-term increases in ambient O3 concentrations are associated with increases in respiratory symptoms in children with asthma. A large body of single-city and single-region studies of asthmatic children provides consistent evidence for associations between short-term increases in ambient O3 concentrations and increased respiratory symptoms and asthma medication use in children with asthma (U.S. EPA, 2013, Figure 6-12, Table 6-20, p. 79). Methodological differences, described in section II.B.2.a.iv of the proposal, among studies make comparisons across recent multicity studies of respiratory symptoms difficult.
Available evidence indicates that O3-associated increases in respiratory symptoms are not confounded by temperature, pollen, or copollutants (primarily PM) (U.S. EPA, 2013, section <IP_ADDRESS>; Table 6-25). However, identifying the independent effects of O3 in some studies was complicated due to the high correlations observed between O3 and PM or different lags and averaging times examined for copollutants. Nonetheless, the ISA noted that the robustness of associations in some studies of individuals with asthma, combined with findings from controlled human exposure studies for the direct effects of O3 exposure, provide substantial evidence supporting the independent effects of short-term ambient O3 exposure on respiratory symptoms (U.S. EPA, 2013, section <IP_ADDRESS>).
In summary, both controlled human exposure and epidemiologic studies have reported respiratory symptoms attributable to short-term O3 exposures. In the last review, the majority of the evidence from controlled human exposure studies in young, healthy adults was for symptoms following exposures to O3 concentrations at or above 80 ppb. Although studies that have become available since the last review have not reported increased respiratory symptoms in young, healthy adults following exposures with moderate exertion to 60 ppb, one recent study did report increased symptoms following exposure to 72 ppb O3. As was concluded in the last review, the collective body of epidemiologic evidence indicates that short-term increases in ambient O3 concentration are associated with increases in respiratory symptoms in children with asthma (U.S. EPA, 2013, section 6.2.4). Recent studies of respiratory symptoms and medication use, primarily in asthmatic children, add to this evidence. In a smaller body of studies, increases in ambient O3 concentration were associated with increases in respiratory symptoms in adults with asthma.
Lung Host Defense
The mammalian respiratory tract has a number of closely integrated defense mechanisms that, when functioning normally, provide protection from the potential health effects of exposures to a wide variety of inhaled particles and microbes. Based on toxicological and human exposure studies, in the last review EPA concluded that available evidence indicates that short-term O3 exposures have the potential to impair host defenses in humans, primarily by interfering with alveolar macrophage function. Any impairment in alveolar macrophage function may lead to decreased clearance of microorganisms or nonviable particles. Compromised alveolar macrophage functions in asthmatics may increase their susceptibility to other O3 effects, the effects of particles, and respiratory infections (U.S. EPA, 2006a).
Relatively few studies conducted since the last review have evaluated the effects of O3 exposures on lung host defense. As presented in section II.B.2.a.v of the proposal (79 FR 75256), when the available evidence is taken as a whole, the ISA concludes that acute O3 exposures impair the host defense capability of animals, primarily by depressing alveolar macrophage function and perhaps also by decreasing mucociliary clearance of inhaled particles and microorganisms. Coupled with limited evidence from controlled human exposure studies, this suggests that humans exposed to O3 could be predisposed to bacterial infections in the lower respiratory tract.
Allergic and Asthma Related Responses
Evidence from controlled human exposure and epidemiologic studies available in the last review indicates that O3 exposure skews immune responses toward an allergic phenotype and could also make airborne allergens more allergenic, as discussed in more detail in the proposal (79 FR 75257). Evidence from controlled human exposure and animal toxicology studies available in the last review indicates that O3 may also increase AHR to specific allergen triggers (75 FR 2970, January 19, 2010). When combined with NO2, O3 has been shown to enhance nitration of common protein allergens, which may increase their allergenicity (Franze et al., 2005).
Hospital Admissions and Emergency Department Visits
The 2006 AQCD concluded that "the overall evidence supports a causal relationship between acute ambient O3 exposures and increased respiratory morbidity resulting in increased emergency department visits and [hospital admissions] during the warm season" (U.S. EPA, 2006a). This conclusion was "strongly supported by the human clinical, animal toxicologic[al], and epidemiologic evidence for [O3-induced] lung function decrements, increased respiratory symptoms, airway inflammation, and airway hyperreactivity" (U.S. EPA, 2006a).
