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National Ambient Air Quality Standards for Ozone

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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 the levels of both standards to 0.070 parts per million (ppm), and retaining their indicators (O3), forms (fourth-highest daily maximum, averaged across three consecutive years) and averaging times (eight hours). 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 December 28, 2015.

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), which has been incorporated by reference into the rulemaking docket. All documents in the docket are listed on the www.regulations.gov Web site. 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 (202) 566-1744 and the telephone number for the Air and Radiation Docket and Information Center is (202) 566-1742. For additional information about EPA's public docket, visit the EPA Docket Center homepage at: http://www.epa.gov/​epahome/​dockets.htm.

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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: (919) 541-1146; fax: (919) 541-0237; email: stone.susan@epa.gov.

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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) Web site (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 O3Start Printed Page 65293

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 (DC 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 Start Printed Page 65294design 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 revising the primary and secondary standards, this action is changing the AQI to reflect the revisions to the 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 provides schedules and information related to implementing the revised standards. Start Printed Page 65295The rule also contains revisions to the schedules associated with exceptional events 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. 7408) directs the Administrator to identify and list certain air pollutants and then to issue air quality criteria for those pollutants. The Administrator is to list those air pollutants that in her “judgment, cause or contribute to air pollution which may reasonably be anticipated to endanger public health or welfare;” “the presence of which in the ambient air results from numerous or diverse mobile or stationary sources;” and “for which . . . [the Administrator] plans to issue air quality criteria . . . .” Air quality criteria are intended to “accurately reflect the latest scientific knowledge useful in indicating the kind and extent of all identifiable effects on public health or welfare which may be expected from the presence of [a] pollutant in the ambient air . . .” 42 U.S.C. 7408(b). Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate “primary” and “secondary” NAAQS for pollutants for which air quality criteria are issued. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on such criteria and allowing an adequate margin of safety, are requisite to protect the public health.” [1] A secondary standard, as defined in section 109(b)(2), must “specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on such criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.” [2]

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) [3] at risk, and the kind and degree of the uncertainties that must be addressed. The selection of any particular approach for providing an adequate margin of safety is a policy choice left specifically to the Administrator's judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62; 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 [4] 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 Start Printed Page 65296to 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),[5] 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 O 3

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,[6] 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 Start Printed Page 65297at 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 Start Printed Page 65298reconsideration with its statutorily required periodic review.[7]

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).[8]

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,[9] 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).[10] 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).[11] The first Start Printed Page 65299draft 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 and welfare 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).Start Printed Page 65300

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 [12] were above the level of the existing health-based (primary) 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 impacts 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.[13] 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.[14] 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 O 3 Standards

For reasons discussed in the proposal, the Administrator proposed to revise the Start Printed Page 65301current 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 O 3 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.Start Printed Page 65302

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 [15] and that a “likely to be causal” relationship exists between long-term exposure to O3 in ambient air and respiratory effects [16] (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 preamble 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-Start Printed Page 65303term 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.[17]

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 [18] (U.S. EPA, 2013, section 6.2.1.1, 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; [19] Schelegle et al., 2009; [20] 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).[21] 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).[22] 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).[23] 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 6.2.1.1, 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%.[24] 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, see also U.S. EPA, 2013, Figures 6-1 and 6-3). 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 Start Printed Page 65304responses 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 6.2.1.2). Some of these studies reported O3-associated lung function decrements accompanied by respiratory symptoms [25] 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 6.2.1.2). As noted in the PA (EPA, 2014c, pp. 4-70 to 4-71), additional research is needed 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 [26] 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 6.2.1.2).

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). Continued cellular damage due to chronic inflammation “may alter the structure and function of pulmonary tissues” (U.S. EPA, 2013, p. 6-161). 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).[27]

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.[28]

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 6.2.3.2). These recent studies form a larger database to establish coherence with findings from controlled human exposure and animal Start Printed Page 65305studies 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 6.2.2.2). 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 6.2.2.2).

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, section 6.2.4.1). 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 6.2.4.5; 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 6.2.4.5).

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), Start Printed Page 65306when 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” [29] (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).[30]

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 6.2.7.1). 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 6.2.7.1). 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 6.2.7.1).

The collective evidence across studies indicates a mostly consistent positive association between O3 exposure and respiratory-related hospital admissions and emergency department visits. Moreover, 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 6.2.7.5).[31]

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 6.2.7.2), 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 6.2.7.3). 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).[32] 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).

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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, sections 6.2.8 and 6.2.9).

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 5.4.2.1 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 7.2.3.2 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 7.2.3.2). 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 5.4.2.4). 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 7.2.3.1). 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 Start Printed Page 65308mortality 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 6.3.2.9).

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).Start Printed Page 65309

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 more recent guidance concludes that transient, reversible loss of lung function in combination with respiratory symptoms should be considered adverse.[33] However, the committee also recommended “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 already have diminished reserve function, and therefore would be at increased risk to further environmental insult (ATS, 2000a, p. 668).

The ATS also concluded in its guidance 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 3.1.2.1).

Application of the ATS guidelines to the least serious category of effects [34] 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 by the EPA 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 Start Printed Page 65310advising 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.[35] However, 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 (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

The currently available evidence expands the understanding of populations that were identified to be at greater risk of O3-related health effects at the time of the last review (i.e., people who are active outdoors, people with lung disease, children and older adults and people with increased responsiveness to O3) and supports the identification of additional factors that may lead to increased risk (U.S. EPA, 2006a, section 6.3; U.S. EPA, 2013, Chapter 8). Populations and lifestages may be at greater risk for O3-related health effects due to factors that contribute to their susceptibility and/or vulnerability to O3. The definitions of susceptibility and vulnerability have been found to vary across studies, but in most instances “susceptibility” refers to biological or intrinsic factors (e.g., lifestage, sex, preexisting disease/conditions) while “vulnerability” refers to non-biological or extrinsic factors (e.g., socioeconomic status [SES]) (U.S. EPA, 2013, p. 8-1; U.S. EPA, 2010, 2009b). In some cases, the terms “at-risk” and “sensitive” have been used to encompass these concepts more generally. In the ISA, PA, and proposal, “at-risk” is the all-encompassing term used to define groups with specific factors that increase their risk of O3-related health effects.

There are multiple avenues by which groups may experience increased risk for O3-induced health effects. A population or lifestage [36] may exhibit greater effects than other populations or lifestages exposed to the same concentration or dose, or they may be at greater risk due to increased exposure to an air pollutant (e.g., time spent outdoors). A group with intrinsically increased risk would have some factor(s) that increases risk through a biological mechanism and, in general, would have a steeper concentration-risk relationship, compared to those not in the group. Factors that are often considered intrinsic include pre-existing asthma, genetic background, and lifestage. A group of people could also have extrinsically increased risk, which would be through an external, non-biological factor, such as socioeconomic status (SES) and diet. Some groups are at risk of increased internal dose at a given exposure concentration, for example, because of breathing patterns. This category would include people who work or exercise outdoors. Finally, there are those who might be placed at increased risk for experiencing greater exposures by being exposed to higher O3 concentrations. This would include, for example, groups of people with greater exposure to ambient O3 due to less availability or use of home air conditioners such that they are more likely to be in locations with open windows on high O3 days. Some groups may be at increased risk of O3-related health effects through a combination of factors. For example, children tend to spend more time outdoors when O3 levels are high, and at higher levels of activity than adults, which leads to increased exposure and dose, and they also have biological, or intrinsic, risk factors (e.g., their lungs are still developing) (U.S. EPA, 2013, Chapter 8). An at-risk population or lifestage is more likely to experience adverse health effects related to O3 exposures and/or, develop more severe effects from exposure than the general population. The populations and lifestages identified by the ISA (U.S. EPA, 2013, section 8.5) identified that have “adequate” evidence for increased O3-related health effects are people with certain genotypes, people with asthma, younger and older age groups, people with reduced intake of certain nutrients, and outdoor workers. These at-risk populations and lifestages are described in more detail in section II.B.4 of the proposal (79 FR 75264-269).

One consideration in the assessment of potential public health impacts is the size of various population groups for which there is adequate evidence of increased risk for health effects associated with O3-related air pollution exposure (U.S. EPA, 2014c, section 3.1.5.2). The factors for which the ISA judged the evidence to be “adequate” with respect to contributing to increased risk of O3-related effects among various populations and lifestages included: Asthma; childhood and older adulthood; diets lower in vitamins C and E; certain genetic variants; and working outdoors (U.S. EPA, 2013, section 8.5). No statistics are available to estimate the size of an at-risk population based on nutritional status or genetic variability.

With regard to asthma, Table 3-7 in the PA (U.S. EPA, 2014c, section 3.1.5.2) summarizes information on the prevalence of current asthma by age in the U.S. adult population in 2010 (Schiller et al. 2012; children—Bloom et al., 2011). Individuals with current asthma constitute a fairly large proportion of the population, including more than 25 million people. Asthma prevalence tends to be higher in children than adults. Within the U.S., approximately 8.2% of adults have reported currently having asthma (Schiller et al., 2012) and 9.5% of Start Printed Page 65311children have reported currently having asthma (Bloom et al., 2011).[37]

With regard to lifestages, based on U.S. census data from 2010 (Howden and Meyer, 2011), about 74 million people, or 24% of the U.S. population, are under 18 years of age and more than 40 million people, or about 13% of the U.S. population, are 65 years of age or older. Hence, a large proportion of the U.S. population (i.e., more than a third) is included in age groups that are considered likely to be at increased risk for health effects from ambient O3 exposure.

With regard to outdoor workers, in 2010, approximately 11.7% of the total number of people (143 million people) employed, or about 16.8 million people, worked outdoors one or more days per week (based on worker surveys).[38] Of these, approximately 7.4% of the workforce, or about 7.8 million people, worked outdoors three or more days per week.

While it is difficult to estimate the total number of people in groups that are at greater risk from exposure to O3, due to the overlap in members of the different at-risk population groups, the proportion of the total population at greater risk is large. The size of the at-risk population combined with the estimates of risk of different health outcomes associated with exposure to O3 can give an indication of the magnitude of O3 impacts on public health.

2. Overview of Human Exposure and Health Risk Assessments

To put judgments about health effects into a broader public health context, the EPA has developed and applied models to estimate human exposures to O3 and O3-associated health risks. Exposure and risk estimates that are output from such models are presented and assessed in the HREA (U.S. EPA, 2014a). Section II.C of the proposal discusses the quantitative assessments of O3 exposures and O3-related health risks that are presented in the HREA (79 FR 75270). Summaries of these discussions are provided below for the approach used to adjust air quality for quantitative exposure and risk analyses in the HREA (II.A.2.a), the HREA assessment of exposures to ambient O3 (II.A.2.b), and the HREA assessments of O3-related health risks (II.A.2.c).

a. Air Quality Adjustment

As discussed in section II.C.1 of the proposal (79 FR 75270), the HREA uses a photochemical model to estimate sensitivities of O3 to changes in precursor emissions in order to estimate ambient O3 concentrations that would just meet the current and alternative standards (U.S. EPA, 2014a, Chapter 4).[39] For the 15 urban study areas evaluated in the HREA,[40] this model-based adjustment approach estimates hourly O3 concentrations at each monitor location when modeled U.S. anthropogenic precursor emissions (i.e., NOX, VOC) [41] are reduced. The HREA estimates air quality that just meets the current and alternative standards for the 2006-2008 and 2008-2010 periods.[42]

As discussed in Chapter 4 of the HREA (U.S. EPA, 2014a), this approach to adjusting air quality models the physical and chemical atmospheric processes that influence ambient O3 concentrations. Compared to the quadratic rollback approach used in previous reviews, it provides more realistic estimates of the spatial and temporal responses of O3 to reductions in precursor emissions. Because ambient NOX can contribute both to the formation and destruction of O3 (U.S. EPA, 2014a, Chapter 4), the response of ambient O3 concentrations to reductions in NOX emissions is more variable than indicated by the quadratic rollback approach. This improved approach to adjusting O3 air quality is consistent with recommendations from the National Research Council of the National Academies (NRC, 2008). In addition, CASAC strongly supported the new approach as an improvement and endorsed the way it was utilized in the HREA, stating that “the quadratic rollback approach has been replaced by a scientifically more valid Higher-order Decoupled Direct Method (HDDM)” and that “[t]he replacement of the quadratic rollback procedure by the HDDM procedure is important and supported by the CASAC” (Frey, 2014a, pp. 1 and 3).

Within urban study areas, the model-based air quality adjustments show reductions in the O3 levels at the upper ends of ambient concentrations and increases in the O3 levels at the lower ends of those distributions (U.S. EPA, 2014a, section 4.3.3.2, Figures 4-9 and 4-10).[43] Seasonal means of daily O3 concentrations generally exhibit only modest changes upon model adjustment, reflecting the seasonal balance between daily decreases in relatively higher concentrations and increases in relatively lower concentrations (U.S. EPA, 2014a, Figures 4-9 and 4-10). The resulting compression in the seasonal distributions of ambient O3 concentrations is evident in all of the urban study areas evaluated, though the degree of compression varies considerably across areas (U.S. EPA, 2014a, Figures 4-9 and 4-10).

As discussed in the PA (U.S. EPA, 2014c, section 3.2.1), adjusted patterns of O3 air quality have important implications for exposure and risk estimates in urban case study areas. Estimates influenced largely by the upper ends of the distribution of ambient concentrations (i.e., exposures of concern and lung function risk estimates, as discussed in sections 3.2.2 and 3.2.3.1 of the PA) will decrease with model-adjustment to the current and alternative standards. In contrast, seasonal risk estimates influenced by the full distribution of ambient O3 concentrations (i.e., epidemiology-based risk estimates, as discussed in section 3.2.3.2 of the PA) either increase or decrease in response to air quality adjustment, depending on the balance between the daily decreases in high O3Start Printed Page 65312concentrations and increases in low O3 concentrations.[44]

To evaluate uncertainties in air quality adjustments, the HREA assessed the extent to which the modeled O3 response to reductions in NOX emissions appropriately represent the trends observed in monitored ambient O3 following actual reductions in NOX emissions, and the extent to which the O3 response to reductions in precursor emissions could differ with emissions reduction strategies that are different from those used in HREA to generate risk estimates.

To evaluate the first issue, the HREA conducted a national analysis evaluating trends in monitored ambient O3 concentrations during a time period when the U.S. experienced large-scale reductions in NOX emissions (i.e., 2001 to 2010). Analyses of trends in monitored O3 indicate that over such a time period, the upper end of the distribution of monitored O3 concentrations (i.e., indicated by the 95th percentile) generally decreased in urban and non-urban locations across the U.S. (U.S. EPA, 2014a, Figure 8-29). During this same time period, median O3 concentrations decreased in suburban and rural locations, and in some urban locations. However, median concentrations increased in some large urban centers (U.S. EPA, 2014a, Figure 8-28). As discussed in the HREA, these increases in median concentrations likely reflect the increases in relatively low O3 concentrations that can occur near important sources of NOX upon reductions in NOX emissions (U.S. EPA, 2014a, section 8.2.3.1). These patterns of monitored O3 during a period when the U.S. experienced large reductions in NOX emissions are qualitatively consistent with the modeled responses of O3 to reductions in NOX emissions.

To evaluate the second issue, the HREA assessed the O3 air quality response to reducing both NOX and VOC emissions (i.e., in addition to assessing reductions in NOX emissions alone) for a subset of seven urban study areas. As discussed in the PA (U.S. EPA, 2014c, section 3.2.1), the addition of VOC reductions generally resulted in larger decreases in mid-range O3 concentrations (25th to 75th percentiles) (U.S. EPA, 2014a, Appendix 4D, section 4.7).[45] In addition, in all seven of the urban study areas evaluated, the increases in low O3 concentrations were smaller for the NOX/VOC scenarios than the NOX alone scenarios (U.S. EPA, 2014a, Appendix 4D, section 4.7). This was most apparent for Denver, Houston, Los Angeles, New York, and Philadelphia. Given the impacts on total risk estimates of increases in low O3 concentrations (discussed below), these results suggest that in some locations optimized emissions reduction strategies could result in larger reductions in O3-associated mortality and morbidity than indicated by HREA estimates.

b. Exposure Assessment

As discussed in section II.C.2 of the proposal, the O3 exposure assessment presented in the HREA (U.S. EPA, 2014a, Chapter 5) provides estimates of the number and percent of people exposed to various concentrations of ambient O3 while at specified exertion levels. The HREA estimates exposures in the 15 urban study areas for four study groups, all school-age children (ages 5 to 18), asthmatic school-age children, asthmatic adults (ages 19 to 95), and all older adults (ages 65 to 95), reflecting the evidence indicating that these populations are at increased risk for O3-attributable effects (U.S. EPA, 2013, Chapter 8; II.A.1.d, above). An important purpose of these exposure estimates is to provide perspective on the extent to which air quality adjusted to just meet the current O3 NAAQS could be associated with exposures to O3 concentrations reported to result in respiratory effects.[46] These analyses of exposure assessment incorporate behavior patterns, including estimates of physical exertion, which are critical in assessing whether ambient concentrations of O3 may pose a public health risk.[47] In particular, exposures to ambient or near-ambient O3 concentrations have only been shown to result in potentially adverse effects if the ventilation rates of people in the exposed populations are raised to a sufficient degree (e.g., through physical exertion) (U.S. EPA, 2013, section 6.2.1.1). Estimates of such “exposures of concern” provide perspective on the potential public health impacts of O3-related effects, including effects that cannot currently be evaluated in a quantitative risk assessment.[48]

The HREA estimates 8-hour exposures at or above benchmark concentrations of 60, 70, and 80 ppb for individuals engaged in moderate or greater exertion (i.e., to approximate conditions in the controlled human exposure studies on which benchmarks are based). Benchmarks reflect exposure concentrations at which O3-induced respiratory effects are known to occur in some healthy adults engaged in moderate, quasi-continuous exertion, based on evidence from controlled human exposure studies (U.S. EPA, 2013, section 6.2; U.S. EPA, 2014c, section 3.1.2.1). The amount of weight to place on the estimates of exposures at or above specific benchmark concentrations depends in part on the weight of the scientific evidence concerning health effects associated with O3 exposures at those benchmark concentrations. It also depends on judgments about the importance, from a public health perspective, of the health effects that are known or can reasonably be inferred to occur as a result of exposures at benchmark concentrations (U.S. EPA, 2014c, sections 3.1.3, 3.1.5).

In considering estimates of O3 exposures of concern at or above benchmarks of 60, 70, and 80 ppb, the PA focuses on modeled exposures for school-age children (ages 5-18), including asthmatic school-age children, which are key at-risk populations identified in the ISA (U.S. EPA, 2014c, section 3.1.5). The percentages of children estimated to experience exposures of concern are considerably larger than the percentages estimated for adult populations (i.e., approximately 3-fold larger across urban Start Printed Page 65313study areas) [49] (U.S. EPA, 2014a, section 5.3.2 and Figures 5-5 to 5-8). The larger exposure estimates for children are due primarily to the larger percentage of children estimated to spend an extended period of time being physically active outdoors when O3 concentrations are elevated (U.S. EPA, 2014a, sections 5.3.2 and 5.4.1).

Although exposure estimates differ between children and adults, the patterns of results across the urban study areas and years are similar among all of the populations evaluated (U.S. EPA, 2014a, Figures 5-5 to 5-8). Therefore, while the PA highlights estimates in children, including asthmatic school-age children, it also notes that the patterns of exposures estimated for children represent the patterns estimated for adult asthmatics and older adults.

Table 1 of the proposal (79 FR 75272 to 75273) summarizes key results from the exposure assessment. This table is reprinted below.

Table 1—Summary of Estimated Exposures of Concern in All School-age Children for the Current and Alternative O3 Standards in Urban Study Areas

Benchmark concentrationStandard level (ppb)Average % children exposed 50Average number of children exposed [average number of asthmatic children] 51% Children—worst year and worst area
One or more exposures of concern per season
≥ 80 ppb750-0.3 (0.1)27,000 [3,000]1.1
700-0.1 (0)3,700 [300]0.2
650 (0)300 [0]0
600 (0)100 52 [0]0
≥ 70 ppb750.6-3.3 (1.9)362,000 [40,000]8.1
700.1-1.2 (0.5)94,000 [10,000]3.2
650-0.2 (0.1)14,000 [2,000]0.5
600 (0)1,400 [200]0.1
≥ 60 ppb759.5-17 (12.2)2,316,000 [246,000]25.8
703.3-10.2 (6.2)1,176,000 [126,000]18.9
650-4.2 (2.1)392,000 [42,000]9.5
600-1.2 (0.4)70,000 [8,000]2.2
Two or more exposures of concern per season
≥ 80 ppb750 (0)600 [100]0.1
700 (0)0 [0]0
650 (0)0 [0]0
600 (0)0 [0]0
≥ 70 ppb750.1-0.6 (0.2)46,000 [5,000]2.2
700-0.1 (0)5,400 [600]0.4
650 (0)300 [100]0
600 (0)0 [0]0
≥ 60 ppb753.1-7.6 (4.5)865,000 [93,000]14.4
700.5-3.5 (1.7)320,000 [35,000]9.2
650-0.8 (0.3)67,000 [7,500]2.8
600-0.2 (0)5,100 [700]0.3

Uncertainties in exposure estimates are summarized in section II.C.2.b of the proposal (79 FR 75273). For example, due to variability in responsiveness, only a subset of individuals who experience exposures at or above a benchmark concentration can be expected to experience health effects.[53] In addition, not all of these effects will be adverse. Given the lack of sufficient exposure-response information for most of the health effects that informed benchmark concentrations, estimates of the number of people likely to experience exposures at or above benchmark concentrations generally cannot be translated into quantitative estimates of the number of people likely to experience specific health effects.[54] The PA views health-relevant exposures as a continuum with greater confidence and less uncertainty about the existence of adverse health effects at higher O3 exposure concentrations, and less confidence and greater uncertainty as one considers lower exposure concentrations (e.g., U.S. EPA, 2014c, Start Printed Page 65314sections 3.1 and 4.6). This view draws from the overall body of available health evidence, which indicates that as exposure concentrations increase, the incidence, magnitude, and severity of effects increases.

Another important uncertainty is that there is very limited evidence from controlled human exposure studies, which provided the basis for health benchmark concentrations for both exposures of concern and lung function decrements, related to clinical responses in at-risk populations. Compared to the healthy young adults included in the controlled human exposure studies, members of at-risk populations could be more likely to experience adverse effects, could experience larger and/or more serious effects, and/or could experience effects following exposures to lower O3 concentrations.[55]

There are also uncertainties associated with the exposure modelling. These are described most fully, and their potential impact characterized, in section 5.5.2 of the HREA (U.S. EPA, 2013, pp. 5-72 to 5-79). These include interpretation of activity patterns set forth in diaries which do not typically distinguish the basis for activity patterns and so may reflect averting behavior,[56] and whether the HREA underestimates exposures for groups spending especially large proportion of time being active outdoors during the O3 season (outdoor workers and especially active children).

c. Quantitative Health Risk Assessments

As discussed in section II.C.3 of the proposal (79 FR 75274), for some health endpoints, there is sufficient scientific evidence and information available to support the development of quantitative estimates of O3-related health risks. In the current review, for short-term O3 concentrations, the HREA estimates lung function decrements; respiratory symptoms in asthmatics; hospital admissions and emergency department visits for respiratory causes; and all-cause mortality (U.S. EPA, 2014a). For long-term O3 concentrations, the HREA estimates respiratory mortality (U.S. EPA, 2014a).[57] Estimates of O3-induced lung function decrements are based on exposure modeling using the MSS model (see section II.1.b.i.(1) above, and 79 FR 75250), combined with exposure-response relationships from controlled human exposure studies (U.S. EPA, 2014a, Chapter 6). Estimates of O3-associated respiratory symptoms, hospital admissions and emergency department visits, and mortality are based on concentration-response relationships from epidemiologic studies (U.S. EPA, 2014a, Chapter 7). As with the exposure assessment discussed above, O3-associated health risks are estimated for recent air quality and for ambient concentrations adjusted to just meet the current and alternative O3 standards, based on 2006-2010 air quality and adjusted precursor emissions. The following sections summarize the discussions from the proposal on the lung function risk assessment (II.A.2.c.i) and the epidemiology-based morbidity and mortality risk assessments (II.A.2.c.ii).

i. Lung Function Risk Assessment

The HREA estimates risks of lung function decrements in school-aged children (ages 5 to 18), asthmatic school-aged children, and the general adult population for the 15 urban study areas. The results presented in the HREA are based on an updated dose-threshold model that estimates FEV1 responses for individuals following short-term exposures to O3 (McDonnell et al., 2012), reflecting methodological improvements since the last review (II.B.2.a.i (1), above; U.S. EPA, 2014a, section 6.2.4). The impact of the dose threshold is that O3-induced FEV1 decrements result primarily from exposures on days with average ambient O3 concentrations above about 40 ppb (U.S. EPA, 2014a, section 6.3.1, Figure 6-9).[58]

Table 2 in the proposal (79 FR 75275), and reprinted below, summarizes key results from the lung function risk assessment. Table 2 presents estimates of the percentages of school-aged children estimated to experience O3-induced FEV1 decrements > 10, 15, or 20% when air quality was adjusted to just meet the current and alternative 8-hour O3 standards. Table 2 also presents the numbers of children, including children with asthma, estimated to experience such decrements.

Table 2—Summary of Estimated O3-Induced Lung Function Decrements for the Current and Potential Alternative O3 Standards in Urban Case Study Areas

Lung function decrementAlternative standard levelAverage % children 59Number of children (5 to 18 years) [number of asthmatic children] 60% Children worst year and area
One or more decrements per season
≥10%7514-193,007,000 [312,000]22
7011-172,527,000 [261,000]20
653-151,896,000 [191,000]18
605-1161 1,404,000 [139,000]13
≥15%753-5766,000 [80,000]7
702-4562,000 [58,000]5
650-3356,000 [36,000]4
601-2225,000 [22,000]3
≥20%751-2285,000 [30,000]2.8
701-2189,000 [20,000]2.1
650-1106,000 [11,000]1.4
600-157,000 [6,000]0.9
Start Printed Page 65315
Two or more decrements per season
≥10%757.5-121,730,000 [179,000]14
705.5-111,414,000 [145,000]13
651.3-8.81,023,000 [102,000]11
602.1-6.4741,000 [73,000]7.3
≥15%751.7-2.9391,000 [40,000]3.8
700.9-2.4276,000 [28,000]3.1
650.1-1.8168,000 [17,000]2.3
600.2-1.0101,000 [10,000]1.4
≥20%750.5-1.1128,000 [13,000]1.5
700.3-0.881,000 [8,000]1.1
650-0.543,000 [4,000]0.8
600-0.221,000 [2,000]0.4

Uncertainties in estimates of lung function risks are summarized in section II.C.3.a.ii of the proposal (79 FR 75275). In addition to the uncertainties noted for exposure estimates, an uncertainty which impacts lung function risk estimates stems from the lack of exposure-response information in children. In the near absence of controlled human exposure data for children, risk estimates are based on the assumption that children exhibit the same lung function response following O3 exposures as healthy 18 year olds (i.e., the youngest age for which controlled human exposure data is generally available) (U.S. EPA, 2014a, section 6.5.3). This assumption is justified in part by the findings of McDonnell et al. (1985), who reported that children (8-11 years old) experienced FEV1 responses similar to those observed in adults (18-35 years old) (U.S. EPA, 2014a, p. 3-10). In addition, as discussed in the ISA (U.S. EPA, 2013, section 6.2.1), summer camp studies of school-aged children reported O3-induced lung function decrements similar in magnitude to those observed in controlled human exposure studies using adults. In extending the risk model to children, the HREA thus fixes the age term in the model at its highest value, the value for age 18. Notwithstanding the information just summarized supporting this approach, EPA acknowledges the uncertainty involved, and notes that the approach could result in either over- or underestimates of O3-induced lung function decrements in children, depending on how children compare to the adults used in controlled human exposure studies (U.S. EPA, 2014a, section 6.5.3).

A related source of uncertainty is that the risk assessment estimates of O3-induced decrements in asthmatics used the exposure-response relationship developed from data collected from healthy individuals. Although the evidence has been mixed (U.S. EPA, 2013, section 6.2.1.1), several studies have reported statistically larger, or a tendency toward larger, O3-induced lung function decrements in asthmatics than in non-asthmatics (Kreit et al., 1989; Horstman et al., 1995; Jorres et al., 1996; Alexis et al., 2000). On this issue, CASAC noted that “[a]sthmatic subjects appear to be at least as sensitive, if not more sensitive, than non-asthmatic subjects in manifesting O3-induced pulmonary function decrements” (Frey, 2014c, p. 4). To the extent asthmatics experience larger O3-induced lung function decrements than the healthy adults used to develop exposure-response relationships, the HREA could underestimate the impacts of O3 exposures on lung function in asthmatics, including asthmatic children. The implications of this uncertainty for risk estimates remain unknown at this time (U.S. EPA, 2014a, section 6.5.4), and could depend on a variety of factors that have not been well-evaluated, including the severity of asthma and the prevalence of medication use. However, the available evidence shows responses to O3 increase with severity of asthma (Horstman et al., 1995) and corticosteroid usage does not prevent O3 effects on lung function decrements or respiratory symptoms in people with asthma (Vagaggini et al., 2001, 2007).

ii. Mortality and Morbidity Risk Assessments

As discussed in section II.C.3.b of the proposal (79 FR 75276), the HREA estimates O3-associated risks in 12 urban study areas [62] using concentration-response relationships drawn from epidemiologic studies. These concentration-response relationships are based on “area-wide” average O3 concentrations.[63] The HREA estimates risks for the years 2007 and 2009 in order to provide estimates of risk for a year with generally higher O3Start Printed Page 65316concentrations (2007) and a year with generally lower O3 concentrations (2009) (U.S. EPA, 2014a, section 7.1.1).

In considering the epidemiology-based risk estimates, the proposal focuses on mortality risks associated with short-term O3 concentrations. The proposal considers estimates of total risk (i.e., based on the full distributions of ambient O3 concentrations) and estimates of risk associated with O3 concentrations in the upper portions of ambient distributions. Both estimates are discussed to provide information that considers risk estimates based on concentration-response relationships being linear over the entire distribution of ambient O3 concentrations, and thus have the greater potential for morbidity and mortality to be affected by changes in relatively low O3 concentrations, as well as risk estimates that are associated with O3 concentrations in the upper portions of the ambient distribution, thus focusing on risk from higher O3 concentrations and placing greater weight on the uncertainty associated with the shapes of concentration-response curves for O3 concentrations in the lower portions of the distribution. These results for O3-associated mortality risk are summarized in Table 3 in the proposal (79 FR 75277).

Important uncertainties in epidemiology-based risk estimates, based on their consideration in the HREA and PA, are discussed in section II.C.3.b.ii of the proposal (79 FR 75277). Compared to estimates of O3 exposures of concern and estimates of O3-induced lung function decrements (discussed above), the HREA conclusions reflect lower confidence in epidemiologic-based risk estimates (U.S. EPA, 2014a, section 9.6). In particular, the HREA highlights the heterogeneity in effect estimates between locations, the potential for exposure measurement errors, and uncertainty in the interpretation of the shape of concentration-response functions at lower O3 concentrations (U.S. EPA, 2014a, section 9.6). The HREA also concludes that lower confidence should be placed in the results of the assessment of respiratory mortality risks associated with long-term O3, primarily because that analysis is based on only one study, though that study is well-designed, and because of the uncertainty in that study about the existence and identification of a potential threshold in the concentration-response function (U.S. EPA, 2014a, section 9.6).[64,65] This section further discusses some of the key uncertainties in epidemiologic-based risk estimates, as summarized in the PA (U.S. EPA, 2014c, section 3.2.3.2), with a focus on uncertainties that can have particularly important implications for the Administrator's consideration of epidemiology-based risk estimates.

The PA notes that reducing NOX emissions generally reduces O3-associated mortality and morbidity risk estimates in locations and time periods with relatively high ambient O3 concentrations and increases risk estimates in locations and time periods with relatively low concentrations (II.A, above). When evaluating uncertainties in epidemiologic risk estimates, the PA considered (1) the extent to which the modeled O3 response to reductions in NOX emissions appropriately represents the trends observed in monitored ambient O3 following actual reductions in NOX emissions, (2) the extent to which the O3 response to reductions in precursor emissions could differ with emissions reduction strategies that are different from those used in HREA to generate risk estimates, and (3) the extent to which estimated changes in risks in urban study areas are representative of the changes that would be experienced broadly across the U.S. population. The first two of these issues are discussed in section II.A.2.c above. The third issue is discussed below.

The HREA conducted national air quality modeling analyses that estimated the proportion of the U.S. population living in locations where seasonal averages of daily O3 concentrations are estimated to decrease in response to reductions in NOX emissions, and the proportion living in locations where such seasonal averages are estimated to increase. Given the close relationship between changes in seasonal averages of daily O3 concentrations and changes in seasonal mortality and morbidity risk estimates, this analysis informs consideration of the extent to which the risk results in urban study areas represent the U.S. population as a whole. This “representativeness analysis” indicates that the majority of the U.S. population lives in locations where reducing NOX emissions would be expected to result in decreases in warm season averages of daily maximum 8-hour ambient O3 concentrations. Because the HREA urban study areas tend to underrepresent the populations living in such areas (e.g., suburban, smaller urban, and rural areas), risk estimates for the urban study areas are likely to understate the average reductions in O3-associated mortality and morbidity risks that would be experienced across the U.S. population as a whole upon reducing NOX emissions (U.S. EPA, 2014a, section 8.2.3.2).

Section 7.4 of the HREA also highlights some additional uncertainties associated with epidemiologic-based risk estimates (U.S. EPA, 2014a). This section of the HREA identifies and discusses sources of uncertainty and presents a qualitative evaluation of key parameters that can introduce uncertainty into risk estimates (U.S. EPA, 2014a, Table 7-4). For several of these parameters, the HREA also presents quantitative sensitivity analyses (U.S. EPA, 2014a, sections 7.4.2 and 7.5.3). Of the uncertainties discussed in Chapter 7 of the HREA, those related to the application of concentration-response functions from epidemiologic studies can have particularly important implications for consideration of epidemiology-based risk estimates, as discussed below.

An important uncertainty is the shape of concentration-response functions at low ambient O3 concentrations (U.S. EPA, 2014a, Table 7-4).[66] In recognition of the ISA's conclusion that certainty in the shape of O3 concentration-response functions decreases at low ambient concentrations, the HREA provides estimates of epidemiology-based mortality risks for entire distributions of ambient O3 concentrations, as well as estimates of total mortality associated with various ambient O3 concentrations. The PA considers both types of risk estimates, recognizing greater public health concern for adverse O3-attributable effects at higher ambient O3 concentrations (which drive higher exposure concentrations, section 3.2.2 of the PA (U.S. EPA, 2014c)), as compared to lower concentrations.

A related consideration is associated with the public health importance of the increases in relatively low O3 concentrations following air quality adjustment. There is uncertainty that relates to the assumption that the concentration response function for O3 is linear, such that total risk estimates are equally influenced by decreasing Start Printed Page 65317high concentrations and increasing low concentrations, when the increases and decreases are of equal magnitude. Even on days with increases in relatively low area-wide average concentrations, resulting in increases in estimated risks, some portions of the urban study areas could experience decreases in high O3 concentrations. To the extent adverse O3-attributable effects are more strongly supported for higher ambient concentrations (which, as noted above, are consistently reduced upon air quality adjustment), the impacts on risk estimates of increasing low O3 concentrations reflect an important source of uncertainty. In addition to the uncertainties discussed above, the proposal also notes uncertainties related to (1) using concentration-response relationships developed for a particular population in a particular location to estimate health risks in different populations and locations; (2) using concentration-response functions from epidemiologic studies reflecting a particular air quality distribution to adjusted air quality necessarily reflecting a different (simulated) air quality distribution; (3) using a national concentration-response function to estimate respiratory mortality associated with long-term O3; and (4) unquantified reductions in risk that could be associated with reductions in the ambient concentrations of pollutants other than O3, resulting from control of NOX (79 FR 75277 to 75279).

B. Need for Revision of the Primary Standard

The initial issue to be addressed in the current review of the primary O3 standard is whether, in view of the advances in scientific knowledge and additional information, it is appropriate to revise the existing standard. This section presents the Administrator's final decision on whether it is “appropriate” to revise the current standard within the meaning of section 109 (d)(1) of the CAA. Section II.B.1 contains a summary discussion of the basis for the proposed conclusions on the adequacy of the primary standard. Section II.B.2 discusses comments received on the adequacy of the primary standard. Section II.B.3 presents the Administrator's final conclusions on the adequacy of the current primary standard.

1. Basis for Proposed Decision

In evaluating whether it is appropriate to retain or revise the current standard, the Administrator's considerations build upon those in the 2008 review, including consideration of the broader body of scientific evidence and exposure and health risk information now available, as summarized in sections II.A to II.C (79 FR 75246-75279) of the proposal and section II.A above.

In developing conclusions on the adequacy of the current primary O3 standard, the Administrator takes into account both evidence-based and quantitative exposure- and risk-based considerations. Evidence-based considerations include the assessment of evidence from controlled human exposure, animal toxicological, and epidemiologic studies for a variety of health endpoints. The Administrator focuses on health endpoints for which the evidence is strong enough to support a “causal” or a “likely to be causal” relationship, based on the ISA's integrative synthesis of the entire body of evidence. The Administrator's consideration of quantitative exposure and risk information draws from the results of the exposure and risk assessments presented in the HREA.

The Administrator's consideration of the evidence and exposure/risk information is informed by the considerations and conclusions presented in the PA (U.S. EPA, 2014c). The purpose of the PA is to help “bridge the gap” between the scientific and technical information assessed in the ISA and HREA, and the policy decisions that are required of the Administrator (U.S. EPA, 2014c, Chapter 1); see also American Farm Bureau Federation, 559 F. 3d at 516, 521 (“[a]lthough not required by the statute, in practice EPA staff also develop a Staff Paper, which discusses the information in the Criteria Document that is most relevant to the policy judgments the EPA makes when it sets the NAAQS”). The PA's evidence-based and exposure-/risk-based considerations and conclusions are briefly summarized below in sections II.B.1.a (evidence-based considerations), II.B.1.b (exposure- and risk-based considerations), and II.B.1.c (PA conclusions on the current standard). Section II.B.1.d summarizes CASAC advice to the Administrator and public commenter views on the current standard. Section II.B.1.e presents a summary of the Administrator's proposed conclusions concerning the adequacy of the public health protection provided by the current standard, and her proposed decision to revise that standard.

a. Evidence-Based Considerations From the PA

In considering the available scientific evidence, the PA evaluates the O3 concentrations in health effects studies (U.S. EPA, 2014c, section 3.1.4). Specifically, the PA characterizes the extent to which health effects have been reported for the O3 exposure concentrations evaluated in controlled human exposure studies, and effects occurring over the distributions of ambient O3 concentrations in locations where epidemiologic studies have been conducted. These considerations, as they relate to the adequacy of the current standard, are presented in detail in section 3.1.4 of the PA (U.S. EPA, 2014c) and are summarized in the proposal (79 FR 75279-75287). The PA's considerations are summarized briefly below for controlled human exposure, epidemiologic panel studies, and epidemiologic population-based studies.

Section II.D.1.a of the proposal discusses the PA's consideration of the evidence from controlled human exposure and panel studies. This evidence is assessed in section 6.2 of the ISA (U.S. EPA, 2013) and is summarized in section 3.1.2 of the PA (U.S. EPA, 2014c). A large number of controlled human exposure studies have reported lung function decrements, respiratory symptoms, air inflammation, airway hyperresponsiveness, and/or impaired lung host defense in young, healthy adults engaged in moderate quasi-continuous exertion, following 6.6-hour O3 exposures. These studies have consistently reported such effects following exposures to O3 concentrations of 80 ppb or greater. In addition to lung function decrements, available studies have evaluated respiratory symptoms or airway inflammation following exposures to O3 concentrations below 75 ppb. Table 3-1 in the PA highlights the group mean results of individual controlled human exposure studies that evaluated exposures to O3 concentrations below 75 ppb. These studies observe the combination of lung function decrements and respiratory symptoms following exposures to O3 concentrations as low as 72 ppb, and lung function decrements and airway inflammation following exposures to O3 concentrations as low as 60 ppb (based on group means).

Based on this evidence, the PA notes that controlled human exposure studies have reported a variety of respiratory effects in young, healthy adults following exposures to a wide range of O3 concentrations for 6.6 hours, including exposures to concentrations below 75 ppb. In particular, the PA further notes that a recent controlled human exposure study reported the combination of lung function decrements and respiratory symptoms in healthy adults engaged in quasi-Start Printed Page 65318continuous, moderate exertion following 6.6 hour exposures to 72 ppb O3, a combination of effects that have been classified as adverse based on ATS guidelines for adversity (ATS, 2000a). In addition, a recent study has also reported lung function decrements and pulmonary inflammation following exposure to 60 ppb O3. Sixty ppb is the lowest exposure concentration for which inflammation has been evaluated and reported to occur, and corresponds to the lowest exposure concentration demonstrated to result in lung function decrements large enough to be judged an abnormal response by ATS (ATS, 2000b). The PA also notes, and CASAC agreed, that these controlled human exposure studies were conducted in healthy adults, while at-risk groups (e.g., children, people with asthma) could experience larger and/or more serious effects. Therefore, the PA concludes that the evidence from controlled human exposure studies provide support that the respiratory effects experienced following exposures to O3 concentrations lower than 75 ppb would be adverse in some individuals, particularly if experienced by members of at-risk populations (e.g., people with asthma, children).

The PA also notes consistent results in some panel studies of O3-associated lung function decrements. In particular, the PA notes that epidemiologic panel studies in children and adults consistently indicate O3-associated lung function decrements when on-site, ambient monitored concentrations were below 75 ppb (although the evidence becomes less consistent at low O3 concentrations, and the averaging periods involved ranged from 10 minutes to 12 hours (U.S. EPA, 2014c, section 3.2.4.2)).

Section II.D.1.b of the proposal summarizes the PA's analyses of monitored O3 concentrations in locations of epidemiologic studies. While the majority of the epidemiologic study areas evaluated would have violated the current standard during study periods, the PA makes the following observations with regard to health effect associations at O3 concentrations likely to have met the current standard:

(1) A single-city study reported positive and statistically significant associations with asthma emergency department visits in children and adults in Seattle, a location that would have met the current standard over the entire study period (Mar and Koenig, 2009).

(2) Additional single-city studies support associations with respiratory morbidity at relatively low ambient O3 concentrations, including when virtually all monitored concentrations were below the level of the current standard (Silverman and Ito, 2010; Strickland et al., 2010).

(3) Canadian multicity studies reported positive and statistically significant associations with respiratory morbidity or mortality when the majority of study cities, though not all study cities, would have met the current standard over the study period in each of these studies (Cakmak et al., 2006; Dales et al., 2006; Katsouyanni et al., 2009; Stieb et al., 2009).

(4) A U.S. multicity study reported positive and statistically significant associations with mortality when ambient O3 concentrations were restricted to those likely to have met the current O3 standard (Bell et al., 2006).

The PA also takes into account important uncertainties in these analyses of air quality in locations of epidemiologic study areas. These uncertainties are summarized in section II.D.1.b.iii of the proposal. Briefly, they include the following: (1) Uncertainty in conclusions about the extent to which multicity effect estimates reflect associations with air quality meeting the current standard, versus air quality violating that standard; (2) uncertainty regarding the potential for thresholds to exist, given that regional heterogeneity in O3 health effect associations could obscure the presence of thresholds, should they exist; (3) uncertainty in the extent to which the PA appropriately recreated the air quality analyses in the published study by Bell et al. (2006); and (4) uncertainty in the extent to which reported health effects are caused by exposures to O3 itself, as opposed to other factors such as co-occurring pollutants or pollutant mixtures, particularly at low ambient O3 concentrations.[67]

In considering the analyses of monitored O3 air quality in locations of epidemiologic studies, as well as the important uncertainties in these analyses, the PA concludes that these analyses provide support for the occurrence of morbidity and mortality associated with short-term ambient O3 concentrations likely to meet the current O3 standard.[68] In considering the evidence as a whole, the PA concludes that (1) controlled human exposure studies provide strong support for the occurrence of adverse respiratory effects following exposures to O3 concentrations below the level of the current standard and (2) epidemiologic studies provide support for the occurrence of adverse respiratory effects and mortality under air quality conditions that would meet the current standard.

b. Exposure- and Risk-Based Considerations in the PA

In order to further inform judgments about the potential public health implications of the current O3 NAAQS, the PA considers the exposure and risk assessments presented in the HREA (U.S. EPA, 2014c, section 3.2). Overviews of these exposure and risk assessments, including brief summaries of key results and uncertainties, are provided in section II.A.2 above. Section II.D.2 of the proposal summarizes key observations from the PA related to the adequacy of the current O3 NAAQS, based on consideration of the HREA exposure assessment, lung function risk assessment, and mortality/morbidity risk assessments (79 FR 75283).

Section II.D.2.a of the proposal summarizes key observations from the PA regarding estimates of O3 exposures of concern (79 FR 75283). Given the evidence for respiratory effects from controlled human exposure studies, the PA considers the extent to which the current standard would be estimated to protect at-risk populations against exposures of concern to O3 concentrations at or above the health benchmark concentrations of 60, 70, and 80 ppb (i.e., based on HREA estimates of one or more and two or more exposures of concern). In doing so, the PA notes the CASAC conclusion that (Frey, 2014c, p. 6):

The 80 ppb-8hr benchmark level represents an exposure level for which there is substantial clinical evidence demonstrating a range of ozone-related effects including lung inflammation and airway responsiveness in healthy individuals. The 70 ppb-8hr benchmark level reflects the fact that in healthy subjects, decreases in lung function and respiratory symptoms occur at concentrations as low as 72 ppb and that these effects almost certainly occur in some people, including asthmatics and others with low lung function who are less tolerant of such effects, at levels of 70 ppb and below. The 60 ppb-8hr benchmark level represents the lowest exposure level at which ozone-Start Printed Page 65319related effects have been observed in clinical studies of healthy individuals.

For exposures of concern at or above 60 ppb, the proposal highlights the following key observations for air quality adjusted to just meet the current standard:

(1) On average over the years 2006 to 2010, the current standard is estimated to allow approximately 10 to 18% of children in urban study areas to experience one or more exposures of concern at or above 60 ppb. Summing across urban study areas, these percentages correspond to almost 2.5 million children experiencing approximately 4 million exposures of concern at or above 60 ppb during a single O3 season. Of these children, almost 250,000 are asthmatics.[69]

(2) On average over the years 2006 to 2010, the current standard is estimated to allow approximately 3 to 8% of children in urban study areas to experience two or more exposures of concern to O3 concentrations at or above 60 ppb. Summing across the urban study areas, these percentages correspond to almost 900,000 children (including almost 90,000 asthmatic children).

(3) In the worst-case years (i.e., those with the largest exposure estimates), the current standard is estimated to allow approximately 10 to 25% of children to experience one or more exposures of concern at or above 60 ppb, and approximately 4 to 14% to experience two or more exposures of concern at or above 60 ppb.

For exposures of concern at or above 70 ppb, the PA highlights the following key observations for air quality adjusted to just meet the current standard:

(1) On average over the years 2006 to 2010, the current standard is estimated to allow up to approximately 3% of children in urban study areas to experience one or more exposures of concern at or above 70 ppb. Summing across urban study areas, almost 400,000 children (including almost 40,000 asthmatic children) are estimated to experience O3 exposure concentrations at or above 70 ppb during a single O3 season.

(2) On average over the years 2006 to 2010, the current standard is estimated to allow less than 1% of children in urban study areas to experience two or more exposures of concern to O3 concentrations at or above 70 ppb.

(3) In the worst-case location and year, the current standard is estimated to allow approximately 8% of children to experience one or more exposures of concern at or above 70 ppb, and approximately 2% to experience two or more exposures of concern, at or above 70 ppb.

For exposures of concern at or above 80 ppb, the PA highlights the observation that the current standard is estimated to allow about 1% or fewer children in urban study areas to experience exposures of concern at or above 80 ppb, even in years with the highest exposure estimates.

Uncertainties in exposure estimates are summarized in section II.C.2.b of the proposal (79 FR 75273), and discussed more fully in the HREA (U.S. EPA, 2014a, section 5.5.2) and the PA (U.S. EPA, 2014c, section 3.2.2). Key uncertainties include the variability in responsiveness following O3 exposures, resulting in only a subset of exposed individuals experiencing health effects, adverse or otherwise, and the limited evidence from controlled human exposure studies conducted in at-risk populations. In addition, there are a number of uncertainties in the exposure modelling approach used in the HREA, contributing to overall uncertainty in exposure estimates.

Section II.D.2.b of the proposal summarizes key observations from the PA regarding the estimated risk of O3-induced lung function decrements (79 FR 75283 to 75284). With respect to the lung function decrements that have been evaluated in controlled human exposure studies, the PA considers the extent to which standards with revised levels would be estimated to protect healthy and at-risk populations against one or more, and two or more, moderate (i.e., FEV1 decrements ≥10% and ≥15%) and large (i.e., FEV1 decrements ≥20%) lung function decrements. As discussed in section 3.1.3 of the PA (U.S. EPA, 2014c), although 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 moderate lung function decrements emerges as the frequency of occurrence increases.

With regard to decrements ≥10%, the PA highlights the following key observations for air quality adjusted to just meet the current standard:

(1) On average over the years 2006 to 2010, the current standard is estimated to allow approximately 14 to 19% of children in urban study areas to experience one or more lung function decrements ≥10%. Summing across urban study areas, this corresponds to approximately 3 million children experiencing 15 million O3-induced lung function decrements ≥10% during a single O3 season. Of these children, about 300,000 are asthmatics.

(2) On average over the years 2006 to 2010, the current standard is estimated to allow approximately 7 to 12% of children in urban study areas to experience two or more O3-induced lung function decrements ≥10%. Summing across the urban study areas, this corresponds to almost 2 million children (including almost 200,000 asthmatic children) estimated to experience two or more O3-induced lung function decrements greater than 10% during a single O3 season.

(3) In the worst-case years, the current standard is estimated to allow approximately 17 to 23% of children in urban study areas to experience one or more lung function decrements ≥10%, and approximately 10 to 14% to experience two or more O3-induced lung function decrements ≥10%.

With regard to decrements ≥15%, the PA highlights the following key observations for air quality adjusted to just meet the current standard:

(1) On average over the years 2006 to 2010, the current standard is estimated to allow approximately 3 to 5% of children in urban study areas to experience one or more lung function decrements ≤15%. Summing across urban study areas, this corresponds to approximately 800,000 children (including approximately 80,000 asthmatic children) estimated to experience at least one O3-induced lung function decrement ≤15% during a single O3 season.

(2) On average over the years 2006 to 2010, the current standard is estimated to allow approximately 2 to 3% of children in urban study areas to experience two or more O3-induced lung function decrements ≤15%.

(3) In the worst-case years, the current standard is estimated to allow approximately 4 to 6% of children in urban study areas to experience one or more lung function decrements ≤15%, and approximately 2 to 4% to experience two or more O3-induced lung function decrements ≤15%.

With regard to decrements ≤20%, the PA highlights the following key observations for air quality adjusted to just meet the current standard:

(1) On average over the years 2006 to 2010, the current standard is estimated to allow approximately 1 to 2% of children in urban study areas to experience one or more lung function decrements ≥20%. Summing across Start Printed Page 65320urban study areas, this corresponds to approximately 300,000 children (including approximately 30,000 asthmatic children) estimated to experience at least one O3-induced lung function decrement ≥20% during a single O3 season.

(2) On average over the years 2006 to 2010, the current standard is estimated to allow less than 1% of children in urban study areas to experience two or more O3-induced lung function decrements ≥20%.

(3) In the worst-case years, the current standard is estimated to allow approximately 2 to 3% of children to experience one or more lung function decrements ≥20%, and less than 2% to experience two or more O3-induced lung function decrements ≥20%.

Uncertainties in lung function risk estimates are summarized in section II.C.3.a of the proposal, and discussed more fully in the HREA (U.S. EPA, 2014a, section 6.5) and the PA (U.S. EPA, 2014c, section 3.2.3.1). In addition to the uncertainties noted above for exposure estimates, the key uncertainties associated with estimates of O3-induced lung function decrements include the paucity of exposure-response information in children and in people with asthma.

Section II.D.2.c of the proposal summarizes key observations from the PA regarding risk estimates of O3-associated mortality and morbidity (79 FR 75284 to 75285). With regard to total mortality or morbidity associated with short-term O3, the PA notes the following for air quality adjusted to just meet the current standard:

(1) When air quality was adjusted to the current standard for the 2007 model year (the year with generally “higher” O3-associated risks), 10 of 12 urban study areas exhibited either decreases or virtually no change in estimates of the number of O3-associated deaths (U.S. EPA, 2014a, Appendix 7B). Increases were estimated in two of the urban study areas (Houston, Los Angeles)[70] (U.S. EPA, 2014a, Appendix 7B).[71]

(2) In focusing on total risk, the current standard is estimated to allow thousands of O3-associated deaths per year in the urban study areas. In focusing on the risks associated with the upper portions of distributions of ambient concentrations (area-wide concentrations ≤ 40, 60 ppb), the current standard is estimated to allow hundreds to thousands of O3-associated deaths per year in the urban study areas.

(3) The current standard is estimated to allow tens to thousands of O3-associated morbidity events per year (i.e., respiratory-related hospital admissions, emergency department visits, and asthma exacerbations).

With regard to respiratory mortality associated with long-term O3, the PA notes the following for air quality adjusted to just meet the current standard:

(1) Based on a linear concentration-response function, the current standard is estimated to allow thousands of O3-associated respiratory deaths per year in the urban study areas.

(2) Based on threshold models, HREA sensitivity analyses indicate that the number of respiratory deaths associated with long-term O3 concentrations could potentially be considerably lower (i.e., by more than 75% if a threshold exists at 40 ppb, and by about 98% if a threshold exists at 56 ppb) (U.S. EPA, 2014a, Figure 7-9).[72]

Compared to the weight given to HREA estimates of exposures of concern and lung function risks, and the weight given to the evidence, the PA places relatively less weight on epidemiologic-based risk estimates. In doing so, the PA notes that the overall conclusions from the HREA likewise reflect less confidence in estimates of epidemiologic-based risks than in estimates of exposures and lung function risks. The determination to attach less weight to the epidemiologic-based estimates reflects the uncertainties associated with mortality and morbidity risk estimates, including the heterogeneity in effect estimates between locations, the potential for exposure measurement errors, and uncertainty in the interpretation of the shape of concentration-response functions at lower O3 concentrations (U.S. EPA, 2014a, section 9.6).

Uncertainty in the shape of concentration-response functions at lower O3 concentrations is particularly important to interpreting risk estimates given the approach used to adjust air quality to just meet the current standard, and potential alternative standards, and the resulting compression in the air quality distributions (i.e., decreasing high concentrations and increasing low concentrations) (II.A.2.a, above). Total risk estimates in the HREA are based on the assumption that the concentration response function for O3 is linear, such that total risk estimates are equally influenced by decreasing high concentrations and increasing low concentrations, when the increases and decreases are of equal magnitude. However, consistent with the PA's consideration of risk estimates, in the proposal the Administrator notes that the overall body of evidence provides stronger support for the occurrence of Start Printed Page 65321O3-attributable health effects following exposures to O3 concentrations corresponding to the upper ends of typical ambient distributions (II.E.4.d of the proposal). In addition, even on days with increases in relatively low area-wide average concentrations, resulting in increases in estimated risks, some portions of the urban study areas could experience decreases in high O3 concentrations. Therefore, to the extent adverse O3-attributable effects are more strongly supported for higher ambient concentrations (which, as noted above, are consistently reduced upon air quality adjustment), the PA notes that the impacts on risk estimates of increasing low O3 concentrations reflect an important source of uncertainty.

c. PA Conclusions on the Current Standard

Section II.D.3 of the proposal summarizes the PA conclusions on the adequacy of the existing primary O3 standard (79 FR 75285). As an initial matter, the PA concludes that reducing precursor emissions to achieve O3 concentrations that meet the current standard will provide important improvements in public health protection. This initial conclusion is based on (1) the strong body of scientific evidence indicating a wide range of adverse health outcomes attributable to exposures to O3 concentrations commonly found in the ambient air and (2) estimates indicating decreased occurrences of O3 exposures of concern and decreased health risks upon meeting the current standard, compared to recent air quality.

In particular, the PA concludes that strong support for this initial conclusion is provided by controlled human exposure studies of respiratory effects, and by quantitative estimates of exposures of concern and lung function decrements based on information in these studies. Analyses in the HREA estimate that the percentages of children (i.e., all children and children with asthma) in urban study areas experiencing exposures of concern, or experiencing abnormal and potentially adverse lung function decrements, are consistently lower for air quality that just meets the current O3 standard than for recent air quality. The HREA estimates such reductions consistently across the urban study areas evaluated and throughout various portions of individual urban study areas, including in urban cores and the portions of urban study areas surrounding urban cores. These reductions in exposures of concern and O3-induced lung function decrements reflect the consistent decreases in the highest O3 concentrations following reductions in precursor emissions to meet the current standard. Thus, populations in both urban and non-urban areas would be expected to experience important reductions in O3 exposures and O3-induced lung function risks upon meeting the current standard.

The PA further concludes that support for this initial conclusion is also provided by estimates of O3-associated mortality and morbidity based on application of concentration-response relationships from epidemiologic studies to air quality adjusted to just meet the current standard. These estimates are based on the assumption that concentration-response relationships are linear over entire distributions of ambient O3 concentrations, an assumption which has uncertainties that complicate interpretation of these estimates (II.A.2.c.ii). However, risk estimates for effects associated with short- and long-term O3 exposures, combined with the HREA's national analysis of O3 responsiveness to reductions in precursor emissions and the consistent reductions estimated for the highest ambient O3 concentrations, suggest that O3-associated mortality and morbidity would be expected to decrease nationwide following reductions in precursor emissions to meet the current O3 standard.

After reaching the initial conclusion that meeting the current primary O3 standard will provide important improvements in public health protection, and that it is not appropriate to consider a standard that is less protective than the current standard, the PA considers the adequacy of the public health protection that is provided by the current standard. In considering the available scientific evidence, exposure/risk information, advice from CASAC (II.B.1.d, below), and input from the public, the PA reaches the conclusion that the available evidence and information clearly call into question the adequacy of public health protection provided by the current primary standard. In reaching this conclusion, the PA notes that evidence from controlled human exposure studies provides strong support for the occurrence of adverse respiratory effects following exposures to O3 concentrations below the level of the current standard. Epidemiologic studies provide support for the occurrence of adverse respiratory effects and mortality under air quality conditions that would likely meet the current standard. In addition, based on the analyses in the HREA, the PA concludes that the exposures and risks projected to remain upon meeting the current standard are indicative of risks that can reasonably be judged to be important from a public health perspective. Thus, the PA concludes that the evidence and information provide strong support for giving consideration to revising the current primary standard in order to provide increased public health protection against an array of adverse health effects that range from decreased lung function and respiratory symptoms to more serious indicators of morbidity (e.g., including emergency department visits and hospital admissions), and mortality. In consideration of all of the above, the PA draws the conclusion that it is appropriate for the Administrator to consider revision of the current primary O3 standard to provide increased public health protection.

d. CASAC Advice

Section II.D.4 of the proposal summarizes CASAC advice regarding the adequacy of the existing primary O3 standard. Following the 2008 decision to revise the primary O3 standard by setting the level at 0.075 ppm (75 ppb), CASAC strongly questioned whether the standard met the requirements of the CAA. In September 2009, the EPA announced its intention to reconsider the 2008 standards, issuing a notice of proposed rulemaking in January 2010 (75 FR 2938). Soon after, the EPA solicited CASAC review of that proposed rule and in January 2011, solicited additional advice. This proposal was based on the scientific and technical record from the 2008 rulemaking, including public comments and CASAC advice and recommendations. As further described above (I.D), in the fall of 2011, the EPA did not revise the standard as part of the reconsideration process but decided to defer decisions on revisions to the O3 standards to the next periodic review, which was already underway. Accordingly, in this section we describe CASAC's advice related to the 2008 final decision and the subsequent reconsideration, as well as its advice on this current review of the O3 NAAQS that was initiated in September 2008.

In April 2008, the members of the CASAC Ozone Review Panel sent a letter to EPA stating “[I]n our most-recent letters to you on this subject—dated October 2006 and March 2007—the CASAC unanimously recommended selection of an 8-hour average Ozone NAAQS within the range of 0.060 to 0.070 parts per million [60 to 70 ppb] for the primary (human health-based) Ozone NAAQS” (Henderson, 2008). In 2010, in response to the EPA's solicitation of advice on the EPA's Start Printed Page 65322proposed rulemaking as part of the reconsideration, CASAC again stated that the current standard should be revised to provide additional protection to the public health (Samet, 2010):

CASAC fully supports EPA's proposed range of 0.060-0.070 parts per million (ppm) for the 8-hour primary ozone standard. CASAC considers this range to be justified by the scientific evidence as presented in the Air Quality Criteria for Ozone and Related Photochemical Oxidants (March 2006) and Review of the National Ambient Air Quality Standards for Ozone: Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper (July 2007). As stated in our letters of October 24, 2006, March 26, 2007 and April 7, 2008 to former Administrator Stephen L. Johnson, CASAC unanimously recommended selection of an 8-hour average ozone NAAQS within the range proposed by EPA (0.060 to 0.070 ppm). In proposing this range, EPA has recognized the large body of data and risk analyses demonstrating that retention of the current standard would leave large numbers of individuals at risk for respiratory effects and/or other significant health impacts including asthma exacerbations, emergency room visits, hospital admissions and mortality.

In response to the EPA's request for additional advice on the reconsideration in 2011, CASAC reaffirmed their conclusion that “the evidence from controlled human and epidemiological studies strongly supports the selection of a new primary ozone standard within the 60-70 ppb range for an 8-hour averaging time” (Samet, 2011, p ii). As requested by the EPA, CASAC's advice and recommendations were based on the scientific and technical record from the 2008 rulemaking. In considering the record for the 2008 rulemaking, CASAC stated the following to summarize the basis for their conclusions (Samet, 2011, pp. ii to iii):

(1) The evidence available on dose-response for effects of O3 shows associations extending to levels within the range of concentrations currently experienced in the United States.

(2) There is scientific certainty that 6.6-hour exposures with exercise of young, healthy, non-smoking adult volunteers to concentrations ≥80 ppb cause clinically relevant decrements of lung function.

(3) Some healthy individuals have been shown to have clinically relevant responses, even at 60 ppb.

(4) Since the majority of clinical studies involve young, healthy adult populations, less is known about health effects in such potentially ozone sensitive populations as the elderly, children and those with cardiopulmonary disease. For these susceptible groups, decrements in lung function may be greater than in healthy volunteers and are likely to have a greater clinical significance.

(5) Children and adults with asthma are at increased risk of acute exacerbations on or shortly after days when elevated O3 concentrations occur, even when exposures do not exceed the NAAQS concentration of 75 ppb.

(6) Large segments of the population fall into what the EPA terms a “sensitive population group,” i.e., those at increased risk because they are more intrinsically susceptible (children, the elderly, and individuals with chronic lung disease) and those who are more vulnerable due to increased exposure because they work outside or live in areas that are more polluted than the mean levels in their communities.

With respect to evidence from epidemiologic studies, CASAC stated “while epidemiological studies are inherently more uncertain as exposures and risk estimates decrease (due to the greater potential for biases to dominate small effect estimates), specific evidence in the literature does not suggest that our confidence on the specific attribution of the estimated effects of ozone on health outcomes differs over the proposed range of 60-70 ppb” (Samet, 2011, p. 10).

Following its review of the second draft PA in the current review, which considers an updated scientific and technical record since the 2008 rulemaking, CASAC concluded that “there is clear scientific support for the need to revise the standard” (Frey, 2014c, p. ii). In particular, CASAC noted the following (Frey, 2014c, p. 5):

[T]he scientific evidence provides strong support for the occurrence of a range of adverse respiratory effects and mortality under air quality conditions that would meet the current standard. Therefore, CASAC unanimously recommends that the Administrator revise the current primary ozone standard to protect public health.[73]

In supporting these conclusions, CASAC judged that the strongest evidence comes from controlled human exposure studies of respiratory effects. The Committee specifically noted that “the combination of decrements in FEV1 together with the statistically significant alterations in symptoms in human subjects exposed to 72 ppb ozone meets the American Thoracic Society's definition of an adverse health effect” (Frey, 2014c, p. 5). CASAC further judged that “if subjects had been exposed to ozone using the 8-hour averaging period used in the standard, adverse effects could have occurred at lower concentration” and that “the level at which adverse effects might be observed would likely be lower for more sensitive subgroups, such as those with asthma” (Frey, 2014c, p. 5). With regard to 60 ppb exposures, CASAC noted that “a level of 60 ppb corresponds to the lowest exposure concentration demonstrated to result in lung function decrements large enough to be judged an abnormal response by ATS and that could be adverse in individuals with lung disease” (Frey, 2014c, p. 7). The CASAC further noted that “a level of 60 ppb also corresponds to the lowest exposure concentration at which pulmonary inflammation has been reported” (Frey, 2014c, p. 7).

In their advice, CASAC also took note of estimates of O3 exposures of concern and the risk of O3-induced lung function decrements. With regard to the benchmark concentrations used in estimating exposures of concern, CASAC stated the following (Frey, 2014c, p. 6):

The 80 ppb-8hr benchmark level represents an exposure level for which there is substantial clinical evidence demonstrating a range of ozone-related effects including lung inflammation and airway responsiveness in healthy individuals. The 70 ppb-8hr benchmark level reflects the fact that in healthy subjects, decreases in lung function and respiratory symptoms occur at concentrations as low as 72 ppb and that these effects almost certainly occur in some people, including asthmatics and others with low lung function who are less tolerant of such effects, at levels of 70 ppb and below. The 60 ppb-8hr benchmark level represents the lowest exposure level at which ozone-related effects have been observed in clinical studies of healthy individuals. Based on its scientific judgment, the CASAC finds that the 60 ppb-8hr exposure benchmark is relevant for consideration with respect to adverse effects on asthmatics.

With regard to lung function risk estimates, CASAC concluded that “estimation of FEV1 decrements of ≥15% is appropriate as a scientifically relevant surrogate for adverse health outcomes in active healthy adults, whereas an FEV1 decrement of ≥10% is a scientifically relevant surrogate for adverse health outcomes for people with asthma and lung disease” (Frey, 2014c, p. 3). The Committee further concluded that “[a]sthmatic subjects appear to be at least as sensitive, if not more sensitive, than non-asthmatic subjects in manifesting O3-induced pulmonary function decrements” (Frey, 2014c, p. 4).

Although CASAC judged that controlled human exposure studies of respiratory effects provide the strongest Start Printed Page 65323evidence supporting their conclusion on the current standard, the Committee judged that there is also “sufficient scientific evidence based on epidemiologic studies for mortality and morbidity associated with short-term exposure to ozone at the level of the current standard” (Frey, 2014c, p. 5) and noted that “[r]ecent animal toxicological studies support identification of modes of action and, therefore, the biological plausibility associated with the epidemiological findings” (Frey, 2014c, p. 5).

e. Administrator's Proposed Decision

Section II.D.5 in the proposal (79 FR 75287-75291) discusses the Administrator's proposed conclusions related to the adequacy of the public health protection provided by the current primary O3 standard, resulting in her proposed decision to revise that standard. These proposed conclusions and her proposed decision, summarized below, were based on the Administrator's consideration of the available scientific evidence, exposure/risk information, the comments and advice of CASAC, and public input that had been received by the time of proposal.

As an initial matter, the Administrator concluded that reducing precursor emissions to achieve O3 concentrations that meet the current primary O3 standard will provide important improvements in public health protection, compared to recent air quality. In reaching this initial conclusion, she noted the discussion in section 3.4 of the PA (U.S. EPA, 2014c). In particular, the Administrator noted that this initial conclusion is supported by (1) the strong body of scientific evidence indicating a wide range of adverse health outcomes attributable to exposures to O3 concentrations commonly measured in the ambient air and (2) estimates indicating decreased occurrences of O3 exposures of concern and decreased O3-associated health risks upon meeting the current standard, compared to recent air quality. Thus, she concluded that it would not be appropriate in this review to consider a standard that is less protective than the current standard.[74]

After reaching the initial conclusion that meeting the current primary O3 standard will provide important improvements in public health protection, and that it is not appropriate to consider a standard that is less protective than the current standard, the Administrator next considered the adequacy of the public health protection that is provided by the current standard. In doing so, the Administrator first noted that studies evaluated since the completion of the 2006 AQCD support and expand upon the strong body of evidence that, in the last review, indicated a causal relationship between short-term O3 exposures and respiratory health effects, the strongest determination under the ISA's hierarchical system for classifying weight of evidence for causation. Together, experimental and epidemiologic studies support conclusions regarding a continuum of O3 respiratory effects ranging from small reversible changes in pulmonary function, and pulmonary inflammation, to more serious effects that can result in respiratory-related emergency department visits, hospital admissions, and premature mortality. The Administrator further noted that recent animal toxicology studies support descriptions of modes of action for these respiratory effects and provide support for biological plausibility for the role of O3 in reported effects. With regard to mode of action, evidence indicates that antioxidant capacity may modify the risk of respiratory morbidity associated with O3 exposure, and that the inherent capacity to quench (based on individual antioxidant capacity) can be overwhelmed, especially with exposure to elevated concentrations of O3. In addition, based on the consistency of findings across studies and evidence for the coherence of results from different scientific disciplines, evidence indicates that certain populations are at increased risk of experiencing O3-related effects, including the most severe effects. These include populations and lifestages identified in previous reviews (i.e., people with asthma, children, older adults, outdoor workers) and populations identified since the last review (i.e., people with certain genotypes related to antioxidant and/or anti-inflammatory status; people with reduced intake of certain antioxidant nutrients, such as Vitamins C and E).

The Administrator further noted that evidence for adverse respiratory health effects attributable to long-term [75] O3 exposures is much stronger than in previous reviews, and noted the ISA's conclusion that there is “likely to be” a causal relationship between such O3 exposures and adverse respiratory health effects (the second strongest causality determination). She noted that the evidence available in this review includes new epidemiologic studies using a variety of designs and analysis methods, conducted by different research groups in different locations, evaluating the relationships between long-term O3 exposures and measures of respiratory morbidity and mortality. New evidence supports associations between long-term O3 exposures and the development of asthma in children, with several studies reporting interactions between genetic variants and such O3 exposures. Studies also report associations between long-term O3 exposures and asthma prevalence, asthma severity and control, respiratory symptoms among asthmatics, and respiratory mortality.

In considering the O3 exposure concentrations reported to elicit respiratory effects, the Administrator agreed with the conclusions of the PA and with the advice of CASAC (Frey, 2014c) that controlled human exposure studies provide the most certain evidence indicating the occurrence of health effects in humans following exposures to specific O3 concentrations. In particular, she noted that the effects reported in controlled human exposure studies are due solely to O3 exposures, and interpretation of study results is not complicated by the presence of co-occurring pollutants or pollutant mixtures.

In considering the evidence from controlled human exposure studies, the Administrator first noted that these studies have reported a variety of respiratory effects in healthy adults following exposures to O3 concentrations of 60, 72, or 80 ppb, and higher. The largest respiratory effects, and the broadest range of effects, have been studied and reported following exposures of healthy adults to 80 ppb O3 or higher, with most exposure studies conducted at these higher concentrations. She further noted that recent evidence includes controlled human exposure studies reporting the combination of lung function decrements and respiratory symptoms in healthy adults engaged in quasi-continuous, moderate exertion following 6.6 hour exposures to concentrations as low as 72 ppb, and lung function decrements and Start Printed Page 65324pulmonary inflammation following exposures to O3 concentrations as low as 60 ppb. As discussed below, compared to the evidence available in the last review, the Administrator viewed these studies as having strengthened support for the occurrence of abnormal and adverse respiratory effects attributable to short-term exposures to O3 concentrations below the level of the current standard. The Administrator stated that such exposures to O3 concentrations below the level of the current standard are potentially important from a public health perspective, given the following:

(1) The combination of lung function decrements and respiratory symptoms reported to occur in healthy adults following exposures to 72 ppb O3 or higher, while at moderate exertion, meet ATS criteria for an adverse response. In specifically considering the 72 ppb exposure concentration, CASAC noted that “the combination of decrements in FEV1 together with the statistically significant alterations in symptoms in human subjects exposed to 72 ppb ozone meets the American Thoracic Society's definition of an adverse health effect” (Frey, 2014c, p. 5).

(2) With regard to 60 ppb O3, CASAC agreed that “a level of 60 ppb corresponds to the lowest exposure concentration demonstrated to result in lung function decrements large enough to be judged an abnormal response by ATS and that could be adverse in individuals with lung disease” (Frey, 2014c, p. 7). CASAC further noted that “a level of 60 ppb also corresponds to the lowest exposure concentration at which pulmonary inflammation has been reported” (Frey, 2014c, p. 7).

(3) The controlled human exposure studies reporting these respiratory effects were conducted in healthy adults, while at-risk groups (e.g., children, people with asthma) could experience larger and/or more serious effects. In their advice to the Administrator, CASAC concurred with this reasoning (Frey, 2014a, p. 14; Frey, 2014c, p. 5).

(4) These respiratory effects are coherent with the serious health outcomes that have been reported in epidemiologic studies evaluating exposure to O3 (e.g., respiratory-related hospital admissions, emergency department visits, and mortality).

As noted above, the Administrator's proposed conclusions regarding the adequacy of the current primary O3 standard placed a large amount of weight on the results of controlled human exposure studies. In particular, given the combination of lung function decrements and respiratory symptoms following 6.6-hour exposures to O3 concentrations as low as 72 ppb, and given CASAC advice regarding effects at 72 ppb, along with ATS adversity criteria, she concluded that the evidence in this review supports the occurrence of adverse respiratory effects following exposures to O3 concentrations lower than the level of the current standard.[76] As discussed below, the Administrator further considered information from the broader body of controlled human exposure studies within the context of quantitative estimates of exposures of concern and O3-induced FEV1 decrements.

While putting less weight on information from epidemiologic studies than on information from controlled human exposure studies, the Administrator also considered what the available epidemiologic evidence indicates with regard to the adequacy of the public health protection provided by the current primary O3 standard. She noted that recent epidemiologic studies provide support, beyond that available in the last review, for associations between short-term O3 exposures and a wide range of adverse respiratory outcomes (including respiratory-related hospital admissions, emergency department visits, and mortality) and with total mortality. Associations with morbidity and mortality are stronger during the warm or summer months, and remain robust after adjustment for copollutants.

In considering information from epidemiologic studies within the context of her conclusions on the adequacy of the current standard, the Administrator considered the extent to which available studies support the occurrence of O3 health effect associations with air quality likely to be allowed by the current standard. Most of the epidemiologic studies considered by the Administrator were conducted in locations likely to have violated the current standard over at least part of the study period. However, she noted three U.S. single-city studies that support the occurrence of O3-associated hospital admissions or emergency department visits at ambient O3 concentrations below the level of the current standard, or when virtually all monitored concentrations were below the level of the current standard (Mar and Koenig, 2009; Silverman and Ito, 2010; Strickland et al., 2010) (section II.D.1 of the proposal). While the Administrator acknowledged greater uncertainty in interpreting air quality for multicity studies, she noted that O3 associations with respiratory morbidity or mortality have been reported when the majority of study locations (though not all study locations) would likely have met the current O3 standard. When taken together, the Administrator reached the initial conclusion at proposal that single-city epidemiologic studies and associated air quality information support the occurrence of O3-associated hospital admissions and emergency department visits for ambient O3 concentrations likely to have met the current standard, and that air quality analyses in locations of multicity studies provide some support for this conclusion for a broader range of effects, including mortality.

Beyond her consideration of the scientific evidence, the Administrator also considered the results of the HREA exposure and risk analyses in reaching initial conclusions regarding the adequacy of the current primary O3 standard. In doing so, as noted above, she focused primarily on exposure and risk estimates based on information from controlled human exposure studies (i.e., exposures of concern and O3-induced lung function decrements) and placed relatively less weight on epidemiologic-based risk estimates.

With regard to estimates of exposures of concern, the Administrator considered the extent to which the current standard provides protection against exposures to O3 concentrations at or above 60, 70, and 80 ppb. Consistent with CASAC advice (Frey, 2014c), the Administrator focused on children in these analyses of O3 exposures, noting that estimates for all children and asthmatic children are virtually indistinguishable, in terms of the percent estimated to experience exposures of concern.[77] Though she focused on children, she also recognized that exposures to O3 concentrations at or above 60 or 70 ppb could be of concern for adults. As discussed in the HREA and PA (and II.C.2.a of the proposal), the patterns of exposure estimates across urban study areas, across years, and across air quality scenarios are similar in adults with asthma, older adults, all children, and children with asthma, though smaller percentages of adult populations are estimated to experience exposures of concern than children and children with asthma. Thus, the Administrator recognized that the exposure patterns for children across years, urban study areas, and air Start Printed Page 65325quality scenarios are indicative of the exposure patterns in a broader group of at-risk populations that also includes asthmatic adults and older adults.

She further noted that while single exposures of concern could be adverse for some people, particularly for the higher benchmark concentrations (70, 80 ppb) where there is stronger evidence for the occurrence of adverse effects, she became increasingly concerned about the potential for adverse responses as the number of occurrences increases (61 FR 75122).[78] In particular, she noted that repeated occurrences of the types of effects shown to occur following exposures of concern can have potentially adverse outcomes. For example, repeated occurrences of airway inflammation could potentially result in the induction of a chronic inflammatory state; altered pulmonary structure and function, leading to diseases such as asthma; altered lung host defense response to inhaled microorganisms; and altered lung response to other agents such as allergens or toxins (U.S. EPA, 2013, section 6.2.3). Thus, the Administrator noted that the types of respiratory effects shown to occur in some individuals following exposures to O3 concentrations from 60 to 80 ppb, particularly if experienced repeatedly, provide a mode of action by which O3 may cause other more serious effects (e.g., asthma exacerbations). Therefore, the Administrator placed the most weight on estimates of two or more exposures of concern (i.e., as a surrogate for the occurrence of repeated exposures), though she also considered estimates of one or more, particularly for the 70 and 80 ppb benchmarks.[79]

As illustrated in Table 1 (above), the Administrator noted that if the 15 urban study areas evaluated in the HREA were to just meet the current O3 standard, fewer than 1% of children in those areas would be estimated to experience two or more exposures of concern at or above 70 ppb, though approximately 3 to 8% of children, including approximately 3 to 8% of asthmatic children, would be estimated to experience two or more exposures of concern to O3 concentrations at or above 60 ppb [80] (based on estimates averaged over the years of analysis). To provide some perspective on these percentages, the Administrator noted that they correspond to almost 900,000 children in urban study areas, including about 90,000 asthmatic children, estimated to experience two or more exposures of concern at or above 60 ppb. Nationally, if the current standard were to be just met, the number of children experiencing such exposures would be larger. In the worst-case year and location (i.e., year and location with the largest exposure estimates), the Administrator noted that over 2% of children are estimated to experience two or more exposures of concern at or above 70 ppb and over 14% are estimated to experience two or more exposures of concern at or above 60 ppb.

Although, as discussed above and in section II.E.4.d of the proposal, the Administrator was less concerned about single occurrences of exposures of concern, she noted that even single occurrences can cause adverse effects in some people, particularly for the 70 and 80 ppb benchmarks. Therefore, she also considered estimates of one or more exposures of concern. As illustrated in Table 1 (above), if the 15 urban study areas evaluated in the HREA were to just meet the current O3 standard, fewer than 1% of children in those areas would be estimated to experience one or more exposures of concern at or above 80 ppb (based on estimates averaged over the years of analysis). However, approximately 1 to 3% of children, including 1 to 3% of asthmatic children, would be estimated to experience one or more exposures of concern to O3 concentrations at or above 70 ppb and approximately 10 to 17% would be estimated to experience one or more exposures of concern to O3 concentrations at or above 60 ppb. In the worst-case year and location, the Administrator noted that over 1% of children are estimated to experience one or more exposures of concern at or above 80 ppb, over 8% are estimated to experience one or more exposures of concern at or above 70 ppb, and about 26% are estimated to experience one or more exposures of concern at or above 60 ppb.

In addition to estimated exposures of concern, the Administrator also considered HREA estimates of the occurrence of O3-induced lung function decrements. In doing so, she particularly noted CASAC advice that “estimation of FEV1 decrements of ≥15% is appropriate as a scientifically relevant surrogate for adverse health outcomes in active healthy adults, whereas an FEV1 decrement of ≥10% is a scientifically relevant surrogate for adverse health outcomes for people with asthma and lung disease” (Frey, 2014c, p. 3). While these surrogates provide perspective on the potential for the occurrence of adverse respiratory effects following O3 exposures, the Administrator agreed with the conclusion in past reviews that a more general consensus view of the adversity of moderate responses emerges as the frequency of occurrence increases (citing to 61 FR 65722-3) (Dec, 13, 1996). Therefore, in the proposal the Administrator expressed increasing concern about the potential for adversity as the frequency of occurrences increased and, as a result, she focused primarily on estimates of two or more O3-induced FEV1 decrements (i.e., as a surrogate for repeated exposures).

When averaged over the years evaluated in the HREA, the Administrator noted that the current standard is estimated to allow about 1 to 3% of children in the 15 urban study areas (corresponding to almost 400,000 children) to experience two or more O3-induced lung function decrements 15%, and to allow about 8 to 12% of children (corresponding to about 180,000 asthmatic children) to experience two or more O3-induced lung function decrements 10%. Nationally, larger numbers of children would be expected to experience such O3-induced decrements if the current standard were to be just met. The current standard is also estimated to allow about 3 to 5% of children in the urban study areas to experience one or more decrements 15% and about 14 to 19% of children to experience one or more decrements 10%. In the worst-case year and location, the current standard is estimated to allow 4% of children in the urban study areas to experience two or more decrements 15% (and 7% to experience one or more such decrements) and 14% of children to experience two or more decrements 10% (and 22% to experience one or more such decrements).[81]

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In further considering the HREA results, the Administrator considered the epidemiology-based risk estimates. Compared to the weight given to HREA estimates of exposures of concern and lung function risks, she placed relatively less weight on epidemiology-based risk estimates. Consistent with the conclusions in the PA, her determination to attach less weight to the epidemiologic-based risk estimates reflected her consideration of key uncertainties, including the heterogeneity in effect estimates between locations, the potential for exposure measurement errors, and uncertainty in the interpretation of the shape of concentration-response functions for O3 concentrations in the lower portions of ambient distributions (U.S. EPA, 2014a, section 9.6) (section II.D.2 of the proposal).

The Administrator focused on estimates of total mortality risk associated with short-term O3 exposures.[82] Given the decreasing certainty in the shape of concentration-response functions for area-wide O3 concentrations at the lower ends of warm season distributions (U.S. EPA, 2013, section 2.5.4.4), the Administrator focused on estimates of risk associated with O3 concentrations in the upper portions of ambient distributions. Even when considering only area-wide O3 concentrations from these upper portions of seasonal distributions, the Administrator noted that the current standard is estimated to allow hundreds to thousands of O3-associated deaths per year in urban study areas (79 FR 75291 citing to section II.C.3 of the proposal).

In addition to the evidence and exposure/risk information discussed above, the Administrator took note of the CASAC advice in the current review and in the 2010 proposed reconsideration of the 2008 decision establishing the current standard. As discussed in more detail above, the current CASAC “finds that the current NAAQS for ozone is not protective of human health” and “unanimously recommends that the Administrator revise the current primary ozone standard to protect public health” (Frey, 2014c, p. 5).

In consideration of all of the above, the Administrator proposed that the current primary O3 standard is not adequate to protect public health, and that it should be revised to provide increased public health protection. This proposed decision was based on the Administrator's initial conclusions that the available evidence and exposure and risk information clearly call into question the adequacy of public health protection provided by the current primary standard and, therefore, that the current standard is not requisite to protect public health with an adequate margin of safety. With regard to the evidence, she specifically noted that (1) controlled human exposure studies provide support for the occurrence of adverse respiratory effects following exposures to O3 concentrations below the level of the current standard (i.e., as low as 72 ppb), and that (2) single-city epidemiologic studies provide support for the occurrence of adverse respiratory effects under air quality conditions that would likely meet the current standard, with multicity studies providing limited support for this conclusion for a broader range of effects (i.e., including mortality). In addition, based on the analyses in the HREA, the Administrator concluded that the exposures and risks projected to remain upon meeting the current standard can reasonably be judged to be important from a public health perspective. Thus, she reached the proposed conclusion that the evidence and information, together with CASAC advice based on their consideration of that evidence and information, provide strong support for revising the current primary standard in order to increase public health protection against an array of adverse effects that range from decreased lung function and respiratory symptoms to more serious indicators of morbidity (e.g., including emergency department visits and hospital admissions), and mortality.

2. Comments on the Need for Revision

The EPA received a large number of comments, more than 430,000 comments, on the proposed decision to revise the current primary O3 standard. These comments generally fell into one of two broad groups that expressed sharply divergent views.

Many commenters asserted that the current primary O3 standard is not sufficient to protect public health, especially the health of sensitive groups, with an adequate margin of safety. These commenters agreed with the EPA's proposed decision to revise the current standard to increase public health protection. Among those calling for revisions to the current primary standard were medical groups (e.g., American Academy of Pediatrics (AAP), American Medical Association, American Lung Association (ALA), American Thoracic Society, American Heart Association, and the American College of Occupational and Environmental Medicine); national, state, and local public health and environmental organizations (e.g., the National Association of County and City Health Officials, American Public Health Association, Physicians for Social Responsibility, Sierra Club, Natural Resources Defense Council, Environmental Defense Fund, Center for Biological Diversity, and Earthjustice); the majority of state and local air pollution control authorities that submitted comments (e.g., agencies from California Air Resources Board and Office of Environmental Health Hazard Assessment, Connecticut, Delaware, Iowa, Illinois, Maryland, Minnesota, New Hampshire, New York, North Dakota, Oregon, Pennsylvania, Tennessee, and Wisconsin); the National Tribal Air Association; State organizations (e.g., National Association of Clean Air Agencies (NACAA), Northeast States for Coordinated Air Use Management, Ozone Transport Commission). While all of these commenters agreed with the EPA that the current O3 standard needs to be revised, many supported a more protective standard than proposed by EPA, as discussed in more detail below (II.C.4). Many individual commenters also expressed similar views.

A second group of commenters, representing industry associations, businesses and some state agencies, opposed the proposed decision to revise the current primary O3 standard, expressing the view that the current standard is adequate to protect public health, including the health of sensitive groups, and to do so with an adequate margin of safety. Industry and business groups expressing this view included the American Petroleum Institute (API), the Alliance of Automobile Manufacturers (AAM), the American Forest and Paper Association, the Dow Chemical Company, the National Association of Manufacturers, the Start Printed Page 65327National Mining Association, the U.S. Chamber of Commerce (in a joint comment with other industry groups), and the Utility Air Regulatory Group (UARG). State environmental agencies opposed to revising the current primary O3 standard included agencies from Arkansas, Georgia, Louisiana, Kansas, Michigan, Mississippi, Nebraska, North Carolina, Ohio, Texas, Virginia, and West Virginia.

The following sections discuss comments submitted by these and other groups, and the EPA's responses to those comments. Comments dealing with overarching issues that are fundamental to EPA's decision-making methodology are addressed in section II.B.2.a. Comments on the health effects evidence, including evidence from controlled human exposure and epidemiologic studies, are addressed in section II.B.2.b. Comments on human exposure and health risk assessments are addressed in section II.B.2.c. Comments on the appropriate indicator, averaging time, form, or level of a revised primary O3 standard are addressed below in section II.C. In addition to the comments addressed in this preamble, the EPA has prepared a Response to Comments document that addresses other specific comments related to standard setting, as well as comments on implementation- and/or cost-related factors that the EPA may not consider as part of the basis for decisions on the NAAQS. This document is available for review in the docket for this rulemaking and through the EPA's OAQPS TTN Web site (http://www.epa.gov/​ttn/​naaqs/​standards/​ozone/​s_​o3_​index.html).

a. Overarching Comments

Some commenters maintained that the proposed rule (and by extension the final rule) is fundamentally flawed because it does not quantify, or otherwise define, what level of protection is “requisite” to protect the public health. These commenters asserted that “EPA has not explained how far above zero-risk it believes is appropriate or how close to background is acceptable. EPA has failed to explain how the current standard is inadequate on this specific basis” (e.g., UARG, p. 10). These commenters further maintained that the failure to quantify a requisite level of protection “drastically reduces the value of public participation” since “the public does not understand what is driving EPA's decision” (e.g., UARG, p. 11).

The EPA disagrees with these comments and notes that industry petitioners made virtually the same argument before the D.C. Circuit in ATA III, on remand from the Supreme Court, arguing that unless EPA identifies and quantifies a degree of acceptable risk, it is impossible to determine if a NAAQS is requisite (i.e., neither too stringent or insufficiently stringent to protect the public health). The D.C. Circuit rejected petitioners' argument, holding that “[a]lthough we recognize that the Clean Air Act and circuit precedent require EPA qualitatively to describe the standard governing its selection of particular NAAQS, we have expressly rejected the notion that the Agency must `establish a measure of the risk to safety it considers adequate to protect public health every time it establish a [NAAQS]'” ATA III, 283 F. 3d at 369 (quoting NRDC v. EPA, 902 F.2d 962, 973 (D.C. Cir. 1990)). The court went on to explain that the requirement is only for EPA to engage in reasoned decision-making, “not that it definitively identify pollutant levels below which risks to public health are negligible.” ATA III, 283 F. 3d at 370.

Thus, the Administrator is required to exercise her judgment in the face of scientific uncertainty to establish the NAAQS to provide appropriate protection against risks to public health, both known and unknown. As discussed below, in the current review, the Administrator judges that the existing primary O3 standard is not requisite to protect public health with an adequate margin of safety, a judgment that is consistent with CASAC's conclusion that “there is clear scientific support for the need to revise the standard” (Frey, 2014c, p. ii). Further, in section II.C.4 below, the Administrator has provided a thorough explanation of her rationale for concluding that a standard with a level of 70 ppb is requisite to protect public health with an adequate margin of safety, explaining the various scientific uncertainties which circumscribe the range of potential alternative standards, and how she exercised her “judgment” (per section 109 (b)(1) of the CAA) in selecting a standard from within that range of scientifically reasonable choices. This “reasoned decision making” is what the Act requires, 283 F. 3d at 370, not the quantification advocated by these commenters.

The EPA further disagrees with the comment that a failure to quantify a requisite level of protection impaired or impeded public notice and comment opportunities. In fact, the EPA clearly gave adequate notice of the bases both for determining that the current standard does not afford requisite protection,[83] and for determining how the standard should be revised. In particular, the EPA explained in detail which evidence it considered critical, and the scientific uncertainties that could cause the Administrator to weight that evidence in various ways (79 FR 75308-75310). There were robust comments submitted by commenters from a range of viewpoints on all of these issues, an indication of the adequacy of notice. The public was also afforded multiple opportunities to comment to the EPA and to CASAC during the development of the ISA, REA, and PA. Thus, the EPA does not agree that lack of quantification of a risk level that is “requisite” has deprived commenters of adequate notice and opportunity to comment in this proceeding.

Various commenters maintained that it was inappropriate to revise the current NAAQS based on their view that natural background concentrations in several states are at or above O3 concentrations associated with meeting a NAAQS set at a level less than 75 ppb (presumably retaining the same indicator, form, and averaging time), making the NAAQS impossible for those states to attain and maintain, a result they claim is legally impermissible. In support for their argument, the commenters cite monitoring and modelling results from various areas in the intermountain west, state that EPA analyses provide underestimates of background O3 and conclude that high concentrations of background O3[84] exist Start Printed Page 65328in many parts of the United States that will “prevent attainment” of a revised standard (NMA, p. 5).

The courts have clearly established that “[a]ttainability and technological feasibility are not relevant considerations in the promulgation of [NAAQS].” API v. EPA, 665 F. 2d 1176, 1185 (D.C. Cir. 1981). Further, the courts have clarified that the EPA may consider proximity to background concentrations as a factor in the decision whether and how to revise the NAAQS only in the context of considering standard levels within the range of reasonable values supported by the air quality criteria and judgments of the Administrator. 79 FR 75242-43 (citing ATA III, 283 F. 3d at 379). In this review, the overall body of scientific evidence and exposure/risk information, as discussed in Section II.B of this notice, is clear and convincing: The existing standard is not adequate to protect public health with an adequate margin of safety and that the standard needs to be revised to reflect a lower level to provide that protection. The EPA analyses indicate that there may be infrequent instances in a limited number of rural areas where background O3 would be appreciable but not the sole contributor to an exceedance of the revised NAAQS, but do not indicate U.S. background (USB) O3 concentrations will prevent attainment of a revised O3 standard with a level of 70 ppb. USB is defined as that O3 that would exist even in the absence of any manmade emissions within the United States.

The EPA's estimates of U.S. background ozone concentrations are based on frequently-utilized, state-of-the-science air quality models and are considered reasonable and reliable, not underestimates. In support of their view, the commenters state that monitored (not modelled) ozone concentrations in remote rural locations include instances of 8-hour average concentrations very occasionally higher than 70 ppb. Monitoring data from places like the Grand Canyon and Yellowstone National Parks, are examples cited in comments. It is inappropriate to assume that monitored O3 concentrations at remote sites can be used as a proxy for background O3. Even at the most remote locations, local O3 concentrations are impacted by anthropogenic emissions from within the U.S. The EPA modeling analyses (U.S. EPA, 2014c, Figure 2-18) estimate that, on a seasonal basis, 10-20% of the O3 at even the most remote locations in the intermountain western U.S. originates from manmade emissions from the U.S., and thus is not part of USB. This conclusion is supported by commenter-submitted recent data analyses of rural O3 observations in Nevada and Utah (NMA, Appendices D and H). These analyses conclude that natural sources, international O3 transport, O3 transported from upwind states, and O3 transported from urban areas within a state all contributed to O3 concentrations at rural sites.[85] Thus, while O3 in high-altitude, rural portions of the intermountain western U.S. can, at times, be substantially influenced by background sources such as wildfires, international transport or the stratosphere, measured O3 in rural locations are also influenced by domestic emissions and so cannot, by themselves, be used to estimate USB concentrations. Accordingly, the fact that 2011-2013 design values in locations like Yellowstone National Park (66 ppb) or Grand Canyon National Park (72 ppb) approach or exceed 70 ppb, does not support the conclusion that a standard with a level of 70 ppb is impossible to attain.

To accurately estimate USB concentrations, it is necessary to use air quality models which can estimate how much of the O3 at any given location originates from sources other than manmade emissions within the U.S. As part of the rulemaking, the EPA has summarized a variety of modeling-based analyses of background O3 (U.S. EPA, 2013, Chapter 3) and conducted our own multi-model assessment of USB concentrations across the U.S. (U.S. EPA, 2014c, Chapter 2). The EPA analyses, which are consistent with the previously-summarized studies highlighted by commenters, concluded that seasonal mean daily maximum 8-hour average concentrations of USB O3 range from 25-50 ppb, with the highest estimates located across the intermountain western U.S.

Importantly, the modeling analyses also indicate that the highest O3 days (i.e., the days most relevant to the form of the NAAQS) generally have similar daily maximum 8-hour average USB concentrations as the seasonal means of this metric, but have larger contributions from U.S. anthropogenic sources. As summarized in the PA, “the highest modeled O3 site-days tend to have background O3 levels similar to mid-range O3 days . . . [T]he days with highest O3 levels have similar distributions (i.e. means, inter-quartile ranges) of background levels as days with lower values, down to approximately 40 ppb. As a result, the proportion of total O3that has background origins is smaller on high O3days (e.g. greater than 60 ppb) than on the more common lower O3days that tend to drive seasonal means” (U.S. EPA, 2014c, p. 2-21, emphasis added). When averaged over the entire U.S., the models estimate that the mean USB fractional contribution to daily maximum 8-hour average O3 concentrations above 70 ppb is less than 35 percent. U.S. anthropogenic emission sources are thus the dominant contributor to the majority of modeled O3 exceedances across the U.S. (U.S. EPA, 2014c, Figures 2-14 and 2-15).

As noted in the PA, and as highlighted by the commenters based on existing modeling, there can be infrequent events where daily maximum 8-hour O3 concentrations approach or exceed 70 ppb largely due to the influence of USB sources like a wildfire or stratospheric intrusion. As discussed below in Section V, the statute and EPA implementing regulations allow for the exclusion of air quality monitoring data from design value calculations when there are exceedances caused by certain event-related U.S. background influences (e.g., wildfires or stratospheric intrusions). As a result, these “exceptional events” will not factor into attainability concerns.

In sum, the EPA believes that the commenters have failed to establish the predicate for their argument. Uncontrollable background concentrations of O3 are not expected to preclude attainment of a revised O3 standard with a level of 70 ppb. The EPA also disagrees with aspects of the specific statements made by the commenters as support for their view that the EPA analyses have underestimated background O3.[86] Thus, even assuming the commenters are correct that the EPA may use proximity to background as a justification for not revising a standard that, in the judgment of the Administrator, is inadequate to protect public health, the commenters' arguments for the justification and need to do so for this review are based on a flawed premise.

b. Comments on the Health Effects Evidence

As noted above, comments on the adequacy of the current standard fell into two broad categories reflecting very Start Printed Page 65329different views of the available scientific evidence. Commenters who expressed support for the EPA's proposed decision to revise the current primary O3 standard generally concluded that the body of scientific evidence assessed in the ISA is much stronger and more compelling than in the last review. These commenters also generally emphasized CASAC's interpretation of the body of available evidence, which formed an important part of the basis for CASAC's reiterated recommendations to revise the O3 standard to provide increased public health protection. In some cases, these commenters supported their positions by citing studies published since the completion of the ISA.

The EPA generally agrees with these commenters regarding the need to revise the current primary O3 standard in order to increase public health protection though, in many cases, not with their conclusions about the degree of protection that is appropriate (II.C.4.b and II.C.4.c, below). The scientific evidence noted by these commenters was generally the same as that assessed in the ISA (U.S. EPA, 2013) and the proposal,[87] and their interpretation of the evidence was often, though not always, consistent with the conclusions of the ISA and CASAC. The EPA agrees that the evidence available in this review provides a strong basis for the conclusion that the current O3 standard is not adequately protective of public health. In reaching this conclusion, the EPA places a large amount of weight on the scientific advice of CASAC, and on CASAC's endorsement of the assessment of the evidence in the ISA (Frey and Samet, 2012).

In contrast, while commenters who opposed the proposed decision to revise the primary O3 standard generally focused on many of the same studies assessed in the ISA, these commenters highlighted different aspects of these studies and reached substantially different conclusions about their strength and the extent to which progress has been made in reducing uncertainties in the evidence since the last review. These commenters generally concluded that information about the health effects of concern has not changed significantly since 2008 and that the uncertainties in the underlying health science have not been reduced since the 2008 review. In some cases, these commenters specifically questioned the EPA's approach to assessing the scientific evidence and to reaching conclusions on the strength of that evidence in the ISA. For example, several commenters asserted that the EPA's causal framework, discussed in detail in the ISA, is flawed and that it has not been applied consistently across health endpoints. Commenters also noted departures from other published causality frameworks (Samet and Bodurow, 2008) and from the criteria for judging causality put forward by Sir Austin Bradford Hill (Hill, 1965).

The EPA disagrees with comments questioning the ISA's approach to assessing the evidence, the causal framework established in the ISA, or the consistent application of that framework across health endpoints. While the EPA acknowledges the ISA's approach departs from assessment and causality frameworks that have been developed for other purposes, such departures reflect appropriate adaptations for the NAAQS. As with other ISAs, the O3 ISA uses a five-level hierarchy that classifies the weight of evidence for causation. In developing this hierarchy, the EPA has drawn on the work of previous evaluations, most prominently the IOM's Improving the Presumptive Disability Decision-Making Process for Veterans (Samet and Bodurow, 2008), EPA's Guidelines for Carcinogen Risk Assessment (U.S. EPA, 2005), and the U.S. Surgeon General's smoking report (CDC, 2004). The ISA's weight of evidence evaluation is based on the integration of findings from various lines of evidence from across the health and environmental effects disciplines. These separate judgments are integrated into a qualitative statement about the overall weight of the evidence and causality. The ISA's causal framework has been developed over multiple NAAQS reviews, based on extensive interactions with CASAC and based on the public input received as part of the CASAC review process. In the current review, the causality framework, and the application of that framework to causality determinations in the O3 ISA, have been reviewed and endorsed by CASAC (Frey and Samet, 2012).

Given these views on the assessment of the evidence in the ISA, it is relevant to note that many of the issues and concerns raised by commenters on the EPA's interpretation of the evidence, and on the EPA's conclusions regarding the extent to which uncertainties have been reduced since the 2008 review, are essentially restatements of issues raised during the development of the ISA, HREA, and/or PA. The CASAC O3 Panel reviewed the interpretation of the evidence, and the EPA's use of information from specific studies, in drafts of these documents. In CASAC's advice to the Administrator, which incorporates its consideration of many of the issues raised by commenters, CASAC approved of the scientific content, assessments, and accuracy of the ISA, REA, and PA, and indicated that these documents provide an appropriate basis for use in regulatory decision making for the O3 NAAQS (Frey and Samet, 2012, Frey, 2014a, Frey, 2014c). Therefore, the EPA's responses to many of the comments on the evidence rely heavily on the process established in the ISA for assessing the evidence, which is the product of extensive interactions with CASAC over a number of different reviews, and on CASAC advice received as part of this review of the O3 NAAQS.

The remainder of this section discusses public comments and the EPA's responses, on controlled human exposure studies (II.B.2.b.i); epidemiologic studies (II.B.2.b.ii); and at-risk populations (II.B.2.b.iii).

i. Evidence From Controlled Human Exposure Studies

This section discusses major comments on the evidence from controlled human exposure studies and provides the Agency's responses to those comments. To support their views on the adequacy of the current standard, commenters often highlighted specific aspects of the scientific evidence from controlled human exposure studies. Key themes discussed by these commenters included the following: (1) The adversity of effects demonstrated in controlled human exposure studies, especially studies conducted at exposure concentrations below 80 ppb; (2) representativeness of different aspects of the controlled human exposure studies for making inferences to the general population and at-risk populations; (3) results of additional analyses of the data from controlled human exposure studies; (4) evaluation of a threshold for effects; and (5) importance of demonstration of inflammation at 60 ppb. This section discusses these key comment themes, and provides the EPA's responses. More detailed discussion of individual comments, and the EPA's responses, is provided in the Response to Comments document.

Adversity

Some commenters who disagreed with the EPA's proposed decision to revise the current primary O3 standard disputed the Agency's characterization Start Printed Page 65330of the adversity of the O3-induced health effects shown to occur in controlled human exposure studies. Some of these commenters contended that the proposal does not provide a clear definition of adversity or that there is confusion concerning what responses the Administrator considers adverse. The EPA disagrees with these comments, and notes that section II.E.4.d of the proposal describes the Administrator's proposed approach to considering the adversity of effects observed in controlled human exposure studies. Her final approach to considering the adversity of these effects, and her conclusions on adversity, are described in detail below (II.C.4.b, II.C.4.c).

Other commenters disagreed with the EPA's judgments regarding adversity and expressed the view that the effects observed in controlled human exposure studies following 6.6-hour exposures to O3 concentrations below the level of the current standard (i.e., 75 ppb) are not adverse.[88] This group of commenters cited several reasons to support their views, including that: (1) The lung function decrements and respiratory symptoms observed at 72 ppb in the study by Schelegle et al. (2009) were not correlated with each other, and therefore were not adverse; and (2) group mean FEV1 decrements observed following exposures below 75 ppb are small (e.g., <10%, as highlighted by some commenters), transient and reversible, do not interfere with daily activities, and do not result in permanent respiratory injury or progressive respiratory dysfunction.

While the EPA agrees that not all effects reported in controlled human exposure studies following exposures below 75 ppb can reasonably be considered to be adverse, the Agency strongly disagrees with comments asserting that none of these effects can be adverse. As an initial matter, the Administrator notes that, when considering the extent to which the current or a revised standard could allow adverse respiratory effects, based on information from controlled human exposure studies, she considers not only the effects themselves, but also quantitative estimates of the extent to which the current or a revised standard could allow such effects. Quantitative exposure and risk estimates provide perspective on the extent to which various standards could allow populations, including at-risk populations such as children and children with asthma, to experience the types of O3 exposures that have been shown in controlled human exposure studies to cause respiratory effects. As discussed further below (II.B.3, II.C.4.b, II.C.4.c), to the extent at-risk populations are estimated to experience such exposures repeatedly, the Administrator becomes increasingly concerned about the potential for adverse responses in the exposed population. Repeated exposures provide a plausible mode of action by which O3 may cause other more serious effects. Thus, even though the Administrator concludes there is important uncertainty in the adversity of some of the effects observed in controlled human exposure studies based on the single exposure periods evaluated in these studies (e.g., FEV1 decrements observed following exposures to 60 ppb O3, as discussed in sections II.C.4.b and II.C.4.c below), she judges that the potential for adverse effects increases as the number of exposures increases. Contrary to the commenters' views noted above, the Administrator considers the broader body of available information (i.e., including quantitative exposure and risk estimates) when considering the extent to which the current or a revised standard could allow adverse respiratory effects (II.B.3, II.C.4.b, II.C.4.c, below).