The results of recent studies largely support the conclusions of the 2006 AQCD (U.S. EPA, 2013, section 6.2.7). Since the completion of the 2006 AQCD, relatively fewer studies, conducted in the U.S., Canada, and Europe, have evaluated associations between short-term O3 concentrations and respiratory hospital admissions and emergency department visits, with a growing number of studies conducted in Asia. This epidemiologic evidence is discussed in detail in the proposal (79 FR 75258) and in the ISA (U.S. EPA, 2013, section 6.2.7).
In considering this body of evidence, the ISA focused primarily on multicity studies because they examine associations with respiratory-related hospital admissions and emergency department visits over large geographic areas using consistent statistical methodologies (U.S. EPA, 2013, section <IP_ADDRESS>). The ISA also focused on single-city studies that encompassed a large number of daily hospital admissions or emergency department visits, included long study-durations, were conducted in locations not represented by the larger studies, or examined population-specific characteristics that may impact the risk of O3-related health effects but were not evaluated in the larger studies (U.S. EPA, 2013, section <IP_ADDRESS>). When examining the association between short-term O3 exposure and respiratory health effects that require medical attention, the ISA distinguishes between hospital admissions and emergency department visits because it is likely that a small percentage of respiratory emergency department visits will be admitted to the hospital; therefore, respiratory emergency department visits may represent potentially less serious, but more common outcomes (U.S. EPA, 2013, section <IP_ADDRESS>).
Although the collective evidence across studies indicates a mostly consistent positive association between O3 exposure and respiratory-related hospital admissions and emergency department visits, the magnitude of these associations may be underestimated to the extent members of study populations modify their behavior in response to air quality forecasts, and to the extent such behavior modification increases exposure misclassification (U.S. EPA, 2013, Section 4.6.6). Studies examining the potential confounding effects of copollutants have reported that O3 effect estimates remained relatively robust upon the inclusion of PM and gaseous pollutants in two-pollutant models (U.S. EPA, 2013, Figure 6-20, Table 6-29). Additional studies that conducted copollutant analyses, but did not present quantitative results, also support these conclusions (Strickland et al., 2010; Tolbert et al., 2007; Medina-Ramon et al., 2006; U.S. EPA, 2013, section <IP_ADDRESS>).
In the last review, studies had not evaluated the concentration-response relationship between short-term O3 exposure and respiratory-related hospital admissions and emergency department visits.  As described in the proposal in section II.B.2.a.vii (79 FR 75257) and in the ISA (U.S. EPA, 2013, section <IP_ADDRESS>), a preliminary examination of this relationship in studies that have become available since the last review found no evidence of a deviation from linearity when examining the association between short-term O3 exposure and asthma hospital admissions (Silverman and Ito, 2010; Strickland et al., 2010). In addition, an examination of the concentration-response relationship for O3 exposure and pediatric asthma emergency department visits found no evidence of a threshold at O3 concentrations as low as 30 ppb (for daily maximum 8-hour concentrations) (U.S. EPA, 2013, section <IP_ADDRESS>). However, in these studies there is uncertainty in the shape of the concentration-response curve at the lower end of the distribution of O3 concentrations due to the low density of data in this range. Further studies at low-level O3 exposures might reduce this uncertainty.
Respiratory Mortality
 Evidence from experimental studies indicates multiple potential pathways of respiratory effects from short-term O3 exposures, which support the continuum of respiratory effects that could potentially result in respiratory-related mortality in adults (U.S. EPA, 2013, section 6.2.8). The evidence in the last review was inconsistent for associations between short-term O3 concentrations and respiratory mortality (U.S. EPA, 2006a). New epidemiologic evidence for respiratory mortality is discussed in detail in the ISA (U.S. EPA, 2013, section 6.6) and summarized below. The majority of recent multicity studies have reported positive associations between short-term O3 exposures and respiratory mortality, particularly during the summer months (U.S. EPA, 2013, Figure 6-36).