In further considering commenters' views on the potential adversity of the respiratory effects themselves (i.e., without considering quantitative estimates), the EPA notes that although the results of controlled human exposure studies provide a high degree of confidence regarding the occurrence of health effects following exposures to O3 concentrations from 60 to 80 ppb, there are no universally accepted criteria by which to judge the adversity of the observed effects. Therefore, as in the proposal, the Administrator relies upon recommendations from the ATS and advice from CASAC to inform her judgments on adversity.

In particular, the Administrator focuses on the ATS recommendation that “reversible loss of lung function in combination with the presence of symptoms should be considered adverse” (ATS, 2000a). The study by Schelegle et al. (2009) reported a statistically significant decrease in group mean FEV1 and a statistically significant increase in respiratory symptoms in healthy adults following 6.6-hour exposures to average O3 concentrations of 72 ppb. In considering these effects, CASAC noted that “the combination of decrements in FEV1 together with the statistically significant alterations in symptoms in human subjects exposed to 72 ppb ozone meets the American Thoracic Society's definition of an adverse health effect” (Frey, 2014c, p. 5).

As mentioned above, some commenters nonetheless maintained that the effects observed in Schelegle et al. (2009) following exposure to 72 ppb O3 (average concentration) were not adverse because the magnitudes of the FEV1 decrements and the increases in respiratory symptoms (as measured by the total subjective symptoms score, TSS) were not correlated across individual study subjects. A commenter submitted an analysis of the individual-level data from the study by Schelegle et al. (2009) to support their position. This analysis indicated that, while the majority of study volunteers (66%) did experience both lung function decrements and increased respiratory symptoms following 6.6-hour exposures to 72 ppb O3, some (33%) did not (e.g., Figure 3 in comments from Gradient).[89] In addition, the study subjects who experienced relatively large lung function decrements did not always also experience relatively large increases in respiratory symptoms. These commenters interpreted the lack of a statistically significant correlation between the magnitudes of decrements and symptoms as meaning that the effects reported by Schelegle et al. (2009) at 72 ppb did not meet the ATS criteria for an adverse response.

However, the ATS recommendation that the combination of lung function decrements and symptomatic responses be considered adverse is not restricted to effects of a particular magnitude nor a requirement that individual responses be correlated. Similarly, CASAC made no such qualifications in its advice on the combination of respiratory symptoms and lung function decrements (See e.g., Frey, 2014c, p. 5). Therefore, as in the proposal and consistent with both CASAC advice and ATS recommendations, the EPA continues to conclude that the finding of both statistically significant decrements in lung function and significant increases in respiratory symptoms following 6.6-hour exposures to an average O3 concentration of 72 ppb provides a strong indication of the Start Printed Page 65331potential for exposed individuals to experience this combination of effects.[90]

In particular, the Administrator notes that lung function provides an objective measure of the respiratory response to O3 exposure while respiratory symptoms are subjective, and as evaluated by Schelegle et al. (2009) were based on a TSS score. If an O3 exposure causes increases in both objectively measured lung function decrements and subjective respiratory symptoms, which indicate that people may modify their behavior in response to the exposure, then the effect is properly viewed as adverse. As noted above, the commenter's analysis shows that the majority of study volunteers exposed to 72 ppb O3 in the study by Schelegle et al. (2009) did, in fact, experience both a decrease in lung function and an increase in respiratory symptoms.

In further considering this comment, the EPA recognizes that, consistent with commenter's analysis, some individuals may experience large decrements in lung function with minimal to no respiratory symptoms (McDonnell et al., 1999), and vice versa. As indicated above and discussed in the proposal (79 FR 75289), the Administrator acknowledges such interindividual variability in responsiveness in her interpretation of estimated exposures of concern. Specifically, she notes that not everyone who experiences an exposure of concern, including for the 70 ppb benchmark, is expected to experience an adverse response. However, she further judges that the likelihood of adverse effects increases as the number of occurrences of O3 exposures of concern increases. In making this judgment, she notes that the types of respiratory effects that can occur following exposures of concern, particularly if experienced repeatedly, provide a plausible mode of action by which O3 may cause other more serious effects.[91] Therefore, her decisions on the primary standard emphasize the public health importance of limiting the occurrence of repeated exposures to O3 concentrations at or above those shown to cause adverse effects in controlled human exposure studies (II.B.3, II.C.4.b, II.C.4.c). The Administrator views this approach to considering the evidence from controlled human exposure studies as being consistent with commenter's analysis indicating that, while the majority did, not all study volunteers exposed to 72 ppb O3 experienced the adverse combination of lung function decrements and respiratory symptoms following the single exposure period evaluated by Schelegle et al. (2009).

Representativeness

A number of commenters raised issues concerning the representativeness of controlled human exposure studies considered by the Administrator in this review, based on different aspects of these studies. These commenters asserted that since the controlled human exposure studies were not representative of real-world exposures, they should not be relied upon as a basis for finding that the current standard is not adequate to protect public health. Some issues highlighted by commenters include: Small size of the study populations; unrealistic activity levels used in the studies; unrealistic exposure scenarios (i.e., triangular exposure protocol) used in some studies, including Schelegle et al. (2009); and differences in study design that limit comparability across studies.

Some commenters noted that the controlled human exposure studies were not designed to have individuals represent portions of any larger group and that the impacts on a small number of people do not implicate the health of an entire subpopulation, particularly when the FEV1 decrements are small, temporary, and reversible. These commenters also noted that the Administrator failed to provide an explanation or justification for why the individuals in these studies can be viewed as representatives of a subpopulation. Further, they asserted that EPA's use of results from individuals, rather than the group mean responses, contradicts the intent of CAA section 109 to protect groups of people, not just the most sensitive individuals in any group (79 FR 75237).

Consistent with CASAC advice (Frey, 2014c, p. 5), the EPA concludes that the body of controlled human exposure studies are sufficiently representative to be relied upon as a basis for finding that the current standard is not adequate to protect public health. These studies generally recruit healthy young adult volunteers, and often expose them to O3 concentrations found in the ambient air under real-world exposure conditions. As described in more detail above in section II.A.1.b, the evidence from controlled human exposure studies to date makes it clear that there is considerable variability in responses across individuals, even in young healthy adult volunteers, and that group mean responses are not representative of more responsive individuals. It is important to look beyond group mean responses to the responses of these individuals to evaluate the potential impact on more responsive members of the population. Moreover, relying on group mean changes to evaluate lung function responses to O3 exposures would mask the responses of the most sensitive groups, particularly where, as here, the group mean reflects responses solely among the healthy young adults who were the study participants. Thus, the studies of exposures below 80 ppb O3 show that 10% of young healthy adults experienced FEV1 decrements >10% following exposures to 60 ppb O3, and 19% experienced such decrements following exposures to 72 ppb (under the controlled test conditions involving moderate exertion for 6.6 hours). These percentages would likely have been higher had people with asthma or other at-risk populations been exposed (U.S. EPA, 2013, pp. 6-17 and 6-18; Frey 2014c, p. 7; Frey, 2014a, p. 14).[92]

Moreover, the EPA may legitimately view the individuals in these studies as representatives of the larger subpopulation of at-risk or sensitive groups. As stated in the Senate Report to the 1970 legislation establishing the NAAQS statutory provisions, “the Committee emphasizes that included among these persons whose health should be protected by the ambient standard are particularly sensitive citizens such as bronchial asthmatics and emphysematics who in the normal course of daily activity are exposed to the ambient environment. In establishing an ambient standard necessary to protect the health of these persons, reference should be made to a representative sample of persons comprising the sensitive group rather than to a single person in such a group. . . . For purposes of this description, a statistically related sample is the number of persons necessary to test in order to detect a deviation in the health of any person within such sensitive group which is attributable to the condition of the ambient air.” S. Rep. No. 11-1196, 91st Start Printed Page 65332Cong. 2d sess. at 10. As just noted above, 10% of healthy young adults in these studies experienced >10% FEV1 decrements following exposure to 60 ppb O3, and the proportion of individuals experiencing such decrements increases with increasing O3 exposure concentrations. This substantial percentage certainly can be viewed as “a representative sample of persons” and as a sufficient number to “detect a deviation in the health of any person within such sensitive group,” especially given that it reflects the percentage of healthy adults who experienced decrements >10%.

These results are consistent with estimates from the MSS model, which makes reliable quantitative predictions of the lung function response to O3 exposures, and reasonably predicts the magnitude of individual lung function responses following such exposures. As described in section II.A.2.c above, and documented in the HREA, when the MSS model was used to quantify the risk of O3-induced FEV1 decrements in 15 urban study areas, the current standard was estimated to allow about 8 to 12% of children to experience two or more O3-induced FEV1 decrements ≥10%, and about 2 to 3% to experience two or more decrements ≥15% (Table 2, above). These percentages correspond to hundreds of thousands of children in urban study areas, and tens of thousands of asthmatic children. While the Administrator judges that there is uncertainty with regard to the adversity of these O3-induced lung function decrements (see II.C.4.b, II.C.4.c, below), such risk estimates clearly indicate that they are a matter of public health importance on a broad scale, not isolated effects on idiosyncratically responding individuals.

Other commenters considered the ventilation rates used in controlled human exposure studies to be unreasonably high and at the extreme of prolonged daily activity. Some of these commenters noted that these scenarios are unrealistic for sensitive populations, such as asthmatics and people with COPD, whose conditions would likely prevent them from performing the intensity of exercise, and therefore experiencing the ventilation rates, required to produce decrements in lung function observed in experimental settings.

The EPA disagrees with these commenters. The activity levels used in controlled human exposure studies were summarized in Table 6-1 of the ISA (U.S. EPA, 2013). The exercise level in the 6.6-hour exposure studies by Adams (2006), Schelegle et al. (2009), and Kim et al. (2011) of young healthy adults was moderate and ventilation rates are typically targeted for 20 L/min-m[2] BSA.[93] Following the exposures to 60 ppb at this activity level, 10% of the individuals had greater than a 10% decrement in FEV1 (U.S. EPA, 2013, p. 6-18). Similar 6.6-hour exposure studies of individuals with asthma are not available to assess either the effects of O3 on their lung function or their ability to perform the required level of moderate exercise.

However, referring to Tables 6-9 and 6-10 of the HREA (U.S. EPA, 2014a), between 42% and 45% of FEV1 decrements ≥ 10% were estimated to occur at exercise levels of <13 L/min-m2 BSA. This corresponds to light exercise, and this level of exercise has been used in a 7.6-hour study of healthy people and people with asthma exposed to 160 ppb O3 (Horstman et al., 1995). In that study, people with asthma exercised with an average minute ventilation of 14.2 L/min-m2 BSA. Adjusted for filtered air responses, an average 19% FEV1 decrement was seen in the people with asthma versus an average 10% FEV1 decrement in the healthy people. In addition, the EPA noted in the HREA that the data underlying the exposure assessment indicate that “activity data for asthmatics [is] generally similar to [that for] non-asthmatics” (U.S. EPA, 2014a, p. 5-75, Tables 5G-2 and 5G-3). Thus, contrary to the commenters' assertion, based on both the HREA and the Horstman et al. (1995) study, people with respiratory disease such as asthma can exercise for a prolonged period under conditions where they would experience >10% FEV1 decrements in response to O3 exposure.

Additionally, a number of commenters asserted that the exposure scenarios in Schelegle et al. (2009), which are based on a so-called triangular study protocol, where O3 concentrations ramp up and down as the study is conducted, are not directly generalizable to most healthy or sensitive populations because of large changes in the O3 concentrations from one hour to the next. Commenters stated that although large fluctuations in O3 are possible in certain locations due to meteorological conditions (e.g., in valleys on very hot, summer days), they believe that, in general, concentrations of O3 do not fluctuate by more than 20-30 ppb from one hour to the next. Thus, commenters suggested the Schelegle et al. (2009) study design could happen in a “worst-case” exposure scenario, but that the exposure protocol was not reflective of conditions in most cities and thus not informative with regard to the adequacy of the current standard.

The EPA disagrees with the comment that these triangular exposure scenarios are not generalizable because of hour-to-hour fluctuations. Adams (2002, 2006) showed that FEV1 responses following 6.6 hours of exposure to 60 and 80 ppb average O3 exposures do not differ between triangular (i.e. ramping concentration up and down) and square-wave (i.e. constant concentration). Schelegle et al. (2009) used the 80 ppb triangular protocol and a slightly modified 60 ppb triangular protocol (concentrations during the third and fourth hours were reversed) from Adams (2006). Therefore, in considering pre- to post-exposure changes in lung function, concerns about the hour-by-hour changes in O3 concentrations at 60 and 80 ppb in the Schelegle et al. (2009) study are unfounded.

Finally, some commenters also stated that the Kim et al. (2011) study is missing critical information and its study design makes comparison to the other studies difficult. That is, the commenter suggests that data at times other than pre- and post-exposure should have been provided.

The EPA disagrees with this comment. With regard to providing data at other time points besides pre- and post-exposure, there is no standard that suggests an appropriate frequency at which lung function should be measured in prolonged 6.6-hour exposure studies. The Adams (2006) study showed that lung function decrements during O3 exposures with moderate exercise become most apparent following the third hour of exposure. As such, it makes little sense to measure lung function during the first couple hours of exposure. However, having data at multiple time points toward the end of an exposure can provide evidence that the mean post-exposure FEV1 response is not a single anomalous data point. The FEV1 response data for the 3-, 4.6-, 5.6-, and 6.6-hour time points of the Kim et al. (2011) study are available in Figure 6 of the McDonnell et al. (2012) paper where they are plotted with the Adams (2006) data for 60 ppb. Similar to the Adams (2006) study, the responses at 5.6 hours are only marginally smaller than the response at 6.6 hours in the Kim et al. (2011) study. This indicates that the post-exposure FEV1 responses in both studies are consistent with responses at an earlier time point and thus not likely to be anomalous data.Start Printed Page 65333

Additional Studies

Several commenters analyzed the data from controlled human exposure studies, or they commented on the EPA's analysis of the data from some of these studies (Brown et al., 2008), to come to a different conclusion than the EPA's interpretation of these studies thereby questioning the proposed decision that the current standard is not adequate to protect public health. One commenter submitted an independent assessment of the scientific evidence and risk, and used this analysis to assert that there are multiple flaws in the underlying studies and their interpretation by the EPA. This commenter stated that the EPA's discussion of the spirometric responses of children and adolescents and older adults to O3 was misleading. They claimed that the EPA did not mention that “the responses of children and adolescents are equivalent to those of young adults (18-35 years old; McDonnell et al., 1985) and that this response diminishes in middle-aged and older adults (Hazucha 1985).” The EPA notes that the commenter misrepresented our characterization of the effect of age on FEV1 responses to O3 and asserted mistakenly that EPA did not mention diminished responses on older adults. In fact, the proposal clearly states that, “Respiratory symptom responses to O3 exposure appears to increase with age until early adulthood and then gradually decrease with increasing age (U.S. EPA, 1996b); lung function responses to O3 exposure also decline from early adulthood (U.S. EPA, 1996b)” (79 FR 75267) (see also U.S. EPA, 2014c p. 3-82). With regard to differences between children and adults, it was clearly stated in the ISA (U.S. EPA, 2013, p. 6-21) that healthy children exposed to filtered air and 120 ppb O3 experienced similar spirometric responses, but lesser symptoms than similarly exposed young healthy adults (McDonnell et al., 1985). In addition, the EPA's approach to modeling the effect of age on responses to O3 is clearly provided in the HREA (U.S. EPA, 2014a, Table 6-2).

The commenter also stated that the EPA's treatment of filtered air responses in the dose-response curve was incorrect. They claimed that when creating a dose-response curve, it is most appropriate to include a zero-dose point and not to subtract the filtered air response from responses to O3. Contrary to this assertion, EPA correctly adjusted FEV1 responses to O3 by responses following filtered air, as was also done in the McDonnell et al. (2012) model. As indicated in the ISA (U.S. EPA, 2013, p. 6-4), the majority of controlled human exposure studies investigating the effects O3 are of a randomized, controlled, crossover design in which subjects were exposed, without knowledge of the exposure condition and in random order, to clean filtered air and, depending on the study, to one or more O3 concentrations. The filtered air control exposure provides an unbiased estimate of the effects of the experimental procedures on the outcome(s) of interest. Comparison of responses following this filtered air exposure to those following an O3 exposure allows for estimation of the effects of O3 itself on an outcome measurement while controlling for independent effects of the experimental procedures, such as ventilation rate. Thus, the commenter's approach does not provide an estimate of the effects of O3 alone. Furthermore, as illustrated in these comments, following “long” filtered air exposures, there is about a 1% improvement in FEV1. By not accounting for this increase in FEV1, the commenter underestimated the FEV1 decrement due to O3 exposure. The commenter's approach thus is fundamentally flawed.

The commenter also asserted that the McDonnell et al. (2012) model and exposure-response (E-R) models incorrectly used only the most responsive people and that EPA's reliance on data from clinical trials that use only the most responsive people irrationally ignores large portions of relevant data. The EPA rejects this assertion that the McDonnell et al. (2012) model and the E-R analysis ignored large portions of relevant data. The McDonnell et al. (2012) model was fit to the FEV1 responses of 741 individuals to O3 and filtered air (i.e., reflecting all available data for O3-induced changes in FEV1). The filtered air responses were subtracted from responses measured during O3 exposures. Subsequently, as illustrated by the figures in the McDonnell et al. (2012) paper and described in the text of paper, the model was fit to all available FEV1 data measured during the course of O3 exposures, including exposures shorter than 6.6 hours. Thus, the model predicts temporal dynamics of FEV1 response to any set of O3 exposure conditions that might reasonably be experienced in the ambient environment, predicting the mean responses and the distribution of responses around the mean. For the HREA (EPA, 2014a), the proportion of individuals, under variable exposure conditions, predicted to have FEV1 decrements ≥10, 15 and 20% was estimated.

Finally, the commenter referenced the exposure-response model on p. 6-18 of the HREA. However, they neglected to note that this was in a section describing the exposure-response function approach used in prior reviews (U.S. EPA, 2014a, starting on p. 6-17). Thus, the commenter confused the exposure-response model used in the last review with the updated approach used in this review.

The commenter also stated that EPA did not properly consider O3 dose when interpreting the human clinical data. Ozone total dose includes three factors: duration of exposure, concentration, and ventilation rate. The commenter claimed the EPA emphasized only concentration without properly considering and communicating duration of exposure and ventilation rate. Further, they asserted that because people are not exposed to the same dose, they cannot be judged to have the same exposure and would therefore not be expected to respond consistently. The EPA rejects the claim that we emphasized only concentration without properly incorporating the other two factors. As noted in the ISA, total O3 dose does not describe the temporal dynamics of FEV1 responses as a function of concentration, ventilation rate, time and age of the exposed individuals (U.S. EPA, 2013, p. 6-5). Thus, the use of total O3 dose is antiquated and the EPA therefore conducted a more sophisticated analysis of FEV1 response to O3 in the HREA. In this review, the HREA estimates risks of lung function decrements in school-aged children (ages 5 to 18), asthmatic school-aged children, and the general adult population for 15 urban study areas. A probabilistic model designed to account for the numerous sources of variability that affect people's exposures was used to simulate the movement of individuals through time and space and to estimate their exposure to O3 while occupying indoor, outdoor, and in-vehicle locations. That information was linked with the McDonnell et al. (2012) model to estimate FEV1 responses over time as O3 exposure concentrations and ventilation rates changed. As noted earlier, CASAC agreed that this approach is both scientifically valid and a significant improvement over approaches used in past O3 reviews (Frey, 2014a, p. 2).

Several commenters criticized the EPA analysis published by Brown et al. (2008). One commenter suggested that the EPA needed to state why the Brown et al. (2008) analysis was relied on rather than Nicolich (2007) or Lefohn et Start Printed Page 65334al. (2010). Further, commenters stated that the analysis of the Adams (2006) data in Brown et al. (2008) was flawed. Among other reasons, one commenter expressed the opinion that it was not appropriate for Brown et al. (2008) to only examine a portion of the Adams (2006) data, citing comments submitted by Gradient.

The EPA disagrees with these commenters.[94] As an initial matter, Nicolich (2007) was a public comment and is not a peer-reviewed publication that would be used to assess the scientific evidence for effects of O3 on lung function in the ISA (U.S. EPA, 2013). The Nicolich (2007) comments were specifically addressed by the EPA on pp. 24-25 in the Response to Comments Document for the 2007 proposed rule (U.S. EPA, 2008). On page A-3 of his comments, Dr. Nicolich stated “that the residuals are not normally distributed and the observations do not meet the assumptions required for the model” and that “the subject-based errors are not independently, identically and normally distributed and the subjects do not meet the assumptions required for the model.” The EPA reasonably chose not to rely on this analysis: “Therefore, given that the underlying statistical assumptions required for his analyses were not met and that significance levels are questionable, in EPA's judgment the analyses presented by Dr. Nicolich are ambiguous” (U.S. EPA, 2008). It is likely that the Lefohn et al. (2010) analysis of the Adams (2006) data would similarly not meet the statistical assumptions of the model (e.g., homoscedasticity). In contrast, recognizing the concerns related to the distribution of responses, Brown et al. (2008) conservatively used a nonparametric sign test to obtain a p-value of 0.002 for the comparison responses following 60 ppb O3 versus filter air. Other common statistical tests also showed significant effects on lung function. In addition, the effects of 60 ppb O3 on FEV1 responses in Brown et al. (2008) remained statistically significant even following the exclusion of three potential outliers.

EPA disagrees with the comment stating that it was not appropriate for Brown et al. (2008) to only examine a portion of the Adams (2006) data. In fact, there is no established single manner or protocol decreeing that data throughout the protocol must be analyzed and included. Furthermore, Brown et al. (2008) was a peer-reviewed journal publication. CASAC also expressed favorable comments in their March 30, 2011, letter to Administrator Jackson. With reference to a memorandum (Brown, 2007) that preceded the Brown et al. (2008) publication, on p. 6 of the CASAC Consensus Responses to Charge Questions CASAC stated, “The results of the Adams et al. study also have been carefully reanalyzed by EPA investigators (Brown et. al., [2008]), and this reanalysis showed a statistically significant group effect on FEV1 after 60 ppb ozone exposure.” On p. A-13, a CASAC panelist and biostatistician stated, “Thus, from my understanding of the statistical analyses that have been conducted, I would argue that the analysis by EPA should be preferred to that of Adams for the specific comparison of the FEV1 effects of 0.06 ppm exposure relative to filtered air exposure.” (Samet 2011, p. a-13)

Threshold

Several commenters used the new McDonnell et al. (2012) and Schelegle et al. (2012) models to support their views about the O3 concentrations associated with a threshold for adverse lung function decrements. For example, one commenter who supported retaining the current standard noted that McDonnell et al. (2012) found that the threshold model fit the observed data better than the original (no-threshold) model, especially at earlier time points and at the lowest exposure concentrations. The commenter expressed the view that the threshold model showed that the population mean FEV1 decrement did not reach 10% until exposures were at least 80 ppb, indicating that O3 exposures of 80 ppb or higher may cause lung function decrements and other respiratory effects.[95]

As described above in section II.A.1.b, the McDonnell et al. (2012) and Schelegle et al. (2012) models represent a significant technological advance in the exposure-response modeling approach since the last review, and these models indicate that a dose-threshold model fits the data better than a non-threshold model. However, the EPA disagrees that using the predicted group mean response from the McDonnell model provides support for retaining the current standard. As discussed above, the group mean responses do not convey information about interindividual variability, or the proportion of the population estimated to experience the larger lung function decrements (e.g., 10 or 15% FEV1 decrements) that could be adverse. In fact, it masks this variability. These variable effects in individuals have been found to be reproducible. In other words, a person who has a large lung function response after exposure to O3 will likely have about the same response if exposed again in a similar manner (raising health concerns, as noted above). Group mean responses are not representative of this segment of the population that has much larger than average responses to O3.

Inflammation

Some commenters asserted that the pulmonary inflammation observed following exposure to 60 ppb in the controlled human exposure study by Kim et al. (2011) was small and unlikely to result in airway damage. It was also suggested that this inflammation is a normal physiological response in all living organisms to stimuli to which people are normally exposed.

The EPA recognized in the proposal (79 FR 75252) and the ISA (U.S. EPA, 2013, p. 6-76) that inflammation induced by a single exposure (or several exposures over the course of a summer) can resolve entirely. Thus, the inflammatory response observed following the single exposure to 60 ppb in the study by Kim et al. (2011) is not necessarily a concern. However, the EPA notes that it is also important to consider the potential for continued acute inflammatory responses to evolve into a chronic inflammatory state and to affect the structure and function of the lung.[96] The Administrator considers this possibility through her consideration of estimated exposures of concern for the 60 ppb benchmark (II.B.3, II.C.4). As discussed in detail below (II.C.4.b), while she judges that there is uncertainty in the adversity of the effects shown to occur following exposures to 60 ppb O3, including the inflammation reported by Kim et al. Start Printed Page 65335(2011), she gives some consideration to estimates of two or more exposures of concern for the 60 ppb benchmark (i.e., as a health-protective surrogate for repeated exposures of concern at or above 60 ppb), particularly when considering the extent to which the current and revised standards incorporate a margin of safety.

ii. Evidence Fom epidemiologic studies

This section discusses key comments on the EPA's assessment of the epidemiologic evidence and provides the Agency's responses to those comments. The focus in this section is on overarching comments related to the EPA's approach to assessing and interpreting the epidemiologic evidence as a whole. Detailed comments on specific studies, or specific methodological or technical issues, are addressed in the Response to Comments document. As discussed above, many of the issues and concerns raised by commenters on the interpretation of the epidemiologic evidence are essentially restatements of issues raised during the development of the ISA, HREA, and/or PA, and in many instances were considered by CASAC in the development of its advice on the current standard. The EPA's responses to these comments rely heavily on the process established in the ISA for assessing the evidence, and on CASAC advice received as part of this review of the O3 NAAQS.

As with evidence from controlled human exposure studies, commenters expressed sharply divergent views on the evidence from epidemiologic studies, and on the EPA's interpretation of that evidence. One group of commenters, representing medical, public health and environmental organizations, and some states, generally supported the EPA's interpretation of the epidemiologic evidence with regard to the consistency of associations, the coherence with other lines of evidence, and the support provided by epidemiologic studies for the causality determinations in the ISA. These commenters asserted that the epidemiologic studies evaluated in the ISA provide valuable information supporting the need to revise the level of the current primary O3 standard in order to increase public health protection. In reaching this conclusion, commenters often cited studies (including a number from the past review) which they interpreted as showing health effect associations in locations with O3 air quality concentrations below the level of the current standard. A second group of commenters, mostly representing industry associations, businesses, and states opposed to revising the primary O3 standard, expressed the general view that while many new epidemiologic studies have been published since the last review of the O3 NAAQS, inconsistencies and uncertainties inherent in these studies as a whole, and in the EPA's assessment of study results, should preclude any reliance on them as justification for a more stringent primary O3 standard. To support their views, these commenters often focused on specific technical or methodological issues that contribute to uncertainty in epidemiologic studies, including the potential for exposure error, confounding by copollutants and by other factors (e.g., weather, season, disease, day of week, etc.), and heterogeneity in results across locations.

The EPA agrees with certain aspects of each of these views. Specifically, while the EPA agrees that epidemiologic studies are an important part of the broader body of evidence that supports the ISA's causality determinations, and that these studies provide support for the decision to revise the current primary O3 standard, the Agency also acknowledges that there are important uncertainties and limitations associated with these epidemiologic studies that should be considered when reaching decisions on the current standard. Thus, although these studies show consistent associations between O3 exposures and serious health effects, including morbidity and mortality, and some of these studies reported such associations with ambient O3 concentrations below the level of the current standard, there are also uncertainties regarding the ambient O3 concentrations in critical studies, such that they lend only limited support to establishing a specific level for a revised standard. (See generally, Mississippi, 744 F. 3d at 1351 (noting that in prior review, EPA reasonably relied on epidemiologic information in determining to revise the standard but appropriately gave the information limited weight in determining a level of a revised standard); see also ATA III, 283 F. 3d at 370 (EPA justified in revising NAAQS when health effect associations are observed in epidemiologic studies at levels allowed by the current NAAQS); Mississippi, 744 F. 3d at 1345 (same)).

Uncertainties in the evidence were considered by the Administrator in the proposal, and contributed to her decision to place less weight on information from epidemiologic studies than on information from controlled human exposure studies when considering the adequacy of the current primary O3 standard (see 79 FR 75281-83). Despite receiving less weight in the proposal, the EPA does not agree with commenters who asserted that uncertainties in the epidemiologic evidence provide a basis for concluding that the current primary standard does not need revision. The Administrator specifically considered the extent to which available studies support the occurrence of O3 health effect associations with air quality likely to be allowed by the current standard, while also considering the implications of important uncertainties, as assessed in the ISA and discussed in the PA. This consideration is consistent with CASAC comments on consideration of these studies in the draft PA (Frey, 2014c, p. 5).

Based on analyses of study area air quality in the PA, the EPA notes that most of the U.S. and Canadian epidemiologic studies evaluated were conducted in locations likely to have violated the current standard over at least part of the study period. Although these studies support the ISA's causality determinations, they provide limited insight into the adequacy of the public health protection provided by the current primary O3 standard. However, as discussed in the proposal, air quality analyses in the locations of three U.S. single-city studies provide support for the occurrence of O3-associated hospital admissions or emergency department visits at ambient O3 concentrations below the level of the current standard.[97] Specifically, a U.S. single-city study reported associations with respiratory emergency department visits in children and adults in a location that would have met the current O3 standard over the entire study period (Mar and Koenig, 2009). In addition, for two studies conducted in locations where the current standard was likely not met (i.e., Silverman and Ito, 2010; Strickland et al., 2010), PA analyses indicate that reported concentration-response functions and available air quality data support the occurrence of O3-health effect associations on subsets of days with virtually all monitored ambient O3 concentrations below the level of the current standard (U.S. EPA, 2014c, Start Printed Page 65336section 3.1.4.2, pp. 3-66 to 67).[98] Thus, the EPA notes that a small number of O3 epidemiologic studies provide support for the conclusion that the current primary standard is not requisite, and that it should be revised to increase public health protection.

As part of a larger set of comments criticizing the EPA's interpretation of the evidence from time series epidemiologic studies, some commenters objected to the EPA's reliance on the studies by Strickland et al. (2010), Silverman and Ito (2010), and Mar and Koenig (2009). These commenters highlighted what they considered to be key uncertainties in interpreting these studies, including uncertainties due to the potential for confounding by co-pollutants, aeroallergens, or the presence of upper respiratory infections; and uncertainties in the interpretation of zero-day lag models (i.e., specifically for Mar and Koenig, 2009).

While the EPA agrees that there are uncertainties associated with interpreting the O3 epidemiologic evidence, as discussed above and elsewhere in this preamble, we disagree with commenters' assertion that these uncertainties should preclude the use of the O3 epidemiologic evidence in general, or the studies by Silverman and Ito, Strickland, or Mar and Koenig in particular, as part of the basis for the Administrator's decision to revise the current primary standard. As a general point, when considering the potential importance of uncertainties in epidemiologic studies, we rely on the broader body of evidence, not restricted to these three studies, and the ISA conclusions based on this evidence. The evidence, the ISA's interpretation of specific studies, and the use of information from these studies in the HREA and PA, was considered by CASAC in its review of drafts of the ISA, HREA, and PA. Based on the assessment of the evidence in the ISA, and CASAC's endorsement of the ISA conclusions, as well as CASAC's endorsement of the approaches to using and considering information from epidemiologic studies in the HREA and PA (Frey, 2014c, p. 5), we do not agree with these commenters' conclusions regarding the usefulness of the epidemiologic studies by Strickland et al. (2010), Silverman and Ito (2010), and Mar and Koenig (2009).

More specifically, with regard to confounding by co-pollutants, we note the ISA conclusion that, in studies of O3-associated hospital admissions and emergency department visits “O3 effect estimates remained relatively robust upon the inclusion of PM . . . and gaseous pollutants in two-pollutant models” (U.S. EPA, 2013, pp. 6-152 and 6-153). This conclusion was supported by several studies that evaluated co-pollutant models including, but not limited to, two of the studies specifically highlighted by commenters (i.e., Silverman and Ito, 2010; Strickland et al., 2010) (U.S. EPA, 2013, section 6.2.7.5; Figure 6-20 and Table 6-29).

Other potential uncertainties highlighted by commenters have been evaluated less frequently (e.g., confounding by allergen exposure, respiratory infections). However, we note that Strickland et al. (2010) did consider the potential for pollen (a common airborne allergen) to confound the association between ambient O3 and emergency department visits. While quantitative results were not presented, the authors reported that “estimates for associations between ambient air pollutant concentrations and pediatric asthma emergency department visits were similar regardless of whether pollen concentrations were included in the model as covariates” (Strickland et al., 2010, p. 309). This suggests a limited impact of aeroallergens on O3 associations with asthma-related emergency department visits and hospital admissions.

With respect to the comment about epidemiologic studies not controlling for respiratory infections in the model, the EPA disagrees with the commenter's assertion. We recognize that asthma is a multi-etiologic disease and that air pollutants, including O3, represent only one potential avenue to trigger an asthma exacerbation. Strickland et al. attempted to further clarify the relationship between short-term O3 exposures and asthma emergency department visits by controlling for the possibility that respiratory infections may lead to an asthma exacerbation. By including the daily count of upper respiratory visits as a covariate in the model, Strickland et al. were able to account for the possibility that respiratory infections contribute to the daily counts of asthma emergency department visits, and to identify the O3 effect on asthma emergency department visits. In models that controlled for upper respiratory infection visits, associations between O3 and emergency department visits remained statistically significant (Strickland et al., Table 4 in published study), demonstrating a relatively limited influence of respiratory infections on the association observed between short-term O3 exposures and asthma emergency department visits, contrary to the commenter's claim.

In addition, with regard to the criticism of the results reported by Mar and Koenig, the EPA disagrees with commenters who questioned the appropriateness of a zero-day lag. These commenters specifically noted uncertainty in the relative timing of the O3 exposure and the emergency department visit when they occurred on the same day. However, based on the broader body of evidence the ISA concludes that the strongest support is for a relatively immediate respiratory response following O3 exposures. Specifically, the ISA states that “[t]he collective evidence indicates a rather immediate response within the first few days of O3 exposure (i.e., for lags days averaged at 0-1, 0-2, and 0-3 days) for hospital admissions and [emergency department] visits for all respiratory outcomes, asthma, and chronic obstructive pulmonary disease in all-year and seasonal analyses” (U.S. EPA, 2013, p. 2-32). Thus, the use of a zero-day lag is consistent with the broader body of evidence supporting the occurrence of O3-associated health effects. In addition, while Mar and Koenig reported the strongest associations for zero-day lags, they also reported positive associations for lags ranging from zero to five days (Mar and Koenig, 2009, Table 5 in the published study). In considering this study, the ISA stated that Mar and Koenig (2009) “found consistent positive associations across individual lag days” and that “[f]or children, consistent positive associations were observed across all lags . . . with the strongest associations observed at lag 0 (33.1% [95% CI: 3.0, 68.5]) and lag 3 (36.8% [95% CI: 6.1, 77.2])” (U.S. EPA, 2013, p. 6-150). Given support for a relatively immediate response to O3 and given the generally consistent results in analyses using various lags, we disagree with commenters who asserted that the use of a zero-day lag represents an important uncertainty in the interpretation of the study by Mar and Koenig (2009).

Given all of the above, we do not agree with commenters who asserted that uncertainties in the epidemiologic evidence in general, or in specific key studies, should preclude the Start Printed Page 65337Administrator from relying on those studies to inform her decisions on the primary O3 standard.

Some commenters also objected to the characterization in the ISA and the proposal that the results of epidemiologic studies are consistent. These commenters contended that the purported consistency of results across epidemiologic studies is the result of inappropriate selectivity on the part of the EPA in focusing on specific studies and specific results within those studies. In particular, commenters contend that EPA favors studies that show positive associations and selectively ignores certain studies that report null results. They also cite a study published after the completion of the ISA (Goodman et al., 2013) suggesting that, in papers where the results of more than one statistical model are reported, the EPA tends to report the results with the strongest associations.

The EPA disagrees that it has inappropriately focused on specific positive studies or specific positive results within individual studies. The ISA appropriately builds upon the assessment of the scientific evidence presented in previous AQCDs and ISAs.[99] When evaluating new literature, “[s]election of studies for inclusion in the ISA is based on the general scientific quality of the study, and consideration of the extent to which the study is informative and policy-relevant” (U.S. EPA, 2013, p. liii). In addition, “the intent of the ISA is to provide a concise review, synthesis, and evaluation of the most policy-relevant science to serve as a scientific foundation for the review of the NAAQS, not extensive summaries of all health, ecological and welfare effects studies for a pollutant” (U.S. EPA, 2013, p. lv). Therefore, not all studies published since the previous review would be appropriate for inclusion in the ISA.[100] With regard to the specific studies that are included in the ISA, and the analyses focused upon within given studies, the EPA notes that the ISA undergoes extensive peer review in a public setting by the CASAC. This process provides ample opportunity for CASAC and the public to comment on studies not included in the ISA, and on the specific analyses focused upon within individual studies. In endorsing the final O3 ISA as adequate for rule-making purposes, CASAC agreed with the selection and presentation of analyses on which to base the ISA's key conclusions.

iii. Evidence Pertaining to At-Risk Populations and Lifestages

A number of groups submitted comments on the EPA's identification of at-risk populations and lifestages. Some industry commenters who opposed revising the current standard disagreed with the EPA's identification of people with asthma or other respiratory diseases as an at-risk population for O3-attributable effects, citing controlled human exposure studies that did not report larger O3-induced FEV1 decrements in people with asthma than in people without asthma. In contrast, comments from medical, environmental, and public health groups generally agreed with the at-risk populations identified by EPA, and also identified other populations that they stated should be considered at risk, including people of lower socio-economic status, people with diabetes or who are obese, pregnant women (due to reproductive and developmental effects, and African American, Asian, Hispanic/Latino or tribal communities. As support for the additional populations, these commenters cited various studies, including some that were not included in the ISA (which we have provisionally considered, as described in section I.C above).

With regard to the former group of comments stating that the evidence does not support the identification of asthmatics as an at-risk population, we disagree. As summarized in the proposal, the EPA's identification of populations at risk of O3 effects is based on a systematic approach that assesses the current scientific evidence across the relevant scientific disciplines (i.e., exposure sciences, dosimetry, controlled human exposure, toxicology, and epidemiology), with a focus on studies that conducted stratified analyses allowing for an evaluation of different populations exposed to similar O3 concentrations within the same study design (U.S. EPA, 2013, pp. 8-1 to 8-3). Based on this established process and framework, the ISA identifies individuals with asthma among the populations and lifestages for which there is “adequate” evidence to support the conclusion of increased risk of O3-related health effects. Other populations for which the evidence is adequate are individuals with certain genotypes, younger and older age groups, individuals with reduced intake of certain nutrients, and outdoor workers. These conclusions are based on consistency in findings across studies and evidence of coherence in results from different scientific disciplines.

For example, with regard to people with asthma, the ISA notes a number of epidemiologic and controlled human exposure studies reporting larger and/or more serious effects in people with asthma than in people without asthma or other respiratory diseases. These include epidemiologic studies of lung function, respiratory symptoms, and medication use, as well as controlled human exposure studies showing larger inflammatory responses and markers indicating altered immune functioning in people with asthma, and also includes evidence from animal models of asthma that informs the EPA's interpretation of the other studies. We disagree with the industry commenters' focus solely on the results of certain studies without an integrated consideration of the broader body of evidence, and wider range of respiratory endpoints. It is such an integrated approach that supports EPA's conclusion that “there is adequate evidence for asthmatics to be an at-risk population” (U.S. EPA, 2013, section 8.2.2).

We also disagree with commenters' misleading reference to various studies cited to support the claim that asthmatics are not at increased risk of O3-related health effects. One of the controlled human studies cited in those comments (Mudway et al. 2001) involved asthmatic adults who were older than the healthy controls, and it is well-recognized that responses to O3 decrease with age (U.S. EPA, 2014c, p. 3-80). Another study (Alexis et al. 2000) used subjects with mild asthma who are unlikely to be as responsive as people with more severe disease (Horstman et al., 1995) (EPA 2014c, p. 3-80). Controlled human exposure studies and epidemiologic studies of adults and children amply confirm that “there is adequate evidence for asthmatics to be an at-risk population” (U.S. EPA, 2014c, p. 3-81).Start Printed Page 65338

We also do not agree with the latter group of commenters that there is sufficient evidence to support the identification of additional populations as at risk of O3-attributable health effects. Specifically with regard to pregnant women, the ISA concluded that the “evidence is suggestive of a causal relationship between exposures to O3 and reproductive and developmental effects” including birth outcomes, noting that “the collective evidence for many of the birth outcomes examined is generally inconsistent” (U.S. EPA, 2013, pp. 7-74 and 7-75). At the time of the completion of the ISA, no studies had been identified that examined the relationship between exposure to O3 and the health of pregnant women (e.g., studies on pre-eclampsia, gestational hypertension). Due to the generally inconsistent epidemiologic evidence for effects on birth outcomes, the lack of studies on the health of pregnant women, and the lack of studies from other disciplines to provide biological plausibility for the effects examined in epidemiologic studies, pregnant women were not considered an at-risk population. Based on the EPA's provisional consideration of studies published since the completion of the ISA (I.C, above), recent studies that examine exposure to O3 and pre-eclampsia and other health effects experienced by pregnant women are not sufficient to materially change the ISA's conclusions on at-risk populations (I.C, above). In addition, as summarized in the proposal, the ISA concluded that the evidence for other populations was either suggestive of increased risk, with further investigation needed (e.g., other genetic variants, obesity, sex, and socioeconomic status), or was inadequate to determine if they were of increased risk of O3-related health effects (influenza/infection, COPD, CVD, diabetes, hyperthyroidism, smoking, race/ethnicity, and air conditioning use) (U.S. EPA, 2013, section 2.5.4.1). The CASAC has concurred with the ISA conclusions (Frey, 2014c).

c. Comments on Exposure and Risk Assessments

This section discusses major comments on the EPA's quantitative assessments of O3 exposures and health risks, presented in the HREA and considered in the PA, and the EPA's responses to those comments. The focus in this section is on overarching comments related to the EPA's approach to assessing exposures and risks, and to interpreting the exposure/risk results within the context of the adequacy of the current primary O3 standard. More detailed discussion of comments and Agency responses is provided in the Response to Comments document. Section II.B.2.c.i discusses comments on estimates of O3 exposures of concern, section II.B.2.c.ii discusses comments on estimates of the risk of O3-induced lung function decrements, and section II.B.2.b.iii discusses comments on estimates of the risk of O3-associated mortality and morbidity.

i. O3 Exposures of Concern

The EPA received a number of comments expressing divergent views on the estimation of, and interpretation of, O3 exposures of concern. In general, comments from industry, business, and some state groups opposed to revising the current primary O3 standard asserted that the approaches and assumptions that went into the HREA assessment result in overestimates of O3 exposures. These commenters highlighted several aspects of the assessment, asserting that the HREA overestimates the proportion of the population expected to achieve ventilation rates high enough to experience an exposure of concern; that the use of out-of-date information on activity patterns results in overestimates of the amount of time people spend being active outdoors; and that exposure estimates do not account for the fact that people spend more time indoors on days with bad air quality (i.e., they engage in averting behavior). In contrast, comments from medical, public health, and environmental groups that supported revision of the current standard asserted that the HREA assessment of exposures of concern, and the EPA's interpretation of exposure estimates, understates the potential for O3 exposures that could cause adverse health effects. These commenters claimed that the EPA's focus on 8-hour exposures understates the O3 impacts on public health since effects in controlled human exposure studies were shown following 6.6-hour exposures; that the HREA exposure estimates do not capture the most highly exposed populations, such as highly active children and outdoor workers; and that the EPA's interpretation of estimated exposures of concern impermissibly relies on the assumption that people stay indoors to avoid dangerous air pollution (i.e., that they engage in averting behavior).

In considering these comments, the EPA first notes that as discussed in the HREA, PA, and the proposal, there are aspects of the exposure assessment that, considered by themselves, can result in either overestimates or underestimates of the occurrence of O3 exposures of concern. Commenters tended to highlight the aspects of the assessment that supported their positions, including aspects that were discussed in the HREA and/or the PA and that were considered by CASAC. In contrast, commenters tended to ignore the aspects of the assessment that did not support their positions. The EPA has carefully described and assessed the significance of the various uncertainties in the exposure analysis (U.S. EPA, 2014a, Table 5-10), noting that, in most instances, the uncertainties could result in either overestimates or underestimates of exposures and that the magnitudes of the impacts on exposure results were either “low,” “low to moderate,” or “moderate” (U.S. EPA, 2014a, Table 5-10).

Consistent with the characterization of uncertainties in the HREA, PA, and the proposal, the EPA agrees with some, though not all, aspects of these commenters' views. For example, the EPA agrees with the comment by groups opposed to revision that the equivalent ventilation rate (EVR) used to characterize individuals as at moderate or greater exertion in the HREA likely leads to overestimates of the number of individuals experiencing exposures of concern (U.S. EPA, 2014a, Table 5-10, p. 5-79). In addition, we note that other physiological processes that are incorporated into exposure estimates are also identified in the HREA as likely leading to overestimates of O3 exposures, based on comparisons with the available scientific literature (U.S. EPA, 2014a, Table 5-10, p. 5-79). These aspects of the exposure assessment are estimated to have either a “moderate” (i.e., EVR) or a “low to moderate” (i.e., physiological processes) impact on exposure estimates (U.S. EPA, 2014a, Table 5-10, p. 5-79). Focusing on these aspects of the assessment, by themselves, could lead to the conclusion that the HREA overstates the occurrence of O3 exposures of concern.

However, the EPA notes that there are also aspects of the HREA exposure assessment that, taken by themselves, could lead to the conclusion that the HREA understates the occurrence of O3 exposures of concern. For example, as noted above, some medical, public health, and environmental groups asserted that the exposure assessment could underestimate O3 exposures for highly active populations, including outdoor workers and children who spend a large portion of time outdoors during summer. In support of these assertions, commenters highlighted sensitivity analyses conducted in the HREA. However, as noted in the HREA (U.S. EPA, 2014a, Table 5-10), this Start Printed Page 65339aspect of the assessment is likely to have a “low to moderate” impact on exposure estimates (i.e., a smaller impact than uncertainty associated with the EVR, and similar in magnitude to uncertainties related to physiological processes, as noted above). Therefore, when considered in the context of all of the uncertainties in exposure estimates, it is unlikely that the HREA's approach to using data on activity patterns leads to overall underestimates of O3 exposures. The implications of this uncertainty are discussed in more detail below (II.C.4.b), within the context of the Administrator's decision on a revised standard level.

In addition, medical, public health, and environmental groups also pointed out that the controlled human exposures studies that provided the basis for health effect benchmarks were conducted in healthy adults, rather than at-risk populations, and these studies evaluated 6.6 hour exposures, rather than the 8-hour exposures evaluated in the HREA exposure analyses. They concluded that adverse effects would occur at lower exposure concentrations in at-risk populations, such as people with asthma, and if people were exposed for 8 hours, rather than 6.6 hours. In its review of the PA, CASAC clearly recognized these uncertainties, which provided part of the basis for CASAC's advice to consider exposures of concern for the 60 ppb benchmark. For example, when considering the results of the study by Schelegle et al. (2009) for 6.6-hour exposures to an average O3 concentration of 72 ppb, CASAC judged that if subjects had been exposed for eight hours, the adverse combination of lung function decrements and respiratory symptoms “could have occurred” at lower O3 exposure concentrations (Frey, 2014c, p. 5). With regard to at-risk populations, CASAC concluded that “based on results for clinical studies of healthy adults, and scientific considerations of differences in responsiveness of asthmatic children compared to healthy adults, there is scientific support that 60 ppb is an appropriate exposure of concern for asthmatic children” (Frey, 2014c, p. 8). As discussed below (II.B.3, II.C.4.b, II.C.4.c), based in large part on CASAC advice, the Administrator does consider exposure results for the 60 ppb benchmark.

Thus, rather than viewing the potential implications of various aspects of the HREA exposure assessment in isolation, as was done by many commenters, the EPA considers them together, along with other issues and uncertainties related to the interpretation of exposure estimates. As discussed above, CASAC recognized the key uncertainties in exposure estimates, as well as in the interpretation of those estimates in the HREA and PA (Frey, 2014a, c). In its review of the 2nd draft REA, CASAC concluded that “[t]he discussion of uncertainty and variability is comprehensive, appropriately listing the major sources of uncertainty and their potential impacts on the APEX exposure estimates” (Frey, 2014a, p. 6). Even considering these and other uncertainties, CASAC emphasized estimates of O3 exposures of concern as part of the basis for their recommendations on the primary O3 NAAQS. In weighing these uncertainties, which can bias exposure results in different directions but tend to have impacts that are similar in magnitude (U.S. EPA, 2014a, Table 5-10), and in light of CASAC's advice based on its review of the HREA and the PA, the EPA continues to conclude that the approach to considering estimated exposures of concern in the HREA, PA, and the proposal reflects an appropriate balance, and provides an appropriate basis for considering the public health protectiveness of the primary O3 standard.

The EPA disagrees with other aspects of commenters' views on HREA estimates of exposures of concern. For example, commenters on both sides of the issue objected to the EPA's handling of averting behavior in exposure estimates. Some commenters who supported retaining the current standard claimed that the HREA overstates exposures of concern because available time-location-activity data do not account for averting behavior. These commenters noted sensitivity analyses in the HREA that estimated fewer exposures of concern when averting behavior was considered. In contrast, commenters supporting revision of the standard criticized the EPA's estimates of exposures of concern, claiming that the EPA “emphasizes the role of averting behavior, noting that it may result in an overestimation of exposures of concern, and cites this behavior (essentially staying indoors or not exercising) in order to reach what it deems an acceptable level of risk” (e.g., ALA et al., p. 120).

The EPA disagrees with both of these comments. In brief, the NAAQS must “be established at a level necessary to protect the health of persons,” not the health of persons refraining from normal activity or resorting to medical interventions to ward off adverse effects of poor air quality (S. Rep. No. 11-1196, 91st Cong. 2d Sess. at 10). On the other hand, ignoring normal activity patterns for a pollutant like O3, where adverse responses are critically dependent on ventilation rates, will result in a standard which provides more protection than is requisite. This issue is discussed in more detail below (II.C.4.b), within the context of the Administrator's decision on a revised standard level.

These commenters also misconstrue the EPA's limited sensitivity analyses on impacts of averting behavior in the HREA. The purpose of the HREA sensitivity analyses was to provide perspective on the potential role of averting behavior in modifying O3 exposures. These sensitivity analyses were limited to a single urban study area, a 2-day period, and a single air quality adjustment scenario (U.S. EPA, 2014a, section 5.4.3.3). In addition, the approach used in the HREA to simulate averting behavior was itself uncertain, given the lack of actual activity pattern data that explicitly incorporated this type of behavioral response. In light of these important limitations, sensitivity analyses focused on averting behavior were discussed in the proposal within the context of the discussion of uncertainties in the HREA assessment of exposures of concern (II.C.2.b in the proposal) and, contrary to the claims of some commenters, they were not used to support the proposed decision.

Some industry groups also claimed that the time-location-activity diaries used by APEX to estimate exposures are out-of-date, and do not represent activity patterns in the current population. These commenters asserted that the use of out-of-date diary information leads to overestimates in exposures of concern. This issue was explicitly addressed in the HREA and the EPA disagrees with commenters' conclusions. In particular, diary data was updated in this review to include data from studies published as late as 2010, directly in response to CASAC concerns. In their review of this data, CASAC stated that “[t]he addition of more recent time activity pattern data addresses a concern raised previously by the CASAC concerning how activity pattern information should be brought up to date” (Frey, 2014a, p. 8). As indicated in the HREA (U.S. EPA, 2014a, Appendix 5G, Figures 5G-7 and Figure 5G-8), the majority of diary days used in exposure simulations of children originate from the most recently conducted activity pattern studies (U.S. EPA, 2014a, Table 5-3). In addition, evaluations included in the HREA indicated that there were not major systematic differences in time-location-activity patterns based on information from older diaries versus those collected more recently (U.S. EPA, Start Printed Page 653402014a, Appendix 5G, Figures 5G-1 and 5G-2). Given all of the above, the EPA does not agree with commenters who claimed that the time-location-activity diaries used by APEX are out-of-date, and result in overestimates of exposures of concern.

ii. Risk of O3-Induced FEV1 Decrements

The EPA also received a large number of comments on the FEV1 risk assessment presented in chapter 6 of the HREA (U.S. EPA, 2014a) and summarized in the proposal (II.C.3.a in the proposal). Commenters representing medical, public health, and environmental groups generally expressed the view that these risk estimates support the need to revise the current primary O3 standard in order to increase public health protection, though these groups also questioned some of the assumptions inherent in the EPA's interpretation of those risk estimates. For example, ALA et al. (p. 127) stated that “[t]he HREA uses a risk function derived from a controlled human exposure study of healthy young adults to estimate lung function decrements in children, including children with asthma. This assumption could result in an underestimate of risk.” On this same issue, commenters representing industry groups opposed to revising the standard also asserted that assumptions about children's responses to O3 exposures are highly uncertain. In contrast to medical and public health groups, these commenters concluded that this uncertainty, along with others discussed below, call into question the use of FEV1 risk estimates to support a decision to revise the current primary O3 standard.

The EPA agrees that an important source of uncertainty is the approach to estimating the risk of FEV1 decrements in children and in children with asthma based on data from healthy adults. However, this issue is discussed at length in the HREA and the PA, and was considered carefully by CASAC in its review of draft versions of these documents. The conclusions of the HREA and PA, and the advice of CASAC, were reflected in the Administrator's interpretation of FEV1 risk estimates in the proposal, as described below. Commenters have not provided additional information that changes the EPA's views on this issue.

As discussed in the proposal (II.C.3.a.ii in the proposal), in the near absence of controlled human exposure data for children, risk estimates are based on the assumption that children exhibit the same lung function response following O3 exposures as healthy 18-year olds (i.e., the youngest age for which sufficient controlled human exposure data is available) (U.S. EPA, 2014a, section 6.5.3). As noted by CASAC (Frey, 2014a, p. 8), this assumption is justified in part by the findings of McDonnell et al. (1985), who reported that children (8-11 years old) experienced FEV1 responses similar to those observed in adults (18-35 years old). The HREA concludes that this approach could result in either over- or underestimates of O3-induced lung function decrements in children, depending on how children compare to the adults used in controlled human exposure studies (U.S. EPA, 2014a, section 6.5.3). With regard to people with asthma, although the evidence has been mixed (U.S. EPA, 2013, section 6.2.1.1), several studies have reported statistically larger, or a tendency for larger, O3-induced lung function decrements in asthmatics than in non-asthmatics (Kreit et al., 1989; Horstman et al., 1995; Jorres et al., 1996; Alexis et al., 2000). On this issue, CASAC noted that “[a]sthmatic subjects appear to be at least as sensitive, if not more sensitive, than non-asthmatic subjects in manifesting O3-induced pulmonary function decrements” (Frey, 2014c, p. 4). To the extent asthmatics experience larger O3-induced lung function decrements than the healthy adults used to develop exposure-response relationships, the HREA could underestimate the impacts of O3 exposures on lung function in asthmatics, including asthmatic children (U.S. EPA, 2014a, section 6.5.4). As noted above, these uncertainties have been considered carefully by the EPA and by CASAC during the development of the HREA and PA. In addition, the Administrator has appropriately considered these and other uncertainties in her interpretation of risk estimates, as discussed further below (II.B.3, II.C.4.b, II.C.4.c).

Some commenters additionally asserted that the HREA does not appropriately characterize the uncertainty in risk estimates for O3-induced lung function decrements. Commenters pointed out that there is statistical uncertainty in model coefficients that is not accounted for in risk estimates. One commenter presented an analysis of this uncertainty, and concluded that there is considerable overlap between risk estimates for standard levels of 75, 70, and 65 ppb, undercutting the confidence in estimated risk reductions for standard levels below 75 ppb.

The Agency recognizes that there are important sources of uncertainty in the FEV1 risk assessment. In some cases, these sources of uncertainty can contribute to substantial variability in risk estimates, complicating the interpretation of those estimates. For example, as discussed in the proposal, the variability in FEV1 risk estimates across urban study areas is often greater than the differences in risk estimates between various standard levels (Table 2, above and 79 FR 75306 n. 164). Given this, and the resulting considerable overlap between the ranges of FEV1 risk estimates for different standard levels, in the proposal the Administrator viewed these risk estimates as providing a more limited basis than exposures of concern for distinguishing between the degree of public health protection provided by alternative standard levels. Thus, although the EPA does not agree with the overall conclusions of industry commenters, their analysis of statistical uncertainty in risk estimates, and the resulting overlap between risk estimates for standard levels of 75, 70, and 65 ppb, tends to reinforce the Administrator's approach, which places greater weight on estimates of O3 exposures of concern than on risk estimates for O3-induced FEV1 decrements.

iii. Risk of O3-Associated Mortality and Morbidity

In the proposal, the Administrator placed the greatest emphasis on the results of controlled human exposure studies and on quantitative analyses based on information from these studies, and less weight on mortality and morbidity risk assessments based on information from epidemiology studies. The EPA received a number of comments on its consideration of epidemiology-based risks, with some commenters expressing support for the Agency's approach and others expressing opposition.

In general, commenters representing industry organizations or states opposed to revising the current primary O3 standard agreed with the Administrator's approach in the proposal to viewing epidemiology-based risk estimates, though these commenters reached a different conclusion than the EPA regarding the adequacy of the current standard. In supporting their views, these commenters highlighted a number of uncertainties in the underlying epidemiologic studies, and concluded that risk estimates based on information from such studies do not provide an appropriate basis for revising the current standard. For example, commenters noted considerable spatial heterogeneity in health effect associations; the potential for co-occurring pollutants (e.g., PM2.5) to confound O3 health effect associations; Start Printed Page 65341and the lack of statistically significant O3 health effect associations in many of the individual cities evaluated as part of multicity analyses. In contrast, some commenters representing medical, public health, or environmental organizations placed greater emphasis than the EPA on epidemiology-based risk estimates. These commenters asserted that risk estimates provide strong support for a lower standard level, and pointed to CASAC advice to support their position.

As in the proposal, the EPA continues to place the greatest weight on the results of controlled human exposure studies and on quantitative analyses based on information from these studies (particularly exposures of concern, as discussed below in II.B.3 and II.C.4), and less weight on risk analyses based on information from epidemiologic studies. In doing so, the Agency continues to note that controlled human exposure studies provide the most certain evidence indicating the occurrence of health effects in humans following specific O3 exposures. In addition, the effects reported in these studies are due solely to O3 exposures, and interpretation of study results is not complicated by the presence of co-occurring pollutants or pollutant mixtures (as is the case in epidemiologic studies). The Agency further notes the CASAC judgment that “the scientific evidence supporting the finding that the current standard is inadequate to protect public health is strongest based on the controlled human exposure studies of respiratory effects” (Frey, 2014c, p. 5). Consistent with this emphasis, the HREA conclusions reflect relatively greater confidence in the results of the exposure and risk analyses based on information from controlled human exposure studies than the results of epidemiology-based risk analyses. As discussed in the HREA (U.S. EPA, 2014a, section 9.6), several key uncertainties complicate the interpretation of these epidemiology-based risk estimates, including the heterogeneity in O3 effect estimates between locations, the potential for exposure measurement errors in these epidemiologic studies, and uncertainty in the interpretation of the shape of concentration-response functions at lower O3 concentrations. Commenters who opposed the EPA's approach in the proposal to viewing the results of quantitative analyses tended to highlight aspects of the evidence and CASAC advice that were considered by the EPA at the time of proposal and nothing in these commenters' views has changed those considerations. Therefore, the EPA continues to place the most emphasis on using the information from controlled human exposure studies to inform consideration of the adequacy of the primary O3 standard.

However, while the EPA agrees that there are important uncertainties in the O3 epidemiology-based risk estimates, the Agency disagrees with industry commenters that these uncertainties support a conclusion to retain the current standard. As discussed below, the decision to revise the current primary O3 standard is based on the EPA's consideration of the broad body of scientific evidence, quantitative analyses of O3 exposures and risks, CASAC advice, and public comments. While recognizing uncertainties in the epidemiology-based risk estimates here, and giving these uncertainties appropriate consideration, the Agency continues to conclude that these risk estimates contribute to the broader body of evidence and information supporting the need to revise the primary O3 standard.

Some commenters opposed to revising the current O3 standard highlighted the fact that, in a few urban study locations, larger risks are estimated for standard levels below 75 ppb than for the current standard with its level of 75 ppb. For example, TCEQ (p. 3) states that “differential effects on ozone in urban areas also lead to the EPA's modeled increases in mortality in Houston and Los Angeles with decreasing ozone standards.” These commenters cited such increases in estimated risk as part of the basis for their conclusion that the current standard should be retained.

For communities across the U.S. (including in the Houston and Los Angeles areas), exposure and risk analyses indicate that reducing emissions of O3 precursors (NOX, VOCs) to meet a revised standard with a level of 70 ppb will substantially reduce the occurrence of adverse respiratory effects and mortality risk attributable to high O3 concentrations (U.S. EPA, 2014a, Appendix 9A; U.S. EPA, 2014c, sections 4.4.2.1 to 4.4.2.3). However, because of the complex chemistry governing the formation and destruction of O3, some NOX control strategies designed to reduce the highest ambient O3 concentrations can also result in increases in relatively low ambient O3 concentrations. As a result of the way the EPA's epidemiology-based risk assessments were conducted (U.S. EPA, 2014a, Chapter 7), increases estimated in low O3 concentrations impacted mortality and morbidity risks, leading to the estimated risk increases highlighted by some commenters. However, while the EPA is confident that reducing the highest ambient O3 concentrations will result in substantial improvements in public health, including reducing the risk of O3-associated mortality, the Agency is far less certain about the public health implications of the changes in relatively low ambient O3 concentrations (79 FR at 75278/3, 75291/1, and 75308/2). Therefore, reducing precursor emissions to meet a lower O3 standard is expected to result in important reductions in O3 concentrations from the part of the air quality distribution where the evidence provides the strongest support for adverse health effects.

Specifically, for area-wide O3 concentrations at or above 40 ppb,[101] a revised standard with a level of 70 ppb is estimated to reduce the number of premature deaths associated with short-term O3 concentrations by about 10%, compared to the current standard. In addition, for area-wide concentrations at or above 60 ppb, a revised standard with a level of 70 ppb is estimated to reduce O3-associated premature deaths by about 50% to 70%.[102] The EPA views these results, which focus on the portion of the air quality distribution where the evidence indicates the most certainty regarding the occurrence of adverse O3-attributable health effects, not only as supportive of the need to revise the current standard (II.B.3, below), but also as showing the benefits of reducing the peak O3 concentrations associated with air quality distributions meeting the current standard (II.C.4, below).

In addition, even considering risk estimates based on the full distribution of ambient O3 concentrations (i.e., estimates influenced by decreases in higher concentrations and increases in lower concentrations), the EPA notes that, compared to the current standard, standards with lower levels are estimated to result in overall reductions in mortality risk across the urban study areas evaluated (U.S. EPA, 2014c, Figure 4-10). As discussed above (II.A.2.a, II.A.2.c), analyses in the HREA indicate that these overall risk reductions could understate the actual reductions that Start Printed Page 65342would be experienced by the U.S. population as a whole.

For example, the HREA's national air quality modeling analyses indicate that the HREA urban study areas tend to underrepresent the populations living in areas where reducing NOX emissions would be expected to result in decreases in warm season averages of daily maximum 8-hour ambient O3 concentrations.[103] Given the strong connection between these warm season average O3 concentrations and risk, risk estimates for the urban study areas are likely to understate the average reductions in O3-associated mortality and morbidity risks that would be experienced across the U.S. population as a whole upon reducing NOX emissions (U.S. EPA, 2014a, section 8.2.3.2).

In addition, in recognizing that the reductions in modeled NOX emissions used in the HREA's core analyses are meant to be illustrative, rather than to imply a particular control strategy for meeting a revised O3 NAAQS, the HREA also conducted sensitivity analyses in which both NOX and VOC emissions reductions were evaluated. In all of the urban study areas evaluated in these analyses, the increases in low O3 concentrations were smaller for the NOX/VOC emission reduction scenarios than the NOX only emission reduction scenario (U.S. EPA, 2014a, Appendix 4D, section 4.7). This was most apparent for Denver, Houston, Los Angeles, New York, and Philadelphia. These results suggest that in some locations, optimized emissions reduction strategies could result in larger reductions in O3-associated mortality and morbidity than indicated by HREA's core estimates.

Thus, the patterns of estimated mortality and morbidity risks across various air quality scenarios and locations have been evaluated and considered extensively in the HREA and the PA, as well as in the proposal. Epidemiology-based risk estimates have also been considered by CASAC, and those considerations are reflected in CASAC's advice. Specifically, in considering epidemiology-based risk estimates in its review of the REA, CASAC stated that “[a]lthough these estimates for short-term exposure impacts are subject to uncertainty, the CASAC is confident that that the evidence of health effects of O3 presented in the ISA and Second Draft HREA in its totality, indicates that there are meaningful reductions in mean, absolute, and relative premature mortality associated with short-term exposures to O3 levels lower than the current standard” (Frey, 2014a, p. 3). Commenters' views on this issue are not based on new information, but on an interpretation of the analyses presented in the HREA that is different from the EPA's, and CASAC's, interpretation. Given this, the EPA's considerations and conclusions related to this issue, as described in the proposal and as summarized briefly above, remain valid. Therefore, the EPA does not agree with commenters who cited increases in estimated risk in some locations as supporting a conclusion that the current standard should be retained.

For risk estimates of respiratory mortality associated with long-term O3, several industry commenters supported placing more emphasis on threshold models, and including these models as part of the core analyses rather than as sensitivity analyses. The EPA agrees with these commenters that an important uncertainty in risk estimates of respiratory mortality associated with long-term O3 stems from the potential for the existence of a threshold. Based on sensitivity analyses included in the HREA in response to CASAC advice, the existence of a threshold could substantially reduce estimated risks. CASAC discussed this issue at length during its review of the REA and supported the EPA's approach to including a range of threshold models as sensitivity analyses (Frey, 2014a p. 3). Based in part on uncertainty in the existence and identification of a threshold, the HREA concluded that lower confidence should be placed in risk estimates for respiratory mortality associated with long-term O3 exposures (U.S. EPA, 2014a, section 9.6). This uncertainty was also a key part of the Administrator's rationale for placing only limited emphasis on risk estimates for long-term O3 exposures. In her final decisions, discussed below (II.B.3, II.C.4.b, II.C.4.c), the Administrator continues to place only limited emphasis on these estimates. The EPA views this approach to considering risk estimates for respiratory mortality as generally consistent with the approach supported by the commenters noted above.

3. Administrator's Conclusions on the Need for Revision

This section discusses the Administrator's conclusions related to the adequacy of the public health protection provided by the current primary O3 standard, and her final decision that the current standard is not requisite to protect public health with an adequate margin of safety. These conclusions, and her final decision, are based on the Administrator's consideration of the available scientific evidence assessed in the ISA (U.S. EPA, 2013), the exposure/risk information presented and assessed in the HREA (U.S. EPA, 2014a), the consideration of that evidence and information in the PA (U.S. EPA, 2014c), the advice of CASAC, and public comments received on the proposal.

As an initial matter, the Administrator concludes that reducing precursor emissions to achieve O3 concentrations that meet the current primary O3 standard will provide important improvements in public health protection, compared to recent air quality. In reaching this conclusion, she notes the discussion in section 3.4 of the PA (U.S. EPA, 2014c). In particular, the Administrator notes that this conclusion is supported by (1) the strong body of scientific evidence indicating a wide range of adverse health outcomes attributable to exposures to O3 at concentrations commonly found in the ambient air and (2) estimates indicating decreased occurrences of O3 exposures of concern and decreased O3-associated health risks upon meeting the current standard, compared to recent air quality. Thus, she concludes that it would not be appropriate in this review to consider a standard that is less protective than the current standard.

After reaching the conclusion that meeting the current primary O3 standard will provide important improvements in public health protection, and that it is not appropriate to consider a standard that is less protective than the current standard, the Administrator next considers the adequacy of the public health protection that is provided by the current standard. In doing so, the Administrator first notes that studies evaluated since the completion of the 2006 AQCD support and expand upon the strong body of evidence that, in the last review, indicated a causal relationship between short-term O3 exposures and respiratory morbidity outcomes (U.S. EPA, 2013, section 2.5). This is the strongest causality finding possible under the ISA's hierarchical system for classifying weight of evidence for causation. In addition, the Administrator notes that the evidence for respiratory health effects attributable to long-term O3 exposures, including the development of asthma in children, is much stronger than in previous reviews, and the ISA concludes that there is “likely to be” a causal relationship Start Printed Page 65343between such O3 exposures and adverse respiratory health effects (the second strongest causality finding).

Together, experimental and epidemiologic studies support conclusions regarding a continuum of O3 respiratory effects ranging from small, reversible changes in pulmonary function, and pulmonary inflammation, to more serious effects that can result in respiratory-related emergency department visits, hospital admissions, and premature mortality. Recent animal toxicology studies support descriptions of modes of action for these respiratory effects and augment support for biological plausibility for the role of O3 in reported effects. With regard to mode of action, evidence indicates that the initial key event is the formation of secondary oxidation products in the respiratory tract, that antioxidant capacity may modify the risk of respiratory morbidity associated with O3 exposure, and that the inherent capacity to quench (based on individual antioxidant capacity) can be overwhelmed, especially with exposure to elevated concentrations of O3.

In addition, based on the consistency of findings across studies and the coherence of results from different scientific disciplines, the available evidence indicates that certain populations are at increased risk of experiencing O3-related effects, including the most severe effects. These include populations and lifestages identified in previous reviews (i.e., people with asthma, children, older adults, outdoor workers) and populations identified since the last review (i.e., people with certain genotypes related to antioxidant and/or anti-inflammatory status; people with reduced intake of certain antioxidant nutrients, such as Vitamins C and E).

In considering the O3 exposure concentrations reported to elicit respiratory effects, as in the proposal, the Administrator agrees with the conclusions of the PA that controlled human exposure studies provide the most certain evidence indicating the occurrence of health effects in humans following specific O3 exposures. In particular, she notes that the effects reported in controlled human exposure studies are due solely to O3 exposures, and interpretation of study results is not complicated by the presence of co-occurring pollutants or pollutant mixtures (as is the case in epidemiologic studies). Therefore, consistent with CASAC advice (Frey, 2014c), she places the most weight on information from controlled human exposure studies in reaching conclusions on the adequacy of the current primary O3 standard.

In considering the evidence from controlled human exposure studies, the Administrator first notes that these studies have reported a variety of respiratory effects in healthy adults following exposures to O3 concentrations of 60, 63,[104] 72,[105] or 80 ppb, and higher. The largest respiratory effects, and the broadest range of effects, have been studied and reported following exposures of healthy adults to 80 ppb O3 or higher, with most exposure studies conducted at these higher concentrations. As discussed above (II.A.1), the Administrator further notes that recent evidence includes controlled human exposure studies reporting the combination of lung function decrements and respiratory symptoms in healthy adults engaged in moderate exertion following 6.6-hour exposures to concentrations as low as 72 ppb, and lung function decrements and pulmonary inflammation following exposures to O3 concentrations as low as 60 ppb.

As discussed in her response to public comments above (II.B.2.b.i), and in detail below (II.C.4.b, II.C.4.c), the Administrator concludes that these controlled human exposure studies indicate that adverse effects are likely to occur following exposures to O3 concentrations below the level of the current standard. The effects observed following such exposures are coherent with the serious health outcomes that have been reported in O3 epidemiologic studies (e.g., respiratory-related hospital admissions, emergency department visits), and the Administrator judges that such effects have the potential to be important from a public health perspective.

In reaching these conclusions, she particularly notes that the combination of lung function decrements and respiratory symptoms reported to occur in healthy adults following exposures to 72 ppb O3 meets ATS criteria for an adverse response (II.B.2.b.i, above). In specifically considering the 72 ppb exposure concentration, CASAC noted that “the combination of decrements in FEV1 together with the statistically significant alterations in symptoms in human subjects exposed to 72 ppb ozone meets the American Thoracic Society's definition of an adverse health effect” (Frey, 2014c, p. 5). In addition, given that the controlled human exposure study reporting these results was conducted in healthy adults, CASAC judged that the adverse combination of lung function decrements and respiratory symptoms “almost certainly occur in some people” (e.g., people with asthma) following exposures to lower O3 concentrations (Frey, 2014c, p. 6).

While the Administrator is less certain regarding the adversity of the lung function decrements and airway inflammation that have been observed following exposures as low as 60 ppb, as discussed in more detail elsewhere in this preamble (II.B.2.b.i, II.C.4.b, II.C.4.c), she judges that these effects also have the potential to be adverse, and to be of public health importance, particularly if they are experienced repeatedly. With regard to this judgment, she specifically notes the ISA conclusion that, while the airway inflammation induced by a single exposure (or several exposures over the course of a summer) can resolve entirely, continued inflammation could potentially result in adverse effects, including the induction of a chronic inflammatory state; altered pulmonary structure and function, leading to diseases such as asthma; altered lung host defense response to inhaled microorganisms; and altered lung response to other agents such as allergens or toxins (U.S. EPA, 2013, section 6.2.3). Thus, the Administrator becomes increasingly concerned about the potential for adverse effects at 60 ppb O3 as the number of exposures increases, though she notes that the available evidence does not indicate a particular number of occurrences of such exposures that would be required to achieve an adverse respiratory effect, and that this number is likely to vary across the population.

In addition to controlled human exposure studies, the Administrator also considers what the available epidemiologic evidence indicates with regard to the adequacy of the public health protection provided by the current primary O3 standard. She notes that recent epidemiologic studies provide support, beyond that available in the last review, for associations between short-term O3 exposures and a wide range of adverse respiratory outcomes (including respiratory-related hospital admissions, emergency department visits, and mortality) and with total mortality. As discussed above in the EPA responses to public comments (II.B.2.b.ii), associations with morbidity and mortality are stronger during the warm or summer months, and remain robust after adjustment for copollutants (U.S. EPA, 2013, Chapter 6).Start Printed Page 65344

In considering information from epidemiologic studies within the context of her conclusions on the adequacy of the current standard, the Administrator specifically considers analyses in the PA that evaluate the extent to which O3 health effect associations have been reported for air quality concentrations likely to be allowed by the current standard. She notes that such analyses can provide insight into the extent to which the current standard would allow the distributions of ambient O3 concentrations that provided the basis for these health effect associations. While the majority of O3 epidemiologic studies evaluated in the PA were conducted in areas that would have violated the current standard during study periods, as discussed above (II.B.2.b.ii), the Administrator observes that the study by Mar and Koenig (2009) reported associations between short-term O3 concentrations and asthma emergency department visits in children and adults in a U.S. location that would have met the current O3 standard over the entire study period.[106] Based on this, she notes the conclusion from the PA that the current primary O3 standard would have allowed the distribution of ambient O3 concentrations that provided the basis for the associations with asthma emergency department visits reported by Mar and Koenig (2009) (U.S. EPA, 2014c, section 3.1.4.2).

In addition, even in some single-city study locations where the current standard was violated (i.e., those evaluated in Silverman and Ito, 2010; Strickland et al., 2010), the Administrator notes that PA analyses of reported concentration-response functions and available air quality data support the occurrence of O3-attributable hospital admissions and emergency department visits on subsets of days with virtually all ambient O3 concentrations below the level of the current standard. PA analyses of study area air quality further support the conclusion that exposures to the ambient O3 concentrations present in the locations evaluated by Strickland et al. (2010) and Silverman and Ito (2010) could have plausibly resulted in the respiratory-related emergency department visits and hospital admissions reported in these studies (U.S. EPA, 2014c, section 3.1.4.2). The Administrator agrees with the PA conclusion that these analyses indicate a relatively high degree of confidence in reported statistical associations with respiratory health outcomes on days when virtually all monitored 8-hour O3 concentrations were 75 ppb or below. She further agrees with the PA conclusion that although these analyses do not identify true design values, the presence of O3-associated respiratory effects on such days provides insight into the types of health effects that could occur in locations with maximum ambient O3 concentrations below the level of the current standard.

Compared to the single-city epidemiologic studies discussed above, the Administrator notes additional uncertainty in interpreting the relationships between short-term O3 air quality in individual study cities and reported O3 multicity effect estimates. In particular, she judges that the available multicity effect estimates in studies of short-term O3 do not provide a basis for considering the extent to which reported O3 health effect associations are influenced by individual locations with ambient O3 concentrations low enough to meet the current O3 standard, versus locations with O3 concentrations that violate this standard.[107] While such uncertainties limit the extent to which the Administrator bases her conclusions on air quality in locations of multicity epidemiologic studies, she does note that O3 associations with respiratory morbidity or premature mortality have been reported in several multicity studies when the majority of study locations (though not all study locations) would have met the current O3 standard (U.S. EPA, 2014c, section 3.1.4.2).

Looking across the body of epidemiologic evidence, the Administrator thus reaches the conclusion that analyses of air quality in study locations support the occurrence of adverse O3-associated effects at ambient O3 concentrations that met, or are likely to have met, the current standard. She further concludes that the strongest support for this conclusion comes from single-city studies of respiratory-related hospital admissions and emergency department visits associated with short-term O3 concentrations, with some support also from multicity studies of morbidity or mortality.

Taken together, the Administrator concludes that the scientific evidence from controlled human exposure and epidemiologic studies calls into question the adequacy of the public health protection provided by the current standard. In reaching this conclusion, she particularly notes that the current standard level is higher than the lowest O3 exposure concentration shown to result in the adverse combination of lung function decrements and respiratory symptoms (i.e., 72 ppb), and that CASAC concluded that such effects “almost certainly occur in some people” following exposures to O3 concentrations below 72 ppb (Frey, 2014c, p. 6). While she also notes that the current standard level is well-above the lowest O3 exposure concentration shown to cause respiratory effects (i.e., 60 ppb), she has less confidence that the effects observed at 60 ppb are adverse (discussed in II.B.2.b.i, II.C.4.b, II.C.4.c). She further considers these effects, and the extent to which the current primary O3 standard could protect against them, within the context of quantitative analyses of O3 exposures (discussed below). With regard to the available epidemiologic evidence, the Administrator notes PA analyses of O3 air quality indicating that, while most O3 epidemiologic studies reported health effect associations with ambient O3 concentrations that violated the current standard, a small number of single-city U.S. studies support the occurrence of asthma-related hospital admissions and emergency department visits at ambient O3 concentrations below the level of the current standard, including one study with air quality that would have met the current standard during the study period. Some support for such O3 associations is also provided by multicity studies of morbidity or mortality. The Administrator further judges that the biological plausibility of associations with clearly adverse morbidity effects is supported by the evidence noted above from controlled human exposure studies conducted at, or in some cases below, typical warm-season ambient O3 concentrations.

Beyond her consideration of the scientific evidence, the Administrator also considers the results of the HREA exposure and risk analyses in reaching final conclusions regarding the adequacy of the current primary O3 standard. In doing so, consistent with Start Printed Page 65345her consideration of the evidence, she focuses primarily on quantitative analyses based on information from controlled human exposure studies (i.e., exposures of concern and risk of O3-induced FEV1 decrements). Consistent with the considerations in the PA, and with CASAC advice (Frey, 2014c), she particularly focuses on exposure and risk estimates in children.[108] As discussed in the HREA and PA (and II.B, above), the patterns of exposure and risk estimates across urban study areas, across years, and across air quality scenarios are similar in children and adults though, because children spend more time being physically active outdoors and are more likely to experience the types of O3 exposures shown to cause respiratory effects, larger percentages of children are estimated to experience exposures of concern and O3-induced FEV1 decrements. Children also have intrinsic risk factors that make them particularly susceptible to O3-related effects (e.g., higher ventilation rates relative to lung volume) (U.S. EPA, 2013, section 8.3.1.1; see section II.A.1.d above). In focusing on exposure and risk estimates in children, the Administrator recognizes that the exposure patterns for children across years, urban study areas, and air quality scenarios are indicative of the exposure patterns in a broader group of at-risk populations that also includes asthmatic adults and older adults. She judges that, to the extent the primary O3 standard provides appropriate protection for children, it will also do so for adult populations,[109] given the larger exposures and intrinsic risk factors in children.

In first considering estimates of exposures of concern, the Administrator considers the extent to which estimates indicate that the current standard limits population exposures to the broader range of O3 concentrations shown in controlled human exposure studies to cause respiratory effects. In doing so, she focuses on estimates of O3 exposures of concern at or above the benchmark concentrations of 60, 70, and 80 ppb. She notes that the current O3 standard can provide some protection against exposures of concern to a range of O3 concentrations, including concentrations below the standard level, given that (1) with the current fourth-high form, most days will have concentrations below the standard level and that (2) exposures of concern depend on both the presence of relatively high ambient O3 concentrations and on activity patterns in the population that result in exposures to such high concentrations while at an elevated ventilation rate (discussed in detail below, II.C.4.b and II.C.4.c).

In considering estimates of O3 exposures of concern allowed by the current standard, she notes that while single exposures of concern could be adverse for some people, particularly for the higher benchmark concentrations (70, 80 ppb) where there is stronger evidence for the occurrence of adverse effects (II.B.2.b.i, II.C.4.b, II.C.4.c, below), she becomes increasingly concerned about the potential for adverse responses as the number of occurrences increases.[110] In particular, as discussed above with regard to inflammation, she notes that the types of lung injury shown to occur following exposures to O3 concentrations from 60 to 80 ppb, particularly if experienced repeatedly, provide a mode of action by which O3 may cause other more serious effects (e.g., asthma exacerbations). Therefore, the Administrator places the most weight on estimates of two or more exposures of concern (i.e., as a surrogate for the occurrence of repeated exposures), though she also considers estimates of one or more exposures for the 70 and 80 ppb benchmarks.

In considering estimates of exposures of concern, the Administrator first notes that if the 15 urban study areas evaluated in the HREA were to just meet the current O3 standard, fewer than 1% of children in those areas would be estimated to experience two or more exposures of concern at or above 70 ppb, based on exposure estimates averaged over the years of analysis, though up to about 2% would be estimated to experience such exposures in the worst-case year and location (i.e., year and location with the largest exposure estimates).[111] Although the Administrator is less concerned about single occurrences of exposures of concern, she notes that even single occurrences could cause adverse effects in some people, particularly for the 70 and 80 ppb benchmarks.[112] As illustrated in Table 1 (above), the current standard could allow up to about 3% of children to experience one or more exposures of concern at or above 70 ppb, averaged over the years of analysis, and up to about 8% in the worst-case year and location. In addition, in the worst-case year and location, the current standard could allow about 1% of children to experience at least one exposure of concern at or above 80 ppb, the highest benchmark evaluated.

While the Administrator has less confidence in the adversity of the effects observed following exposures to 60 ppb O3 (II.B.2.b.i, II.C.4.b, II.C.4.c), particularly for single exposures, she judges that the potential for adverse effects increases as the number of exposures of concern increases. With regard to the 60 ppb benchmark, she particularly notes that the current standard is estimated to allow approximately 3 to 8% of children in urban study areas, including approximately 3 to 8% of asthmatic children, to experience two or more exposures of concern to O3 concentrations at or above 60 ppb, based on estimates averaged over the years of analysis. To provide some perspective on the average percentages estimated, the Administrator notes that they correspond to almost 900,000 children in urban study areas, including about 90,000 asthmatic children. Nationally, if the current standard were to be just met, the number of children experiencing such exposures would be larger.

Based on her consideration of these estimates within the context of her judgments on adversity, as discussed in her responses to public comments (II.B.2.b.i, II.C.4.b), the Administrator concludes that the exposures projected to remain upon meeting the current standard can reasonably be judged to be important from a public health perspective. In particular, given that the average percent of children estimated to experience two or more exposures of concern for the 60 ppb benchmark approaches 10% in some areas, even based on estimates averaged over the Start Printed Page 65346years of the analysis, she concludes that the current standard does not incorporate an adequate margin of safety against the potentially adverse effects that can occur following repeated exposures at or above 60 ppb. Although she has less confidence that the effects observed at 60 ppb are adverse, compared to the effects at and above 72 ppb, she judges that this approach to considering the results for the 60 ppb benchmark is appropriate given CASAC advice, which clearly focuses the EPA on considering the effects observed at 60 ppb (Frey, 2014c) (II.C.4.b, II.C.4.c below).[113] This approach to considering estimated exposures of concern is consistent with setting standards that provide some safeguard against dangers to human health that are not fully certain (i.e., standards that incorporate an adequate margin of safety) (See, e.g., State of Mississippi, 744 F. 3d at 1353).

In addition to estimated exposures of concern, the Administrator also considers HREA estimates of the risk of O3-induced FEV1 decrements ≥10 and 15%. In doing so, she particularly notes CASAC advice that “estimation of FEV1 decrements of ≥15% is appropriate as a scientifically relevant surrogate for adverse health outcomes in active healthy adults, whereas an FEV1 decrement of ≥10% is a scientifically relevant surrogate for adverse health outcomes for people with asthma and lung disease” (Frey, 2014c, p. 3). The Administrator notes that while single occurrences of O3-induced lung function decrements could be adverse for some people, as discussed above (II.B.1), she agrees with the judgment in past reviews that a more general consensus view of the potential adversity of such decrements emerges as the frequency of occurrences increases. Therefore, as in the proposal, the Administrator focuses primarily on the estimates of two or more O3-induced lung function decrements. When averaged over the years evaluated in the HREA, the Administrator notes that the current standard is estimated to allow about 1 to 3% of children in the 15 urban study areas (corresponding to almost 400,000 children) to experience two or more O3-induced lung function decrements ≥15%, and to allow about 8 to 12% of children (corresponding to about 180,000 asthmatic children) to experience two or more O3-induced lung function decrements ≥10%.

In further considering the HREA results, the Administrator considers the epidemiology-based risk estimates. As discussed in the proposal, compared to the weight given to HREA estimates of exposures of concern and lung function risks, she places relatively less weight on epidemiology-based risk estimates. In giving some consideration to these risk estimates, as discussed in the proposal and above in the EPA's responses to public comments (II.B.2.b.iii), the Administrator focuses on the risks associated with O3 concentrations in the upper portions of ambient distributions. In doing so, she notes the increasing uncertainty associated with the shapes of concentration-response curves for O3 concentrations in the lower portions of ambient distributions and the evidence from controlled human exposure studies, which provide the strongest support for O3-induced effects following exposures to O3 concentrations corresponding to the upper portions of typical ambient distributions (i.e., 60 ppb and above). Even when considering only area-wide O3 concentrations from the upper portions of seasonal distributions (i.e., ≥40, 60 ppb, Table 3 in the proposal), the Administrator notes that the general magnitude of mortality risk estimates suggests the potential for a substantial number of O3-associated deaths and adverse respiratory events to occur nationally, even when the current standard is met (79 FR 75277 and II.B.2.c.iii above).

In addition to the evidence and exposure/risk information discussed above, the Administrator also takes note of the CASAC advice in the current review, in the 2008 review and decision establishing the current standard, and in the 2010 reconsideration of the 2008 decision. As discussed in more detail above, the current CASAC “finds that the current NAAQS for ozone is not protective of human health” and “unanimously recommends that the Administrator revise the current primary ozone standard to protect public health” (Frey, 2014c, p. 5). The prior CASAC O3 Panel likewise recommended revision of the current standard to one with a lower level due to the lack of protectiveness of the current standard. This earlier recommendation was based entirely on the evidence and information in the record for the 2008 standard decision, which, as discussed above, has been substantially strengthened in the current review (Samet, 2011; Frey and Samet, 2012).

In consideration of all of the above, the Administrator concludes that the current primary O3 standard is not requisite to protect public health with an adequate margin of safety, and that it should be revised to provide increased public health protection. This decision is based on the Administrator's conclusions that the available evidence and exposure and risk information clearly call into question the adequacy of public health protection provided by the current primary standard such that it is not appropriate, within the meaning of section 109(d)(1) of the CAA, to retain the current standard. With regard to the evidence, she particularly notes that the current standard level is higher than the lowest O3 exposure concentration shown to result in the adverse combination of lung function decrements and respiratory symptoms (i.e., 72 ppb), and also notes CASAC's advice that at-risk groups (e.g., people with asthma) could experience adverse effects following exposure to lower concentrations. In addition, while the Administrator is less certain about the adversity of the effects that occur following lower exposure concentrations, she judges that recent controlled human exposure studies at 60 ppb provide support for a level below 75 ppb in order to provide an increased margin of safety, compared to the current standard, against effects with the potential to be adverse, particularly if they are experienced repeatedly. With regard to O3 epidemiologic studies, she notes that while most available studies reported health effect associations with ambient O3 concentrations that violated the current standard, a small number provide support for the occurrence of adverse respiratory effects at ambient O3 concentrations below the level of the current standard.[114]

Based on the analyses in the HREA, the Administrator concludes that the exposures and risks projected to remain upon meeting the current standard can reasonably be judged to be important from a public health perspective. In particular, this conclusion is based on her judgment that it is appropriate to set a standard that would be expected to eliminate, or almost eliminate, exposures of concern at or above 70 and 80 ppb. In addition, given that the average percent of children estimated to experience two or more exposures of concern for the 60 ppb benchmark approaches 10% in some urban study areas, the Administrator concludes that the current standard does not incorporate an adequate margin of safety Start Printed Page 65347against the potentially adverse effects that could occur following repeated exposures at or above 60 ppb. Beyond estimated exposures of concern, the Administrator concludes that the HREA risk estimates (FEV1 risk estimates, mortality risk estimates) further support a conclusion that the O3-associated health effects estimated to remain upon just meeting the current standard are an issue of public health importance on a broad national scale. Thus, she concludes that O3 exposure and risk estimates, when taken together, support a conclusion that the exposures and health risks associated with just meeting the current standard can reasonably be judged important from a public health perspective, such that the current standard is not sufficiently protective and does not incorporate an adequate margin of safety.

In the next section, the Administrator considers what revisions are appropriate in order to set a standard that is requisite to protect public health with an adequate margin of safety.

C. Conclusions on the Elements of a Revised Primary Standard

Having reached the conclusion that the current O3 standard is not requisite to protect public health with an adequate margin of safety, based on the currently available scientific evidence and exposure/risk information, the Administrator next considers the range of alternative standards supported by that evidence and information. Consistent with her consideration of the adequacy of the current standard, the Administrator's conclusions on the elements of the primary standard are informed by the available scientific evidence assessed in the ISA, exposure/risk information presented and assessed in the HREA, the evidence-based and exposure-/risk-based considerations and conclusions in the PA, CASAC advice, and public comments. The sections below discuss the evidence and exposure/risk information, CASAC advice and public input, and the Administrator's proposed conclusions, for the major elements of the NAAQS: Indicator (II.C.1), averaging time (II.C.2), form (II.C.3), and level (II.C.4).

1. Indicator

In the 2008 review, the EPA focused on O3 as the most appropriate indicator for a standard meant to provide protection against ambient photochemical oxidants. In this review, while the complex atmospheric chemistry in which O3 plays a key role has been highlighted, no alternatives to O3 have been advanced as being a more appropriate indicator for ambient photochemical oxidants. More specifically, the ISA noted that O3 is the only photochemical oxidant (other than NO2) that is routinely monitored and for which a comprehensive database exists (U.S. EPA, 2013, section 3.6). Data for other photochemical oxidants (e.g., peroxyacetyl nitrate, hydrogen peroxide, etc.) typically have been obtained only as part of special field studies. Consequently, no data on nationwide patterns of occurrence are available for these other oxidants; nor are extensive data available on the relationships of concentrations and patterns of these oxidants to those of O3 (U.S. EPA, 2013, section 3.6). In its review of the second draft PA, CASAC stated “The indicator of ozone is appropriate based on its causal or likely causal associations with multiple adverse health outcomes and its representation of a class of pollutants known as photochemical oxidants” (Frey, 2014c, p. ii).

In addition, the PA notes that meeting an O3 standard can be expected to provide some degree of protection against potential health effects that may be independently associated with other photochemical oxidants, even though such effects are not discernible from currently available studies indexed by O3 alone (U.S. EPA, 2014c, section 4.1). That is, since the precursor emissions that lead to the formation of O3 generally also lead to the formation of other photochemical oxidants, measures leading to reductions in population exposures to O3 can generally be expected to lead to reductions in population exposures to other photochemical oxidants. In considering this information, and CASAC's advice, the Administrator reached the proposed conclusion that O3 remains the most appropriate indicator for a standard meant to provide protection against photochemical oxidants.[115]

The EPA received very few comments on the indicator of the primary standard. Those who did comment supported the proposed decision to retain O3 as the indicator, noting the rationale put forward in the preamble to the proposed rule. These commenters generally expressed support for retaining the current indicator in conjunction with retaining other elements of the current standard, such as the averaging time and form. After considering the available evidence, CASAC advice, and public comments, the Administrator concludes that O3 remains the most appropriate indicator for a standard meant to provide protection against photochemical oxidants. Therefore, she is retaining O3 as the indicator for the primary standard in this final rule.

2. Averaging Time

The EPA established the current 8-hour averaging time [116] for the primary O3 NAAQS in 1997 (62 FR 38856). The decision on averaging time in that review was based on numerous controlled human exposure and epidemiologic studies reporting associations between adverse respiratory effects and 6- to 8-hour O3 concentrations (62 FR 38861). The EPA also noted that a standard with a maximum 8-hour averaging time is likely to provide substantial protection against respiratory effects associated with 1-hour peak O3 concentrations. The EPA reached similar conclusions in the last O3 NAAQS review and thus, the EPA retained the 8-hour averaging time in 2008.

In reaching a proposed conclusion on averaging time in the current review, the Administrator considered the extent to which the available evidence continues to support the appropriateness of a standard with an 8-hour averaging time (79 FR 75292). Specifically, the Administrator considered the extent to which the available information indicates that a standard with the current 8-hour averaging time provides appropriate protection against short- and long-term O3 exposures. These considerations from the proposal are summarized below in sections II.C.2.a (short-term) and II.C.2.b (long-term). Section II.C.2.c summarizes the Administrator's proposed decision on averaging time. Section II.C.2.d discusses comments received on averaging time. Section II.C.2.e presents the Administrator's final decision regarding averaging time.

a. Short-Term

As an initial consideration with respect to the most appropriate averaging time for the O3 NAAQS, in the proposal the Administrator noted that the strongest evidence for O3-associated health effects is for respiratory effects following short-term exposures. More specifically, the Administrator noted the ISA conclusion that the evidence is “sufficient to infer a causal relationship” between short-term O3 exposures and respiratory effects. The ISA also judges that for short-term O3 exposures, the evidence indicates “likely to be causal” relationships with Start Printed Page 65348both cardiovascular effects and mortality (U.S. EPA, 2013, section 2.5.2). Therefore, as in past reviews, the Administrator noted that the strength of the available scientific evidence provides strong support for a standard that protects the public health against short-term exposures to O3.

In first considering the level of support available for specific short-term averaging times, the Administrator noted in the proposal the evidence available from controlled human exposure studies. As discussed in more detail in Chapter 3 of the PA, substantial health effects evidence from controlled human exposure studies demonstrates that a wide range of respiratory effects (e.g., pulmonary function decrements, increases in respiratory symptoms, lung inflammation, lung permeability, decreased lung host defense, and airway hyperresponsiveness) occur in healthy adults following 6.6-hour exposures to O3 (U.S. EPA, 2013, section 6.2.1.1). Compared to studies evaluating shorter exposure durations (e.g., 1-hour), studies evaluating 6.6-hour exposures in healthy adults have reported respiratory effects at lower O3 exposure concentrations and at more moderate levels of exertion.

The Administrator also noted in the proposal the strength of evidence from epidemiologic studies that evaluated a wide variety of populations (e.g., including at-risk lifestages and populations, such as children and people with asthma, respectively). A number of different averaging times have been used in O3 epidemiologic studies, with the most common being the max 1-hour concentration within a 24-hour period (1-hour max), the max 8-hour average concentration within a 24-hour period (8-hour max), and the 24-hour average. These studies are assessed in detail in Chapter 6 of the ISA (U.S. EPA, 2013). Limited evidence from time-series and panel epidemiologic studies comparing risk estimates across averaging times does not indicate that one exposure metric is more consistently or strongly associated with respiratory health effects or mortality, though the ISA notes some evidence for “smaller O3 risk estimates when using a 24-hour average exposure metric” (U.S. EPA, 2013, section 2.5.4.2; p. 2-31). For single- and multi-day average O3 concentrations, lung function decrements were associated with 1-hour max, 8-hour max, and 24-hour average ambient O3 concentrations, with no strong difference in the consistency or magnitude of association among the averaging times (U.S. EPA, 2013, p. 6-71). Similarly, in studies of short-term exposure to O3 and mortality, Smith et al. (2009) and Darrow et al. (2011) have reported high correlations between risk estimates calculated using 24-hour average, 8-hour max, and 1-hour max averaging times (U.S. EPA, 2013, p. 6-253). Thus, the Administrator noted that the epidemiologic evidence alone does not provide a strong basis for distinguishing between the appropriateness of 1-hour, 8-hour, and 24-hour averaging times.

Considering the health information discussed above, in the proposal the Administrator concluded that an 8-hour averaging time remains appropriate for addressing health effects associated with short-term exposures to ambient O3. An 8-hour averaging time is similar to the exposure periods evaluated in controlled human exposure studies, including recent studies that provide evidence for respiratory effects following exposures to O3 concentrations below the level of the current standard. In addition, epidemiologic studies provide evidence for health effect associations with 8-hour O3 concentrations, as well as with 1-hour and 24-hour concentrations. As in previous reviews, the Administrator noted that a standard with an 8-hour averaging time (combined with an appropriate standard form and level) would also be expected to provide substantial protection against health effects attributable to 1-hour and 24-hour exposures (e.g., 62 FR 38861, July 18, 1997). This conclusion is consistent with the advice received from CASAC that “the current 8-hour averaging time is justified by the combined evidence from epidemiologic and clinical studies” (Frey, 2014c, p. 6).

b. Long-Term

The ISA concludes that the evidence for long-term O3 exposures indicates that there is “likely to be a causal relationship” with respiratory effects (U.S. EPA, 2013, chapter 7). Thus, in this review the Administrator also considers the extent to which currently available evidence and exposure/risk information suggests that a standard with an 8-hour averaging time can provide protection against respiratory effects associated with longer term exposures to ambient O3.

In considering this issue in the 2008 review of the O3 NAAQS, the Staff Paper noted that “because long-term air quality patterns would be improved in areas coming into attainment with an 8-hr standard, the potential risk of health effects associated with long-term exposures would be reduced in any area meeting an 8-hr standard” (U.S. EPA, 2007, p. 6-57). In the current review, the PA further evaluates this issue, with a focus on the long-term O3 metrics reported to be associated with mortality or morbidity in recent epidemiologic studies. As discussed in section 3.1.3 of the PA (U.S. EPA, 2014c, section 4.2), much of the recent evidence for such associations is based on studies that defined long-term O3 in terms of seasonal averages of daily maximum 1-hour or 8-hour concentrations.

As an initial consideration, in the proposal the Administrator noted the risk results from the HREA for respiratory mortality associated with long-term O3 concentrations. These HREA analyses indicate that as air quality is adjusted to just meet the current 8-hour standard, most urban study areas are estimated to experience reductions in respiratory mortality associated with long-term O3 concentrations based on the seasonal averages of 1-hour daily maximum O3 concentrations evaluated in the study by Jerrett et al. (2009) (U.S. EPA, 2014a, chapter 7).[117] As air quality is adjusted to meet lower alternative standard levels, for standards based on 3-year averages of the annual fourth-highest daily maximum 8-hour O3 concentrations, respiratory mortality risks are estimated to be reduced further in urban study areas. This analysis indicates that an O3 standard with an 8-hour averaging time, when coupled with an appropriate form and level, can reduce respiratory mortality reported to be associated with long-term O3 concentrations.

In further considering the study by Jerrett et al. (2009), in the proposal the Administrator noted the PA comparison of long-term O3 concentrations following model adjustment in urban study areas (i.e., adjusted to meet the current and alternative 8-hour standards) to the concentrations present in study cities that provided the basis for the positive and statistically significant association with respiratory mortality. As indicated in Table 4-3 of the PA (U.S. EPA, 2014c, section 4.2), this comparison suggests that a standard with an 8-hour averaging time can decrease seasonal averages of 1-hour daily maximum O3 concentrations, and can maintain those O3 concentrations below the seasonal average concentration where the study indicates the most confidence in the reported concentration-response relationship with respiratory mortality (U.S. EPA, 2014c, sections 4.2 and 4.4.1).Start Printed Page 65349

The Administrator also noted in the proposal that the HREA conducted analyses evaluating the impacts of reducing regional NOX emissions on the seasonal averages of daily maximum 8-hour O3 concentrations. Seasonal averages of 8-hour daily max O3 concentrations reflect long-term metrics that have been reported to be associated with respiratory morbidity effects in several recent O3 epidemiologic studies (e.g., Islam et al., 2008; Lin et al., 2008a, 2008b; Salam et al., 2009). The HREA analyses indicate that the large majority of the U.S. population lives in locations where reducing NOX emissions would be expected to result in decreases in seasonal averages of daily max 8-hour ambient O3 concentrations (U.S. EPA, 2014a, chapter 8). Thus, consistent with the respiratory mortality risk estimates noted above, these analyses suggest that reductions in O3 precursor emissions in order to meet a standard with an 8-hour averaging time would also be expected to reduce the long-term O3 concentrations that have been reported in recent epidemiologic studies to be associated with respiratory morbidity.

c. Administrator's Proposed Conclusion on Averaging Time

In the proposal the Administrator noted that, when taken together, the analyses summarized above indicate that a standard with an 8-hour averaging time, coupled with the current fourth-high form and an appropriate level, would be expected to provide appropriate protection against the short- and long-term O3 concentrations that have been reported to be associated with respiratory morbidity and mortality. The CASAC agreed with this conclusion, stating that “[t]he current 8-hour averaging time is justified by the combined evidence from epidemiologic and clinical studies” and that “[t]he 8-hour averaging window also provides protection against the adverse impacts of long-term ozone exposures, which were found to be “likely causal” for respiratory effects and premature mortality” (Frey, 2014c, p. 6). Therefore, considering the available evidence and exposure risk information, and CASAC's advice, the Administrator proposed to retain the current 8-hour averaging time, and not to set an additional standard with a different averaging time.

d. Comments on Averaging Time

Most public commenters did not address the issue of whether the EPA should consider additional or alternative averaging times. Of those who did address this issue, some commenters representing state agencies or industry groups agreed with the proposed decision to retain the current 8-hour averaging time, generally noting the supportive evidence discussed in the preamble to the proposed rule. In contrast, several medical organizations and environmental groups questioned the degree of health protection provided by a standard based on an 8-hour averaging time. For example, one group asserted that “[a]veraging over any time period, such as 8 hours, is capable of hiding peaks that may be very substantial if they are brief enough.”

The EPA agrees with these commenters that an important issue in the current review is the appropriateness of using a standard with an 8-hour averaging time to protect against adverse health effects that are attributable to a wide range of O3 exposure durations, including those shorter and longer than 8 hours. This is an issue that has been thoroughly evaluated by the EPA in past reviews, as well as in the current review.

The 8-hour O3 NAAQS was originally set in 1997, as part of revising the then-existing standard with its 1-hour averaging time, and was retained in the review completed in 2008 (73 FR 16472). In both of these reviews, several lines of evidence and information provided support for an 8-hour averaging time rather than a shorter averaging time. For example, substantial health evidence demonstrated associations between a wide range of respiratory effects and 6- to 8-hour exposures to relatively low O3 concentrations (i.e., below the level of the 1-hour O3 NAAQS in place prior to the review completed in 1997). A standard with an 8-hour averaging time was determined to be more directly associated with health effects of concern at lower O3 concentrations than a standard with a 1-hour averaging time. In addition, results of quantitative analyses showed that a standard with an 8-hour averaging time can effectively limit both 1- and 8-hour exposures of concern, and that an 8-hour averaging time results in a more uniformly protective national standard than a 1-hour averaging time. In past reviews, CASAC has agreed that an 8-hour averaging time is appropriate.