Recent multicity studies from the U.S. (Zanobetti and Schwartz, 2008), Europe (Samoli et al., 2009), Italy (Stafoggia et al., 2010), and Asia (Wong et al., 2010), as well as a multi-continent study (Katsouyanni et al., 2009), reported associations between short-term O3 concentrations and respiratory mortality (U.S. EPA, 2013, Figure 6-37, page 6-259). With respect to respiratory mortality, summer-only analyses were consistently positive and most were statistically significant. All-year analyses had more mixed results, but most were positive.
Of the studies evaluated, only two studies analyzed the potential for copollutant confounding of the O3-respiratory mortality relationship (Katsouyanni et al., (2009); Stafoggia et al., (2010)). Based on the results of these analyses, the O3 respiratory mortality risk estimates appear to be moderately to substantially sensitive (e.g., increased or attenuated) to inclusion of PM10. However, in the APHENA study (Katsouyanni et al., 2009), the mostly every-6th-day sampling schedule for PM10 in the Canadian and U.S. datasets greatly reduced their sample size and limits the interpretation of these results (U.S. EPA, 2013, section 6.2.8).
The evidence for associations between short-term O3 concentrations and respiratory mortality has been strengthened since the last review, with the addition of several large multicity studies. The biological plausibility of the associations reported in these studies is supported by the experimental evidence for respiratory effects.
ii. Respiratory Effects  -  Long-Term Exposure
Since the last review, the body of evidence indicating the occurrence of respiratory effects due to long-term O3 exposure has been strengthened. This evidence is discussed in detail in the ISA (U.S. EPA, 2013, Chapter 7) and summarized below for new-onset asthma and asthma prevalence, asthma hospital admissions, pulmonary structure and function, and respiratory mortality.
Asthma is a heterogeneous disease with a high degree of temporal variability. The onset, progression, and symptoms can vary within an individual's lifetime, and the course of asthma may vary markedly in young children, older children, adolescents, and adults. In the previous review, longitudinal cohort studies that examined associations between long-term O3 exposures and the onset of asthma in adults and children indicated a direct effect of long-term O3 exposures on asthma risk in adults and effect modification by O3 in children. Since then, additional studies have evaluated associations with new onset asthma, further informing our understanding of the potential gene-environment interactions, mechanisms, and biological pathways associated with incident asthma.
In children, the relationship between long-term O3 exposure and new-onset asthma has been extensively studied in the Children's Health Study (CHS), a long-term study that was initiated in the early 1990's which has evaluated effects in several cohorts of children. For this review, recent studies from the CHS provide evidence for gene-environment interactions in effects on new-onset asthma by indicating that the lower risks associated with specific genetic variants are found in children who live in lower O3 communities. Described in detail in the proposal (79 FR 75259) and in the ISA (U.S. EPA, 2013, section 7.2.1), these studies indicate that the risk for new-onset asthma is related in part to genetic susceptibility, as well as behavioral factors and environmental exposure. Cross-sectional studies by Akinbami et al. (2010) and Hwang et al. (2005) provide further evidence relating O3 exposures with asthma prevalence. Gene-environment interactions are discussed in detail in Section <IP_ADDRESS> in the ISA (U.S. EPA, 2013).
In the 2006 AQCD (U.S. EPA, 2006a), studies on O3-related hospital discharges and emergency department visits for asthma and respiratory disease mainly looked at short-term (daily) metrics. Recent studies continue to indicate that there is evidence for increases in both hospital admissions and emergency department visits in children and adults related to all respiratory outcomes, including asthma, with stronger associations in the warm months.
In the 2006 AQCD (U.S. EPA, 2006a), few epidemiologic studies had investigated the effect of chronic O3 exposure on pulmonary function. As discussed in the proposal, epidemiologic studies of long-term exposures in both children and adults provide mixed results about the effects of long-term O3 exposure on pulmonary function and the growth rate of lung function.