In reaching her proposed decision to retain the 8-hour averaging time in the current review, the Administrator again considered the body of evidence for adverse effects attributable to a wide range of O3 exposure durations, including studies specifically referenced by public commenters who questioned the protectiveness of a standard with an 8-hour averaging time. For example, as noted above a substantial body of health effects evidence from controlled human exposure studies demonstrates that a wide range of respiratory effects occur in healthy adults following 6.6-hour exposures to O3 (U.S. EPA, 2013, section 6.2.1.1). Compared to studies evaluating shorter exposure durations (e.g., 1-hour), studies evaluating 6.6-hour exposures in healthy adults have reported respiratory effects at lower O3 exposure concentrations and at more moderate levels of exertion. The Administrator also noted the strength of evidence from epidemiologic studies that evaluated a number of different averaging times, with the most common being the maximum 1-hour concentration within a 24-hour period (1-hour max), the maximum 8-hour average concentration within a 24-hour period (8-hour max), and the 24-hour average. Evidence from time-series and panel epidemiologic studies comparing risk estimates across averaging times does not indicate that one exposure metric is more consistently or strongly associated with respiratory health effects or mortality (U.S. EPA, 2013, section 2.5.4.2; p. 2-31). For single- and multi-day average O3 concentrations, lung function decrements were associated with 1-hour max, 8-hour max, and 24-hour average ambient O3 concentrations, with no strong difference in the consistency or magnitude of association among the averaging times (U.S. EPA, 2013, p. 6-71). Similarly, in studies of short-term exposure to O3 and mortality, Smith et al. (2009) and Darrow et al. (2011) have reported high correlations between risk estimates calculated using 24-hour average, 8-hour max, and 1-hour max averaging times (U.S. EPA, 2013, p. 6-253). Thus, the epidemiologic evidence does not provide a strong basis for distinguishing between the appropriateness of 1-hour, 8-hour, and 24-hour averaging times.

In addition, quantitative exposure and risk analyses in the HREA are based on an air quality adjustment approach that estimates hourly O3 concentrations, and on scientific studies that evaluated health effects attributable to a wide range of O3 exposure durations. For example, the risk of lung function decrements is estimated using a model based on controlled human exposure studies with exposure durations ranging from 2 to 7.6 hours (U.S. EPA, 2013, section 6.2.1.1). Epidemiology-based risk estimates are based on studies that reported health effect associations with short-term ambient O3 concentrations ranging from 1-hour to 24-hours and with long-term seasonal average concentrations (U.S. EPA, 2014a, Table 7-2). Thus, the HREA estimated health Start Printed Page 65350risks associated with a wide range of O3 exposure durations and the Administrator's conclusions on averaging time in the current review are based, in part, on consideration of these estimates.

When taken together, the evidence and analyses indicate that a standard with an 8-hour averaging time, coupled with the current fourth-high form and an appropriate level, would be expected to provide appropriate protection against the short- and long-term O3 concentrations that have been reported to be associated with respiratory morbidity and mortality. The CASAC agreed with this, stating the following (Frey, 2014c, p. 6):

The current 8-hour averaging time is justified by the combined evidence from epidemiologic and clinical studies referenced in Chapter 4. Results from clinical studies, for example, show a wide range of respiratory effects in healthy adults following 6.6 hours of exposure to ozone, including pulmonary function decrements, increases in respiratory symptoms, lung inflammation, lung permeability, decreased lung host defense, and airway hyperresponsiveness. These findings are supported by evidence from epidemiological studies that show causal associations between short-term exposures of 1, 8 and 24-hours and respiratory effects and “likely to be causal” associations for cardiovascular effects and premature mortality. The 8-hour averaging window also provides protection against the adverse impacts of long-term ozone exposures, which were found to be “likely causal” for respiratory effects and premature mortality.

Given all of the above, the EPA disagrees with commenters who question the protectiveness of an O3 standard with an 8-hour averaging time, particularly for an 8-hour standard with the revised level of 70 ppb that is being established in this review, as discussed below (II.C.4).

e. Administrator's Final Decision Regarding Averaging Time

In considering the evidence and information summarized in the proposal and discussed in detail in the ISA, HREA, and PA; CASAC's views; and public comments, the Administrator concludes that a standard with an 8-hour averaging time can effectively limit health effects attributable to both short- and long-term O3 exposures. As was the case in the proposal, this final conclusion is based on (1) the strong evidence that continues to support the importance of protecting public health against short-term O3 exposures (e.g., ≤ 1-hour to 24-hour) and (2) analyses in the HREA and PA supporting the conclusion that the current 8-hour averaging time can effectively limit long-term O3 exposures. Furthermore, the Administrator observes that the CASAC Panel agreed with the choice of averaging time (Frey, 2014c). Therefore, in the current review, the Administrator concludes that it is appropriate to retain the 8-hour averaging time and to not set a separate standard with a different averaging time in this final rule.

3. Form

The “form” of a standard defines the air quality statistic that is to be compared to the level of the standard in determining whether an area attains that standard. The foremost consideration in selecting a form is the adequacy of the public health protection provided by the combination of the form and the other elements of the standard. In this review, the Administrator considers the extent to which the available evidence and/or information continue to support the appropriateness of a standard with the current form, defined by the 3-year average of annual fourth-highest 8-hour daily maximum O3 concentrations. Section II.C.3.a below summarizes the basis for the current form. Section II.C.3.b discusses the Administrator's proposed decision to retain the current form. Section II.C.3.c discusses public comments received on the form of the primary standard. Section II.C.3.d discusses the Administrator's final decision on form.

a. Basis for the Current Form

The EPA established the current form of the primary O3 NAAQS in 1997 (62 FR 38856). Prior to that time, the standard had a “1-expected-exceedance” form.[118] An advantage of the current concentration-based form recognized in the 1997 review is that such a form better reflects the continuum of health effects associated with increasing ambient O3 concentrations. Unlike an expected exceedance form, a concentration-based form gives proportionally more weight to years when 8-hour O3 concentrations are well above the level of the standard than years when 8-hour O3 concentrations are just above the level of the standard.[119] The EPA judged it appropriate to give more weight to higher O3 concentrations, given that available health evidence indicated a continuum of effects associated with exposures to varying concentrations of O3, and given that the extent to which public health is affected by exposure to ambient O3 is related to the actual magnitude of the O3 concentration, not just whether the concentration is above a specified level.

During the 1997 review, the EPA considered a range of alternative “concentration-based” forms, including the second-, third-, fourth- and fifth-highest daily maximum 8-hour concentrations in an O3 season. The fourth-highest daily maximum was selected, recognizing that a less restrictive form (e.g., fifth-highest) would allow a larger percentage of sites to experience O3 peaks above the level of the standard, and would allow more days on which the level of the standard may be exceeded when the site attains the standard (62 FR 38856). The EPA also considered setting a standard with a form that would provide a margin of safety against possible but uncertain chronic effects, and would provide greater stability to ongoing control programs.[120] A more restrictive form was not selected, recognizing that the differences in the degree of protection afforded by the alternatives were not well enough understood to use any such differences as a basis for choosing the most restrictive forms (62 FR 38856).

In the 2008 review, the EPA additionally considered the potential value of a percentile-based form. In doing so, the EPA recognized that such a statistic is useful for comparing datasets of varying length because it samples approximately the same place in the distribution of air quality values, whether the dataset is several months or several years long. However, the EPA concluded that a percentile-based statistic would not be effective in ensuring the same degree of public health protection across the country. Specifically, a percentile-based form would allow more days with higher air quality values in locations with longer O3 seasons relative to locations with shorter O3 seasons. Thus, in the 2008 review, the EPA concluded that a form based on the nth-highest maximum O3 concentration would more effectively ensure that people who live in areas Start Printed Page 65351with different length O3 seasons receive the same degree of public health protection.

Based on analyses of forms specified in terms of an nth-highest concentration (n ranged from 3 to 5), advice from CASAC, and public comment, the Administrator concluded that a fourth-highest daily maximum should be retained (73 FR 16465, March 27, 2008). In reaching this decision, the Administrator recognized that “there is not a clear health-based threshold for selecting a particular nth-highest daily maximum form of the standard” and that “the adequacy of the public health protection provided by the combination of the level and form is a foremost consideration” (73 FR 16475, March 27, 2008). Based on this, the Administrator judged that the existing form (fourth-highest daily maximum 8-hour average concentration) should be retained, recognizing the increase in public health protection provided by combining this form with a lower standard level (i.e., 75 ppb).

The Administrator also recognized that it is important to have a form that provides stability with regard to implementation of the standard. In the case of O3, for example, he noted the importance of a form insulated from the impacts of extreme meteorological events that are conducive to O3 formation. Such events could have the effect of reducing public health protection, to the extent they result in frequent shifts in and out of attainment due to meteorological conditions. The Administrator noted that such frequent shifting could disrupt an area's ongoing implementation plans and associated control programs (73 FR 16474, March 27, 2008). In his final decision, the Administrator judged that a fourth-high form “provides a stable target for implementing programs to improve air quality” (id. at 16475).

b. Proposed Decision on Form

In the proposal for the current review, the Administrator considered the extent to which newly available information provides support for the current form (79 FR 75293). In so doing, she took note of the conclusions of prior reviews summarized above. She recognized the value of an nth-high statistic over that of an expected exceedance or percentile-based form in the case of the O3 standard, for the reasons summarized above. The Administrator additionally took note of the importance of stability in implementation to achieving the level of protection specified by the NAAQS. Specifically, she noted that to the extent areas engaged in implementing the O3 NAAQS frequently shift from meeting the standard to violating the standard, it is possible that ongoing implementation plans and associated control programs could be disrupted, thereby reducing public health protection.

In light of this, while giving foremost consideration to the adequacy of public health protection provided by the combination of all elements of the standard, including the form, the Administrator considered particularly the findings from prior reviews with regard to the use of the nth-high metric. As noted above, the EPA selected the fourth-highest daily maximum, recognizing the public health protection provided by this form, when coupled with an appropriate averaging time and level, and recognizing that such a form can provide stability for implementation programs. In the proposal the Administrator concluded that the currently available evidence and information do not call into question these conclusions from previous reviews. In reaching this initial conclusion, the Administrator noted that CASAC concurred that the O3 standard should be based on the fourth-highest, daily maximum 8-hour average value (averaged over 3 years), stating that this form “provides health protection while allowing for atypical meteorological conditions that can lead to abnormally high ambient ozone concentrations which, in turn, provides programmatic stability” (Frey, 2014c, p. 6). Thus, a standard with the current fourth-high form, coupled with a level lower than 75 ppb as discussed below, would be expected to increase public health protection relative to the current standard while continuing to provide stability for implementation programs. Therefore, the Administrator proposed to retain the current fourth-highest daily maximum form for an O3 standard with an 8-hour averaging time and a revised level.

c. Public Comments on Form

Several commenters focused on the stability of the standard to support their positions regarding form. Some industry associations and state agencies support changing to a form that would allow a larger number of exceedances of the standard level than are allowed by the current fourth-high form. In some cases, these commenters argued that a standard allowing a greater number of exceedances would provide the same degree of public health protection as the current standard. Some commenters advocated a percentile-based form, such as the 98th percentile. These commenters cited a desire for consistency with short-term standards for other criteria pollutants (e.g., PM2.5, NO2), as well as a desire to allow a greater number of exceedances of the standard level, thus making the standard less sensitive to fluctuations in background O3 concentrations and to extreme meteorological events.

Other commenters submitted analyses purporting to indicate that a fourth-high form provides only a small increase in stability, relative to forms that allow fewer exceedances of the standard level (i.e., first-high, second-high). These commenters also called into question the degree of health protection achieved by a standard with a fourth-high form and a level in the proposed range (i.e., 65 to 70 ppb). They pointed out that a fourth-high form will, by definition, allow 3 days per year, on average, with 8-hour O3 concentrations above the level of the standard. Commenters further stated that “[i]f ozone levels on these peak days are appreciably higher than on the fourth-highest day, given EPA's acknowledged concerns regarding single or multiple (defined by EPA as 2 or more) exposures to elevated ozone concentrations, EPA must account for the degree of under-protection in setting the level of the NAAQS” (e.g., ALA et al., p. 138).

For the reasons discussed in the proposal, and summarized above, the EPA disagrees with commenters who supported a percentile-based form, such as the 98th percentile, for the O3 NAAQS. As noted above, a percentile-based statistic would not be effective in ensuring the same degree of public health protection across the country. Rather, a percentile-based form would allow more days with higher air quality values in locations with longer O3 seasons relative to locations with shorter O3 seasons. Thus, as in the 2008 review, in the current review the EPA concludes that a form based on the nth-highest maximum O3 concentration would more effectively ensure that people who live in areas with different length O3 seasons receive the same degree of public health protection.

In considering various nth-high values, as in past reviews (e.g., 73 FR 16475, March 27, 2008), the EPA recognizes that there is not a clear health-based threshold for selecting a particular nth-highest daily maximum form. Rather, the primary consideration is the adequacy of the public health protection provided by the combination of all of the elements of the standard, including the form. Environmental and public health commenters are correct that a standard with the current fourth-high form will allow 3 days per year, on average, with 8-hour O3 concentrations higher than the standard level. However, the EPA disagrees with these Start Printed Page 65352commenters' assertion that using a fourth-high form results in a standard that is under-protective. The O3 exposure and risk estimates that informed the Administrator's consideration of the degree of public health protection provided by various standard levels were based on air quality that “just meets” various standards with the current 8-hour averaging time and fourth-high, 3-year average form (U.S. EPA, 2014a, section 4.3.3). Therefore, air quality adjusted to meet various levels of the standard with the current form and averaging time will include days with concentrations above the level of the standard, and these days contribute to exposure and risk estimates. In this way, the Administrator has reasonably considered the public health protection provided by the combination of all of the elements of the standard, including the fourth-high form.

In past reviews, EPA selected the fourth-highest daily maximum form in recognition of the public health protection provided by this form, when coupled with an appropriate averaging time and level, and recognizing that such a form can provide stability for ongoing implementation programs. As noted above, some commenters submitted analyses suggesting that a fourth-high form provides only a small increase in stability, relative to a first- or second-high form. The EPA has conducted analyses of ambient O3 monitoring data to further consider these commenters' assertions regarding stability. The EPA's analyses of nth-high concentrations ranging from first-high to fifth-high have been summarized in a memo to the docket (Wells, 2015a). Consistent with commenters' analyses, Wells (2015a) indicates a progressive decrease in the variability of O3 concentrations, and an increase in the stability of those concentrations, as “n” increases. Based on these analyses, there is no clear threshold for selecting a particular nth-high form based on stability alone. Rather, as in past reviews, the decision on form in this review focuses first and foremost on the Administrator's judgments on public health protection, with judgments regarding stability of the standard being a legitimate, but secondary consideration. The Administrator's final decision on form is discussed below.

d. Administrator's Final Decision Regarding Form

In reaching a final decision on the form of the primary O3 standard, as described in the proposal and above, the Administrator recognizes that there is not a clear health-based rationale for selecting a particular nth-highest daily maximum form. Her foremost consideration is the adequacy of the public health protection provided by the combination of all of the elements of the standard, including the form. In this regard, the Administrator recognizes the support from analyses in previous reviews, and from the CASAC in the current review, for the conclusion that the current fourth-high form of the standard, when combined with a revised level as discussed below, provides an appropriate balance between public health protection and a stable target for implementing programs to improve air quality. In particular, she notes that the CASAC concurred that the O3 standard should be based on the fourth-highest, daily maximum 8-hour average value (averaged over 3 years), stating that this form “provides health protection while allowing for atypical meteorological conditions that can lead to abnormally high ambient ozone concentrations which, in turn, provides programmatic stability” (Frey, 2014c, p. 6). Based on these considerations, and on consideration of public comments on form as discussed above, the Administrator judges it appropriate to retain the current fourth-high form (fourth-highest daily maximum 8-hour O3 concentration, averaged over 3 years) in this final rule.

4. Level

This section summarizes the basis for the Administrator's proposed decision to revise the current standard level (II.C.4.a); discusses public comments, and the EPA's responses, on that proposed decision (II.C.4.b); and presents the Administrator's final decision regarding the level of the primary O3 standard (II.C.4.c).

a. Basis for the Administrator's Proposed Decision on Level

In conjunction with her proposed decisions to retain the current indicator, averaging time, and form (II.C.1 to II.C.3, above), the Administrator proposed to revise the level of the primary O3 standard to within the range of 65 to 70 ppb. In proposing this range of standard levels, as discussed in section II.E.4 of the proposal, the Administrator carefully considered the scientific evidence assessed in the ISA (U.S. EPA, 2013); the results of the exposure and risk assessments in the HREA (U.S. EPA, 2014a); the evidence-based and exposure-/risk-based considerations and conclusions in the PA (U.S. EPA, 2014c); CASAC advice and recommendations, as reflected in CASAC's letters to the Administrator and in public discussions of drafts of the ISA, HREA, and PA (Frey and Samet, 2012; Frey, 2014 a, c); and public input received during the development of these documents.

The Administrator's proposal to revise the standard level built upon her proposed conclusion that the overall body of scientific evidence and exposure/risk information calls into question the adequacy of public health protection afforded by the current primary O3 standard, particularly for at-risk populations and lifestages. In reaching proposed conclusions on alternative levels for the primary O3 standard, the Administrator considered the extent to which various alternatives would be expected to protect the public, including at-risk populations, against the wide range of adverse health effects that have been linked with short- or long-term O3 exposures.

As was the case for her consideration of the adequacy of the current primary O3 standard (II.B.3, above), the Administrator placed the greatest weight on the results of controlled human exposure studies and on exposure and risk analyses based on information from these studies. In doing so, she noted that controlled human exposure studies provide the most certain evidence indicating the occurrence of health effects in humans following exposures to specific O3 concentrations. The effects reported in these studies are due solely to O3 exposures, and interpretation of study results is not complicated by the presence of co-occurring pollutants or pollutant mixtures (as is the case in epidemiologic studies). She further noted the CASAC judgment that “the scientific evidence supporting the finding that the current standard is inadequate to protect public health is strongest based on the controlled human exposure studies of respiratory effects” (Frey, 2014c, p. 5).

In considering the evidence from controlled human exposure studies, the Administrator first noted that the largest respiratory effects, and the broadest range of effects, have been studied and reported following exposures to 80 ppb O3 or higher, with most exposure studies conducted at these higher concentrations. Exposures of healthy adults to O3 concentrations of 80 ppb or higher have been reported to decrease lung function, increase airway inflammation, increase respiratory symptoms, result in airway hyperresponsiveness, and decrease lung host defenses. The Administrator further noted that O3 exposure concentrations as low as 72 ppb have been shown to both decrease lung function and increase respiratory Start Printed Page 65353symptoms (Schelegle et al., 2009),[121] a combination that meets the ATS criteria for an adverse response, and that exposures as low as 60 ppb have been reported to decrease lung function and increase airway inflammation.

Based on this evidence, the Administrator reached the initial conclusion that the results of controlled human exposure studies strongly support setting the level of a revised O3 standard no higher than 70 ppb. In reaching this conclusion, she placed a large amount of weight on the importance of setting the level of the standard well below 80 ppb, the exposure concentration at which the broadest range of effects have been studied and reported, and below 72 ppb, the lowest exposure concentration shown to result in the adverse combination of lung function decrements and respiratory symptoms. She placed significant weight on this combination of effects, as did CASAC, in making judgments regarding the potential for adverse responses.

In further considering the potential public health implications of a standard with a level of 70 ppb, the Administrator also considered quantitative estimates of the extent to which such a standard would be expected to limit population exposures to the broader range of O3 concentrations shown in controlled human exposure studies to cause respiratory effects. In doing so, she focused on estimates of O3 exposures of concern at or above the benchmark concentrations of 60, 70, and 80 ppb. The Administrator judged that the evidence supporting the occurrence of adverse respiratory effects is strongest for exposures at or above the 70 and 80 ppb benchmarks. Therefore, she placed a large amount of emphasis on the importance of setting a standard that limits exposures of concern at or above these benchmarks.

The Administrator expressed less confidence that adverse effects will occur following exposures to O3 concentrations as low as 60 ppb. In reaching this conclusion, she highlighted the fact that statistically significant increases in respiratory symptoms, combined with lung function decrements, have not been reported following exposures to 60 or 63 ppb O3, though several studies have evaluated the potential for such effects (Kim et al., 2011; Schelegle et al., 2009; Adams, 2006).[122] The proposal specifically stated that “[t]he Administrator has decreasing confidence that adverse effects will occur following exposures to O3 concentrations below 72 ppb. In particular, compared to O3 exposure concentrations at or above 72 ppb, she has less confidence that adverse effects will occur following exposures to O3 concentrations as low as 60 ppb” (79 FR 73304-05).

However, she noted the possibility for adverse effects following such exposures given that: (1) CASAC judged the adverse combination of lung function decrements and respiratory symptoms “almost certainly occur in some people” following exposures to O3 concentrations below 72 ppb (though CASAC did not specify or otherwise indicate how far below) (Frey, 2014c, p. 6); (2) CASAC indicated the moderate lung function decrements (i.e., FEV1 decrements ≥ 10%) that occur in some healthy adults following exposures to 60 ppb O3 could be adverse to people with lung disease; and (3) airway inflammation has been reported following exposures as low as 60 ppb O3. She also took note of CASAC advice that the occurrence of exposures of concern at or above 60 ppb is an appropriate consideration for people with asthma (Frey, 2014c, p. 6). Therefore, while the Administrator expressed less confidence that adverse effects will occur following exposures to O3 concentrations as low as 60 ppb, compared to 70 ppb and above, based on the evidence and CASAC advice she also gave some consideration to exposures of concern for the 60 ppb benchmark.

Due to interindividual variability in responsiveness, the Administrator further noted that not every occurrence of an exposure of concern will result in an adverse effect, and that repeated occurrences of some of the effects demonstrated following exposures of concern could increase the likelihood of adversity (U.S. EPA, 2013, section 6.2.3). Therefore, the Administrator was most concerned about protecting at-risk populations against repeated occurrences of exposures of concern. Based on the above considerations, the Administrator focused on the extent to which a revised standard with a level of 70 ppb would be expected to protect populations from experiencing two or more O3 exposures of concern (i.e., as a surrogate for repeated exposures).

As illustrated in Table 1 in the proposal (and Table 1 above), the Administrator noted that, in urban study areas, a revised standard with a level of 70 ppb is estimated to eliminate the occurrence of two or more exposures of concern to O3 concentrations at and above 80 ppb and to virtually eliminate the occurrence of two or more exposures of concern to O3 concentrations at and above 70 ppb, even in the worst-case urban study area and year evaluated. Though the Administrator acknowledged greater uncertainty with regard to the occurrence of adverse effects following exposures to 60 ppb, she noted that a revised standard with a level of 70 ppb would also be expected to protect the large majority of children in the urban study areas (i.e., about 96% to more than 99% of children in individual urban study areas) from experiencing two or more exposures of concern at or above the 60 ppb benchmark. Compared to the current standard, this represents a reduction of more than 60%.[123]

In further evaluating the potential public health impacts of a standard with a level of 70 ppb, the Administrator also considered the HREA estimates of O3-induced lung function decrements. To inform her consideration of these decrements, the Administrator took note of CASAC advice that “estimation of FEV1 decrements of ≥ 15% is appropriate as a scientifically relevant surrogate for adverse health outcomes in active healthy adults, whereas an FEV1 decrement of ≥ 10% is a scientifically relevant surrogate for adverse health outcomes for people with asthma and lung disease” (Frey, 2014c, p. 3).

Although these FEV1 decrements provide perspective on the potential for the occurrence of adverse respiratory effects following O3 exposures, the Administrator agreed with the conclusion in past reviews that a more general consensus view of the adversity of moderate responses emerges as the frequency of occurrence increases (61 FR 65722-3, Dec, 13, 1996). Specifically, she judged that not every estimated occurrence of an O3-induced FEV1 decrement will be adverse and Start Printed Page 65354that repeated occurrences of moderate responses could lead to more serious illness. Therefore, the Administrator noted increasing concern about the potential for adversity as the number of occurrences increases and, as a result, she focused primarily on estimates of two or more O3-induced FEV1 decrements (i.e., as a surrogate for repeated exposures).[124]

The Administrator noted that a revised O3 standard with a level of 70 ppb is estimated to protect about 98 to 99% of children in urban study areas from experiencing two or more O3-induced FEV1 decrements 15%, and about 89 to 94% from experiencing two or more decrements 10%. She judged that these estimates reflect important risk reductions, compared to the current standard. Given these estimates, as well as estimates of one or more decrements per season (about which she was less concerned (79 FR 75290, December 17, 2014)), the Administrator concluded that a revised standard with a level of 70 ppb would be expected to provide substantial protection against the risk of O3-induced lung function decrements, and would be expected to result in important reductions in such risks, compared to the current standard. The Administrator further noted, however, that the variability in lung function risk estimates across urban study areas is often greater than the differences in risk estimates between various standard levels (Table 2, above). Given this, and the resulting considerable overlap between the ranges of lung function risk estimates for different standard levels, in the proposal the Administrator viewed lung function risk estimates as providing a more limited basis than exposures of concern for distinguishing between the degrees of public health protection provided by alternative standard levels (79 FR 75306 n. 164).

In next considering the additional protection that would be expected from standard levels below 70 ppb, the Administrator evaluated the extent to which a standard with a level of 65 ppb would be expected to further limit O3 exposures of concern and O3-induced lung function decrements. In addition to eliminating almost all exposures of concern to O3 concentrations at or above 80 and 70 ppb, even in the worst-case years and locations, the Administrator noted that a revised standard with a level of 65 ppb would be expected to protect more than 99% of children in urban study areas from experiencing two or more exposures of concern at or above 60 ppb and to substantially reduce the occurrence of one or more such exposures, compared to the current standard. With regard to O3-induced lung function decrements, an O3 standard with a level of 65 ppb is estimated to protect about 98% to more than 99% of children from experiencing two or more O3-induced FEV1 decrements 15% and about 91 to 99% from experiencing two or more decrements 10%.[125]

Taken together, the Administrator concluded that the evidence from controlled human exposure studies, and the information from quantitative analyses that draw upon these studies, provide strong support for standard levels from 65 to 70 ppb. In particular, she based this conclusion on the fact that such standard levels would be well below the O3 exposure concentration shown to result in the widest range of respiratory effects (i.e., 80 ppb),[126] and below the lowest O3 exposure concentration shown to result in the adverse combination of lung function decrements and respiratory symptoms (i.e., 72 ppb). A standard with a level from 65 to 70 ppb would also be expected to result in important reductions, compared to the current standard, in the occurrence of O3 exposures of concern for all of the benchmarks evaluated (i.e., 60, 70, and 80 ppb) and in the risk of O3-induced lung function decrements 10 and 15%.

In further considering the evidence and exposure/risk information, the Administrator considered the extent to which the epidemiologic evidence also provides support for standard levels from 65 to 70 ppb. In particular, the Administrator noted analyses in the PA (U.S. EPA, 2014c, section 4.4.1) indicating that a revised standard with a level of 65 or 70 ppb would be expected to maintain distributions of short-term ambient O3 concentrations below those present in the locations of all the single-city epidemiologic studies of hospital admissions or emergency department visits analyzed. She concluded that a revised standard with a level at least as low as 70 ppb would result in improvements in public health, beyond the protection provided by the current standard, in the locations of the single-city epidemiologic studies that reported significant health effect associations.[127]

The Administrator noted additional uncertainty in interpreting air quality in locations of multicity epidemiologic studies of short-term O3 for the purpose of evaluating alternative standard levels (II.D.1 and U.S. EPA, 2014c, section 4.4.1). While acknowledging this uncertainty, and therefore placing less emphasis on these analyses of study location air quality, she noted that PA analyses suggest that standard levels of 65 or 70 ppb would require reductions, beyond those required by the current standard, in ambient O3 concentrations present in several of the locations that provided the basis for statistically significant O3 health effect associations in multicity studies.

In further evaluating information from epidemiologic studies, the Administrator considered the HREA's epidemiology-based risk estimates for O3-associated morbidity or mortality (U.S. EPA, 2014a, Chapter 7). Compared to the weight given to the evidence from controlled human exposure studies, and to HREA estimates of exposures of concern and lung function risks, she placed relatively less weight on epidemiology-based risk estimates. In doing so, she noted that the overall conclusions from the HREA likewise reflect relatively less confidence in estimates of epidemiology-based risks than in estimates of exposures of concern and lung function risks.

In considering epidemiology-based risk estimates, the Administrator focused on risks associated with O3 concentrations in the upper portions of ambient distributions, given the greater uncertainty associated with the shapes of concentration-response curves for O3 concentrations in the lower portions of ambient distributions (i.e., below about 20 to 40 ppb depending on the O3 metric, health endpoint, and study population) (U.S. EPA, 2013, section 2.5.4.4). The Administrator further noted that experimental studies provide the strongest evidence for O3-induced effects following exposures to O3 concentrations corresponding to the upper portions of typical ambient Start Printed Page 65355distributions. In particular, as discussed above, she noted controlled human exposure studies showing respiratory effects following exposures to O3 concentrations at or above 60 ppb (79 FR 75308, December 17, 2014). Therefore, in considering risks associated with O3 concentrations in the upper portions of ambient distributions, the Administrator focused on the extent to which revised standards with levels of 70 or 65 ppb are estimated to reduce the risk of premature deaths associated with area-wide O3 concentrations at or above 40 ppb and 60 ppb.

Given all of the above evidence, exposure/risk information, and advice from CASAC, the Administrator proposed to revise the level of the current primary O3 standard to within the range of 65 to 70 ppb. In considering CASAC advice on the range of standard levels, the Administrator placed a large amount of weight on CASAC's conclusion that there is adequate scientific evidence to consider a range of levels for a primary standard that includes an upper end at 70 ppb. She also noted that although CASAC expressed concern about the margin of safety at a level of 70 ppb, it further acknowledged that the choice of a level within the range recommended based on scientific evidence is a policy judgment (Frey, 2014c, p. ii). While she agreed with CASAC that it is appropriate to consider levels below 70 ppb, as reflected in her range of proposed levels from 65 to 70 ppb, for the reasons discussed above she also concluded that a standard level as high as 70 ppb, which CASAC concluded could be supported by the scientific evidence, could reasonably be judged to be requisite to protect public health with an adequate margin of safety.

In considering the appropriateness of standard levels below 65 ppb, the Administrator noted the conclusions of the PA and the advice of CASAC that it would be appropriate for her to consider standard levels as low as 60 ppb. In making the decision to not propose levels below 65 ppb, she focused on CASAC's rationale for a level of 60 ppb, which focused on the importance of limiting exposures to O3 concentrations as low as 60 ppb (Frey, 2014c, p. 7). As discussed above, the Administrator agreed that it is appropriate to consider the implications of a revised standard level for estimated exposures of concern at or above 60 ppb. She noted that standards within the proposed range of 65 to 70 ppb would be expected to substantially limit the occurrence of exposures of concern to O3 concentrations at or above 60 ppb, particularly the occurrence of two or more exposures. When she further considered that not all exposures of concern lead to adverse effects, and that the NAAQS are not meant to be zero-risk or background standards, the Administrator judged that alternative standard levels below 65 ppb are not needed to further reduce such exposures.

b. Comments on Level

A number of groups representing medical, public health, or environmental organizations; some state agencies; and many individuals submitted comments on the appropriate level of a revised primary O3 standard.[128] Virtually all of these commenters supported setting the standard level within the range recommended by CASAC (i.e., 60 to 70). Some expressed support for the overall CASAC range, without specifying a particular level within that range, while others expressed a preference for the lower part of the CASAC range, often emphasizing support for a level of 60 ppb. Some of these commenters stated that if the EPA does not set the level at 60 ppb, then the level should be set no higher than 65 ppb (i.e., the lower bound of the proposed range of standard levels).

To support their views on the level of a revised standard, some commenters focused on overarching issues related to the statutory requirements for the NAAQS. For example, some commenters maintained that the primary NAAQS must be set at a level at which there is an absence of adverse effects in sensitive populations. While this argument has some support in the case law and in the legislative history to the 1970 CAA (see Lead Industries Ass'n v. EPA, 647 F. 2d 1147, 1153 (D.C. Cir. 1980)), it is well established that the NAAQS are not meant to be zero risk standards. See Lead Industries v. EPA, 647 F.2d at 1156 n.51; Mississippi v. EPA, 744 F. 3d at 1351. From the inception of the NAAQS standard-setting process, the EPA and the courts have acknowledged that scientific uncertainties in general, and the lack of clear thresholds in pollutant effects in particular, preclude any such definitive determinations. Lead Industries, 647 F. 2d at 1156 (setting standard at a level which would remove most but not all sub-clinical effects). Likewise, the House report to the 1977 amendments addresses this question (H. Rep. 95-294, 95th Cong. 1st sess. 127): [129]

Some have suggested that since the standards are to protect against all known or anticipated effects and since no safe threshold can be established, the ambient standards should be set at zero or background levels. Obviously, this no-risk philosophy ignores all economic and social consequences and is impractical. This is particularly true in light of the legal requirement for mandatory attainment of the national primary standards within 3 years.

Thus, post-1970 jurisprudence makes clear the impossibility, and lack of legal necessity, for NAAQS removing all health risk. See ATA III, 283 F. 3d at 360 (“[t]he lack of a threshold concentration below which these pollutants are known to be harmless makes the task of setting primary NAAQS difficult, as EPA must select standard levels that reduce risks sufficiently to protect public health even while recognizing that a zero-risk standard is not possible”); Mississippi, 744 F. 3d at 1351 (same); see also id. at 1343 (“[d]etermining what is `requisite' to protect the `public health' with an `adequate' margin of safety may indeed require a contextual assessment of acceptable risk. See Whitman, 531 U.S. at 494-95 (Breyer J. concurring)”).

In this review, EPA is setting a standard based on a careful weighing of available evidence, including a weighing of the strengths and limitations of the evidence and underlying scientific uncertainties therein. The Administrator's choice of standard level is rooted in her evaluation of the evidence, which reflects her legitimate uncertainty as to the O3 concentrations at which the public would experience adverse health effects. This is a legitimate, and well recognized, exercise of “reasoned decision-making.” ATA III. 283 F. 3d at 370; see also id. at 370 (“EPA's inability to guarantee the accuracy or increase the precision of the . . . NAAQS in no way undermines the standards' validity. Rather, these limitations indicate only that significant scientific uncertainty remains about the health effects of fine particulate matter at low atmospheric concentration. . . .”); Mississippi, 744 F. 3d at 1352-53 (appropriate for EPA to balance scientific uncertainties in determining level of revised O3 NAAQS).Start Printed Page 65356

In an additional overarching comment, some commenters also fundamentally objected to the EPA's consideration of exposure estimates in reaching conclusions on the primary O3 standard. These commenters' general assertion was that NAAQS must be established so as to be protective, with an adequate margin of safety, regardless of the activity patterns that feed into exposure estimates. They contended that “[a]ir quality standards cannot rely on avoidance behavior in order to protect the public health and sensitive groups” and that “[i]t would be unlawful for EPA to set the standard at a level that is contingent upon people spending most of their time indoors” (e.g., ALA et al., p. 124). To support these comments, for example, ALA et al. analyzed ambient monitoring data from Core-Based Statistical Areas (CBSAs) with design values between 66-70 ppb (Table 17, pp. 145-151 in ALA et al.) and 62-65 ppb (Table 18, pp. 153-154 in ALA et al.) and pointed out that there are many more days with ambient concentrations above the benchmark levels than were estimated in the EPA's exposure analysis (i.e., at and above the benchmark level of 60, 70 and 80 ppb).

The EPA disagrees with these commenters' conclusions regarding the appropriateness of considering exposure estimates, and notes that NAAQS must be “requisite” (i.e., “sufficient, but not more than necessary” (Whitman, 531 U.S. at 473)) to protect the “public health” (“the health of the public” (Whitman, 531 U.S. at 465)). Estimating exposure patterns based on extensive available data [130] is a reasonable means of ascertaining that standards are neither under- nor over-protective, and that standards address issues of public health rather than health issues pertaining only to isolated individuals.[131] Behavior patterns are critical in assessing whether ambient concentrations of O3 may pose a public health risk.[132] Exposures to ambient or near-ambient O3 concentrations have only been shown to result in potentially adverse effects if the ventilation rates of people in the exposed populations are raised to a sufficient degree (e.g., through physical exertion) (U.S. EPA, 2013, section 6.2.1.1).[133] Ignoring whether such elevated ventilation rates are actually occurring, as advocated by these commenters, would not provide an accurate assessment of whether the public health is at risk. Indeed, a standard established without regard to behavior of the public would likely lead to a standard which is more stringent than necessary to protect the public health.

While setting the primary O3 standard based only on ambient concentrations, without consideration of activity patterns and ventilation rates, would likely result in a standard that is over-protective, the EPA also concludes that setting a standard based on the assumption that people will adjust their activities to avoid exposures on high-pollution days would likely result in a standard that is under-protective. The HREA's exposure assessment does not make this latter assumption.[134] The time-location-activity diaries that provided the basis for exposure estimates reflect actual variability in human activities. While some diary days may reflect individuals spending less time outdoors than would be typical for them, it is similarly likely that some days reflect individuals spending more time outdoors than would be typical. Considering the actual variability in time-location-activity patterns is at the least a permissible way of identifying standards that are neither over- nor under-protective.[135]

Further, the EPA sees nothing in the CAA that prohibits consideration of the O3 exposures that could result in effects of public health concern. While a number of judicial opinions have upheld the EPA's decisions in other NAAQS reviews to place little weight on particular risk or exposure analyses (i.e., because of scientific uncertainties in those analyses), none of these opinions have suggested that such analyses are irrelevant because actual exposure patterns do not matter. See, e.g. Mississippi, 744 F. 3d at 1352-53; ATA III, 283 F. 3d at 373-74. Therefore, because behavior patterns are critical in assessing whether ambient concentrations of O3 may pose a public health risk, the EPA disagrees with the views expressed by these commenters objecting to the consideration of O3 exposures in reaching decisions on the primary O3 standard.

In addition to these overarching comments, a number of commenters supported their views on standard level by highlighting specific aspects of the scientific evidence, exposure/risk information, and/or CASAC advice. Key themes expressed by these commenters included the following: (1) Controlled human exposure studies provide strong evidence of adverse lung function decrements and airway inflammation in healthy adults following exposures to O3 concentrations as low as 60 ppb, and at-risk populations would be likely to experience more serious effects or effects at even lower concentrations; (2) epidemiologic studies provide strong evidence for associations with mortality and morbidity in locations with ambient O3 concentrations below 70 ppb, and in many cases in locations with concentrations near and below 60 ppb; (3) quantitative analyses in the HREA are biased such that they understate O3 exposures and risks, and the EPA's interpretation of lung function risk estimates is not appropriate and not consistent with other NAAQS; and (4) the EPA must give deference to CASAC advice, particularly CASAC's policy advice to set the standard level below 70 ppb. The next sections discuss comments related to each of these points, and provide the EPA's responses to those comments. More detailed discussion of individual comments, and the EPA's responses, is provided in the Response to Comments document.

i. Effects in Controlled Human Exposure Studies

Some commenters who advocated for a level of 60 ppb (or absent that, for 65 ppb) asserted that controlled human exposure studies have reported adverse respiratory effects in healthy adults following exposures to O3 concentrations as low as 60 ppb. These commenters generally based their conclusions on the demonstration of FEV1 decrements ≥ 10% and increased airway inflammation following exposures of healthy adults to 60 ppb O3. They concluded that even more serious effects would occur in at-risk Start Printed Page 65357populations exposed to 60 ppb O3, and that such populations would experience adverse effects following exposures to O3 concentrations below 60 ppb.

While the EPA agrees that information from controlled human exposure studies conducted at 60 ppb can help to inform the Administrator's decision on the standard level, the Agency does not agree that this information necessitates a level below 70 ppb. In fact, as discussed in the proposal, a revised O3 standard with a level of 70 ppb can be expected to provide substantial protection against the effects shown to occur following various O3 exposure concentrations, including those observed following exposures to 60 ppb. This is because the degree of protection provided by any NAAQS is due to the combination of all of the elements of the standard (i.e., indicator, averaging time, form, level). In the case of the fourth-high form of the O3 NAAQS, which the Administrator is retaining in the current review (II.C.3), the large majority of days in areas that meet the standard will have 8-hour O3 concentrations below the level of the standard, with most days well below the level. Therefore, as discussed in the proposal, in considering the degree of protection provided by an O3 standard with a particular level, it is important to consider the extent to which that standard would be expected to limit population exposures of concern to the broader range of O3 exposure concentrations shown in controlled human exposure studies to result in health effects. The Administrator's consideration of such exposures of concern is discussed below (II.C.4.c).

Another important part of the Administrator's consideration of exposure estimates is the extent to which she judges that adverse effects could occur following specific O3 exposures. While controlled human exposure studies provide a high degree of confidence regarding the extent to which specific health effects occur following exposures to O3 concentrations from 60 to 80 ppb, the Administrator notes that there are no universally accepted criteria by which to judge the adversity of the observed effects. Therefore, in making judgments about the extent to which the effects observed in controlled human exposure studies have the potential to be adverse, the Administrator considers the recommendations of ATS and advice from CASAC (II.A.1.c, above).

As an initial matter, with regard to the effects shown in controlled human exposure studies following O3 exposures, the Administrator notes the following:

1. The largest respiratory effects, and the broadest range of effects, have been studied and reported following exposures to 80 ppb O3 or higher, with most exposure studies conducted at these higher concentrations. Specifically, 6.6-hour exposures of healthy young adults to 80 ppb O3, while engaged in quasi-continuous, moderate exertion, can decrease lung function, increase airway inflammation, increase respiratory symptoms, result in airway hyperresponsiveness, and decrease lung host defenses.

2. Exposures of healthy young adults for 6.6 hours to O3 concentrations as low as 72 ppb, while engaged in quasi-continuous, moderate exertion, have been shown to both decrease lung function and result in respiratory symptoms.

3. Exposures of healthy young adults for 6.6 hours to O3 concentrations as low as 60 ppb, while engaged in quasi-continuous, moderate exertion, have been shown to decrease lung function and to increase airway inflammation.

To inform her judgments on the potential adversity to public health of these effects reported in controlled human exposure studies, as in the proposal, the Administrator considers the ATS recommendation that “reversible loss of lung function in combination with the presence of symptoms should be considered adverse” (ATS, 2000a). She notes that this combination of effects has been shown to occur following 6.6-hour exposures to O3 concentrations at or above 72 ppb. In considering these effects, CASAC observed that “the combination of decrements in FEV1 together with the statistically significant alterations in symptoms in human subjects exposed to 72 ppb ozone meets the American Thoracic Society's definition of an adverse health effect” (Frey, 2014c, p. 5).

Regarding the potential for adverse effects following exposures to lower concentrations, the Administrator notes the CASAC judgment that the adverse combination of lung function decrements and respiratory symptoms “almost certainly occur in some people” following exposures to O3 concentrations below 72 ppb (Frey, 2014c, p. 6). In particular, when commenting on the extent to which the study by Schelegle et al. (2009) suggests the potential for adverse effects following O3 exposures below 72 ppb, CASAC judged that:

[I]f subjects had been exposed to ozone using the 8-hour averaging period used in the standard [rather than the 6.6-hour exposures evaluated in the study], adverse effects could have occurred at lower concentration. Further, in our judgment, the level at which adverse effects might be observed would likely be lower for more sensitive subgroups, such as those with asthma (Frey, 2014c, p. 5).

Though CASAC did not provide advice as to how far below 72 ppb adverse effects would likely occur, the Administrator agrees that such effects could occur following exposures at least somewhat below 72 ppb.

The Administrator notes that while adverse effects could occur following exposures at least somewhat below 72 ppb, the combination of statistically significant increases in respiratory symptoms and decrements in lung function has not been reported following 6.6-hour exposures to average O3 concentrations of 60 ppb or 63 ppb, though studies have evaluated the potential for such effects (Adams, 2006; Schelegle et al., 2009; Kim et al., 2011). In the absence of this combination, the Administrator looks to additional ATS recommendations and CASAC advice in order to inform her judgments regarding the potential adversity of the effects that have been observed following O3 exposures as low as 60 ppb.

With regard to ATS, she first notes the recommendations that “a small, transient loss of lung function, by itself, should not automatically be designated as adverse” and that “[f]ew . . . biomarkers have been validated sufficiently that their responses can be used with confidence to define the point at which a response should be equated to an adverse effect warranting preventive measures” (ATS, 2000a).[136] Based on these recommendations, compared to effects following exposures at or above 72 ppb, the Administrator has less confidence in the adversity of the respiratory effects that have been observed following exposures to 60 or 63 ppb.

She further notes that some commenters who advocated for a level of 60 ppb also focused on ATS recommendations regarding population-level risks. These commenters specifically stated that lung function decrements “may be adverse in terms of `population risk,' where exposure to air pollution increases the risk to the population even though it might not harm lung function to a degree that is, on its own, `clinically important' to an individual” (e.g., ALA et al., p. 118). These commenters asserted that the EPA Start Printed Page 65358has not appropriately considered the potential for such population-level risk. Contrary to the views expressed by these commenters, the Administrator carefully considers the potential for population risk, particularly within the context of the ATS recommendation 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). Given that exposures to 60 ppb O3 have been shown in controlled human exposure studies to cause transient and reversible decreases in group mean lung function, the Administrator notes the potential for such exposures to result in similarly transient and reversible shifts in the risk profile of an exposed population. However, in contrast to commenters who advocated for a level of 60 ppb, the Administrator also notes that the available evidence does not provide information on the extent to which a short-term, transient decrease in lung function in a population, as opposed to a longer-term or permanent decrease, could affect the risk of other, more serious respiratory effects (i.e., change the risk profile of the population). This uncertainty, together with the additional ATS recommendations noted above, indicates to the Administrator that her judgment that there is uncertainty in the adversity of the effects shown to occur at 60 ppb is consistent with ATS recommendations.[137]

With regard to CASAC advice, the Administrator notes that, while CASAC clearly advised the EPA to consider the health effects shown to occur following exposures to 60 ppb O3, its advice regarding the adversity of those effects is less clear. In particular, she notes that CASAC was conditional about whether the lung function decrements observed in some people at 60 ppb (i.e., FEV1 decrements ≥ 10%) are adverse. Specifically, CASAC stated that these decrements “could be adverse in individuals with lung disease” (Frey, 2014c, p. 7, emphasis added) and that they provide a “surrogate for adverse health outcomes for people with asthma and lung disease” (Frey, 2014c, p. 3, emphasis added). Further, CASAC did not recommend considering standard levels low enough to eliminate O3-induced FEV1 decrements ≥ 10% (Frey, 2014c). With regard to the full range of effects shown to occur at 60 ppb (i.e., FEV1 decrements, airway inflammation), CASAC stated that exposures of concern for the 60 ppb benchmark are “relevant for consideration” with respect to people with asthma (Frey, 2014c, p. 6, italics added). In addition, “[t]he CASAC concurs with EPA staff regarding the finding based on scientific evidence that a level of 60 ppb corresponds to the lowest exposure concentration demonstrated to result in lung function decrements large enough to be judged an abnormal response by ATS and that could be adverse in individuals with lung disease” (Frey, 2014c, p. 7, italics added). The Administrator contrasts these statements with CASAC's clear advice that “the combination of decrements in FEV1 together with the statistically significant alterations in symptoms in human subjects exposed to 72 ppb ozone meets the American Thoracic Society's definition of an adverse health effect” (Frey, 2014c, p. 5).

Based on her consideration of all of the above recommendations and advice noted above, the Administrator judges that, compared to exposure concentrations at and above 72 ppb, there is greater uncertainty with regard to the adversity of effects shown to occur following O3 exposures as low as 60 ppb. However, based on the effects that have been shown to occur at 60 ppb (i.e., lung function decrements, airway inflammation), and CASAC advice indicating the importance of considering these effects (though its advice regarding the adversity of effects at 60 ppb is less clear), she concludes that it is appropriate to give some consideration to the extent to which a revised standard could allow such effects.

In considering estimates of exposures of concern for the 60, 70, and 80 ppb benchmarks within the context of her judgments on adversity, the Administrator notes that, due to interindividual variability in responsiveness, not every occurrence of an exposure of concern will result in an adverse effect. As discussed above (II.B.2.b.i), this point was highlighted by some commenters who opposed revision of the current standard, based on their analysis of effects shown to occur following exposures to 72 ppb O3. This point was also highlighted by some commenters who advocated for a level of 60 ppb, based on the discussion of O3-induced inflammation in the proposal. In particular, this latter group of commenters highlighted discussion from the proposal indicating that “[i]nflammation induced by a single O3 exposure can resolve entirely but, as noted in the ISA (U.S. EPA, 2013, p. 6-76), `continued acute inflammation can evolve into a chronic inflammatory state'” (e.g., ALA et al., p. 48). Consistent with these comments, and with her consideration of estimated exposurs of concern in the proposal, the Administrator judges that the types of respiratory effects that can occur following exposures of concern, particularly if experienced repeatedly, provide a plausible mode of action by which O3 may cause other more serious effects. Because of this, as in the proposal, the Administrator is most concerned about prote cting against repeated occurrences of exposures of concern.

The Administrator's consideration of estimated exposures of concern is discussed in more detail below (II.C.4.b.iv, II.C.4.c). In summary, contrary to the conclusions of commenters who advocated for a level of 60 ppb, the Administrator judges that a revised standard with a level of 70 ppb will effectively limit the occurrence of the O3 exposures for which she is most confident in the adversity of the resulting effects (i.e., based on estimates for the 70 and 80 ppb benchmarks). She further concludes that such a standard will provide substantial protection against the occurrence of O3 exposures for which there is greater uncertainty in the adversity of effects (i.e., based on estimates for the 60 ppb benchmark).

As noted above, commenters also pointed out that benchmark concentrations are based on studies conducted in healthy adults, whereas at-risk populations are likely to experience more serious effects and effects at lower O3 exposure concentrations. In considering this issue, the EPA notes CASAC's endorsement of 60 ppb as the lower end of the range of benchmarks for evaluation, and its advice that “the 60 ppb-8hr exposure benchmark is relevant for consideration with respect to adverse effects on asthmatics” (Frey, 2014c, p. 6). As discussed in detail below (II.C.4.c), the Administrator has carefully considered estimated exposures of concern for the 60 ppb benchmark. In addition, though the available information does not support the identification of specific benchmarks below 60 ppb that could be appropriate for consideration for at-risk populations, and though CASAC did not recommend consideration of any such benchmarks, the EPA expects that a revised standard with a level of 70 ppb will also reduce the occurrence of exposures to O3 concentrations at least somewhat below 60 ppb (U.S. EPA, Start Printed Page 653592014a, Figures 4-9 and 4-10).[138] Thus, even if some members of at-risk populations may experience effects following exposures to O3 concentrations somewhat below 60 ppb, a revised level of 70 ppb would be expected to reduce the occurrence of such exposures.[139] Therefore, the EPA has considered O3 exposures that could be relevant for at-risk populations such as children and people with asthma, and does not agree that controlled human exposure studies reporting respiratory effects in healthy adults following exposures to 60 ppb O3 necessitate a standard level below 70 ppb.

ii. Epidemiologic Studies

Commenters representing environmental and public health organizations also highlighted epidemiologic studies that, in their view, provide strong evidence for associations with mortality and morbidity in locations with ambient O3 concentrations near and below 60 ppb. These commenters focused both on the epidemiologic studies evaluated in the PA's analyses of study location air quality (U.S. EPA, 2014c, Chapter 4) and on studies that were not explicitly analyzed in the PA, and in some cases on studies that were not included in the ISA.

The EPA agrees that epidemiologic studies can provide perspective on the degree to which O3-associated health effects have been identified in areas with air quality likely to have met various standards. However, as discussed below, we do not agree with the specific conclusions drawn by these commenters regarding the implications of epidemiologic studies for the standard level. As an initial matter in considering epidemiologic studies, the EPA notes its decision, consistent with CASAC advice, to place the most emphasis on information from controlled human exposure studies (II.B.2 and II.B.3, above). This decision reflects the greater certainty in using information from controlled human exposure studies to link specific O3 exposures with health effects, compared to using air quality information from epidemiologic studies of O3 for this purpose.