Long-term studies in animals allow for greater insight into the potential effects of prolonged exposure to O3 that may not be easily measured in humans, such as structural changes in the respiratory tract. Despite uncertainties, epidemiologic studies observing associations of O3 exposure with functional changes in humans can attain biological plausibility in conjunction with long-term toxicological studies, particularly O3-inhalation studies performed in non-human primates whose respiratory systems most closely resemble that of the human. An important series of studies, discussed in section <IP_ADDRESS> of the ISA (U.S. EPA, 2013), have used nonhuman primates to examine the effect of O3 alone, or in combination with an inhaled allergen, house dust mite antigen, on morphology and lung function. Animals exhibit the hallmarks of allergic asthma defined for humans (NHLBI, 2007). These studies and others have demonstrated changes in pulmonary function and airway morphology in adult and infant nonhuman primates repeatedly exposed to environmentally relevant concentrations of O3 (U.S. EPA, 2013, section <IP_ADDRESS>). As discussed in more detail in the proposal, the studies provide evidence of an O3-induced change in airway resistance and responsiveness and provide  biological plausibility of long-term exposure, or repeated short-term exposures, to O3 contributing to the effects of asthma in children.
Collectively, evidence from animal studies strongly suggests that chronic O3 exposure is capable of damaging the distal airways and proximal alveoli, resulting in lung tissue remodeling and leading to apparent irreversible changes. Potentially, persistent inflammation and interstitial remodeling play an important role in the progression and development of chronic lung disease. Further discussion of the modes of action that lead to O3-induced morphological changes and the mechanisms involved in lifestage susceptibility and developmental effects can be found in the ISA (U.S. EPA, 2013, section 5.3.7, section <IP_ADDRESS>). The findings reported in chronic animal studies offer insight into potential biological mechanisms for the suggested association between seasonal O3 exposure and reduced lung function development in children as observed in epidemiologic studies (U.S. EPA, 2013, section <IP_ADDRESS>). Further research could help fill in the gaps in our understanding of the mechanisms involved in lifestage susceptibility and developmental effects in children of seasonal or long-term exposure to O3.
A limited number of epidemiologic studies have assessed the relationship between long-term exposure to O3 and mortality in adults. The 2006 AQCD concluded that an insufficient amount of evidence existed "to suggest a causal relationship between chronic O3 exposure and increased risk for mortality in humans" (U.S. EPA, 2006a). Though total and cardio-pulmonary mortality were considered in these studies, respiratory mortality was not specifically considered.
In a recent follow-up analysis of the American Cancer Society cohort (Jerrett et al., 2009), cardiopulmonary deaths were separately subdivided into respiratory and cardiovascular deaths, rather than combined as in the Pope et al. (2002) work. Increased O3 exposure was associated with the risk of death from respiratory causes, and this effect was robust to the inclusion of PM2.5. Additionally, a recent multicity time series study (Zanobetti and Schwartz, 2011), which followed (from 1985 to 2006) four cohorts of Medicare enrollees with chronic conditions that might predispose to O3-related effects, observed an association between long-term (warm season) exposure to O3 and elevated risk of mortality in the cohort that had previously experienced an emergency hospital admission due to chronic obstructive pulmonary disease (COPD). A key limitation of this study is the inability to control for PM2.5, because data were not available in these cities until 1999.
iii. Cardiovascular Effects  -  Short-Term Exposure
A relatively small number of studies have examined the potential effect of short-term O3 exposure on the cardiovascular system. The 2006 AQCD (U.S. EPA, 2006a, p. 8-77) concluded that "O3 directly and/or indirectly contributes to cardiovascular-related morbidity," but added that the body of evidence was limited. This conclusion was based on a controlled human exposure study that included hypertensive adult males; a few epidemiologic studies of physiologic effects, heart rate variability, arrhythmias, myocardial infarctions, and hospital admissions; and toxicological studies of heart rate, heart rhythm, and blood pressure.
More recently, the body of scientific evidence available that has examined the effect of O3 on the cardiovascular system has expanded. There is an emerging body of animal toxicological evidence demonstrating that short-term exposure to O3 can lead to autonomic nervous system alterations (in heart rate and/or heart rate variability) and suggesting that proinflammatory signals may mediate cardiovascular effects. Interactions of O3 with respiratory tract components result in secondary oxidation product formation and subsequent production of inflammatory mediators, which have the potential to penetrate the epithelial barrier and to initiate toxic effects systemically. In addition, animal toxicological studies of long-term exposure to O3 provide evidence of enhanced atherosclerosis and ischemia/reperfusion (I/R) injury, corresponding with development of a systemic oxidative, proinflammatory environment. Recent experimental and epidemiologic studies have investigated O3-related cardiovascular events and are summarized in the ISA (U.S. EPA, 2013, section 6.3).
Controlled human exposure studies discussed in previous reviews have not demonstrated any consistent extrapulmonary effects. In this review, evidence from controlled human exposure studies suggests cardiovascular effects in response to short-term O3 exposure (U.S. EPA, 2013, section 6.3.1) and provides some coherence with evidence from animal toxicology studies. Controlled human exposure studies also support the animal toxicological studies by demonstrating O3-induced effects on blood biomarkers of systemic inflammation and oxidative stress, as well as changes in biomarkers that can indicate the potential for increased clotting following O3 exposures. Increases and decreases in high frequency heart rate variability (HRV) have been reported. These changes in cardiac function observed in animal and human studies provide preliminary evidence for O3-induced modulation of the autonomic nervous system through the activation of neural reflexes in the lung (U.S. EPA, 2013, section 5.3.2).
      Overall, the ISA concludes that the available body of epidemiologic evidence examining the relationship between short-term exposures to O3 concentrations and cardiovascular morbidity is inconsistent (U.S. EPA, 2013, section <IP_ADDRESS>).
Despite the inconsistent evidence for an association between O3 concentration and cardiovascular disease (CVD) morbidity, mortality studies indicate a consistent positive association between short-term O3 exposure and cardiovascular mortality in multicity studies and in a multi-continent study. When examining mortality due to CVD, epidemiologic studies consistently observe positive associations with short-term exposure to O3. Additionally, there is some evidence for an association between long-term exposure to O3 and mortality, although the association between long-term ambient O3 concentrations and cardiovascular mortality can be confounded by other pollutants (U.S. EPA, 2013). The ISA (U.S. EPA, 2013, section 6.3.4) states that taken together, the overall body of evidence across the animal and human studies is sufficient to conclude that there is likely to be a causal relationship between relevant short-term exposures to O3 and cardiovascular system effects.
iv. Premature Mortality  -  Short-Term Exposure
The 2006 AQCD concluded that the overall body of evidence was highly suggestive that short-term exposure to O3 directly or indirectly contributes to nonaccidental and cardiopulmonary-related mortality in adults, but additional research was needed to more fully establish underlying mechanisms by which such effects occur (U.S. EPA, 2006a; U.S. EPA, 2013, p. 2-18). In building on the evidence for mortality from the last review, the ISA states (U.S. EPA, 2013, p. 6-261):
The evaluation of new multicity studies that examined the association between short-term O3 exposures and mortality found evidence that supports the conclusions of the 2006 AQCD. These new studies reported consistent positive associations between short-term O3 exposure and all-cause (nonaccidental) mortality, with associations persisting or increasing in magnitude during the warm season, and provide additional support for associations between O3 exposure and cardiovascular and respiratory mortality.
The 2006 AQCD reviewed a large number of time-series studies of associations between short-term O3 exposures and total mortality including single- and multicity studies, and meta-analyses. Available studies reported some evidence for heterogeneity in O3 mortality risk estimates across cities and across studies. Studies that conducted seasonal analyses reported larger O3 mortality risk estimates during the warm or summer season. Overall, the 2006 AQCD identified robust associations between various measures of daily ambient O3 concentrations and all-cause mortality, which could not be readily explained by confounding due to time, weather, or copollutants. With regard to cause-specific mortality, consistent positive associations were reported between short-term O3 exposure and cardiovascular mortality, with less consistent evidence for associations with respiratory mortality. The majority of the evidence for associations between O3 and cause-specific mortality were from single-city studies, which had small daily mortality counts and subsequently limited statistical power to detect associations. The 2006 AQCD concluded that "the overall body of evidence is highly suggestive that O3 directly or indirectly contributes to nonaccidental and cardiopulmonary-related mortality" (U.S. EPA, 2013, section 6.6.1).