While being aware of the uncertainties discussed above (II.B.2.b.ii), in considering what epidemiologic studies can tell us, the EPA notes analyses in the PA (U.S. EPA, 2014c, section 4.4.1) indicating that a revised standard with a level at or below 70 ppb would be expected to maintain distributions of short-term ambient O3 concentrations below those present in the locations of all of the single-city epidemiologic studies analyzed. As discussed in the PA (U.S. EPA, 2014c, section 4.4.1), this includes several single-city studies conducted in locations that would have violated the current standard, and the study by Mar and Koenig (2009) that reported positive and statistically significant associations with respiratory emergency department visits with children and adults in a location that would have met the current standard over the entire study period, but would have violated a standard with a level of 70 ppb.[140] While these analyses provide support for a level at least as low as 70 ppb, the Administrator judges that they do not provide a compelling basis for distinguishing between the appropriateness of 70 ppb and lower standard levels.

As in the proposal, the EPA acknowledges additional uncertainty in interpreting air quality in locations of multicity epidemiologic studies of short-term O3 for the purpose of evaluating alternative standard levels (U.S. EPA, 2014c, sections 3.1.4.2, 4.4.1). In particular, the PA concludes that interpretation of such air quality information is complicated by uncertainties in the extent to which multicity effect estimates (i.e., which are based on combining estimates from multiple study locations) can be attributed to ambient O3 in the subset of study locations that would have met a particular standard, versus O3 in the study locations that would have violated the standard. While giving only limited weight to air quality analyses in these study areas because of this uncertainty, the EPA also notes PA analyses indicating that a standard level at or below 70 ppb would require additional reductions, beyond those required by the current standard, in the ambient O3 concentrations that provided the basis for statistically significant O3 health effect associations in multicity epidemiologic studies. As was the case for the single-city studies, and contrary to the views expressed by the commenters noted above, the Administrator judges that these studies do not provide a compelling basis for distinguishing between the appropriateness of alternative standard levels at or below 70 ppb.

In some cases, commenters highlighted studies that were assessed in the 2008 review of the O3 NAAQS, but were not included in the ISA in the current review. These commenters asserted that such studies support the occurrence of O3 health effect associations in locations with air quality near or, in some cases, below 60 ppb. Specifically, commenters highlighted a number of studies included in the 2007 Staff Paper that were not included in the ISA, claiming that these studies support a standard level below 70 ppb, and as low as 60 ppb.

As an initial matter with regard to these studies, the EPA notes that the focus of the ISA is on assessing the most policy-relevant scientific evidence. In the current review, the ISA considered over 1,000 new studies that have been published since the last review. Thus, it is not surprising that, as the body of evidence has been strengthened since the last review, some of the studies considered in the last review are no longer among the most policy relevant. However, based on the information included in the 2007 Staff Paper, the EPA does not agree that the studies highlighted by commenters provide compelling support for a level below 70 ppb. In fact, as discussed in the Staff Paper in the last review (U.S. EPA, 2007, p. 6-9; Appendix 3B), the O3 concentrations reported for these studies, and the concentrations highlighted by commenters, were based on averaging across multiple monitors in study areas. Given that the highest monitor in an area is used to determine whether that area meets or violates the NAAQS, the averaged concentrations reported in the Staff Paper are thus not appropriate for direct comparison to the level of the O3 standard. When the Staff Paper considered the O3 concentrations measured at individual monitors for the subset of these study areas with particularly low concentrations, they were almost universally found to be above, and in many cases well above, even the current standard level of 75 ppb.[141] Based on the above Start Printed Page 65360considerations, and consistent with the Administrator's overall decision to place less emphasis on air quality in locations of epidemiologic studies to select a standard level, the EPA disagrees with commenters who asserted that epidemiologic studies included in the last review, but not cited in the ISA or PA in this review, necessitate a level below 70 ppb. In fact, the EPA notes that these studies are consistent with the majority of the U.S. studies evaluated in the PA in the current review, in that most were conducted in locations that would have violated the current O3 NAAQS over at least part of the study periods.

iii. Exposure and Risk Assessments

Some commenters supporting levels below 70 ppb also asserted that quantitative analyses in the HREA are biased such that they understate O3 exposures of concern and risks of O3-induced FEV1 decrements. Many of these comments are discussed above within the context of the adequacy of the current standard (II.B.2.b.i), including comments pointing out that exposure and risk estimates are based on information from healthy adults rather than at-risk populations; comments noting that the exposure assessment evaluates 8-hour O3 exposures rather than the 6.6-hour exposures used in controlled human exposure studies; and comments asserting that the EPA's exposure and risk analyses rely on people staying indoors on high pollution days (i.e., averting behavior).

As discussed in section II.B.2.b.i above, while the EPA agrees with certain aspects of these commenters' assertions, we do not agree with their overall conclusions. In particular, there are aspects of the HREA's quantitative analyses that, if viewed in isolation, would tend to either overstate or understate O3 exposures and/or health risks. While commenters tended to focus on those aspects of the assessments that support their position, they tended to ignore aspects of the assessments that do not support their position (points that were often raised by commenters on the other side of the issue). Rather than viewing the potential implications of these aspects of the HREA assessments in isolation, the EPA considers them together, along with other issues and uncertainties related to the interpretation of exposure and risk estimates.

For example, some commenters who advocated for a level below 70 ppb asserted that the exposure assessment could underestimate O3 exposures for highly active populations, including outdoor workers and children who spend a large portion of time outdoors during summer. In support of these assertions, commenters highlighted sensitivity analyses conducted in the HREA. However, as noted in the HREA (U.S. EPA, 2014a, Table 5-10), this aspect of the assessment is likely to have only a “low to moderate” impact on the magnitude of exposure estimates. To put this magnitude in perspective, HREA sensitivity analyses conducted in a single urban study area indicate that, regardless of whether exposure estimates for children are based on all available diaries or on a subset of diaries restricted to simulate highly exposed children, a revised standard with a level of 70 ppb is estimated to protect more than 99% of children from experiencing two or more exposures of concern at or above 70 ppb (U.S. EPA, 2014a, Chapter 5 Appendices, Figure 5G-9).[142 143] In contrast to the focus of commenters who supported a level below 70 ppb, other aspects of quantitative assessments, some of which were highlighted by commenters who opposed revising the current standard (II.B.2), tend to result in overestimates of O3 exposures. These aspects are characterized in the HREA as having either a “low,” a “low-to-moderate,” or a “moderate” impact on the magnitudes of exposure estimates.

In its reviews of the HREA and PA, CASAC recognized many of the uncertainties and issues highlighted by commenters. Even considering these uncertainties, CASAC endorsed the approaches adopted by the EPA to assess O3 exposures and health risks, and CASAC used exposure and risk estimates as part of the basis for their recommendations on the primary O3 NAAQS (Frey, 2014c). Thus, as discussed in section II.B.2.b.i above, the EPA disagrees with commenters who claim that the aspects of the quantitative assessments that they highlight lead to overall underestimates of exposures or health risks.[144]

Some commenters further contended that the level of the primary O3 standard should be set below 70 ppb in order to compensate for the use of a form that allows multiple days with concentrations higher than the standard level. These groups submitted air quality analyses to support their point that the current fourth-high form allows multiple days per year with ambient O3 concentrations above the level of the standard. While the EPA does not dispute the air quality analyses submitted by these commenters, and agrees that fourth-high form allows multiple days per year with ambient O3 concentrations above the level of the standard (3 days per year, on average over a 3-year period), the Agency disagrees with commenters' assertion that, because of this, the level of the primary O3 standard should be set below 70 ppb. As discussed above (II.A.2), the quantitative assessments that informed the Administrator's proposed decision, presented in the HREA and considered in the PA and by CASAC, estimated O3 exposures and health risks associated with air quality that “just meets” various standards with the current 8-hour averaging time and fourth-high, 3-year average form. Thus, in considering the degree of public health protection appropriate for the primary O3 standard, the Administrator has considered quantitative exposure and risk estimates that are based a fourth-high form, and therefore on a standard that, as these commenters point out, allows multiple days per year with ambient O3 concentrations above the level of the standard.

iv. CASAC Advice

Many commenters, including those representing major medical, public health, or environmental groups; some state agencies; and a large number of individual commenters, focused on CASAC advice in their rationale supporting levels below 70 ppb, and as low as 60 ppb. These commenters generally asserted that the EPA must Start Printed Page 65361give deference to CASAC. In some cases, these commenters expressed strong objections to a level of 70 ppb, noting CASAC policy advice that such a level would provide little margin of safety.

The EPA agrees that CASAC advice is an important consideration in reaching a decision on the standard level (see e.g. CAA section 307 (d)(3)),[145] though not with commenters' conclusion that CASAC advice necessitates a standard level below 70 ppb. As discussed above (II.C.4.a), the Administrator carefully considered CASAC advice in the proposal, and she judged that her proposed decision to revise the level to within the range of 65 to 70 ppb was consistent with CASAC advice, based on the available science.

As in the proposal, in her final decision on level the Administrator notes CASAC's overall conclusion that “based on the scientific evidence from clinical studies, epidemiologic studies, animal toxicology studies, as summarized in the ISA, the findings from the exposure and risk assessments as summarized in the HREA, and the interpretation of the implications of all of these sources of information as given in the Second Draft PA . . . there is adequate scientific evidence to recommend a range of levels for a revised primary ozone standard from 70 ppb to 60 ppb” (Frey, 2014c, p. 8). Thus, CASAC used the health evidence and exposure/risk information to inform its range of recommended standard levels, a range that included an upper bound of 70 ppb based on the scientific evidence, and it did not use the evidence and information to recommend setting the primary O3 standard at any specific level within the range of 70 to 60 ppb. In addition, CASAC further stated that “the choice of a level within the range recommended based on scientific evidence [i.e., 70 to 60 ppb] is a policy judgment under the statutory mandate of the Clean Air Act” (Frey, 2014c, p. ii).

In addition to its advice based on the scientific evidence, CASAC offered the “policy advice” to set the level below 70 ppb, stating that a standard level of 70 ppb “may not meet the statutory requirement to protect public health with an adequate margin of safety” (Frey, 2014c, p. ii). In supporting its policy advice to set the level below 70 ppb, CASAC noted the respiratory effects that have been shown to occur in controlled human exposure studies following exposures from 60 to 80 ppb O3, and the extent to which various standard levels are estimated to allow the occurrence of population exposures that can result in such effects (Frey, 2014c, pp. 7-8).

The EPA agrees that an important consideration when reaching a decision on level is the extent to which a revised standard is estimated to allow the types of exposures shown in controlled human exposure studies to cause respiratory effects. In reaching her final decision that a level of 70 ppb is requisite to protect public health with an adequate margin of safety (II.C.4.c, below), the Administrator carefully considers the potential for such exposures and effects. In doing so, she emphasizes the importance of setting a standard that limits the occurrence of the exposures about which she is most concerned (i.e., those for which she has the most confidence in the adversity of the resulting effects, which are repeated exposures of concern at or above 70 or 80 ppb, as discussed above in II.C.4.b.i). Based on her consideration of information from controlled human exposure studies in light of CASAC advice and ATS recommendations, the Administrator additionally judges that there is important uncertainty in the extent to which the effects shown to occur following exposures to 60 ppb O3 are adverse to public health (discussed above, II.C.4.b.i and II.C.4.b.iii). However, based on the effects that have been shown to occur, CASAC advice indicating the importance of considering these effects, and ATS recommendations indicating the potential for adverse population-level effects (II.C.4.b.i, II.C.4.b.iii), she concludes that it is appropriate to give some consideration to the extent to which a revised standard could allow the respiratory effects that have been observed following exposures to 60 ppb O3.

When considering the extent to which a revised standard could allow O3 exposures that have been shown in controlled human exposures studies to result in respiratory effects, the Administrator is most concerned about protecting the public, including at-risk populations, against repeated occurrences of such exposures of concern (II.C.4.b.i, above). In considering the appropriate metric for evaluating repeated occurrences of exposures of concern, the Administrator acknowledges that it is not clear from the evidence, or from the ATS recommendations, CASAC advice, or public comments, how particular numbers of exposures of concern could impact the seriousness of the resulting effects, especially at lower exposure concentrations. Therefore, the Administrator judges that focusing on HREA estimates of two or more exposures of concern provides a health-protective approach to considering the potential for repeated occurrences of exposures of concern that could result in adverse effects. She notes that other possible metrics for considering repeated occurrences of exposures of concern (e.g., 3 or more, 4 or more, etc.) would result in smaller exposure estimates.

As discussed further below (II.C.4.c), the Administrator notes that a revised standard with a level of 70 ppb is estimated to eliminate the occurrence of two or more exposures of concern to O3 concentrations at or above 80 ppb and to virtually eliminate the occurrence of two or more exposures of concern to O3 concentrations at or above 70 ppb (Table 1, above). For the 70 ppb benchmark, this reflects about a 90% reduction in the number of children estimated to experience two or more exposures of concern, compared to the current standard.[146] Even considering the worst-case urban study area and worst-case year evaluated in the HREA, a standard with a level of 70 ppb is estimated to protect more than 99% of children from experiencing two or more exposures of concern to O3 concentrations at or above 70 ppb (Table 1).

Though the Administrator judges that there is greater uncertainty with regard to the occurrence of adverse effects following exposures as low as 60 ppb, she notes that a revised standard with a level of 70 ppb is estimated to protect the vast majority of children in urban study areas (i.e., about 96% to more than 99% in individual areas) from experiencing two or more exposures of concern at or above 60 ppb. Compared to the current standard, this represents a reduction of more than 60% in exposures of concern for the 60 ppb benchmark (Table 1). Given the Administrator's uncertainty regarding the adversity of the effects following exposures to 60 ppb O3, and her health-protective approach to considering repeated occurrences of exposures of concern, the Administrator judges that this degree of protection is appropriate and that it reflects substantial protection against the occurrence of O3-induced effects, including effects for which she judges the adversity to public health is uncertain.Start Printed Page 65362

While being less concerned about single occurrences of exposures of concern, especially at lower exposure concentrations, the Administrator also notes that a standard with a level of 70 ppb is estimated to (1) virtually eliminate all occurrences of exposures of concern at or above 80 ppb; (2) protect ≥ about 99% of children in urban study areas from experiencing any exposures of concern at or above 70 ppb; and (3) to achieve substantial reductions (i.e., about 50%), compared to the current standard, in the occurrence of one or more exposures of concern at or above 60 ppb (Table 1).

Given the information and advice noted above (and in II.C.4.b.i, II.C.4.b.iii), the Administrator judges that a revised standard with a level of 70 ppb will effectively limit the occurrence of the O3 exposures for which she has the most confidence in the adversity of the resulting effects (i.e., based on estimates for the 70 and 80 ppb benchmarks). She further judges that such a standard will provide a large degree of protection against O3 exposures for which there is greater uncertainty in the adversity of effects (i.e., those observed following exposures to 60 ppb O3), contributing to the margin of safety of the standard. See M ississippi, 744 F. 3d at 1353 (“By requiring an `adequate margin of safety', Congress was directing EPA to build a buffer to protect against uncertain and unknown dangers to human health”). Given the considerable protection provided against repeated exposures of concern for all of the benchmarks evaluated, including the 60 ppb benchmark, the Administrator judges that a standard with a level of 70 ppb will provide an adequate margin of safety against the adverse O3-induced effects shown to occur following exposures at or above 72 ppb, and judged by CASAC likely to occur following exposures somewhat below 72 ppb.[147]

Contrary to the conclusions of commenters who advocated for a level below 70 ppb, the Administrator notes that her final decision is consistent with CASAC's advice, based on the scientific evidence, and with CASAC's focus on setting a revised standard to further limit the occurrence of the respiratory effects observed in controlled human exposure studies, including effects observed following exposures to 60 ppb O3. Given her judgments and conclusions discussed above, and given that the CAA reserves the choice of the standard that is requisite to protect public health with an adequate margin of safety for the judgment of the EPA Administrator, she disagrees with commenters who asserted that CASAC advice necessitates a level below 70 ppb, and as low as 60 ppb. The Administrator's final conclusions on level are discussed in more detail below (II.C.4.c).

c. Administrator's Final Decision Regarding Level

Having carefully considered the public comments on the appropriate level of the primary O3 standard, as discussed above and in the Response to Comments document, the Administrator believes her scientific and policy judgments in the proposal remain valid. In conjunction with her decisions to retain the current indicator, averaging time, and form (II.C.1 to II.C.3, above), the Administrator is revising the level of the primary O3 standard to 70 ppb. In doing so, she is selecting a primary O3 standard that is requisite to protect public health with an adequate margin of safety, in light of her judgments based on an interpretation of the scientific evidence and exposure/risk information that neither overstates nor understates the strengths and limitations of that evidence and information and the appropriate inferences to be drawn therefrom.

The Administrator's decision to revise the level of the primary O3 standard to 70 ppb builds upon her conclusion that the overall body of scientific evidence and exposure/risk information calls into question the adequacy of public health protection afforded by the current standard, particularly for at-risk populations and lifestages (II.B.3).[148] Consistent with the proposal, her decision on level places the greatest emphasis on the results of controlled human exposure studies and on quantitative analyses based on information from these studies, particularly analyses of O3 exposures of concern. As in the proposal, and as discussed further below, she views the results of the lung function risk assessment, analyses of O3 air quality in locations of epidemiologic studies, and epidemiology-based quantitative health risk assessments as providing information in support of her decision to revise the current standard, but a more limited basis for selecting a particular standard level among a range of options. See Mississippi, 744 F. 3d at 1351-52 (studies can legitimately support a decision to revise the standard, but not provide sufficient information to justify their use in setting the level of a revised standard).

Given her consideration of the evidence, exposure/risk information, advice from CASAC, and public comments, the Administrator judges that a standard with a level of 70 ppb is requisite to protect public health with an adequate margin of safety. She notes that the determination of what constitutes an adequate margin of safety is expressly left to the judgment of the EPA Administrator. See Lead Industries Association v. EPA, 647 F.2d at 1161-62; Mississippi, 744 F. 3d at 1353. She further notes that in evaluating how particular standards address the requirement to provide an adequate margin of safety, it is appropriate to consider 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 present (I.B, above). Consistent with past practice and long-standing judicial precedent, the Administrator takes the need for an adequate margin of safety into account as an integral part of her decision-making on the appropriate level, averaging time, form, and indicator of the standard.[149]

In considering the need for an adequate margin of safety, the Administrator notes that a standard with a level of 70 ppb O3 would be expected to provide substantial improvements in public health, including for at-risk groups such as children and people with asthma. The following paragraphs summarize the basis for the Administrator's conclusion that a revised primary O3 standard with a level of 70 ppb is requisite to protect the public health with an adequate margin of safety.

As an initial matter, consistent with her conclusions on the need for revision of the current standard (II.B.3), in reaching a decision on level the Administrator places the most weight on information from controlled human exposure studies. In doing so, she notes that controlled human exposure studies provide the most certain evidence indicating the occurrence of health Start Printed Page 65363effects in humans following specific O3 exposures. In particular, she notes that the effects reported in controlled human exposure studies are due solely to O3 exposures, and interpretation of study results is not complicated by the presence of co-occurring pollutants or pollutant mixtures (as is the case in epidemiologic studies). The Administrator also observes that her emphasis on information from controlled human exposure studies is consistent with CASAC's advice and interpretation of the scientific evidence (Frey, 2014c).

With regard to the effects shown in controlled human exposure studies following specific O3 exposures, as discussed in more detail above (II.B, II.C.4.b.i), the Administrator notes that (1) the largest respiratory effects, and the broadest range of effects, have been studied and reported following exposures to 80 ppb O3 or higher (i.e., decreased lung function, increased airway inflammation, increased respiratory symptoms, AHR, and decreased lung host defense); (2) exposures to O3 concentrations as low as 72 ppb have been shown to both decrease lung function and result in respiratory symptoms; and (3) exposures to O3 concentrations as low as 60 ppb have been shown to decrease lung function and to increase airway inflammation.

While such controlled human exposure studies provide a high degree of confidence regarding the occurrence of health effects following exposures to O3 concentrations from 60 to 80 ppb, there are no universally accepted criteria by which to judge the adversity of the observed effects. To inform her judgments on the potential adversity to public health of effects reported in controlled human exposure studies, the Administrator considers ATS recommendations and CASAC advice, as described in detail above (II.B.2, II.C.4.b.i, II.C.4.b.iii, II.C.4.b.iv). Based on her consideration of such recommendations and advice, the Administrator is confident that the respiratory effects that have been observed following exposures to 72 ppb O3 or above can be adverse. In addition, she judges that adverse effects are likely to occur following exposures somewhat below 72 ppb (II.C.4.b.i). However, as described above (II.C.4.b.i, II.C.4.b.iii, II.C.4.b.iv), the Administrator is notably less confident in the adversity to public health of the respiratory effects that have been observed following exposures to O3 concentrations as low as 60 ppb, given her consideration of the following: (1) ATS recommendations indicating uncertainty in judging adversity based on lung function decrements alone; (2) uncertainty in the extent to which a short-term, transient population-level decrease in FEV1 would increase the risk of other, more serious respiratory effects in that population (i.e., per ATS recommendations on population-level risk); and (3) compared to 72 ppb, CASAC advice is less clear regarding the potential adversity of effects at 60 ppb.

Taken together, the Administrator concludes that the evidence from controlled human exposure studies provides strong support for her conclusion that a revised standard with a level of 70 ppb is requisite to protect the public health with an adequate margin of safety. She bases this conclusion, in part, on the fact that such a standard level would be well below the O3 exposure concentration shown to result in the widest range of respiratory effects (i.e., 80 ppb), and below the lowest O3 exposure concentration shown to result in the adverse combination of lung function decrements and respiratory symptoms (i.e., 72 ppb). See Lead Industries, 647 F. 2d at 1160 (setting NAAQS at level well below the level where the clearest adverse effects occur, and at a level eliminating most “sub-clinical effects” provides an adequate margin of safety).

As discussed above (II.C.4.b.i), the Administrator also notes that a revised O3 standard with a level of 70 ppb can provide substantial protection against the broader range of O3 exposure concentrations that have been shown in controlled human exposure studies to result in respiratory effects, including exposure concentrations below 70 ppb. The degree of protection provided by any NAAQS is due to the combination of all of the elements of the standard (i.e., indicator, averaging time, form, level) and, in the case of the fourth-high form of the revised primary O3 standard (II.C.3), the large majority of days in areas that meet the revised standard will have 8-hour O3 concentrations below 70 ppb, with most days having 8-hour O3 concentrations well below this level. In addition, the degree of protection provided by the O3 NAAQS is also dependent on the extent to which people experience health-relevant O3 exposures in locations meeting the NAAQS. As discussed above, for a pollutant like O3 where adverse responses are critically dependent on ventilation rates, the Administrator notes that it is important to consider activity patterns in the exposed population. Not considering activity patterns, and corresponding ventilation rates, can result in a standard that provides more protection than is requisite. Therefore, as discussed in the proposal, in considering the degree of protection provided by a revised primary O3 standard, the Administrator considers the extent to which that standard would be expected to limit population exposures of concern (i.e., which take into account activity patterns and estimated ventilation rates) to the broader range of O3 exposure concentrations shown to result in health effects.

Due to interindividual variability in responsiveness, the Administrator notes that not every occurrence of an exposure of concern will result in an adverse effect (II.C.4.b.i). Moreover, repeated occurrences of some of the effects demonstrated following exposures of concern could increase the likelihood of adversity (U.S. EPA, 2013, Section 6.2.3, p. 6-76). In particular, she notes that the types of respiratory effects that can occur following exposures of concern, particularly if experienced repeatedly, provide a plausible mode of action by which O3 may cause other more serious effects. Therefore, as in the proposal, the Administrator is most concerned about protecting at-risk populations against repeated occurrences of exposures of concern. In considering the appropriate metric for evaluating repeated occurrences of exposures of concern, the Administrator acknowledges that it is not clear from the evidence, or from the ATS recommendations, CASAC advice, or public comments, how particular numbers of exposures of concern could impact the seriousness of the resulting effects, especially at lower exposure concentrations. Therefore, the Administrator judges that focusing on HREA estimates of two or more exposures of concern provides a health-protective approach to considering the potential for repeated occurrences of exposures of concern that could result in adverse effects.

Based on her consideration of adversity discussed above, the Administrator places the most emphasis on setting a standard that appropriately limits repeated occurrences of exposures of concern at or above the 70 and 80 ppb benchmarks. She notes that a revised standard with a level of 70 ppb is estimated to eliminate the occurrence of two or more exposures of concern to O3 concentrations at or above 80 ppb and to virtually eliminate the occurrence of two or more exposures of concern to O3 concentrations at or above 70 ppb for all children and children with asthma, even in the worst-case year and location evaluated.

While she is less confident that adverse effects will occur following exposures to O3 concentrations as low as 60 ppb, as discussed above, the Start Printed Page 65364Administrator judges that it is also appropriate to consider estimates of exposures of concern for the 60 ppb benchmark. Consistent with this judgment, although CASAC advice regarding the potential adversity of effects at 60 ppb was less definitive than for effects at 72 ppb, CASAC did clearly advise the EPA to consider the extent to which a revised standard is estimated to limit the effects observed following 60 ppb exposures (Frey, 2014c). Therefore, the Administrator considers estimated exposures of concern for the 60 ppb benchmark, particularly considering the extent to which the health protection provided by a revised standard includes a margin of safety against the occurrence of adverse O3-induced effects. The Administrator notes that a revised standard with a level of 70 ppb is estimated to protect the vast majority of children in urban study areas (i.e., about 96% to more than 99% of children in individual areas) from experiencing two or more exposures of concern at or above 60 ppb. Compared to the current standard, this represents a reduction of more than 60%.

Given the considerable protection provided against repeated exposures of concern for all of the benchmarks evaluated, including the 60 ppb benchmark, the Administrator judges that a standard with a level of 70 ppb will incorporate a margin of safety against the adverse O3-induced effects shown to occur following exposures at or above 72 ppb, and judged likely to occur following exposures somewhat below 72 ppb.

While the Administrator is less concerned about single occurrences of O3 exposures of concern, especially for the 60 ppb benchmark, she judges that estimates of one or more exposures of concern can provide further insight into the margin of safety provided by a revised standard. In this regard, she notes that a standard with a level of 70 ppb is estimated to (1) virtually eliminate all occurrences of exposures of concern at or above 80 ppb; (2) protect the vast majority of children in urban study areas from experiencing any exposures of concern at or above 70 ppb (i.e., ≥ about 99%, based on mean estimates; Table 1); and (3) to achieve substantial reductions, compared to the current standard, in the occurrence of one or more exposures of concern at or above 60 ppb (i.e., about a 50% reduction; Table 1). The Administrator judges that these results provide further support for her conclusion that a standard with a level of 70 ppb will incorporate an adequate margin of safety against the occurrence of O3 exposures that can result in effects that are adverse to public health.

The Administrator additionally judges that a standard with a level of 70 ppb would be expected to result in important reductions, compared to the current standard, in the population-level risk of O3-induced lung function decrements (≥10%, ≥15%) in children, including children with asthma. Specifically, a revised standard with a level of 70 ppb is estimated to reduce the risk of two or more O3-induced decrements by about 30% and 20% for decrements ≥15 and 10%, respectively (Table 2, above). However, as discussed above (II.C.4.b.i), the Administrator judges that there are important uncertainties in using lung function risk estimates as a basis for considering the occurrence of adverse effects in the population given (1) the ATS recommendation that “a small, transient loss of lung function, by itself, should not automatically be designated as adverse” (ATS, 2000a); (2) uncertainty in the extent to which a transient population-level decrease in FEV1 would increase the risk of other, more serious respiratory effects in that population (i.e., per ATS recommendations on population-level risk); and (3) that CASAC did not advise considering a standard that would be estimated to eliminate O3-induced lung function decrements ≥10 or 15% (Frey, 2014c). Moreover, as at proposal, the Administrator notes that the variability in lung function risk estimates across urban study areas is often greater than the differences in risk estimates between various standard levels (Table 2, above).[150] Given this, and the resulting considerable overlap between the ranges of lung function risk estimates for different standard levels, the Administrator puts limited weight on the lung function risk estimates for distinguishing between the degrees of public health protection provided by alternative standard levels. Therefore, the Administrator judges that while a standard with a level of 70 ppb would be expected to result in important reductions, compared to the current standard, in the population-level risk of O3-induced lung function decrements (> 10%, 15%) in children, including children with asthma, she also judges that estimated risks of O3-induced lung function decrements provide a more limited basis than exposures of concern for distinguishing between the appropriateness of the health protection afforded by a standard level of 70 ppb versus lower levels.

The Administrator also considers the epidemiologic evidence and the quantitative risk estimates based on information from epidemiologic studies. As discussed in the proposal, and above in the EPA's responses to significant comments, although the Administrator acknowledges the important uncertainties in using the O3 epidemiologic studies as a basis for selecting a standard level, she notes that these studies can provide perspective on the degree to which O3-associated health effects have been identified in areas with air quality likely to have met various standards. Specifically, the Administrator notes analyses in the PA (U.S. EPA, 2014c, section 4.4.1) indicating that a revised standard with a level of 70 ppb would be expected to require additional reductions, beyond those required by the current standard, in the short- and long-term ambient O3 concentrations that provided the basis for statistically significant O3 health effect associations in both the single-city and multicity epidemiologic studies evaluated. As discussed above in the response to comments, while the Administrator concludes that these analyses support a level at least as low as 70 ppb, based on a study reporting health effect associations in a location that met the current standard over the entire study period but that would have violated a revised standard with a level of 70 ppb,[151] she further judges that they are of more limited utility for distinguishing between the appropriateness of the health protection estimated for a standard level of 70 ppb and the protection estimated for lower levels. Thus, the Administrator notes that a revised standard with a level of 70 ppb will provide additional public health protection, beyond that provided by the current standard, against the clearly adverse effects reported in Start Printed Page 65365epidemiologic studies. She judges that a standard with a level of 70 ppb strikes an appropriate balance between setting the level to require reductions in the ambient O3 concentrations associated with statistically significant health effects in epidemiologic studies, while not being more protective than necessary in light of her considerable uncertainty in the extent to which studies clearly show O3-attributable effects at lower ambient O3 concentrations. This judgment is consistent with the Administrator's conclusions based on information from controlled human exposure studies, as discussed above.

With regard to epidemiology-based risk estimates, the Administrator takes note of the CASAC conclusion that “[a]lthough the estimates for short-term exposure impacts are subject to uncertainty, the data supports a conclusion that there are meaningful reductions in mean premature mortality associated with ozone levels lower than the current standard” (Frey, 2014a, p. 10). While she concludes that epidemiology-based risk analyses provide only limited support for any specific standard level, consistent with CASAC advice the Administrator judges that, compared to the current standard, a revised standard with a level of 70 ppb will result in meaningful reductions in the mortality and respiratory morbidity risk that is associated with short-or long-term ambient O3 concentrations.

Given all of the evidence and information discussed above, the Administrator judges that a standard with a level of 70 ppb is requisite to protect public health with an adequate margin of safety, and that a level below 70 ppb would be more than “requisite” to protect the public health. In reaching this conclusion, she notes that a decision to set a lower level would place a large amount of emphasis on the potential public health importance of (1) further reducing the occurrence of O3 exposures of concern, though the exposures about which she is most concerned are estimated to be almost eliminated with a level of 70 ppb, and lower levels would be expected to achieve virtually no additional reductions in these exposures (see Table 1, above); (2) further reducing the risk of O3-induced lung function decrements > 10 and 15%, despite having less confidence in judging the potential adversity of lung function decrements alone and the considerable overlap between risk estimates for various standard levels that make it difficult to distinguish between the risk reductions achieved; (3) further reducing ambient O3 concentrations, relative to those in locations of epidemiologic studies, though associations have not been reported for air quality that would have met a standard with a level of 70 ppb across all study locations and over entire study periods, and despite her consequent judgment that air quality analyses in epidemiologic study locations are not informative regarding the additional degree of public health protection that would be afforded by a standard set at a level below 70 ppb; and (4) further reducing epidemiology-based risk estimates, despite the important uncertainties in those estimates. As discussed in this section and in the responses to significant comments above, the Administrator does not agree that it is appropriate to place significant weight on these factors or to use them to support the appropriateness of standard levels below 70 ppb O3. Compared to an O3 standard level of 70 ppb, the Administrator concludes that the extent to which lower standard levels could result in further public health improvements becomes notably less certain.

Thus, having carefully considered the evidence, information, CASAC advice, and public comments relevant to her decision on the level of the primary O3 standard, as discussed above and in the Response to Comments document, the Administrator is revising the level of the primary O3 standard to 70 ppb. She is mindful that the selection of a primary O3 standard that is requisite to protect public health with an adequate margin of safety requires judgments based on an interpretation of the scientific evidence and exposure/risk information that neither overstate nor understate the strengths and limitations of that evidence and information and the appropriate inferences to be drawn therefrom. Her decision places the greatest emphasis on the results of controlled human exposure studies and on quantitative analyses based on information from these studies, particularly analyses of O3 exposures of concern. As in the proposal, and as discussed above, she views the results of the lung function risk assessment, analyses of O3 air quality in locations of epidemiologic studies, and epidemiology-based quantitative health risk assessments as providing information in support of her decision to revise the current standard, but a more limited basis for selecting a particular standard level among a range of options.

In making her decision to revise the level of the primary O3 standard to 70 ppb, the Administrator judges that a revised standard with a level of 70 ppb strikes the appropriate balance between limiting the O3 exposures about which she is most concerned and not going beyond what would be required to effectively limit such exposures. Specifically, the Administrator judges it appropriate to set a standard estimated to eliminate, or almost eliminate, repeated occurrences of exposures of concern for the 70 and 80 ppb benchmarks. She further judges that a lower standard level would not be appropriate given that lower levels would be expected to achieve virtually no additional reductions in repeated occurrences of exposures of concern for these benchmarks. For the 60 ppb benchmark, a level of 70 ppb is estimated to protect the vast majority of children (including children with asthma) in urban study areas from experiencing two or more exposures of concern, reflecting important reductions in such exposures compared to the current standard and indicating that the revised primary O3 standard provides an adequate margin of safety. Given these results, including the considerable protection provided against repeated exposures of concern for the 60 ppb benchmark, the Administrator judges that a standard with a level of 70 ppb incorporates an adequate margin of safety against the occurrence of adverse O3-induced effects.

For all of the above reasons, the Administrator concludes that a primary O3 standard with an 8-hour averaging time; a 3-year average, fourth-high form; and a level of 70 ppb is requisite to protect public health, including the health of at-risk populations, with an adequate margin of safety. Therefore, in this final rule she is setting the level of the primary O3 standard at 70 ppb.

D. Decision on the Primary Standard

For the reasons discussed above, and taking into account information and assessments presented in the ISA, HREA, and PA, the advice and recommendations of the CASAC Panel, and the public comments, the Administrator has decided to revise the existing 8-hour primary O3 standard. Specifically, the Administrator is revising the level of the primary O3 standard to 70 ppb. The revised 8-hour primary standard, with a level of 70 ppb, would be met at an ambient air monitoring site when the 3-year average of the annual fourth-highest daily maximum 8-hour average O3 concentration is less than or equal to 70 ppb. Data handling conventions are specified in the new Appendix U that is adopted, as discussed in section V below.Start Printed Page 65366

At this time, EPA is also promulgating revisions to the Air Quality Index (AQI) for O3 to be consistent with the revisions to the primary O3 standard and the health information evaluated in this review of the standards. These revisions are discussed below in section III.

III. Communication of Public Health Information

Information on the public health implications of ambient concentrations of criteria pollutants is currently made available primarily through EPA's AQI program. The AQI has been in use since its inception in 1999 (64 FR 42530). It provides accurate, timely, and easily understandable information about daily levels of pollution. It is designed to tell individual members of the public how clean or unhealthy their air is, whether health effects might be a concern, and, if so, measures individuals can take to reduce their exposure to air pollution.[152] See CAA section 127. The AQI focuses on health effects individuals may experience within a few hours or days after breathing unhealthy air. The AQI establishes a nationally uniform system of indexing pollution concentrations for O3, CO, NO2, PM and SO2. The AQI converts pollutant concentrations in a community's air to a number on a scale from 0 to 500. Reported AQI values enable the public to know whether air pollution concentrations in a particular location are characterized as good (0-50), moderate (51-100), unhealthy for sensitive groups (101-150), unhealthy (151-200), very unhealthy (201-300), or hazardous (301-500). The AQI index value of 100 typically corresponds to the level of the short-term NAAQS for each pollutant. For the 2008 O3 NAAQS, an 8-hour average concentration of 75 ppb corresponds to an AQI value of 100. An AQI value greater than 100 means that a pollutant is in one of the unhealthy categories (i.e., unhealthy for sensitive groups, unhealthy, very unhealthy, or hazardous) on a given day; an AQI value at or below 100 means that a pollutant concentration is in one of the satisfactory categories (i.e., moderate or good). An additional consideration in selecting breakpoints is for each category to span at least a 15 ppb range to allow for more accurate air pollution forecasting. Decisions about the pollutant concentrations at which to set the various AQI breakpoints, that delineate the various AQI categories, draw directly from the underlying health information that supports the NAAQS review.

A. Proposed Revisions to the AQI

Recognizing the importance of revising the AQI in a timely manner to be consistent with any revisions to the NAAQS, EPA proposed conforming changes to the AQI, in connection with the Agency's proposed decision on revisions to the O3 NAAQS. These conforming changes included setting the 100 level of the AQI at the same level as the revised primary O3 NAAQS and also making adjustments based on health information from this NAAQS review to AQI breakpoints at the lower end of each range (i.e., AQI values of 50, 150, 200 and 300). The EPA did not propose to change the level at the top of the index (i.e., AQI value of 500) that typically is set equal to the Significant Harm Level (40 CFR 51.16), which would apply to state contingency plans.

The EPA proposed to revise the AQI for O3 by setting an AQI value of 100 equal to the level of the revised O3 standard (65-70 ppb). The EPA also proposed to revise the following breakpoints: an AQI value of 50 to within a range from 49-54 ppb; an AQI value of 150 to 85 ppb; an AQI value of 200 to 105 ppb, and an AQI value of 300 to 200 ppb. All these levels are averaged over 8 hours. The EPA proposed to set an AQI value of 50, the breakpoint between the good and moderate categories, at 15 ppb below the value of the proposed standard, i.e. to within a range from 49 to 54 ppb. The EPA took comment on what level within this range to select, recognizing that there is no health message for either at-risk or healthy populations in the good category. Thus, the level selected should be below the lowest concentration (i.e., 60 ppb) that has been shown in controlled human exposure studies of young, healthy adults exposed to O3 while engaged in quasi-continuous moderate exercise for 6.6 hours to cause moderate lung function decrements (i.e., FEV1 decrements ≥ 10%, which could be adverse to people with lung disease) and airway inflammation.[153] The EPA proposed to set an AQI value of 150, the breakpoint between the unhealthy for sensitive groups and unhealthy categories, at 85 ppb. At this level, controlled human exposure studies of young, healthy adults indicate that up to 25% of exposed people are likely to have moderate lung function decrements (i.e., 25% have FEV1 decrements ≥ 10%; 12% have FEV1 decrements ≥ 15%) and up to 7% are likely to have large lung function decrements (i.e., FEV1 decrements ≥ 20%) (McDonnell et al., 2012; Figure 7). Large lung function decrements would likely interfere with normal activity for many healthy people. For most people with lung disease, large lung function decrements would not only interfere with normal activity but would increase the likelihood that they would seek medical treatment (72 FR 37850, July 11, 2007). The EPA proposed to set an AQI value of 200, the breakpoint between the unhealthy and very unhealthy categories, at 105 ppb. At this level, controlled human exposure studies of young, healthy adults indicate that up to 38% of exposed people are likely to have moderate lung function decrements (i.e., 38% have FEV1 decrements ≥ 10%; 22% have FEV1 decrements ≥ 15%) and up to 13% are likely to have large lung function decrements (i.e., FEV1 decrements ≥ 20%). The EPA proposed to set an AQI value of 300, the breakpoint between the very unhealthy and hazardous categories, at 200 ppb. At this level, controlled human exposure studies of healthy adults indicate that up to 25% of exposed individuals are likely to have large lung function decrements (i.e., FEV1 decrements ≥ 20%), which would interfere with daily activities for many of them and likely cause people with lung disease to seek medical attention.

EPA stated that the proposed breakpoints reflect an appropriate balance between reflecting the health evidence that is the basis for the proposed primary O3 standard and providing category ranges that are large enough to be forecasted accurately, so Start Printed Page 65367that the new AQI for O3 can be implemented more easily in the public forum for which the AQI ultimately exists. However, the EPA recognized alternative approaches to viewing the evidence and information and solicited comment on the proposed revisions to the AQI.

With respect to reporting requirements (40 CFR part 58, section 58.50), EPA proposed to revise 40 CFR part 58, section 58.50 (c) to determine the areas subject to AQI reporting requirements based on the latest available census figures, rather than the most recent decennial U.S. census.[154] This change is consistent with our current practice of using the latest population figures to make monitoring requirements more responsive to changes in population.

B. Comments on Proposed Revisions to the AQI

EPA received many comments on the proposed changes to the AQI. Three issues came up in the comments, including: (1) Whether the AQI should be revised at all, even if the primary standard is revised; (2) whether an AQI value of 100 should be set equal to the level of the primary standard and the other breakpoints adjusted accordingly; and, (3) whether the AQI reporting requirements should be based on the latest available census figures rather than the most recent decennial census.

With respect to the first issue, some industry commenters stated that the AQI should not be revised at all, even if the level of the primary O3 standard is revised. In support of this position, these commenters stated that the proposed conforming changes to the AQI would lower O3 levels in each category, and would mean that air quality that is actually improving would be reported as less healthy. According to commenters, the revised AQI would fail to capture these improvements and potentially mislead the public into thinking that air quality has degraded and that EPA and state regulators are not doing their jobs. These commenters noted that there is no requirement to revise the AQI, and that the CAA does not tie the AQI to the standards, stating that the purpose of section 319(a) of the CAA is to provide a consistent, uniform means of gauging air quality. These commenters further asserted that EPA's proposed changes run counter to that uniformity by changing the air quality significance of a given index value and category and that retention of the current AQI breakpoints would allow continued uniform information on air quality. Commenters stated that it is important that the EPA clearly communicates that the immediate increases in moderate rated days are due to AQI breakpoint adjustment and not due to a sudden decline in air quality. One commenter estimated the increased proportion of days in the moderate category and above in 10 metropolitan areas for 2013 and also for 2025 for 4 cities from the original 10 that were estimated to attain a standard below 70 ppb, to compare with 2013. This commenter noted that the change in the proposed AQI breakpoint between “good” and “moderate” would result in a larger number of days that did not meet the “good” criteria. They went further to claim that the change in breakpoints would result in fewer “good” days in the year 2025 (using the new breakpoint) than occurred in 2013 (using the old breakpoints) despite substantial improvement in air quality over that time period.

On the other hand, state and local agencies and their organizations, environmental and medical groups, and members of the public overwhelmingly supported revising the AQI when the level of the standard is revised. Even state agencies that did not support revising the standard, expressed support for revising the AQI at the same time as the standard, if the standard is revised.

Recognizing the importance of the AQI as a communication tool that allows members of the public to take exposure reduction measures when air quality poses health risks, the EPA agrees with these comments about revising the AQI at the same time as the primary standard. The EPA agrees with state and local agency commenters that its historical approach of setting an AQI value of 100 equal to the level of the revised 8-hour primary O3 standard is appropriate, both from a public health and a communication perspective.

EPA disagrees with commenters who stated that the AQI should not be linked to the primary standards. As noted in the August 4, 1999, rulemaking (64 FR 149, 42531) that established the current AQI, the EPA established the nationally uniform air quality index, called the Pollutant Standards Index (PSI), in 1976 to meet the needs of state and local agencies with the following advantages: It sends a clear and consistent message to the public by providing nationally uniform information on air quality; it is keyed as appropriate to the NAAQS and the Significant Harm Level which have a scientific basis relating air quality and public health; it is simple and easily understood by the public; it provides a framework for reflecting changes to the NAAQS; and it can be forecasted to provide advance information on air quality. Both the PSI and AQI have historically been normalized across pollutants by defining an index value of 100 as the numerical level of the short-term (i.e., averaging time of 24-hours or less) primary NAAQS for each pollutant. Moreover, this approach does not mislead the public. Since the establishment of the AQI, the EPA and state and local air agencies and organizations have developed experience in educating the public about changes in the standards and, concurrently, related changes to AQI breakpoints and advisories. When the standards change, EPA and state and local agencies have tried to help the public understand that air quality is not getting worse, it's that the health evidence underlying the standards and the AQI has changed. EPA's Air Quality System (AQS), the primary repository for air quality monitoring data, is also adjusted to reflect the revised breakpoints. Specifically, all historical AQI values in AQS are recomputed with the revised breakpoints, so that all data queries and reports downstream of AQS will show appropriate trends in AQI values over time.[155]

In general, commenters who supported revising the AQI when the standard is revised, also supported setting an AQI value of 100 equal to the level of the 8-hour primary O3 standard. The EPA agrees with these commenters. With respect to an AQI value of 100, the EPA is taking final action to set an AQI value of 100 equal to the level of the 8-hour primary standard at 70 ppb O3.

With respect to proposed changes to other AQI breakpoints, some state and local agency commenters expressed general support for all the changes in O3 breakpoints (in Table 2 of Appendix G). In addition, we received a few comments specifically about the breakpoint between the good and moderate categories. One state expressed the view that forecasting the AQI for O3 is not an exact science, so it is important to provide a range large enough to reasonably predict O3Start Printed Page 65368concentrations for the following day (≥ 20 ppb). Although not supporting revision of the standard, this state recommended that if the primary standard was revised to 70 ppb, the lower end of moderate category should be set at 50 ppb to allow for a 20 ppb spread in that category. Several commenters recommending a breakpoint between the good and moderate categories of no higher than 50 ppb stated that this breakpoint should be set on health information, pointing to epidemiologic data and the World Health organization guidelines. The Agency agrees that AQI breakpoints should take into consideration health information when possible, and also that it is important for AQI categories to span ranges large enough to support accurate forecasting. The EPA is setting the breakpoint at the lower end of the moderate category at 55 ppb, which is 15 ppb below the level of the standard of 70 ppb. This is consistent with past practice of making a proportional adjustment to this AQI breakpoint, relative to an AQI value of 100 (i.e., 70 ppb), and also retains the current practice of providing a 15 ppb range in the moderate category to allow for accurate forecasting. This level is below the lowest concentration (i.e., 60 ppb) that has been shown in controlled human exposure studies of healthy adults to cause moderate lung function decrements (i.e., FEV1 decrements ≥ 10%, which could be adverse to people with lung disease), large lung function decrements (i.e., FEV1 decrements ≥ 20%) in a small proportion of people, and airway inflammation, notwithstanding the Administrator's judgment that there is uncertainty in the adversity of the effects shown to occur at 60 ppb.

We received fewer comments on proposed changes to the AQI values of 150, 200 and 300. Again, some state and local agency commenters expressed general support for proposed changes to the AQI. Some states specifically supported these breakpoints. However, a commenter suggested setting an AQI value at the lower end of the unhealthy category, at a level much lower than 85 ppb, since they state that it is a key threshold that is often used in air quality action day programs as a trigger to encourage specific behavior modifications or reduce emissions of O3 precursors (e.g., by taking public transportation to work). This commenter stated that setting the breakpoint at 85 ppb would, in the Agency's own rationale, not require the triggering of these pollution reduction measures until air quality threatened to impact 25% of people exposed. We disagree with this commenter because EPA does not have any requirements for voluntary programs. State and local air agencies have discretion to set the trigger for voluntary action programs at whatever level they choose, and they are currently set at different levels, not just at the unhealthy breakpoint specified in the comment. For example, Houston, Galveston and Brazoria TX metropolitan area calls ozone action days when air quality reaches the unhealthy for sensitive groups category. For more information about action days programs across the U.S. see the AirNow Web site (www.airnow.gov) and click on the link to AirNow Action Days. The unhealthy category represents air quality where there are general population-level effects. We believe that setting the breakpoint between the unhealthy for sensitive groups and unhealthy categories, at 85 ppb where, as discussed in section IIIA above, controlled human exposure studies of young, healthy adults exposed to O3 while engaged in quasi-continuous moderate exercise for 6.6 hours indicate that up to 25% of exposed people are likely to have moderate lung function decrements and up to 7% are likely to have large lung function decrements (McDonnell et al., 2012; Figure 7) is appropriate. A smaller proportion of inactive or less active individuals would be expected to experience lung function decrements at 85 ppb. Moreover, a breakpoint at 85 ppb allows for category ranges large enough for accurate forecasting. Accordingly, the EPA is adopting the proposed revisions to the AQI values of 150, 200 and 300.

As noted earlier, the EPA proposed to revise 40 CFR part 58, section 58.50(c) to determine the areas subject to AQI reporting requirements based on the latest available census figures, rather than the most recent decennial U.S. census.

A total of five state air monitoring agencies provided comments on this proposed change. Four agencies supported the proposal. One state commenter did not support the proposal, noting that the change would unnecessarily complicate AQI reporting and possibly increase reporting burdens in an unpredictable manner.

The EPA notes that the majority of monitoring network minimum requirements listed in Appendix D to Part 58 include a reference to “latest available census figures.” Minimum network requirements for O3, PM2.5, SO2, and NO2 all include this language in the regulatory text and monitoring agencies have successfully adopted these processes into their planning activities and the subsequent revision of their annual monitoring network plans which are posted for public review. Annual population estimates are easily obtainable from the U.S. Census Bureau and the EPA does not believe the burden in tracking these annual estimates is excessive or complicated.[156] Although the changes in year to year estimates are typically modest, there are MSAs that are approaching (or have recently exceeded) the 350,000 population AQI reporting limit and there is great value in having the AQI reported for these areas when the population threshold is exceeded versus waiting potentially up to 10 years for a revision to the decennial census. Accordingly, the EPA is finalizing the proposed revision to 40 CFR part 58, section 58.50(c) to require the AQI reporting requirements to be based on the latest available census figures.

One state requested additional guidance on the frequency of updating the AQI reporting threshold, and recommended linking the AQI reporting requirement evaluation with the annual air monitoring network plan requirements, and recommended requiring AQI reporting to begin no later than January 1 of the following year. The EPA notes that the census bureau estimates appear to be released around July 1 of each year which would not provide sufficient time for monitoring agencies to incorporate AQI reporting in their annual plans for that year, which are also due by July 1 each year. EPA believes that it should be unnecessary for monitoring agencies to wait until the implementation of the following year's annual plan (i.e., approximately 18 months later) to begin AQI reporting. Accordingly, EPA is not at this time including a specific deadline for commencement of AQI reporting for newly-subject areas in 40 CFR part 58, but will work with agencies to implement additional AQI reporting as needed to ensure that information is being disseminated in a timely fashion.

C. Final Revisions to the AQI

For the reasons discussed above, the EPA is revising the AQI for O3 by setting an AQI value of 100 equal to 70 ppb, 8-hour average, the level of the revised primary O3 standard. The EPA is also revising the following breakpoints: An AQI value of 50 is set at 54 ppb; an AQI value of 150 is set at 85 ppb; an AQI value of 200 is set at 105 ppb; and an AQI value of 300 is set at 200 ppb. All of these levels are averaged over 8 hours. The revisions to all of the Start Printed Page 65369breakpoints are based on estimated health outcomes at relevant ambient concentrations and to allow for each category to span at least a 15-20 ppb category range to allow for more accurate air pollution forecasting. The EPA believes that the revised breakpoints provide a balance between adjustments to reflect the health information supporting the revised O3 standard and providing category ranges that are large enough to be forecasted accurately, so that the AQI can be implemented more easily in the public forum for which the AQI ultimately exists. With respect to AQI reporting requirements (40 CFR part 58, section 58.50), the EPA is revising 40 CFR part 58, section 58.50(c) to make the AQI reporting requirements based on the latest available census figures, rather than the most recent decennial U.S. census. This change is consistent with our current practice of using the latest population figures to make monitoring requirements more responsive to changes in population.

IV. Rationale for Decision on the Secondary Standard

A. Introduction

This section (IV) presents the rationale for the Administrator's decisions regarding the need to revise the current secondary standard for O3, and the appropriate revision. Based on her consideration of the full body of welfare effects evidence and related analyses, including the evidence of effects associated with cumulative seasonal exposures of the magnitudes allowed by the current standard, the Administrator has concluded that the current secondary standard for O3 does not provide the requisite protection of public welfare from known or anticipated adverse effects. She has decided to revise the level of the current secondary standard to 0.070 ppm, in conjunction with retaining the current indicator, averaging time and form.

The Administrator has made 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 so doing, she has focused 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 from adverse effects to public welfare will be provided by a standard that limits cumulative seasonal exposures to 17 ppm-hrs or lower, in terms of a 3-year W126 index, in nearly all instances, and she has also concluded that such control of cumulative seasonal exposures may be achieved by revising the level of the current standard to 70 ppb. Based on all of these considerations, the Administrator has decided that a secondary standard with a level of 0.070 ppm, and the current form and averaging time, will provide the requisite protection of public welfare from known or anticipated adverse effects.

As discussed more fully below, this decision is based on a thorough review, in the ISA, of the latest scientific information on O3-induced environmental effects. This decision also takes into account (1) staff assessments in the PA of the most policy-relevant information in the ISA regarding evidence of adverse effects of O3 to vegetation and ecosystems, information on biologically-relevant exposure metrics, WREA analyses of air quality, exposure, and ecological risks and associated ecosystem services, and staff analyses of relationships between levels of a W126-based metric and a metric based on the form and averaging time of the current standard summarized in the PA and in the proposal notice; (2) CASAC advice and recommendations; and (3) public comments received during the development of these documents, either in connection with CASAC meetings or separately, and on the proposal notice.

This decision draws on the ISA's integrative synthesis of the entire body of evidence, generally published through July 2011, on environmental effects associated with the presence of O3 and related photochemical oxidants in the ambient air (U.S. EPA, 2013, ISA chapters 9-10), and includes more than four hundred new studies that build on the extensive evidence base from the last review. In addition to reviewing the most recent scientific information as required by the CAA, this rulemaking incorporates the EPA's response to the judicial remand of the 2008 secondary O3 standard in State of Mississippi v. EPA, 744 F. 3d 1334 (D.C. Cir. 2013) and, in accordance with the court's decision in that case, fully explains the Administrator's conclusions as to the level of air quality that provides the requisite protection of public welfare from known or anticipated adverse effects. In drawing conclusions on the secondary standard, the decision described in this rulemaking is a public welfare policy judgment made by the Administrator. The Administrator's decision draws upon the available scientific evidence for O3-attributable welfare effects and on analyses of exposures and public welfare risks based on impacts to vegetation, ecosystems and their associated services, as well as judgments about the appropriate weight to place on the range of uncertainties inherent in the evidence and analyses. As described in sections IV.B.3 and IV.C.3 below, such judgments in the context of this review include judgments on the weight to place on the evidence of specific vegetation-related effects estimated to result across a range of cumulative seasonal concentration-weighted O3 exposures; on the weight to give associated uncertainties, including those related to the variability in occurrence of such effects in areas of the U.S., especially areas of particular public welfare significance; and on the extent to which such effects in such areas may be considered adverse to public welfare.

Information related to vegetation and ecosystem effects, biologically relevant exposure indices, and vegetation exposure and risk assessments were summarized in sections IV.A through IV.C of the proposal (79 FR at 75314-75329), respectively, and key observations from the proposal are briefly outlined in sections IV.A.1 to IV.A.3 below. Subsequent sections of this preamble provide a more complete discussion of the Administrator's rationale, in light of key issues raised in public comments, for concluding that the current standard is not requisite to protect public welfare from known or anticipated adverse effects (section IV.B), and that it is appropriate to revise the current secondary standard to provide additional public welfare protection by revising the level while retaining the current indicator, form and averaging time (section IV.C). A summary of the final decisions on revisions to the secondary standard is presented in section IV.D.

1. Overview of Welfare Effects Evidence

a. Nature of Effects

In the more than fifty years that have followed identification of O3's phytotoxic effects, extensive research has been conducted both in and outside of the U.S. to examine the impacts of O3 on plants and their associated ecosystems (U.S. EPA, 1978, 1986, 1996a, 2006a, 2013). As was established in prior reviews, O3 can interfere with carbon gain (photosynthesis) and allocation of carbon within the plant, making fewer carbohydrates available Start Printed Page 65370for plant growth, reproduction, and/or yield. For seed-bearing plants, these reproductive effects will culminate in reduced seed production or yield (U.S. EPA, 1996a, pp. 5-28 and 5-29). Recent studies, assessed in the ISA, together with this longstanding and well-established literature on O3-related vegetation effects, further contribute to the coherence and consistency of the vegetation effects evidence (U.S. EPA, 2013, chapter 9).

The strongest evidence for effects from O3 exposure on vegetation is from controlled exposure studies, which “have clearly shown that exposure to O3 is causally linked to visible foliar injury, decreased photosynthesis, changes in reproduction, and decreased growth” in many species of vegetation (U.S. EPA, 2013, p. 1-15). Such effects at the plant scale can also be linked to an array of effects at larger spatial scales, with the currently available evidence indicating that “ambient O3 exposures can affect ecosystem productivity, crop yield, water cycling, and ecosystem community composition” (U.S. EPA, 2013, p. 1-15; Chapter 9, section 9.4). The current body of O3 welfare effects evidence confirms and strengthens support for the conclusions reached in the last review on the nature of O3-induced welfare effects and is summarized in the ISA as follows (U.S. EPA, 2013, p. 1-8).

The welfare effects of O3 can be observed across spatial scales, starting at the subcellular and cellular level, then the whole plant and finally, ecosystem-level processes. Ozone effects at small spatial scales, such as the leaf of an individual plant, can result in effects along a continuum of larger spatial scales. These effects include altered rates of leaf gas exchange, growth, and reproduction at the individual plant level, and can result in broad changes in ecosystems, such as productivity, carbon storage, water cycling, nutrient cycling, and community composition.

Based on assessment of this extensive body of science, the EPA has determined that, with respect to vegetation and ecosystems, a causal relationship exists between exposure to O3 in ambient air and visible foliar injury effects on vegetation, reduced vegetation growth, reduced productivity in terrestrial ecosystems, reduced yield and quality of agricultural crops and alteration of below-ground biogeochemical cycles (U.S. EPA, 2013, Table 1-2). In consideration of the evidence of O3 exposure and alterations in stomatal performance, “which may affect plant and stand transpiration and therefore possibly affecting hydrological cycling,” the ISA concludes that “[a]lthough the direction of the response differed among studies,” the evidence is sufficient to conclude a likely causal relationship between O3 exposure and the alteration of ecosystem water cycling (U.S. EPA, 2013, section 2.6.3). The evidence is also sufficient to conclude a likely causal relationship between O3 exposure and the alteration of community composition of some terrestrial ecosystems (U.S. EPA, 2013, section 2.6.5). Related to the effects on vegetation growth, productivity and, to some extent, below-ground biogeochemical cycles, the EPA has additionally determined that a likely causal relationship exists between exposures to O3 in ambient air and reduced carbon sequestration (also termed carbon storage) in terrestrial ecosystems (U.S. EPA, 2013, p. 1-10 and section 2.6.2). Modeling studies available in this review consistently found negative impacts of O3 on carbon sequestration, although the severity of impact was influenced by “multiple interactions of biological and environmental factors” (U.S. EPA, 2013, p. 2-39).

Ozone in the troposphere is also a major greenhouse gas and radiative forcing agent,[157] with the ISA formally concluding that “the evidence supports a causal relationship between changes in tropospheric O3 concentrations and radiative forcing” (U.S. EPA, 2013, p. 1-13 and section 2.7.1). While tropospheric O3 has been ranked third in importance after carbon dioxide and methane, there are “large uncertainties in the magnitude of the radiative forcing estimate attributed to tropospheric O3, making the impact of tropospheric O3 on climate more uncertain than the effect of the longer-lived greenhouse gases” (U.S. EPA, 2013, p. 2-47). The ISA notes that “[e]ven with these uncertainties, global climate models indicate that tropospheric O3 has contributed to observed changes in global mean and regional surface temperatures” and concludes that “[a]s a result of such evidence presented in climate modeling studies, there is likely to be a causal relationship between changes in tropospheric O3 concentrations and effects on climate” (U.S. EPA, 2013, p. 2-47).[158] The ISA additionally states that “[i]mportant uncertainties remain regarding the effect of tropospheric O3 on future climate change” (U.S. EPA, 2013, p. 10-31).

b. Vegetation Effects

Given the strong evidence base and the findings of causal or likely causal relationships with O3 in ambient air, including the quantitative assessments of relationships between O3 exposure and occurrence and magnitude of effects, this review has given primary consideration to three main kinds of vegetation effects, some of which contribute to effects at scales beyond the plant level, such as at the ecosystem level and on ecosystem services. The three kinds of effects are addressed below in the following order: 1) Visible foliar injury, 2) impacts on tree growth, productivity and carbon storage, and 3) crop yield loss.

Visible foliar injury resulting from exposure to O3 has been well characterized and documented over several decades of research on many tree, shrub, herbaceous, and crop species (U.S. EPA, 2013, p. 1-10; U.S. EPA, 2006a, 1996a, 1986, 1978). Ozone-induced visible foliar injury symptoms on certain plant species, such as black cherry, yellow-poplar and common milkweed, are considered diagnostic of exposure to O3 based on the consistent association established with experimental evidence (U.S. EPA, 2013, p. 1-10). The evidence has found that visible foliar injury occurs only when sensitive plants are exposed to elevated O3 concentrations in a predisposing environment; a major modifying factor is the amount of available soil moisture during the year (U.S. EPA, 2013, section 9.4.2).

The significance of O3 injury at the leaf and whole plant levels depends on an array of factors, and therefore, it is difficult to quantitatively relate visible foliar injury symptoms to vegetation effects such as individual tree growth, or effects at population or ecosystem levels (U.S. EPA, 2013, p. 9-39). The ISA notes that visible foliar injury “is not always a reliable indicator of other negative effects on vegetation” (U.S. EPA, 2013, p. 9-39). Factors that influence the significance to the leaf and whole plant include the amount of total leaf area affected, age of plant, size, developmental stage, and degree of functional redundancy among the existing leaf area (U.S. EPA, 2013, section 9.4.2). Although there remains a lack of robust exposure-response functions that would allow prediction of visible foliar injury severity and incidence under varying air quality and environmental conditions, “[e]xperimental evidence has clearly Start Printed Page 65371established a consistent association of visible injury with O3 exposure, with greater exposure often resulting in greater and more prevalent injury” (U.S. EPA, 2013, section 9.4.2, p. 9-41).

By far the most extensive field-based dataset of visible foliar injury incidence is that obtained by the U.S. Forest Service Forest Health Monitoring/Forest Inventory and Analysis (USFS FHM/FIA) biomonitoring network program (U.S. EPA, 2013, section 9.4.2.1; Smith, 2012; Coulston et al., 2007). A recently published trend analysis of data from the sites located in 24 states of the northeast and north central U.S. for the 16-year period from 1994 through 2009 (Smith, 2012) describes evidence of visible foliar injury occurrence in the field as well as some insight into the influence of changes in air quality and soil moisture on visible foliar injury and the difficulty inherent in predicting foliar injury response under different air quality and soil moisture scenarios (Smith, 2012; U.S. EPA, 2013, section 9.4.2.1). Study results showed that incidence and severity of foliar injury were dependent on local site conditions for soil moisture availability and O3 exposure (U.S. EPA, 2013, p. 9-41). Although the study indicated that moderate O3 exposures continued to cause visible foliar injury at sites throughout the study area, there was an overall declining trend in the incidence of visible foliar injury as peak O3 concentrations declined (U.S. EPA, 2013, p. 9-40).

Ozone has been shown to affect a number of important U.S. tree species with respect to growth, productivity, and carbon storage. Ambient O3 concentrations have long been known to cause decreases in photosynthetic rates and plant growth. As discussed in the ISA, research published since the 2006 AQCD substantiates prior conclusions regarding O3-related effects on forest tree growth, productivity and carbon storage, and further strengthens the support for those conclusions. A variety of factors in natural environments can either mitigate or exacerbate predicted O3-plant interactions and are recognized sources of uncertainty and variability. Such factors include multiple genetically influenced determinants of O3 sensitivity, changing sensitivity to O3 across vegetative growth stages, co-occurring stressors and/or modifying environmental factors (U.S. EPA, 2013, section 9.4.8). In considering of the available evidence, the ISA states, “previous O3 AQCDs concluded that there is strong evidence that exposure to O3 decreases photosynthesis and growth in numerous plant species” and that “[s]tudies published since the 2008 review support those conclusions” (U.S. EPA, 2013, p. 9-42). The available studies come from a variety of different study types that cover an array of different species, effects endpoints, levels of biological organization and exposure methods and durations. The O3-induced effects at the scale of the whole plant may translate to the ecosystem scale, with changes in productivity and carbon storage. As stated in the ISA, “[s]tudies conducted during the past four decades have demonstrated unequivocally that O3 alters biomass allocation and plant reproduction” (U.S. EPA, 2013, p. 1-10).

The strong evidence of O3 impacts on trees includes robust exposure-response (E-R) functions for reduced growth, termed relative biomass loss (RBL),[159] in seedlings of 11 species. These functions were developed under the National Health and Environmental Effects Research Laboratory-Western Ecology Division program, a series of experiments that used open top chambers (OTCs) to investigate seedling growth response for a single growing season under a variety of O3 exposures (ranging from near background to well above current ambient concentrations) and growing conditions (U.S. EPA, 2013, section 9.6.2; Lee and Hogsett, 1996). The evidence from these studies shows that there is a wide range in sensitivity across the studied species in the seedling growth stage over the course of a single growing season, with some species being extremely sensitive and others being very insensitive over the range of cumulative O3 exposures studied (U.S. EPA, 2014c, Figure 5-1). At the other end of the organizational spectrum, field-based studies of species growing in natural stands have compared observed plant responses across a number of different sites and/or years when exposed to varying ambient O3 exposure conditions. For example, a study conducted in forest stands in the southern Appalachian Mountains during a period when O3 concentrations exceeded the current standard found that the cumulative effects of O3 decreased seasonal stem growth (measured as a change in circumference) by 30-50 percent for most of the examined tree species (i.e., tulip poplar, black cherry, red maple, sugar maple) in a high-O3 year in comparison to a low-O3 year (U.S. EPA, 2013, section 9.4.3.1; McLaughlin et al., 2007a). The study also reported that high ambient O3 concentrations can increase whole-tree water use and in turn reduce late-season streamflow (McLaughlin et al., 2007b; U.S. EPA, 2013, p. 9-43).

The magnitude of O3 impact on ecosystem productivity and on forest composition can vary among plant communities based on several factors, including the type of stand or community in which the sensitive species occurs (e.g., single species versus mixed canopy), the role or position of the species in the stand (e.g., dominant, sub-dominant, canopy, understory), and the sensitivity of co-occurring species and environmental factors (e.g., drought and other factors). For example, recent studies found O3 to have little impact on white fir, but to greatly reduce growth of ponderosa pine in southern California locations, with associated reductions in ponderosa pine abundance in the community, and to cause decreased net primary production of most forest types in the mid-Atlantic region, with only small impacts on spruce-fir forest (U.S. EPA, 2013, section 9.4.3.4).

There is previously and newly available evidence of the potential for O3 to alter biomass allocation and plant reproduction in seasons subsequent to exposure (U.S. EPA, 2013, section 9.4.3). For example, several studies published since the 2006 AQCD further demonstrate that O3 can alter the timing of flowering and the number of flowers, fruits and seeds in herbaceous and woody plant species (U.S. EPA, 2013, section 9.4.3.3). Further, limited evidence in previous reviews reported that vegetation effects from a single year of exposure to elevated O3 could be observed in the following year. For example, growth affected by a reduction in carbohydrate storage in one year may result in the limitation of growth in the following year. Such “carry-over” effects have been documented in the growth of some tree seedlings and in roots (U.S. EPA, 2013, section 9.4.8; Andersen et al., 1997). In the current review, additional field-based evidence expands the EPA's understanding of the consequences of single and multi-year O3 exposures in subsequent years.

A number of studies were conducted at a planted forest at the Aspen free-air carbon-dioxide and ozone enrichment (FACE) experiment site in Wisconsin. These studies, which occurred in a field setting (more similar to natural forest stands than OTC studies), observed tree growth responses when grown in single or two species stands within 30-m diameter rings and exposed over a period of ten years to existing ambient conditions and elevated O3Start Printed Page 65372concentrations. Some studies indicate the potential for carry-over effects, such as those showing that the effects of O3 on birch seeds (reduced weight, germination, and starch levels) could lead to a negative impact on species regeneration in subsequent years, and that the O3-attributable effect of reduced aspen bud size might have been related to the observed delay in spring leaf development. These effects suggest that elevated O3 exposures have the potential to alter carbon metabolism of overwintering buds, which may have subsequent effects in the following year (Darbah, et al., 2008, 2007; Riikonen et al., 2008; U.S. EPA, 2013, section 9.4.3). Other studies found that, in addition to affecting tree heights, diameters, and main stem volumes in the aspen community, elevated O3 over a 7-year study period was reported to increase the rate of conversion from a mixed aspen-birch community to a community dominated by the more tolerant birch, leading the authors to conclude that elevated O3 may alter intra- and inter-species competition within a forest stand (U.S. EPA, 2013, section 9.4.3; Kubiske et al., 2006; Kubiske et al., 2007). These studies confirm earlier FACE results of aspen growth reductions from exposure to elevated O3 during the first seven years of stand growth and of cumulative biomass impacts associated with changes in annual production in studied tree communities (U.S. EPA, 2013, section 9.4.3; King et al., 2005).

Robust and well-established E-R functions for RBL are available for 11 tree species: black cherry, Douglas fir, loblolly pine, ponderosa pine, quaking aspen, red alder, red maple, sugar maple, tulip poplar, Virginia pine, and white pine (U.S. EPA, 2013; U.S. EPA, 2014c). While these 11 species represent only a small fraction (0.8 percent) of the total number of native tree species in the contiguous U.S. (1,497), this small subset includes eastern and western species, deciduous and coniferous species, and species that grow in a variety of ecosystems and represent a range of tolerance to O3 (U.S. EPA, 2013, section 9.6.2; U.S. EPA, 2014b, section 6.2, Figure 6-2, Table 6-1). Supporting the E-R functions for each of these species are studies in OTCs, with most species studied multiple times under a wide range of exposure and/or growing conditions, with separate E-R functions developed for each combination of species, exposure condition and growing condition scenario (U.S. EPA, 2013, section 9.6.1). Based on these separate E-R functions, species-specific composite E-R functions have been developed and successfully used to predict the biomass loss response from tree seedling species over a range of cumulative exposure conditions (U.S. EPA, 2013, section 9.6.2). These 11 composite functions, as well as the E-R function for eastern cottonwood (derived from a field study in which O3 and climate conditions were not controlled),[160] are described in the ISA and graphed in the WREA to illustrate the predicted responses of these species over a wide range of cumulative exposures (U.S. EPA, 2014b, section 6.2, Table 6-1 and Figure 6-2; U.S. EPA, 2013, section 9.6.2). For some of these species, the E-R function is based on a single study (e.g., red maple), while for other species there were as many as 11 studies available (e.g., ponderosa pine). In total, the E-R functions developed for these 12 species (the 11 with robust composite E-R functions plus eastern cottonwood) reflect 52 tree seedling studies. A stochastic analysis in the WREA, summarized in section IV.C of the proposal, indicates the potential for within-species variability in these relationships for each species. Consideration of biomass loss estimates in the PA and in discussions below, however, is based on conventional methods and focuses on estimates for the 11 species for which the robust datasets from OTC experiments are available, in consideration of CASAC advice.

The “detrimental effect of O3 on crop production has been recognized since the 1960s” (U.S. EPA, 2013, p. 1-10, section 9.4.4). On the whole, the newly available evidence supports and strengthens previous conclusions that exposure to O3 reduces growth and yield of crops. The ISA describes average crop yield loss reported across a number of recently published meta-analyses and identifies several new exposure studies that support prior findings for a variety of crops of decreased yield and biomass with increased O3 exposure (U.S. EPA, 2013, section 9.4.4.1, Table 9-17). Studies have also “linked increasing O3 concentration to decreased photosynthetic rates and accelerated aging in leaves, which are related to yield” and described effects of O3 on crop quality, such as nutritive quality of grasses, macro- and micronutrient concentrations in fruits and vegetable crops and cotton fiber quality (U.S. EPA, 2013, p. 1-10, section 9.4.4). The findings of the newly available studies do not change the basic understanding of O3-related crop yield loss since the last review and little additional information is available in this review on factors that influence associations between O3 levels and crop yield loss (U.S. EPA, 2013, section 9.4.4.). However, the evidence available in this review continues to support the conclusion that O3 in ambient air can reduce the yield of major commodity crops in the U.S. Further, the recent evidence increases our confidence in the use of crop E-R functions based on OTC experiments to characterize the quantitative relationship between ambient O3 concentrations and yield loss (U.S. EPA, 2013, section 9.4.4).

The new evidence has strengthened support for previously established E-R functions for 10 crops (barley, field corn, cotton, kidney bean, lettuce, peanut, potato, grain sorghum, soybean and winter wheat), reducing two important areas of uncertainty, especially for soybean, as summarized in more detail in section IV.A of the proposal. The established E-R functions for relative yield loss (RYL)[161] were developed from OTC-type experiments from the National Crop Loss Assessment Network (NCLAN) (U.S. EPA, 2013, section 9.6.3; U.S. EPA, 2014b, section 6.2; U.S. EPA, 2014c, Figure 5-4 and section 6.3). With regard to the first area of uncertainty reduced, evaluations in the ISA found that yield loss in soybean from O3 exposure at the SoyFACE (Soybean Free Air Concentration Enrichment) field experiment was reliably predicted by soybean E-R functions developed from NCLAN data (U.S. EPA, 2013, section 9.6.3.1),[162] demonstrating a robustness of the NCLAN-based E-R functions for predicting relative yield loss from O3 exposure. A second area of uncertainty that was reduced is that regarding the Start Printed Page 65373application of the NCLAN E-R functions to more recent cultivars currently growing in the field. Recent studies, especially those focused on soybean, provide little evidence that crops are becoming more tolerant of O3 (U.S. EPA, 2006a; U.S. EPA, 2013, sections 9.6.3.1 and 9.6.3.4 and p. 9-59). The ISA comparisons of NCLAN and SoyFACE data referenced above also “confirm that the response of soybean yield to O3 exposure has not changed in current cultivars” (U.S. EPA, 2013, p. 9-59; section 9.6.3.1). Additionally, a recent assessment of the relationship between soybean yield loss and O3 in ambient air over the contiguous area of Illinois, Iowa, and Indiana found a relationship that correlates well with previous results from FACE- and OTC-type experiments (U.S. EPA, 2013, section 9.4.4.1).

c. Biologically Relevant Exposure Metric

In assessing biologically based indices of exposure pertinent to O3 effects on vegetation, the ISA states the following (U.S. EPA, 2013, p. 2-44).

The main conclusions from the 1996 and 2006 O3 AQCDs [Air Quality Criteria Documents] regarding indices based on ambient exposure remain valid. These key conclusions can be restated as follows: ozone effects in plants are cumulative; higher O3 concentrations appear to be more important than lower concentrations in eliciting a response; plant sensitivity to O3 varies with time of day and plant development stage; [and] quantifying exposure with indices that cumulate hourly O3 concentrations and preferentially weight the higher concentrations improves the explanatory power of exposure/response models for growth and yield, over using indices based on mean and peak exposure values.

The long-standing body of available evidence upon which these conclusions are based includes a wealth of information on aspects of O3 exposure that are important in influencing plant response (U.S. EPA, 1996a; U.S. EPA, 2006a; U.S. EPA, 2013). Specifically, a variety of “factors with known or suspected bearing on the exposure-response relationship, including concentration, time of day, respite time, frequency of peak occurrence, plant phenology, predisposition, etc.,” have been identified (U.S. EPA, 2013, section 9.5.2). In addition, the importance of the duration of the exposure and the relatively greater importance of higher concentrations over lower concentrations in determining plant response to O3 have been consistently well documented (U.S. EPA, 2013, section 9.5.3). Based on improved understanding of the biological basis for plant response to O3 exposure, a large number of “mathematical approaches for summarizing ambient air quality information in biologically meaningful forms for O3 vegetation effects assessment purposes” have been developed (U.S. EPA, 2013, section 9.5.3), including those that cumulate exposures over some specified period while weighting higher concentrations more than lower (U.S. EPA, 2013, section 9.5.2). As with any summary statistic, these exposure indices retain information on some, but not all, characteristics of the original observations.

Based on extensive review of the published literature on different types of exposure-response metrics, including comparisons between metrics, the EPA has focused on cumulative, concentration-weighted indices, recognizing them as the most appropriate biologically based metrics to consider in this context (U.S. EPA, 1996a; U.S. EPA, 1996b; U.S. EPA, 2006a; U.S. EPA, 2013). In the last two reviews of the O3 NAAQS, the EPA concluded that the risk to vegetation comes primarily from cumulative exposures to O3 over a season or seasons [163] and focused on metrics intended to characterize such exposures: SUM06 [164] in the 1997 review (61 FR 65716, December 13, 1996) and W126 in the 2008 review (72 FR 37818, July 11, 2007). Although in both reviews the policy decision was made not to revise the form and averaging time of the secondary standard, the Administrator, in both cases, also concluded, consistent with CASAC advice, that a cumulative, seasonal index was the most biologically relevant way to relate exposure to plant growth response (62 FR 38856, July 18, 1997; 73 FR 16436, March 27, 2008). This approach for characterizing O3 exposure concentrations that are biologically relevant with regard to potential vegetation effects received strong support from CASAC in the last review and again in this review, including strong support for use of such a metric as the form for the secondary standard (Henderson, 2006, 2008; Samet, 2010; Frey, 2014c).

Alternative methods for characterizing O3 exposure to predict plant response have, in recent years, included flux models, which some researchers have claimed may “better predict vegetation responses to O3 than exposure-based approaches” because they estimate the ambient O3 concentration that actually enters the leaf (i.e., flux or deposition). However, the ISA notes that “[f]lux calculations are data intensive and must be carefully implemented” (U.S. EPA, 2013, p. 9-114). Further, the ISA states, “[t]his uptake-based approach to quantify the vegetation impact of O3 requires inclusion of those factors that control the diurnal and seasonal O3 flux to vegetation (e.g., climate patterns, species and/or vegetation-type factors and site-specific factors)” (U.S. EPA, 2013, p. 9-114). In addition to these data requirements, each species has different amounts of internal detoxification potential that may protect species to differing degrees. The lack of detailed species- and site-specific data required for flux modeling in the U.S. and the lack of understanding of detoxification processes have continued to make this technique less viable for use in vulnerability and risk assessments at the national scale in the U.S. (U.S. EPA, 2013, section 9.5.4).

Therefore, consistent with the ISA conclusions regarding the appropriateness of considering cumulative exposure indices that preferentially weight higher concentrations over lower for predicting O3 effects of concern based on the well-established conclusions and supporting evidence described above, and in light of continued CASAC support, we continue to focus on cumulative concentration-weighted indices as the most biologically relevant metrics for consideration of O3 exposures eliciting vegetation-related effects. Quantifying exposure in this way “improves the explanatory power of exposure/response models for growth and yield over using indices based on mean and peak exposure values” (U.S. EPA, 2013, section 2.6.6.1, p. 2-44). In this review, as in the last review, we use the W126-based cumulative, seasonal metric (U.S. EPA, 2013, sections 2.6.6.1 and 9.5.2) for consideration of the effects evidence and in the exposure and risk analyses in the WREA.

This metric, commonly called the W126 index, is a non-threshold approach described as the sigmoidally weighted sum of all hourly O3 concentrations observed during a specified daily and seasonal time window, where each hourly O3 concentration is given a weight that increases from zero to one with increasing concentration (U.S. EPA, 2014c, p. 5-6; U.S. EPA 2013, p. 9-101). Start Printed Page 65374The first step in calculating the seasonal W126 index, as described and considered in this review, is to sum the weighted ambient O3 concentrations during daylight hours (defined as 8:00 a.m. to 8:00 p.m.) within each calendar month, resulting in monthly index values (U.S. EPA, 2014b, pp. 4-5 to 4-6). As more completely described in the WREA, the monthly W126 index values are calculated from hourly O3 concentrations as follows:

where N is the number of days in the month, d is the day of the month (d = 1, 2, . . ., N), h is the hour of the day (h = 0, 1, . . ., 23), and Cdh is the hourly O3 concentration observed on day d, hour h, in parts per million. The seasonal W126 index value for a specific year is the maximum sum of the monthly index values for three consecutive months. Three-year W126 index values are calculated by taking the average of seasonal W126 index values for three consecutive years (U.S. EPA, 2014b, pp. 4-5 to 4-6; Wells, 2014a).

2. Overview of Welfare Exposure and Risk Assessment

This section outlines the information presented in section IV.C of the proposal regarding the WREA conducted for this review, which built upon similar analyses performed in the last review. The WREA focuses primarily on analyses related to two types of effects on vegetation: Reduced growth (biomass loss) in both trees and agricultural crops, and foliar injury. The assessments of O3-associated reduced growth in native trees and crops (specifically, RBL and RYL, respectively) include analysis of associated changes in related ecosystem services, including pollution removal, carbon sequestration or storage, and hydrology, as well as economic impacts on the forestry and agriculture sectors of the economy. The foliar injury assessments include cumulative analyses of the proportion of USFS biosite index scores [165] above zero (or five, in a separate set of analyses) with increasing W126 exposure index estimates, with and without consideration of soil moisture conditions. The implications of visible foliar injury in national parks were considered in a screening level assessment and three case studies.[166]

Growth-related effects were assessed for W126-based exposure estimates in five scenarios of national-scale [167] air quality: Recent conditions (2006 to 2008), the existing secondary standard, and W126 index values of 15 ppm-hrs, 11 ppm-hrs, and 7 ppm-hrs, using 3-year averages (U.S. EPA, 2014b, chapter 4). For each of these scenarios, 3-year average W126 exposure index values were estimated for 12 kilometer (km) by 12 km grid cells in a national-scale spatial surface. The method for creating these grid cell estimates generally involved two steps (summarized in Table 5-4 of the PA).

The first step in creating the grid cell estimates for each scenario was calculation of the average W126 index value (across the three years) at each monitor location. For the recent conditions scenario, this value was based on unadjusted O3 concentrations from monitoring data. For the other four scenarios, the W126 index value for each monitor location was calculated from model-adjusted hourly O3 concentrations. The adjusted concentrations were based on model-predicted relationships between O3 at each monitor location and reductions in NOX. Adjustments were applied independently for each of the nine U.S. regions (see U.S. EPA, 2014b, section 4.3.4.1).[168] The existing standard scenario was created first, with the result being a national dataset for which the highest monitor location in each U.S. region had a design value equal to the level of the current standard.[169] The W126 scenarios were created from the hourly concentrations used to create the existing standard scenario, with model-based adjustments made at all monitor sites in those regions with a site not already at or below the target W126 value for that scenario (U.S. EPA, 2014b, section 4.3.4.1).[170]

After completing step one for all the scenarios, the second step involved creating the national-scale spatial surfaces (composed of 3-year W126 index values at grid cell centroids). These were created by applying the Voronoi Neighbor Averaging (VNA) spatial interpolation technique to the monitor-location, 3-year W126 index values (described in step 1).[171] This step of creating the gridded spatial surfaces resulted in further reduction of the highest values in each modeling region, as demonstrated by comparing the W126 index values from steps one and two for the existing standard scenario. After the step-one adjustment of the monitor location concentrations such that the highest location in each NOAA region just met the existing standard (using relationships mentioned above), the maximum 3-year average W126 values in the nine regions ranged from 18.9 ppm-hrs in the West region to 2.6 ppm-hrs in the Northeast region (U.S. EPA, 2014b, Table 4-3). After application of the VNA technique in the second step, however, the highest 3-year average W126 values across the national surface grid cells, which were in the Southwest region, were below 15 ppm-hrs (U.S. EPA, 2014b, Figure 4-7).[172]

All of the assessments based on growth impacts relied on the W126 index estimates from the national-scale spatial surfaces (created from the 3-year average monitor location values as described above). Among the analyses related to visible foliar injury, a small component of the screening-level Start Printed Page 65375national park assessment and also the three national park case studies involved summarizing 3-year W126 index estimates from the four air quality scenarios. However, the visible foliar injury cumulative proportion analyses and a component of the national park screening-level assessment relied on national-scale spatial surfaces of single-year, unadjusted W126 index values created for each year from 2006 through 2010 using the VNA interpolation technique applied to the monitor location index values for these years (U.S. EPA, 2014b, section 4.3.2, Appendix 4A).

Because the W126 estimates generated for the different air quality scenarios assessed are inputs to the vegetation risk analyses for tree biomass and crop yield loss, and also used in some components of the visible foliar injury assessments, limitations and uncertainties in the air quality analyses, which are discussed in detail in the WREA and some of which are mentioned here, are propagated into those analyses (U.S. EPA, 2014b, chapters 4 and 8 and section 8.5, Table 4-5). An important uncertainty in the analyses is the application of regionally determined emissions reductions to meet the existing standard (U.S. EPA, 2014b, section 8.5.1). The model adjustments are based on emissions reductions in NOx and characterize only one potential distribution of air quality across a region when all monitor locations meet the standard, as well as for the W126 scenarios (U.S. EPA, 2014b, section 4.3.4.2).[173]

An additional uncertainty related to the W126 index estimates in the national surfaces for each air quality scenario, and to the estimates for the single-year surfaces used in the visible foliar injury cumulative analysis, comes with the creation of the national-scale spatial surfaces of grid cells from the monitor-location O3 data.[174] In general, spatial interpolation techniques perform better in areas where the O3 monitoring network is denser. Therefore, the W126 index values estimated using this technique in rural areas in the West, Northwest, Southwest, and West North Central regions where there are few or no monitors (U.S. EPA, 2014b, Figure 2-1) are more uncertain than those estimated for areas with denser monitoring. Further, as described above, this interpolation method generally underpredicts the highest W126 exposure index values. Due to the important influence of higher exposures in determining risks to plants, the potential for the VNA interpolation approach to dampen peak W126 index values could result in an underestimation of risks to vegetation in some areas.[175]

The vegetation analyses performed in the WREA, along with key observations, insights, uncertainties and limitations were summarized in sections IV.C.2 through IV.C.3 of the proposal. Highlights for the three categories of biomass loss and foliar injury assessments are summarized here.

a. Tree Growth, Productivity and Carbon Storage

These assessments rely on the species-specific E-R functions described in section IV.A.1.b above. For the air quality scenarios described above, the WREA applied the species-specific E-R functions to develop estimates of O3-associated RBL and associated effects on productivity, carbon storage and associated ecosystem services (U.S. EPA, 2014b, Chapter 6). More specifically, the WREA derived species-specific and weighted RBL estimates for grid cells across the continental U.S. and summarized the estimates by counties and national parks. Additional WREA case study analyses focused on selected urban areas. The WREA estimates indicate substantial heterogeneity in plant responses to O3, both within species (e.g., study-specific variation), between species, and across regions of the U.S. National variability in the estimates (e.g., eastern vs western U.S.) is influenced by there being different sets of resident species (with different E-R functions) in different areas of the U.S., as well as differences in number of national parks and O3 monitors. For example, the eastern U.S. has different resident species compared to the western U.S., and the eastern U.S. has far more such species. Additionally, there are more national parks in the western than the eastern U.S., yet fewer O3 monitors (U.S. EPA, 2014b, chapter 8).

Relative biomass loss nationally (across all of the air quality surface grid cells) was estimated for each of the 12 studied species from the composite E-R functions for each species described above and information on the distribution of those species across the U.S. (U.S. EPA, 2014b, section 6.2.1.3 and Appendix 6A). In consideration of CASAC advice (summarized in section IV.A.1.b above), the WREA derived RBL and weighted RBL (wRBL) estimates separately, both with and without the eastern cottonwood, and the PA and proposal gave primary focus to analyses that exclude cottonwood. These analyses provided estimates of per-species and cross-species RBL in the different air quality scenarios. Air quality scenario estimates were also developed in terms of proportion of basal area affected at different magnitudes of RBL. The wRBL analysis integrated the species-specific estimates, providing an indication of potential magnitude of ecological effect possible in some ecosystems. The county analyses also included analyses focused on the median species response. The WREA also used the E-R functions to estimate RBL across tree lifespans and the resulting changes in consumer and producer/farmer economic surplus in the forestry and agriculture sectors of the economy. Case studies in five urban areas provided comparisons across air quality scenarios of estimates for urban tree pollutant removal and carbon storage or sequestration.

The array of uncertainties associated with estimates from these tree RBL analyses are summarized in the proposal and described in detail in the WREA, including the potential for the air quality scenarios to underestimate the higher W126 index values and associated implications for the RBL-related estimates, as referenced above.

b. Crop Yield Loss

These assessments rely on the species-specific E-R functions described in section IV.A.1.b above. For the different air quality scenarios, the WREA applied the species-specific E-R functions to develop estimates of O3 impacts related to crop yield, including annual yield losses estimated for 10 commodity crops grown in the U.S. and how these losses affect producer and consumer economic surpluses (U.S. EPA, 2014b, sections 6.2, 6.5). The WREA derived estimates of crop RYL nationally and in a county-specific analysis, relying on information regarding crop distribution (U.S. EPA, 2014b, section 6.5). As with the tree analyses described above, the county analysis included estimates based on Start Printed Page 65376the median O3 response across the studied crop species (U.S. EPA, 2014b, section 6.5.1, Appendix 6B).

Overall effects on agricultural yields and producer and consumer surplus depend on the ability of producers/farmers to substitute other crops that are less O3 sensitive, and the responsiveness, or elasticity, of demand and supply (U.S. EPA, 2014b, section 6.5). The WREA discusses multiple areas of uncertainty associated with the crop yield loss estimates, including those associated with the model-based adjustment methodology as well as those associated with the projection of yield loss using the Forest and Agriculture Sector Optimization Model (with greenhouse gases) at the estimated O3 concentrations (U.S. EPA, 2014b, Table 6-27, section 8.5). Because the W126 index estimates generated in the air quality scenarios are inputs to the vegetation risk analyses for crop yield loss, any uncertainties in the air quality scenario estimation of W126 index values are propagated into those analyses (U.S. EPA, 2014b, Table 6-27, section 8.5). Therefore, the air quality scenarios in the crop yield analyses have the same uncertainties and limitations as in the biomass loss analyses (summarized above), including those associated with the model-based adjustment methodology (U.S. EPA, 2014b, section 8.5).

c. Visible Foliar Injury

The WREA presents a number of analyses of O3-related visible foliar injury and associated ecosystem services impacts (U.S. EPA, 2014b, Chapter 7). In the initial analysis, the WREA used the biomonitoring site data from the USFS FHM/FIA Network (USFS, 2011),[176] associated soil moisture data during the sample years, and national surfaces of ambient air O3 concentrations based on spatial interpolation of monitoring data from 2006 to 2010 in a cumulative analysis of the proportion of biosite records with any visible foliar injury, as indicated by a nonzero biosite index score (U.S. EPA, 2014b, section 7.2). This analysis was done for all records together, and also for subsets based on soil moisture conditions (normal, wet or dry).

In each cumulative analysis, the biosite records were ordered by W126 index and then, moving from low to high W126 index, the records were cumulated into a progressively larger dataset. With the addition of each new data point (composed of biosite index score and W126 index value for a biosite and year combination) to the cumulative dataset, the percentage of sites with a nonzero biosite index score was derived and plotted versus the W126 index estimate for the just added data point. The cumulative analysis for all sites indicates that (1) as the cumulative set of sites grows with addition of sites with progressively higher W126 index values, the proportion of the dataset for which no foliar injury was recorded changes (increases) noticeably prior to about 10 ppm-hrs (10.46 ppm-hrs), and (2) as the cumulative dataset grows still larger with the addition of records for higher W126 index estimates, the proportion of the cumulative dataset with no foliar injury remains relatively constant (U.S. EPA, 2014b, Figure 7-10). The data for normal moisture years are very similar to the dataset as a whole, with an overall proportion of about 18 percent for presence of any foliar injury. The data for relatively wet years have a much higher proportion of biosites showing injury, approximately 25% when all data are included, and a proportion of approximately 20% when data for W126 index estimates up to about 5-8 ppm-hrs are included (U.S. EPA, 2014b, Figure 7-10).[177] The overall proportion showing injury for the subset for relatively dry conditions is much lower, less than 15% for the subset (U.S. EPA, 2014b, section 7.2.3, Figures 7-10). While these analyses indicate the potential for foliar injury to occur under conditions that meet the current standard, the extent of foliar injury that might be expected under different exposure conditions is unclear from these analyses.

Criteria derived from the cumulative analyses were then used in two additional analyses. The national-scale screening-level assessment compared W126 index values estimated within 214 national parks using the VNA technique described above for the individual years from 2006 to 2010 with benchmark criteria developed from the biosite data analysis (U.S. EPA, 2014b, Appendix 7A and section 7.3). Separate case study analyses described visits, as well as visitor uses and expenditures for three national parks, and the 3-year W126 index estimates in those parks for the four air quality scenarios (U.S. EPA, 2014b, section 7.4). Uncertainties associated with these analyses, included those associated with the W126 index estimates, are discussed in the WREA, sections 7.5 and 8.5.3, and in WREA Table 7-24, and also summarized in the PA (e.g., U.S. EPA, 2014c, section 6.3).

3. Potential Impacts on Public Welfare

As provided in the CAA, section 109(b)(2), the secondary standard is to “specify a level of air quality the attainment and maintenance of which in the judgment of the Administrator . . . is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of such air pollutant in the ambient air.” Effects on welfare include, but are not limited to, “effects on soils, water, crops, vegetation, man-made materials, animals, wildlife, weather, visibility, and climate, damage to and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal comfort and well-being” (CAA section 302(h)). The secondary standard is not meant to protect against all known or anticipated O3-related effects, but rather those that are judged to be adverse to the public welfare, and a bright-line determination of adversity is not required in judging what is requisite (78 FR 8312, January 15, 2013; see also 73 FR 16496, March 27, 2008). Thus, the level of protection from known or anticipated adverse effects to public welfare that is requisite for the secondary standard is a public welfare policy judgment to be made by the Administrator. In the current review, the Administrator's judgment is informed by conclusions drawn with regard to adversity of effects to public welfare in decisions on secondary O3 standards in past reviews.

As indicated by the Administrator in the 2008 decision, the degree to which O3 effects on vegetation should be considered to be adverse to the public welfare depends on the intended use of the vegetation and the significance of the vegetation to the public welfare (73 FR 16496, March 27, 2008). Such judgments regarding public welfare significance in the last O3 NAAQS decision gave particular consideration to O3 effects in areas with special federal protections, and lands set aside by states, tribes and public interest groups to provide similar benefits to the public welfare (73 FR 16496, March 27, 2008). For example, in reaching his conclusion regarding the need for revision of the secondary standard in the 2008 review, the Administrator took Start Printed Page 65377note of “a number of actions taken by Congress to establish public lands that are set aside for specific uses that are intended to provide benefits to the public welfare, including lands that are to be protected so as to conserve the scenic value and the natural vegetation and wildlife within such areas, and to leave them unimpaired for the enjoyment of future generations” (73 FR 16496, March 27, 2008). As further recognized in the 2008 notice, “[s]uch public lands that are protected areas of national interest include national parks and forests, wildlife refuges, and wilderness areas” (73 FR 16496, March 27, 2008).[178] [179] Such areas include Class I areas[180] which are federally mandated to preserve certain air quality related values. Additionally, as the Administrator recognized, “States, Tribes and public interest groups also set aside areas that are intended to provide similar benefits to the public welfare, for residents on State and Tribal lands, as well as for visitors to those areas” (73 FR 16496, March 27, 2008). The Administrator took note of the “clear public interest in and value of maintaining these areas in a condition that does not impair their intended use and the fact that many of these lands contain O3-sensitive species” (73 FR 16496, March 27, 2008).

The concept described in the 2008 notice regarding the degree to which effects on vegetation in specially protected areas, such as those identified above, may be judged adverse also applies beyond the species level to the ecosystem level, such that judgments can depend on the intended use[181] for, or service (and value) of, the affected vegetation, ecological receptors, ecosystems and resources and the significance of that use to the public welfare (73 FR 16496, March 27, 2008). Uses or services provided by areas that have been afforded special protection can flow in part or entirely from the vegetation that grows there. Aesthetic value and outdoor recreation depend, at least in part, on the perceived scenic beauty of the environment (U.S. EPA, 2014b, chapters 5 and 7). Further, analyses have reported that the American public values—in monetary as well as nonmonetary ways—the protection of forests from air pollution damage. In fact, studies that have assessed willingness-to-pay for spruce-fir forest protection in the southeastern U.S. from air pollution and insect damage have found that values held by the survey respondents for the more abstract services (existence, option and bequest)[182] were greater than those for recreation or other services (U.S. EPA, 2014b, Table 5-6; Haefele et al., 1991; Holmes and Kramer, 1995).

The spatial, temporal and social dimensions of public welfare impacts are also influenced by the type of service affected. For example, a national park can provide direct recreational services to the thousands of visitors that come each year, but also provide an indirect value to the millions who may not visit but receive satisfaction from knowing it exists and is preserved for the future (U.S. EPA, 2014b, chapter 5, section 5.5.1). Similarly, ecosystem services can be realized over a range of temporal scales. An evaluation of adversity to the public welfare might also consider the likelihood, type, and magnitude of the effect, as well as the potential for recovery and any uncertainties relating to these conditions, as stated in the preamble of the 2012 final notice of rulemaking on the secondary standards for oxides of nitrogen and sulfur (77 FR 20232, April 3, 2012).

The three main categories of effects on vegetation discussed in section IV.A.1.b above differ with regard to aspects important to judging their public welfare significance. Judgments regarding crop yield loss, for example, depend on considerations related to the heavy management of agriculture in the U.S., while judgments regarding the other categories of effects generally relate to considerations regarding forested areas. For example, while both tree growth-related effects and visible foliar injury have the potential to be significant to the public welfare through impacts in Class I and other protected areas, they differ in how they might be significant and with regard to the clarity of the data that describe the relationship between the effect and the services potentially affected.

With regard to effects on tree growth, reduced growth is associated with effects on an array of ecosystem services including reduced productivity, altered forest and forest community (plant, insect and microbe) composition, reduced carbon storage and altered water cycling (U.S. EPA, 2013, Figure 9-1, sections 9.4.1.1 and 9.4.1.2; U.S. EPA, 2014b, section 6.1). For example, forest or forest community composition can be affected through O3 effects on growth and reproductive success of sensitive species in the community, with the extent of compositional changes dependent on factors such as competitive interactions (U.S. EPA, 2013, sections 9.4.3 and 9.4.3.1). Depending on the type and location of the affected ecosystem, services benefitting the public in other ways can be affected as well. For example, other services valued by people that can be affected by reduced tree growth, productivity and carbon storage include aesthetic value, food, fiber, timber, other forest products, habitat, recreational opportunities, climate and water regulation, erosion control, air pollution removal, and desired fire regimes (U.S. EPA 2013, sections 9.4.1.1 and 9.4.1.2; U.S. EPA, 2014b, section 6.1, Figure 6-1, section 6.4, Table 6-13). Further, impacts on some of these services (e.g., forest or forest community composition) may be considered of greater public welfare significance when occurring in Class I or other protected areas.

Consideration of the magnitude of tree growth effects that might cause or contribute to adverse effects for trees, forests, forested ecosystems or the public welfare is complicated by aspects Start Printed Page 65378of, or limitations in, the available information. For example, the evidence on tree seedling growth effects, deriving from the E-R functions for 11 species (described in section IV.A.1 above), provides no clear threshold or breakpoint in the response to O3 exposure. Additionally, there are no established relationships between magnitude of tree seedling growth reduction and forest ecosystem impacts and, as noted in section IV.A.1.b above, other factors can influence the degree to which O3-induced growth effects in a sensitive species affect forest and forest community composition and other ecosystem service flows from forested ecosystems. These include (1) the type of stand or community in which the sensitive species is found (i.e., single species versus mixed canopy); (2) the role or position the species has in the stand (i.e., dominant, sub-dominant, canopy, understory); (3) the O3 sensitivity of the other co-occurring species (O3 sensitive or tolerant); and (4) environmental factors, such as soil moisture and others. The lack of such established relationships complicates judgments as to the extent to which different estimates of impacts on tree seedling growth would indicate significance to the public welfare and thus be an important consideration in the level of protection for the secondary standard.

During the 1997 review of the secondary standard, views related to this issue were provided by a 1996 workshop of 16 leading scientists in the context of discussing their views for a secondary O3 standard (Heck and Cowling, 1997). In their consideration of tree growth effects as an indicator for forest ecosystems and crop yield reduction as an indicator of agricultural systems, the workshop participants identified annual percentages, of RBL for forest tree seedlings and RYL for agricultural crops, considered important to their judgments on the standard. With regard to forest ecosystems and seedling growth effects as an indicator, the participants selected a range of 1-2% RBL per year “to avoid cumulative effects of yearly reductions of 2%.” With regard to crops, they indicated an interest in protecting against crop yield reductions of 5% RYL yet noted uncertainties surrounding such a percentage which led them to identifying 10% RYL for the crop yield endpoint (Heck and Cowling, 1997). The workshop report provides no explicit rationale for the percentages identified (1-2% RBL and 5% or 10% RYL); nor does it describe their connection to ecosystem impacts of a specific magnitude or type, nor to judgments on significance of the identified effects for public welfare, e.g., taking into consideration the intended use and significance of the affected vegetation (Heck and Cowling, 1997). In recognition of the complexity of assessing the adversity of tree growth effects and effects on crop yield in the broader context of public welfare, the EPA's consideration of those effects in both the 1997 and 2008 reviews extended beyond the consideration of various benchmark responses for the studied species, and, with regard to crops, additionally took note of their extensive management (62 FR 38856, July 18, 1997; 73 FR 16436, March 27, 2008).

While, as noted above, public welfare benefits of forested lands can be particular to the type of area in which the forest occurs, some of the potential public welfare benefits associated with forest ecosystems are not location dependent. A potentially extremely valuable ecosystem service provided by forested lands is carbon storage, a regulating service that is “of paramount importance for human society” (U.S. EPA, 2013, section 2.6.2.1 and p. 9-37). As noted above, the EPA has concluded that this ecosystem service has a likely causal relationship with O3 in ambient air. The service of carbon storage is potentially important to the public welfare no matter in what location the sensitive trees are growing or what their intended current or future use. In other words, the benefit exists as long as the tree is growing, regardless of what additional functions and services it provides. Another example of locations potentially vulnerable to O3-related impacts but not necessarily identified for such protection might be forested lands, both public and private, where trees are grown for timber production. Forests in urbanized areas also provide a number of services that are important to the public in those areas, such as air pollution removal, cooling, and beautification. There are also many other tree species, such as species identified by the USFS and various ornamental and agricultural species (e.g., Christmas trees, fruit and nut trees), that provide ecosystem services that may be judged important to the public welfare but whose vulnerability to O3 impacts has not been quantitatively characterized (U.S. EPA, 2014b, Chapter 6).

As noted above, in addition to tree growth-related effects, O3-induced visible foliar injury also has the potential to be significant to the public welfare through impacts in Class I and other similarly protected areas. Visible foliar injury is a visible bioindicator of O3 exposure in species sensitive to this effect, with the injury affecting the physical appearance of the plant. Accordingly visible foliar injury surveys are used by federal land managers as tools in assessing potential air quality impacts in Class I areas. These surveys may focus on plant species that have been identified as potentially sensitive air quality related values (AQRVs) due to their sensitivity to O3-induced foliar injury (USFS, NPS, FWS, 2010). An AQRV is defined by the National Park Service as a “resource, as identified by the [federal land manager] for one or more Federal areas that may be adversely affected by a change in air quality,” and the resource “may include visibility or a specific scenic, cultural, physical, biological, ecological, or recreational resource identified by the [federal land manager] for a particular area” (USFS, NPS, USFWS, 2010).[183] No criteria have been established, however, regarding a level or prevalence of visible foliar injury considered to be adverse to the affected vegetation, and, as noted in section IV.A.1.b above, there is not a clear relationship between visible foliar injury and other effects, such as reduced growth and productivity.[184] Thus, key considerations with regard to public welfare significance of this endpoint Start Printed Page 65379have related to qualitative consideration of the plant's aesthetic value in protected forested areas. Depending on the extent and severity, O3-induced visible foliar injury might be expected to have the potential to impact the public welfare in scenic and/or recreational areas during the growing season, particularly in areas with special protection, such as Class I areas.