Recent studies have strengthened the body of evidence that supports the association between short-term O3 concentrations and mortality in adults. This evidence includes a number of studies reporting associations with nonaccidental as well as cause-specific mortality. Multi-continent and multicity studies have consistently reported positive and statistically significant associations between short-term O3 concentrations and all-cause mortality, with evidence for larger mortality risk estimates during the warm or summer months (79 FR 75262; U.S. EPA, 2013 Figure 6-27; Table 6-42). Similarly, evaluations of cause-specific mortality have reported consistently positive associations with O3, particularly in analyses restricted to the warm season (79 FR 75262; U.S. EPA, 2013 Fig. 6-37; Table 6-53).
In the previous review, multiple uncertainties remained regarding the relationship between short-term O3 concentrations and mortality, including the extent of residual confounding by copollutants; characterization of the factors that modify the O3-mortality association; the appropriate lag structure for identifying O3-mortality effects; and the shape of the O3-mortality concentration-response function and whether a threshold exists. Many of the studies, published since the last review, have attempted to address one or more of these uncertainties and are described in more detail in the proposal (79 FR 75262 and in the ISA (U.S. EPA, 2013, section 6.6.2).
In particular, recent studies have evaluated different statistical approaches to examine the shape of the O3-mortality concentration-response relationship and to evaluate whether a threshold exists for O3-related mortality. These studies are detailed in the proposal (79 FR 75262) and in the ISA (U.S. EPA, 2013, p. 2-32). The ISA reaches the following overall conclusions that the epidemiologic studies identified in the ISA indicated a generally linear C-R function with no indication of a threshold but that there is a lack of data at lower O3 concentrations and therefore, less certainty in the shape of the C-R curve at the lower end of the distribution (U.S. EPA, 2013, p. 2-32).
c. Adversity of Effects
In making judgments as to when various O3-related effects become regarded as adverse to the health of individuals, in previous NAAQS reviews, the EPA has relied upon the guidelines published by the ATS and the advice of CASAC. In 2000, the ATS published an official statement on "What Constitutes an Adverse Health Effect of Air Pollution?" (ATS, 2000a), which updated and built upon its earlier guidance (ATS, 1985). The earlier guidance defined adverse respiratory health effects as "medically significant physiologic changes generally evidenced by one or more of the following: (1) interference with the normal activity of the affected person or persons, (2) episodic respiratory illness, (3) incapacitating illness, (4) permanent respiratory injury, and/or (5) progressive respiratory dysfunction," while recognizing that perceptions of "medical significance" and "normal activity" may differ among physicians, lung physiologists and experimental subjects (ATS, 1985). The guidance concludes that transient, reversible loss of lung function in combination with respiratory symptoms should be considered adverse. They also note that: "However, the committee recommends that a small, transient loss of lung function, by itself, should not automatically be designated as adverse" (ATS, 2000a, p. 670).
There is also a more specific consideration of population risk in the 2000 guidance. Specifically, the committee considered that a shift in the risk factor distribution, and hence the risk profile of the exposed population, should be considered adverse, even in the absence of the immediate occurrence of frank illness (ATS, 2000a, p. 668). For example, a population of asthmatics could have a distribution of lung function such that no individual has a level associated with clinically important impairment. Exposure to air pollution could shift the distribution to lower levels of lung function that still do not bring any individual to a level that is associated with clinically relevant effects. However, this would be considered to be adverse because individuals within the population would have diminished reserve function, and therefore would be at increased risk to further environmental insult (ATS, 2000a, p. 668).
The ATS also concluded that elevations of biomarkers such as cell numbers and types, cytokines, and reactive oxygen species may signal risk for ongoing injury and more serious effects or may simply represent transient responses, illustrating the lack of clear boundaries that separate adverse from nonadverse events. More subtle health outcomes also may be connected mechanistically to health effects that are clearly adverse, so that small changes in physiological measures may not appear clearly adverse when considered alone, but may be part of a coherent and biologically plausible chain of related health outcomes that include responses that are clearly adverse, such as mortality (U.S. EPA, 2014c, section <IP_ADDRESS>).
Application of the ATS guidelines to the least serious category of effects related to ambient O3 exposures, which are also the most numerous and, therefore, are also important from a public health perspective, involves judgments about which medical experts on CASAC panels and public commenters have in the past expressed diverse views. To help frame such judgments, in past reviews, the EPA has defined gradations of individual functional responses (e.g., decrements in FEV1 and airway responsiveness) and symptomatic responses (e.g., cough, chest pain, wheeze), together with judgments as to the potential impact on individuals experiencing varying degrees of severity of these responses. These gradations were used in the 1997 O3 NAAQS review and slightly revised in the 2008 review (U.S. EPA, 1996b, p. 59; U.S. EPA, 2007, p. 3-72; 72 FR 37849, July 11, 2007). These gradations and impacts are summarized in Tables 3-2 and 3-3 in the 2007 O3 Staff Paper (U.S. EPA, 2007, pp. 3-74 to 3-75).
For the purpose of estimating potentially adverse lung function decrements in active healthy people, the CASAC panel in the 2008 O3 NAAQS review indicated that a focus on the mid to upper end of the range of moderate levels of functional responses is most appropriate (e.g., FEV1 decrements >= 15% but < 20%) (Henderson, 2006; U.S. EPA, 2007, p. 3-76). In this review, CASAC reiterated that the "[e]stimation of FEV1 decrements of >=15% is appropriate as a scientifically relevant surrogate for adverse health outcomes in active healthy adults" (Frey, 2014c, p. 3).
For the purpose of estimating potentially adverse lung function decrements in people with lung disease, the CASAC panel in the 2008 O3 NAAQS review indicated that a focus on the lower end of the range of moderate levels of functional responses is most appropriate (e.g., FEV1 decrements >=10%) (Henderson, 2006; U.S. EPA, 2007, p. 3-76). In their letter advising the Administrator on the reconsideration of the 2008 final decision, CASAC stated that "[a] 10% decrement in FEV1 can lead to respiratory symptoms, especially in individuals with pre-existing pulmonary or cardiac disease. For example, people with chronic obstructive pulmonary disease have decreased ventilatory reserve (i.e., decreased baseline FEV1) such that a >= 10% decrement could lead to moderate to severe respiratory symptoms" (Samet, 2011). In this review, CASAC provided similar advice, stating that "[a]n FEV1 decrement of >= 10% is a scientifically relevant surrogate for adverse health outcomes for people with asthma and lung disease", and that such decrements "could be adverse for people with lung disease" (Frey, 2014c, pp. 3, 7).
In judging the extent to which these impacts represent effects that should be regarded as adverse to the health status of individuals, in previous NAAQS reviews, the EPA has also considered whether effects were experienced repeatedly during the course of a year or only on a single occasion (U.S. EPA, 2007). While some experts would judge single occurrences of moderate responses to be a "nuisance," especially for healthy individuals, a more general consensus view of the adversity of such moderate responses emerges as the frequency of occurrence increases. In particular, not every estimated occurrence of an O3-induced FEV1 decrement will be adverse and repeated occurrences of moderate responses, even in otherwise healthy individuals, may be considered to be adverse since they could set the stage for more serious illness. Thus, it has been judged that repeated occurrences of moderate responses, even in otherwise healthy individuals, may be considered to be adverse since they could well set the stage for more serious illness (61 FR 65723). The CASAC panel in the 1997 NAAQS review expressed a consensus view that these "criteria for the determination of an adverse physiological response were reasonable" (Wolff, 1995). In the review completed in 2008, as in the current review (II.B, II.C below), estimates of repeated occurrences continued to be an important public health policy factor in judging the adversity of moderate lung function decrements in healthy and asthmatic people (72 FR 37850, July 11, 2007).
d. Ozone-Related Impacts on Public Health