The ecosystem services most likely to be affected by O3-induced visible foliar injury (some of which are also recognized above for tree growth-related effects) are cultural services, including aesthetic value and outdoor recreation. In addition, several tribes have indicated that many of the species identified as O3 sensitive (including bioindicator species) are culturally significant (U.S. EPA, 2014c, Table 5-1). The geographic extent of protected areas that may be vulnerable to such public welfare effects of O3 is potentially appreciable. Sixty-six plant species that occur on U.S. National Park Service (NPS) and U.S. Fish and Wildlife Service lands [185] have been identified as sensitive to O3-induced visible foliar injury, and some also have particular cultural importance to some tribes (U.S. EPA, 2014c, Table 5-1 and Appendix 5-A; U.S. EPA, 2014b, section 6.4.2). Not all species are equally sensitive to O3, however, and quantitative E-R relationships for O3 exposure and other important effects, such as seedling growth reduction, are only available for a subset of 12 of the 66, as summarized in section IV.A.1.b above. A diverse array of ecosystem services has been identified for these twelve species (U.S. EPA, 2014c, Table 5-1). Two species in this group that are slightly more sensitive than the median for the group with regard to effects on growth are the ponderosa pine and quaking aspen (U.S. EPA, 2014b, section 6.2), the ranges for which overlap with many lands that are protected or preserved for enjoyment of current and future generations (consistent with the discussion above on Class I and other protected areas), including such lands located in the west and southwest regions of the U.S. where ambient O3 concentrations and associated cumulative seasonal exposures can be highest (U.S. EPA, 2014c, Appendix 2B).[186]

With regard to agriculture-related effects, the EPA has recognized other complexities, stating that the degree to which O3 impacts on vegetation that could occur in areas and on species that are already heavily managed to obtain a particular output (such as commodity crops or commercial timber production) would impair the intended use at a level that might be judged adverse to the public welfare has been less clear (73 FR 16497, March 27, 2008). As noted in section IV.B.2 of the proposal, while having sufficient crop yields is of high public welfare value, important commodity crops are typically heavily managed to produce optimum yields. Moreover, based on the economic theory of supply and demand, increases in crop yields would be expected to result in lower prices for affected crops and their associated goods, which would primarily benefit consumers. These competing impacts on producers and consumers complicate consideration of these effects in terms of potential adversity to the public welfare (U.S. EPA, 2014c, sections 5.3.2 and 5.7). When agricultural impacts or vegetation effects in other areas are contrasted with the emphasis on forest ecosystem effects in Class I and similarly protected areas, it can be seen that the Administrator has in past reviews judged the significance to the public welfare of O3-induced effects on sensitive vegetation growing within the U.S. to differ depending on the nature of the effect, the intended use of the sensitive plants or ecosystems, and the types of environments in which the sensitive vegetation and ecosystems are located, with greater significance ascribed to areas identified for specific uses and benefits to the public welfare, such as Class I areas, than to areas for which such uses have not been established (FR 73 16496-16497, March 27, 2008).

In summary, several considerations are recognized as important to judgments on the public welfare significance of the array of effects of different O3 exposure conditions on vegetation. While there are complexities associated with the consideration of the magnitude of key vegetation effects that might be concluded to be adverse to ecosystems and associated services, there are numerous locations where O3-sensitive tree species are present that may be vulnerable to impacts from O3 on tree growth, productivity and carbon storage and their associated ecosystems and services. Cumulative exposures that may elicit effects and the significance of the effects in specific situations can vary due to differences in exposed species sensitivity, the importance of the observed or predicted O3-induced effect, the role that the species plays in the ecosystem, the intended use of the affected species and its associated ecosystem and services, the presence of other co-occurring predisposing or mitigating factors, and associated uncertainties and limitations. These factors contribute to the complexity of the Administrator's judgments regarding the adversity of known and anticipated effects to the public welfare.

B. Need for Revision of the Secondary Standard

The initial issue to be addressed in this review of the secondary standard for O3 is whether, in view of the currently available scientific evidence, exposure and risk information and air quality analyses, as reflected in the record, the standard should be retained or revised. In drawing conclusions on adequacy of the current O3 secondary standard, the Administrator has taken into account both evidence-based and quantitative exposure- and risk-based considerations, as well as advice from CASAC and public comment. Evidence-based considerations draw upon the EPA's assessment and integrated synthesis of the scientific evidence from experimental and field studies evaluating welfare effects related to O3 exposure, with a focus on policy-relevant considerations, as discussed in the PA. Air quality analyses inform these considerations with regard to cumulative, seasonal exposures occurring in areas of the U.S. that meet the current standard. Exposure- and risk-based considerations draw upon the EPA assessments of risk of key welfare effects, including O3 effects on forest growth, productivity, carbon storage, crop yield and visible foliar injury, expected to occur in model-based scenarios for the current standard, with appropriate consideration of associated uncertainties.

In evaluating whether it is appropriate to revise the current standard, the Administrator's considerations build on the general approach used in the last review, as summarized in section IV.A of the proposal, and reflect the body of evidence and information available during this review. The approach used is based on an integration of the information on vegetation effects associated with exposure to O3 in ambient air, as well as policy judgments on the adversity of such effects to public welfare and on when the standard is requisite to protect public welfare from known or anticipated adverse effects. Such judgments are informed by air quality and related analyses, quantitative assessments, when available, and qualitative assessment of impacts that could not be quantified. The Administrator has taken into Start Printed Page 65380account both evidence of effects on vegetation and ecosystems and public uses of these entities that may be important to the public welfare. The decision on adequacy of the protection provided by the current standard has also considered the 2013 remand of the secondary standard by the D.C. Circuit such that this decision incorporates the EPA's response to this remand.

Section IV.B.1 below summarizes the basis for the proposed decision by the Administrator that the current secondary standard should be revised. Significant comments received from the public on the proposal are discussed in section IV.B.2 and the Administrator's final decision is described in section IV.B.3.

1. Basis for Proposed Decision

In evaluating whether it was appropriate to propose to retain or revise the current standard, as discussed in section IV.D of the proposal, the Administrator carefully considered the assessment of the current evidence in the ISA, findings of the WREA, including associated limitations and uncertainties, considerations and staff conclusions and associated rationales presented in the PA, views expressed by CASAC, and public comments that had been offered up to that point. In the paragraphs below, we summarize the proposal presentation of the PA considerations with regard to adequacy of the current secondary standard, advice from the CASAC, and the Administrator's proposed conclusions, drawing from section IV.D of the proposal, where a fuller discussion is presented.

a. Considerations and Conclusions in the PA

The PA evaluation is based on the longstanding evidence for O3 effects and the associated conclusions in the current review of causal and likely causal relationships between O3 in ambient air and an array of welfare effects at a range of biological and ecological scales of organization, as summarized in section IV.A.1 above (and described in detail in the ISA). Drawing from the ISA and CASAC advice, the PA emphasizes the strong support in the evidence for the conclusion that effects on vegetation are attributable to cumulative seasonal O3 exposures, taking note of the improved “explanatory power” (for effects on vegetation) of the W126 index over other exposure metrics, as summarized in section IV.A.1.c above. The PA further recognizes the strong basis in the evidence for the conclusion that it is appropriate to use a cumulative seasonal exposure metric, such as the W126 index, to judge impacts of O3 on vegetation; related effects on ecosystems and services, such as carbon storage; and the level of public welfare protection achieved for such effects (U.S. EPA, 2014c, p. 5-78). As a result, based on the strong support in the evidence and advice from CASAC in the current and past reviews, the PA concludes that the most appropriate and biologically relevant way to relate O3 exposure to plant growth, and to determine what would be adequate protection for public welfare effects attributable to the presence of O3 in ambient air, is to characterize exposures in terms of a cumulative seasonal form, and in particular the W126 metric (U.S. EPA, 2014c, pp. 5-7 and 5-78). Accordingly, in considering the evidence with regard to level of protection provided by the current secondary standard, the PA considers air quality data and exposure-response relationships for vegetation effects, particularly those related to forest tree growth, productivity and carbon storage, in terms of the W126 index (U.S. EPA, 2014c, section 5.2; 79 FR 75330-75333, December 17, 2014).

In considering the extent to which such growth-related effects might be expected to occur under conditions that meet the current secondary standard, the PA focused particularly on tree seedling RBL estimates for the 11 species for which robust E-R functions have been developed, noting the CASAC concurrence with use of O3-related tree biomass loss as a surrogate for related effects extending to the ecosystem scale (U.S. EPA, 2014c, p. 5-80, Frey, 2014c, p. 10). The PA evaluation relied on RBL estimates for these 11 species derived using the robust OTC-based E-R functions, noting that analyses newly performed in this review have reduced the uncertainty associated with using OTC E-R functions to predict tree growth effects in the field (U.S. EPA, 2014c, section 5.2.1; U.S. EPA, 2013, section 9.6.3.2).

In considering the RBL estimates for different O3 conditions associated with the current standard, the PA focused primarily on the median of the species-specific (composite) E-R functions. In so doing, in the context of considering the adequacy of protection afforded by the current standard, the PA takes note of CASAC's view regarding a 6% median RBL (Frey, 2014c, p. 12). Based on the summary of RBL estimates in the PA, the PA notes that the median species RBL estimate, across the 11 estimates derived from the robust species-specific E-R functions, is at or above 6% for W126 index values of 19 ppm-hrs and higher (U.S. EPA, 2014c, Tables 6-1 and 5C-3).

In recognition of the potential significance to public welfare of vegetation effects in Class I areas, the proposal described in detail findings of the PA analysis of the occurrence of O3 concentrations associated with the potential for RBL estimates above benchmarks of interest in Class I areas that meet the current standard, focusing on 22 Class I areas for which air quality data indicated the current standard was met and cumulative seasonal exposures, in terms of a 3-year average W126 index, were at or above 15 ppm-hrs (79 FR 75331-75332, Table 7, December 17, 2014; U.S. EPA, 2014c, Table 5-2). The PA noted that W126 index values (both annual and 3-year average values) in many such areas, distributed across multiple states and NOAA climatic regions, were above 19 ppm-hrs. The highest 3-year average value was over 22 ppm-hrs and the highest annual value was over 27 ppm-hrs, exposure values for which the corresponding median species RBL estimates markedly exceed 6%, which CASAC has termed “unacceptably high” (U.S. EPA, 2014c, section 5.2). The PA additionally considered the species-specific RBL estimates for two tree species (quaking aspen and ponderosa pine) that are found in many of these Class I areas and that have a sensitivity to O3 exposure that places them slightly more sensitive than the median of the group for which robust E-R functions have been established (U.S. EPA, 2014c, sections 5.2 and 5.7). As further summarized in the proposal, the PA describes the results of this analysis, particularly in light of advice from CASAC regarding the significance of the 6% RBL benchmark, as evidence of the occurrence in Class I areas, during periods when the current standard is met, of cumulative seasonal O3 exposures of a magnitude for which the tree growth impacts indicated by the associated RBL estimates might reasonably be concluded to be important to public welfare (79 FR 75332; U.S. EPA, 2014c, sections 5.2.1 and 5.7).

The proposal also noted that the PA additionally considered findings of the WREA analyses of O3 effects on tree growth and an array of ecosystem services provided by forests, including timber production, carbon storage and air pollution removal (79 FR 75332-75333; U.S. EPA, 2014b, sections 6.2-6.8; U.S. EPA, 2014c, section 5.2). While recognizing that these analyses provide quantitative estimates of impacts on tree growth and associated services for several different air quality scenarios, Start Printed Page 65381the PA takes note of the large uncertainties associated with these analyses (see U.S. EPA, 2014b, Table 6-27) and the potential for these findings to underestimate the response at the national scale. While noting the potential usefulness of considering predicted and anticipated impacts to these services in assessing the extent to which the current information supports or calls into question the adequacy of the protection afforded by the current standard, the PA also recognizes significant uncertainties associated with the absolute magnitude of the estimates for these ecosystem service endpoints which limited the weight staff placed on these results (U.S. EPA, 2014c, sections 5.2 and 5.7).

As described in the proposal, the PA also considered O3 effects on crops, taking note of the extensive and long-standing evidence of the detrimental effect of O3 on crop production, which continues to be confirmed by evidence newly available in this review (79 FR 75333; U.S. 2014c, sections 5.3 and 5.7). With regard to consideration of the quantitative impacts of O3 exposures under exposure conditions associated with the current standard, the PA focused on RYL estimates that had strong support in the current evidence (as characterized in the ISA, section 9.6) in light of CASAC comments regarding RYL benchmarks (Frey, 2014c, pp. iii and 14). In considering such evidence-based analyses, as well as the exposure/risk-based information for crops, the PA notes the CASAC comments regarding the use of crop yields as a surrogate for consideration of public welfare impacts, which noted that “[c]rops provide food and fiber services to humans” and that “[e]valuation of market-based welfare effects of O3 exposure in forestry and agricultural sectors is an appropriate approach to take into account damage that is adverse to public welfare” (Frey, 2014c, p. 10; U.S. EPA, 2014c, section 5.7). The PA additionally notes, however, as recognized in section IV.A.3 above that the determination of the point at which O3-induced crop yield loss becomes adverse to the public welfare is still unclear, given that crops are heavily managed (e.g., with fertilizer, irrigation) for optimum yields, have their own associated markets and that benefits can be unevenly distributed between producers and consumers (79 FR 75322; U.S. EPA, 2014c, sections 5.3 and 5.7).

With regard to visible foliar injury, as summarized in the proposal, the PA recognizes the long-standing evidence that has established that O3 causes diagnostic visible foliar injury symptoms on studied bioindicator species and also recognizes that such O3-induced impacts have the potential to impact the public welfare in scenic and/or recreational areas, with visible foliar injury associated with important cultural and recreational ecosystem services to the public, such as scenic viewing, wildlife watching, hiking, and camping, that are of significance to the public welfare and enjoyed by millions of Americans every year, generating millions of dollars in economic value (U.S. EPA, 2014b, section 7.1). In addition, several tribes have indicated that many of the O3-sensitive species (including bioindicator species) are culturally significant (U.S. EPA, 2014c, Table 5-1). Similarly, the PA notes CASAC comments that “visible foliar injury can impact public welfare by damaging or impairing the intended use or service of a resource,” including through “visible damage to ornamental or leafy crops that affects their economic value, yield, or usability; visible damage to plants with special cultural significance; and visible damage to species occurring in natural settings valued for scenic beauty or recreational appeal” (Frey, 2014c, p. 10). Given the above, and taking note of CASAC views, the PA recognizes visible foliar injury as an important O3 effect which, depending on severity and spatial extent, may reasonably be concluded to be of public welfare significance, especially when occurring in nationally protected areas, such as national parks and other Class I areas.

As summarized in the proposal, the PA additionally takes note of the evidence described in the ISA regarding the role of soil moisture conditions that can decrease the incidence and severity of visible foliar injury under dry conditions (U.S. EPA, 2014c, sections 5.4 and 5.7). As recognized in the PA, this area of uncertainty complicates characterization of the potential for visible foliar injury and its severity or extent of occurrence for given air quality conditions and thus complicates identification of air quality conditions that might be expected to provide a specific level of protection from this effect (U.S. EPA, 2014c, sections 5.4 and 5.7). While noting the uncertainties associated with describing the potential for visible foliar injury and its severity or extent of occurrence for any given air quality conditions, the PA notes the occurrence of O3-induced visible foliar injury in areas, including federally protected Class I areas that meet the current standard, and suggests it may be appropriate to consider revising the standard for greater protection. In so doing, however, the PA recognizes that the degree to which O3-induced visible foliar injury would be judged important and potentially adverse to public welfare is uncertain (U.S. EPA, 2014c, section 5.7).

As noted in the proposal, with regard to other welfare effects, for which the ISA determined a causal or likely causal relationships with O3 in ambient air, such as alteration of ecosystem water cycling and changes in climate, the PA concludes there are limitations in the available information that affect our ability to consider potential impacts of air quality conditions associated with the current standard.

Based on the considerations described in the PA, summarized in the proposal and outlined here, the PA concludes that the currently available evidence and exposure/risk information call into question the adequacy of the public welfare protection provided by the current standard and provide support for considering potential alternative standards to provide increased public welfare protection, especially for sensitive vegetation and ecosystems in federally protected Class I and similarly protected areas. In this conclusion, staff gives particular weight to the evidence indicating the occurrence in Class I areas that meet the current standard of cumulative seasonal O3 exposures associated with estimates of tree growth impacts of a magnitude that may reasonably be considered important to public welfare.

b. CASAC Advice

The proposal also summarized advice offered by the CASAC in the current review, based on the updated scientific and technical record since the 2008 rulemaking. The CASAC stated that it “[supports] the conclusion in the Second Draft PA that the current secondary standard is not adequate to protect against current and anticipated welfare effects of ozone on vegetation” (Frey, 2014c, p. iii) and that the PA “clearly demonstrates that ozone-induced injury may occur in areas that meet the current standard” (Frey, 2014c, p. 12). The CASAC further stated “[w]e support the EPA's continued emphasis on Class I and other protected areas” (Frey, 2014c, p. 9). Additionally, the CASAC indicated support for the concept of ecosystem services “as part of the scope of characterizing damage that is adverse to public welfare” and “concur[red] that trees are important from a public welfare perspective because they provide valued services to humans, including aesthetic value, food, fiber, timber, other forest products, habitat, recreational opportunities, climate regulation, erosion control, air Start Printed Page 65382pollution removal, and hydrologic and fire regime stabilization” (Frey, 2014c, p. 9). Similar to comments from CASAC in the last review, and comments on the proposed reconsideration, the current CASAC also endorsed the PA discussions and conclusions on biologically relevant exposure metrics and the focus on the W126 index accumulated over a 12-hour period (8 a.m.-8 p.m.) over the 3-month summation period of a year resulting in the maximum value (Frey, 2014c, p. iii).

In addition, CASAC stated that “relative biomass loss for tree species, crop yield loss, and visible foliar injury are appropriate surrogates for a wide range of damage that is adverse to public welfare,” listing an array of related ecosystem services (Frey, 2014c, p. 10). With respect to RBL for tree species, CASAC states that it is appropriate to identify in the PA “a range of levels of alternative W126-based standards that include levels that aim for not greater than 2% RBL for the median tree species” and that a median tree species RBL of 6% is “unacceptably high” (Frey, 2014c, pp. 13 and 14). With respect to crop yield loss, CASAC points to a benchmark of 5%, stating that a crop RYL for median species over 5% is “unacceptably high” and described crop yield as a surrogate for related services (Frey, 2014c, p. 13).

c. Administrator's Proposed Conclusions

At the time of proposal, the Administrator took into account the information available in the current review with regard to the nature of O3-related effects on vegetation and the adequacy of protection provided by the current secondary standard. The Administrator recognized the appropriateness and usefulness of the W126 metric in evaluating O3 exposures of potential concern for vegetation effects, additionally noting support conveyed by CASAC for such a use for this metric. Further, the Administrator took particular note of (1) the PA analysis of the magnitude of tree seedling growth effects (biomass loss) estimated for different cumulative, seasonal, concentration-weighted exposures in terms of the W126 metric; (2) the monitoring analysis in the PA of cumulative exposures (in terms of W126 index) occurring in locations where the current standard is met, including those locations in or near Class I areas, and associated estimates of tree seedling growth effects; and (3) the analyses in the WREA illustrating the geographic distribution of tree species for which E-R functions are available and estimates of O3-related growth impacts for different air quality scenarios, taking into account the identified potential for the WREA's existing standard scenario to underestimate the highest W126-based O3 values that would be expected to occur.

With regard to considering the adequacy of public welfare protection provided by the current secondary standard at the time of proposal, the Administrator focused first on welfare effects related to reduced native plant growth and productivity in terrestrial systems, taking note of the following: (a) The ISA conclusion of a causal relationship between O3 in the ambient air and these welfare effects, and supporting evidence related to O3 effects on vegetation growth and productivity, including the evidence from OTC studies of tree seedling growth that support robust E-R functions for 11 species; (b) the evidence, described in section IV.D.1 of the proposal and summarized above, of the occurrence of cumulative seasonal O3 exposures for which median species RBL estimates are of a magnitude that CASAC has termed “unacceptably high” in Class I areas during periods where the current standard is met; (c) actions taken by Congress to establish public lands that are set aside for specific uses intended to provide benefits to the public welfare, including lands that are to be protected so as to conserve the scenic value and the natural vegetation and wildlife within such areas for the enjoyment of future generations, such as national parks and forests, wildlife refuges, and wilderness areas (many of which have been designated Class I areas); and (d) PA conclusions that the current information calls into question the adequacy of the current standard, based particularly on impacts on tree growth (and the potential for associated ecosystem effects), estimated for Class I area conditions meeting the current standard, that are reasonably concluded to be important from a public welfare standpoint in terms of both the magnitude of the vegetation effects and the significance to public welfare of such effects in such areas.

At the time of proposal, the Administrator also recognized the causal relationships between O3 in the ambient air and visible foliar injury, reduced yield and quality of agricultural crops, and alteration of below-ground biogeochemical cycles associated with effects on growth and productivity. As to visible foliar injury, she took note of the complexities and limitations in the evidence base regarding characterizing air quality conditions with respect to the magnitude and extent of risk for visible foliar injury, and she additionally recognized the challenges of associated judgments with regard to adversity of such effects to public welfare. In taking note of the conclusions with regard to crops, she recognized the complexity of considering adverse O3 impacts to public welfare due to the heavy management common for achieving optimum yields and market factors that influence associated services and additionally took note of the PA conclusions that placing emphasis on the protection afforded to trees inherently also recognizes a level of protection afforded for crops.

Based on her consideration of the conclusions in the PA, and with particular weight given to PA findings pertaining to tree growth-related effects, as well as with consideration of CASAC's conclusion that the current standard is not adequate, the Administrator proposed to conclude that the current standard is not requisite to protect public welfare from known or anticipated adverse effects and that revision is needed to provide the requisite public welfare protection, especially for sensitive vegetation and ecosystems in federally protected Class I areas and in other areas providing similar public welfare benefits. The Administrator further concluded that the scientific evidence and quantitative analyses on tree growth-related effects provide strong support for consideration of alternative standards that would provide increased public welfare protection beyond that afforded by the current O3 secondary standard. She further noted that a revised standard would provide increased protection for other growth-related effects, including for carbon storage and for areas for which it is more difficult to determine public welfare significance, as recognized in section IV.B.2 of the proposal, as well as other welfare effects of O3, including visible foliar injury and crop yield loss.

2. Comments on the Need for Revision

In considering comments on the need for revision, we first note the advice and recommendations from CASAC with regard to the adequacy of the current standard. In its review of the second draft PA, CASAC stated that it “supports the scientific conclusion in the Second Draft PA that the current secondary standard is not adequate to protect against current and anticipated welfare effects of ozone on vegetation” (Frey, 2014c).

General comments received from the public on the proposal that are based on relevant factors and either supported or opposed the proposed decision to revise Start Printed Page 65383the current O3 secondary standard are addressed in this section. Comments on specific issues or information that relate to consideration of the appropriate elements of a revised secondary standard are addressed below in section IV.C. Other specific comments related to standard setting, as well as general comments based on implementation-related factors that are not a permissible basis for considering the need to revise the current standard, are addressed in the Response to Comments document.

Public comments on the proposal were divided with regard to support for the Administrator's proposed decision to revise the current secondary standard. Many state and local environmental agencies or government bodies, tribal agencies and organizations, and environmental organizations agreed with the EPA's proposed conclusion on the need to revise the current standard, stating that the available scientific information shows that O3-induced vegetation and ecosystem effects are occurring under air quality conditions allowed by the current standard and, therefore, provides a strong basis and support for the conclusion that the current secondary standard is not adequate. In support of their view, these commenters relied on the entire body of evidence available for consideration in this review, including evidence assessed previously in the 2008 review. These commenters variously pointed to the information and analyses in the PA and the conclusions and recommendations of CASAC as providing a clear basis for concluding that the current standard does not provide adequate protection of public welfare from O3-related effects. Many of these commenters generally noted their agreement with the rationale provided in the proposal with regard to the Administrator's proposed conclusion on adequacy of the current standard, and some gave additional emphasis to several aspects of that rationale, including the appropriateness of the EPA's attention to sensitive vegetation and ecosystems in Class I areas and other public lands that provide similar public welfare benefits and of the EPA's reliance on the strong evidence of impacts to tree growth and growth-related effects.

Comments from tribal organizations additionally noted that many Class I areas are of sacred value to tribes or provide treaty-protected benefits to tribes, including the exercise of gathering rights. Tribal organizations also noted the presence in Class I areas of large numbers of culturally important plant species, which they indicate to be impacted by air quality conditions allowed by the current standard. The impacts described include visible foliar injury, loss in forest growth and crop yield loss, which these groups describe as especially concerning when occurring on lands set aside for the benefit of the public or that are of sacred value to tribes or provide treaty-protected benefits to tribes.

As described in section IV.B.3 below, the EPA generally agrees with the view of these commenters regarding the need for revision of the current secondary standard and with CASAC that the evidence provides support for the conclusions that the current secondary standard is not adequate to protect public welfare from known or anticipated adverse effects, particularly with respect to effects on vegetation.

A number of industries, industry associations, or industry consultants, as well as some state governors, attorneys general and environmental agencies, disagreed with the EPA's proposed conclusion on the adequacy of the current standard and recommended against revision. In support of their position, these commenters variously stated that the available evidence is little changed from that available at the time of the 2008 decision, and that the evidence is too uncertain, including with regard to growth-related effects and visible foliar injury, to support revision, and does not demonstrate adverse effects to public welfare for conditions associated with the current standard, with some commenters stating particularly that the EPA analysis of Class I areas did not document adverse effects to public welfare. They also cited the WREA modeling analyses as indicating that any welfare improvements associated with a revised standard would be marginal; in particular, compared to the benefits of achieving the current standard. Further, they state that, because of long-range transport of O3 and precursors, it is not appropriate for the EPA to draw conclusions about the level of protection offered by the current standard based on current air quality conditions; in support of this view, these commenters point to different modeling analyses as demonstrating that under conditions where the current standard is met throughout the U.S., the associated W126 values would all be below the upper end of the range proposed as providing requisite public welfare protection and nearly all below the lower end of 13 ppm-hrs.

As an initial matter, we note that, as noted in sections I.C and IV.A above, the EPA's 2008 decision on the secondary standard was remanded back to the Agency because in setting the 2008 secondary standard, the EPA failed to specify what level of air quality was requisite to protect public welfare from known or anticipated adverse effects or explain why any such level would be requisite. So, in addressing the court remand, the EPA has more explicitly considered the extent to which protection is provided from known or anticipated effects that the Administrator may judge to be adverse to public welfare, and has described how the air quality associated with the revised standard would provide requisite public welfare protection, consistent with CAA section 109(b)(2) and the court's decision remanding the 2008 secondary standard. In undertaking this review, consistent with the direction of the CAA, the EPA has considered the current air quality criteria.

While we recognize, as stated in the proposal, that the evidence newly available in this review is largely consistent with the evidence available at the time of the last review (completed in 2008) with regard to the welfare effects of O3, we disagree with the commenters' interpretations of the evidence and analyses available in this review and with their views on the associated uncertainties. As summarized in section IV.A above, the ISA has determined causal relationships to exist between several vegetation and ecosystem endpoints and O3 in ambient air (U.S. 2013, section 9.7). The ISA characterized the newly available evidence as largely consistent with and supportive of prior conclusions, as summarized in section IV.A above. This is not to say, however, that there is no newly available evidence and information in this review or that it is identical to that available in the last review. In some respects, the newly available evidence has strengthened the evidence available in the last review and reduced important uncertainties. As summarized in section IV.A.1.b above, newly available field studies confirm the cumulative effects and effects on forest community composition over multiple seasons. Additionally, among the newly available evidence for this review are analyses documented in the ISA that evaluate the RBL and RYL E-R functions for aspen and soybean, respectively, with experimental datasets that were not used in the derivation of the functions (U.S. 2013, section 9.6.3). These evaluations confirm the pertinence of the tree seedling RBL estimates for aspen, a species with sensitivity roughly midway in the range of sensitivities for the studied species, across multiple years in older trees. Start Printed Page 65384With regard to crops, the ISA evaluations demonstrate a robustness of the E-R functions to predict O3-attributable RYL and confirm the relevance of the crop RYL estimates for more recent cultivars currently growing in the field. Together, the information newly available in this review confirms the basis for the E-R functions and strengthens our confidence in interpretations drawn from their use in other analyses newly available in this review that have been described in the WREA and PA.

With regard to comments on uncertainties associated with estimates of RBL, we first note that these established, robust E-R functions, which the EPA gave particular emphasis in this review, are available for seedling growth for 11 tree species native to the U.S., as summarized in section IV.A.1.b above and described in the proposal. These E-R functions are based on studies of multiple genotypes of 11 tree species grown for up to three years in multiple locations across the U.S. (U.S. EPA, 2013, section 9.6.1). We have recognized the uncertainty regarding the extent to which the studied species encompass the O3 sensitive species in the U.S. and also the extent to which they represent U.S. vegetation as a whole (U.S. EPA, 2014b, section 6.9). However, the studied species include both deciduous and coniferous trees with a wide range of sensitivities and species native to every region across the U.S. and in most cases are resident across multiple states and NOAA climatic regions (U.S. EPA, 2014b, Appendix 6A). While the CASAC stated that there is “considerable uncertainty in extrapolating from the [studied] forest tree species to all forest tree species in the U.S.,” it additionally expressed the view that it should be anticipated that there are highly sensitive vegetation species for which we do not have E-R functions and others that are insensitive.[187] In so doing, the CASAC stated that it “should not be assumed that species of unknown sensitivity are tolerant to ozone” and “[i]t is more appropriate to assume that the sensitivity of species without E-R functions might be similar to the range of sensitivity for those species with E-R functions” (Frey, 2014c, p. 11). Accordingly, we disagree with commenters' view that effects on these species are not appropriate considerations for evaluation of the adequacy of the current standard.

In support of their view that RBL estimates are too uncertain to inform a conclusion that the current standard is not adequately protective of public welfare, some commenters state that some of the 11 E-R functions are based on as few as one study. The EPA agrees that there are two species for which there is only one study supporting the E-R function (Virginia pine and red maple). We also note, however, that those two species are appreciably less sensitive than the median (Lee and Hogsett, 1996; U.S. EPA, 2014c, Table 5C-1). Thus, in the relevant analyses, they tend to influence the median toward a relatively less (rather than more) sensitive response. Further, there are four species for which the E-R functions are based on more than five studies,[188] contrary to the commenters' claims of there being no functions supported by that many studies. That said, the EPA has noted the relatively greater uncertainty in the species for which fewer studies are available, and it is in consideration of such uncertainties that the EPA focused in the proposal on the median E-R function across the 11 species, rather than a function for a species much more (or less) sensitive than the median. The EPA additionally notes that it gave less emphasis to the E-R function available for one species, eastern cottonwood, based on CASAC advice that the study results supporting that E-R function were not as strong as the results of the other experiments that support the other, robust E-R functions and that the eastern cottonwood study results showed extreme sensitivity to O3 compared to other studies (Frey, 2014c, p. 10). Accordingly, the EPA has appropriately considered the strength of the scientific evidence and the associated uncertainties in considering revision of the secondary standard.

Other commenters stated that the scientific evidence does not support revising the NAAQS, pointing to uncertainty related to interpretation of the RBL estimates (based on tree seedling studies) with regard to effects on older tree lifestages. Some of these commenters' claim that mature canopy trees experience reduced O3 effects. The EPA agrees that the quantitative information for O3 growth effects on older tree lifestages is available for a more limited set of species than that available for tree seedlings. We note, however, that this is an area for which there is information newly available in this review. A detailed analysis of study data for seedlings and older lifestages of aspen shows close agreement between the O3-attributable reduced growth observed in the older trees and reductions predicted from the seedling E-R function (U.S. EPA, 2013, section 9.6.3.2; discussed in the PA, section 5.2.1 as noted in the proposal, p. 75330). This finding, newly available in this review and documenting impacts on mature trees, improves our confidence in conclusions drawn with regard to the significance of RBL estimates for this species, which is prevalent across multiple regions of the U.S.[189] It is also noteworthy that this species is generally more sensitive to O3 effects on growth than the median of the 11 species with robust E-R functions (as shown in U.S. EPA 2014c, Table 5C-1). Other newly available studies, summarized in section IV.A.1.b above and section IV.B.1.b of the proposal, provide additional evidence of O3 impacts on mature trees, including a meta-analysis reporting older trees to be more affected by O3 than younger trees (U.S. EPA, 2013, p. 9-42; Wittig et al., 2007). We additionally note that CASAC “concur[red] that biomass loss in trees is a relevant surrogate for damage to tree growth that affects ecosystem services such as habitat provision for wildlife, carbon storage, provision of food and fiber, and pollution removal” additionally stating that “[b]iomass loss may also have indirect process-related effects such as on nutrient and hydrologic cycles” leading them to conclude that “[t]herefore, biomass loss is a scientifically valid surrogate of a variety of adverse effects to public welfare” (Frey, 2014c, p. 10).

As noted in section IV.A above and discussed below, the Administrator's final decision on the adequacy of the current standard draws upon, among other things, the available evidence and quantitative analyses as well as judgments about the appropriate weight to place on the range of uncertainties inherent in the evidence and analyses. The strengthening in this review, as compared with the last review, of the basis for the robust E-R functions for tree seedling RBL, as well as other newly available quantitative analyses, Start Printed Page 65385will, accordingly, contribute to judgments made by the Administrator with regard to these effects in reaching her final decisions in this review.

Amongst the newly available information in this review is a new analysis describing W126-based exposures occurring in counties containing Class I areas for which monitoring data indicated compliance with the current standard. The PA gave particular attention to this analysis in consideration of the adequacy of the current standard, and this analysis was also described in the proposal (U.S. EPA, 2014c, Appendix 5B and pp. 5-27 to 5-29; 79 FR 75331-75332, December 17, 2014). Some of the commenters who disagreed with the EPA's conclusion on adequacy of the current standard variously stated that this analysis does not demonstrate growth effects are occurring in Class I areas and that the analysis is too uncertain for reliance on by the Administrator in her judgment on adequacy of the current standard. While the EPA agrees with commenters that data on the occurrence of growth effects in the areas and time periods identified are not part of this analysis, we note that this is because such data have not been collected and consequently cannot be included. As a result, the EPA has utilized measurements of O3 in or near these areas in combination with the established E-R functions to estimate the potential for growth impacts in these areas under conditions where the current standard is met. The EPA additionally notes that species for which E-R functions have been developed have been documented to occur within these areas (see Table 3).

The EPA disagrees with commenters regarding the appropriateness of this analysis for the Administrator's consideration. This analysis documents the occurrence of cumulative growing season exposures in these ecosystems which the EPA and CASAC have interpreted, through the use of the established E-R functions for tree seedling growth effects summarized in section IV.A.1.b above (and described in the ISA, PA and proposal), as indicating the potential for growth effects of significance in these protected areas. To the extent that these comments imply that the Administrator may only consider welfare effects that are certain in judging the adequacy of the current standard, we note that section 109(b)(2) of the CAA plainly provides for consideration of both known and anticipated adverse effects in establishing or revising secondary NAAQS.

In support of some commenters' view that this analysis is too uncertain to provide a basis for the Administrator's proposed conclusion that the current standard is not adequate, one commenter observed that the O3 monitors used for six of the 22 Class I areas in the analysis, although in the same county, were sited outside of the Class I areas. This was the case due to the analysis being focused on the highest monitor in the county that met the current standard. To clarify the presentation, however, we have refocused the presentation, restricting it to data for monitors sited in or within 15 kilometers of a Class I area,[190] and note that the results are little changed, continuing to call into question the adequacy of the current standard. As shown in Table 3, the dataset in the refocused presentation, which now spans 1998 up through 2013, includes 17 Class I areas for which monitors were identified in this manner. For context, we note that this represents nearly a quarter of the Class I areas for which there are O3 monitors within 15 km.[191]

In recognition of the influence that other environmental factors can exert in the natural environment on the relationship between ambient O3 exposures and RBL, potentially modifying the impact predicted by the E-R functions, the PA and proposal took particular note of the occurrence of 3-year average W126 index values at or above 19 ppm-hrs. In the re-focused analysis in Table 3, there are 11 areas, distributed across four states in two NOAA climatic regions, for which the 3-year W126 exposure index values ranged at or above 19 ppm-hrs, a value for which the corresponding median species RBL estimate for a growing season's exposure is 6%, a magnitude termed “unacceptably high” by CASAC (Frey, 2014c, p. 13). The highest 3-year W126 index values in these 11 areas ranged from 19.0 up to 22.2 ppm-hrs, a cumulative seasonal exposure for which the median species RBL estimate is 9% for a single growing season. The annual W126 index values range above 19 ppm-hrs in 15 of the areas in the re-focused table provided here; these areas are distributed across six states (AZ, CA, CO, KY, SD, UT) and four regions (West, Southwest, West North Central and Central).[192] The highest index values in the areas with annual index values above 19 ppm-hrs range from 19.1 to 26.9 ppm-hrs. As is to be expected from the focus on a smaller dataset, the number of states with 1-year W126 index values above 19 ppm-hrs is smaller in the refocused analysis (15 as compared to 20), although the number of regions affected is the same. More importantly, however, the number of areas with 3-year W126 index values at or above 19 ppm-hrs is the same, 11 Class I areas across two regions, supporting the prior conclusions.

Table 3—O3 Concentrations for Class I Areas During Period From 1998 to 2013 That Met the Current Standard and Where 3-Year Average W126 Index Value Was at or Above 15 ppm-hrs

Class I area (distance away, if monitor is not at/within boundaries)State/ CountyDesign value (ppb)*3-Year average W126 (ppm-hrs)* (# ≥ 19 ppm-hrs, range)Annual W126 (ppm-hrs)* (# ≥ 19 ppm-hrs, range)Number of 3-year periods
Bridger Wilderness AreaQA, DF (8.9 km)WY/Sublette70-7216.2-17.013.9-18.84
Canyonlands National ParkQA, DF, PPUT/San Juan70-7315.4-19.5 (2, 19.1-19.5)9.6-23.6 (4, 19.2-23.6)8
Chiricahua National MonumentDF, PP (12 km)AZ/Cochise69-7315.2-19.8 (1, 19.8)11.7-21.9 (2, 19.8-21.9)10
Grand Canyon National ParkQA, DF, PPAZ/Coconino68-7415.3-22.2 (7, 19.1-22.2)10.1-26.9 (6, 19.8-26.9)12
Desolation WildernessPP (3.9 km)CA/El Dorado7519.8 (1, 19.8)15.6-22.9 (2, 21.0-22.9)1
Start Printed Page 65386
Lassen Volcanic National ParkDF, PPCA/Shasta72-7415.3-15.611.5-19.1 (1, 19.1)2
Mammoth Cave National ParkBC, C, LP, RM, SM, VP, YP (0.1 km)KY/Edmonson7415.712.3-22.0 (1, 22.0)1
Maroon Bells-Snowmass Wilderness AreaQA, DF (0.8 km)CO/Gunnison68-7315.6-20.2 (1, 20.2)13.0-23.8 (3, 21.3-23.8)8
Mazatzal WildernessDF, PP (10.9 km)AZ/Maricopa74-7517.8-19.9 (1, 19.9)10.3-26.2 (3, 19.7-26.2)2
Mesa Verde National ParkDFCO/Montezuma67-7315.4-20.7 (1, 20.7)10.7-23.4 (4, 19.5-23.4)11
Petrified Forest National ParkCAZ/Navajo7015.4-16.912.7-18.62
Rocky Mountain National ParkQA, DF, PP (0.9 km)CO/Larimer73-7415.3-18.48.3-26.2 (4, 19.4-26.2)5
Saguaro National ParkDF, PP (0.1 km)**AZ/Pima69-7415.4-19.0 (1, 19.0)7.3-22.9 (3, 19.6-22.9)6
AZ/Gila72-7516.6-20.9 (2, 19.0-20.9)13.8-25.5 (4, 19.0-25.5)5
Superstition Wilderness AreaPP (6.3, 14.9 km and 7.2 km)**AZ/Maricopa70-7515-20.2 (1, 20.2)6.3-23.9 (4, 19.6-23.9)4
AZ/Pinal72-7515.3-21.1 (1, 21.1)10.2-24.7 (4, 21.4-24.7)7
Weminuche Wilderness AreaQA, DF, PP (14.9 km)CO/La Plata70-7415.1-19.1 (1, 19.1)10.8-21.0 (2, 20.8-21.0)6
Wind Cave National ParkQA, PPSD/Custer7015.412.3-20.5 (1, 20.5)1
Zion National ParkQA, DF, PP (3.6 km)UT/Washington70-7317.0-20.1 (2, 19.4-20.1)14.2-23.2 (3, 19.8-23.2)6
* Based on hourly O3 concentration data retrieved from AQS on June 25, 2014, and additional CASTNET data downloaded from http://java.epa.gov/​castnet/​epa_​jsp/​prepackageddata.jsp on June 25, 2014. Design values shown above are derived in accordance with Appendix P to 40 CFR Part 50. Annual W126 index values are derived as described in section IV.A.1 above; three consecutive year annual values are averaged for 3-year averages. Prior to presentation, both types of W126 index values are rounded to one decimal place. The full list of monitoring site identifiers and individual statistics is available in the docket for this rulemaking.
** No monitor was sited within these Areas and multiple monitors were sited within 15 km. Data for the closest monitor per county are presented.
Superscript letters refer to species present for which E-R functions have been developed. QA=Quaking Aspen, BC=Black Cherry, C=Cottonwood, DF=Douglas Fir, LP=Loblolly Pine, PP=Ponderosa Pine, RM=Red Maple, SM=Sugar Maple, VP=Virginia Pine, YP=Yellow (Tulip) Poplar. Sources include USDA-NRCS (2014, http://plants.usda.gov), USDA-FS (2014, http://www.fs.fed.us/​foresthealth/​technology/​nidrm2012.shtml) UM-CFCWI (2014, http://www.wilderness.net/​printFactSheet.cfm?​WID=​583), NPS (http://www.nps.gov/​pefo/​planyourvisit/​upload/​Common-Plants-Site-Bulletin-sb-2013.pdf) and Phillips and Comus (2000).

As support for their view that the Class I area analysis is too uncertain to provide a basis for the Administrator's proposed conclusion that the current standard is not adequate, some commenters stated that forests in Class I areas were composed of mature trees and that the tree seedling E-R functions do not predict growth impacts in mature forests. The EPA disagrees with the commenters' statement that Class I areas are only made up of mature trees. Seedlings exist throughout forests as part of the natural process of replacing aging trees and overstory trees affected by periodic disturbances.[193] Seedlings also tend to occur in areas affected by natural disturbances, such as fires, insect infestations and flooding, and such disturbances are common in many natural forests. As noted above, information newly available in this review strengthens our understanding regarding O3 effects on mature trees for aspen, an important and O3-sensitive species (U.S. EPA, 2013, section 9.6.3.2).

One commenter additionally stated that the EPA has not shown reduced biomass to be adverse to public welfare, variously citing individual studies, most of which are not considering O3, as support for their view that such an effect of O3 may not occur in the environment and may be of no significance if it does. With regard to the occurrence of O3-related reduced growth in the field, we note the strength of the evidence from field OTC studies on which the E-R functions are based, and evidence from comparative studies with open-air chamberless control treatments suggests that characteristics particular to the OTC did not significantly affect plant response (U.S. EPA, 2013, p. 9-5). Thus, we view the OTC systems as combining aspects of controlled exposure systems with field conditions to facilitate a study providing data that represent the role of the studied pollutant in a natural system.

Further, we disagree with the commenters on the significance of O3-attributable reduced growth in natural ecosystems. Even in the circumstances cited by the commenter (e.g., subsequent to large-scale disturbances, nutrient limited system, multigeneration exposure), O3 can affect growth of seedlings and older trees, with the potential for effects on ecosystem productivity, handicapping the sensitive species and affecting community dynamics and associated community composition, as well as ecosystem hydrologic cycles (U.S. EPA, 2013, p. 1-8). For example, two recent studies report on the role of O3 exposure in affecting water use in a mixed deciduous forest and indicated that O3 increased water use in the forest and also reduced growth rate (U.S. EPA, 2013, p. 9-43, McLaughlin, 2007a, 2007b). Contrary to the lesser effects implied by the commenters, the authors of these two studies noted implications of their findings with regard to the potential for effects to be amplified under conditions of increased temperature and associated reduced water availability (McLaughlin, 2007a). We additionally note comments from Start Printed Page 65387the CASAC, summarized above, in which it concurs with a focus on biomass loss and the use of RBL estimates, calling biomass loss in trees a “relevant surrogate for damage to tree growth” that affects an array of ecosystem services (Frey, 2014c, p. 10), and identifies 6% RBL as “unacceptably high” (Frey, 2014c, p. 13). The evidence we presented includes evidence related to RBL estimates above that benchmark. Thus, while we agree that some reductions in tree growth may not be concluded to be adverse to public welfare, we disagree with commenters that we have not presented the evidence, which includes RBL estimates well above the 6% magnitude identified by CASAC, that supports the Administrator's judgments on adversity that may be indicated by such estimates and her conclusion that adequate protection is not provided by the current standard, as described in section IV.B.3 below.

Some commenters disagree with the EPA's consideration of the Class I areas analysis, stating that it is not appropriate for the EPA to evaluate the level of protection offered by the current primary O3 standard under current conditions due to the long-range transport of O3 and O3 precursors to Class I areas from upwind non-attainment areas. It is the view of these commenters that once the upwind areas make emissions reductions to attain the current standard, downwind areas will see improvements in air quality and decreasing W126 levels. In support of this view, commenters point to several modeling analyses. Some commenters point to air quality modeling conducted by an environmental consultant that projects all sites to have W126 index values below 13 ppm-hrs when emissions are adjusted such that all upwind monitors are modeled to meet the current standard. Detailed methodology, results and references for the commenter's modeling analysis were not provided, precluding a thorough evaluation and comparison to the EPA's modeling. While the EPA agrees that transport of O3 and O3 precursors can affect downwind monitors, we disagree with commenters regarding the conclusions that are appropriate to draw from modeling simulations for the reasons noted below.

As support for their view that the current standard provides adequate protection, some commenters pointed to estimates drawn from the EPA's air quality modeling performed for the RIA, stating that this modeling for an alternative standard level of 70 ppb indicates “only a handful” of monitoring sites approaching as high as 13 ppm-hrs as a 3-year average (e.g., UARG, p. 76). These commenters further point to the WREA modeling, noting that those estimates project that attainment of the current standard would result in only 5 sites above 15 ppm-hrs. Based on these statements, these commenters state that the current standard is likely to provide conditions with no site having a monitor over 17 ppm-hrs and a “minimal number” likely exceeding 13 ppm-hrs (e.g., UARG, p. 77). We disagree with commenters' interpretation of the modeling information from the two different assessments. As we summarized in section IV.C.1 of the proposal with regard to the WREA modeling, the modeling estimates are each based on a single set of precursor emissions reductions that are estimated to achieve the desired target conditions, which is also the case for the RIA modeling[194] (U.S. EPA, 2014c, pp. 5-40 to 5-41; see also section 1.2.2 of the 2014 RIA).

As noted in section IV.A.2 above, and in the proposal, the model-adjusted air quality in the WREA scenario for the current standard does not represent an optimized control scenario that just meets the current standard, but rather characterizes one potential distribution of air quality across a region when all monitor locations meet the standard (79 FR 75322; U.S. EPA, 2014b, section 4.3.4.2). Alternate precursor emissions reductions would be expected to produce different patterns of O3 concentrations and associated differences in W126 index values. Specifically, the precursor emissions reductions scenarios examined in the WREA focuses on regional reductions over broad areas rather than localized cuts that may focus more narrowly on areas violating the current standard (U.S. EPA, 2014b, p. 4-35). The assumption of regionally determined across-the-board emissions reductions is a source of potential uncertainty with the potential to overestimate W126 scenario benefits (U.S. EPA, 2014b, Table 4-5 [row G]). The application of emissions reductions to all locations in each region to bring down the highest monitor in the region to meet the current standard could potentially lead to W126 index underestimates at some locations, as noted in the WREA: “[w]hile the scenarios implemented in this analysis show that [] bringing down the highest monitor in a region would lead to reductions below the targeted level through the rest of the region, to the extent that the regional reductions from on-the-books controls are supplemented with more local controls the additional benefit may be overestimated” (U.S. EPA, 2014b, p. 4-36; U.S. EPA, 2014c, pp. 5-40 to 5-41). This point was emphasized by CASAC in their comments on the 2nd draft WREA. CASAC noted that, “[m]eeting a target level at the highest monitor requires substantial reductions below the targeted level through the rest of the region” and stated that “[t]his artificial simulation does not represent an actual control strategy and may conflate differences in control strategies required to meet different standards” (Frey, 2014b, p. 2).

Due to the uncertainty about what actual future emissions control strategies might be and their associated emissions reductions, and the impact such uncertainty might have on modeling estimates involving reductions from recent conditions, we believe it is important to place weight on ambient air monitoring data for recent conditions in drawing conclusions regarding W126 index values that would be expected in areas that meet the current standard. The analysis of air quality data for Class I areas described in the proposal, and updated in Table 3 above (1998-2013), indicates the occurrence of 3-year W126 exposure index values well above 19 ppm-hrs, a cumulative exposure value for which CASAC termed the associated median RBL estimate “unacceptably high,” in multiple Class I areas that meet the current standard (79 FR 75312, December 17, 2014, Table 7; updated in Table 3 above). Additionally, analysis of recent air quality data (2011-2013) for all locations across the U.S. indicates 10 monitor locations distributed across two NOAA climatic regions that meet the current standard and at which 3-year W126 index values are above 19 ppm-hrs, with the highest values extending up to 23 ppm-hrs (Wells, 2015b).

In support of their view that the EPA's modeling supports the conclusion that W126 index values of interest are achieved under the current secondary standard, some commenters additionally state that the W126 values in the WREA are overestimated in unmonitored rural areas due to the much greater prevalence of urban monitors across the U.S. The EPA Start Printed Page 65388disagrees with this conclusion. In order to estimate O3 concentrations in grid cells across a national-scale spatial surface, the WREA applied the VNA spatial interpolation technique after applying the HDDM technique to adjust O3 concentrations at monitoring sites based on the emissions reductions necessary to just meet the current standard. In estimating concentrations in unmonitored areas, the VNA method considers only the “neighboring” monitors, using an inverse distance squared weighting formula, which assigns the greatest influence to the nearest neighboring monitor (U.S. EPA, 2014b, p. 4A-6). By this approach, monitors in less-densely monitored areas contribute to the concentration estimates over much larger areas than do monitors in more-densely monitored areas. In an urban area, neighboring monitors may be quite close to one another, such that any one monitor may only be influencing concentration estimates for a handful of spatial grid cells in the immediate vicinity. By contrast, monitors in rural areas may influence hundreds of grid cells. A specific example of this is the monitor in Great Basin National Park in eastern Nevada. The VNA algorithm assigns very high weights to this monitor for all of the grid cells covering a 100 km radius around it, simply because there are no other monitors in that area and it is the closest. On the other hand, a monitor near downtown Las Vegas may only get a high weight for, and thus exert influence on the concentration estimate in, the one grid cell containing it. We agree with the commenter that urban monitors may influence the spatial surface for some distance away from the urban areas, although the influence wanes with increasing distance from that area and decreasing distance to the next closest monitor. As we lack data for the intervening locations, however, we have no reason to conclude that the VNA surface is overestimating the W126 index values. Further, as was summarized in section IV.A.2 above, and in the WREA, the PA and the proposal (U.S. EPA, 2014b, Table 6-27, section 8.5; U.S. EPA, 2014c, p. 5-49; 79 FR 75323, December 17, 2014), the VNA approach results in a lowering of the highest W126 index values at monitoring sites, which contributes to underestimates of the highest W126 index values in each region.

In support of their view that the current standard is adequate, some industry commenters additionally cite WREA analyses for the current standard scenario, including the W126 index estimates in national parks, as showing that the current standard provides more than adequate protection, with alternative scenarios providing only marginal and increasingly uncertain benefits. As we noted in the proposal and section IV.A.2 above, there are an array of uncertainties associated with the W126 index estimates, in the current standard scenario and in the other scenarios, which, as they are inputs to the vegetation risk analyses, are propagated into those analyses (79 FR 75323; December 17, 2014). As a result, consistent with the approach in the proposal, the Administrator has not based her decision with regard to adequacy of the current standard in this review on these air quality scenario analyses.

In support of their view that the current standard provides adequate protection and should not be revised, some commenters described their concerns with any consideration of visible foliar injury in the decision regarding the secondary standard. These commenters variously stated that visible foliar injury cannot be reliably evaluated for adversity given lack of available information, is not an adverse effect on public welfare that must be addressed through a secondary standard, and is not directly relatable to growth suppression (and the EPA's use of RBL captures that effect anyway). Additionally, some state that any associated ecosystem services effects are not quantifiable. In sum, the view of these commenters is that it is not appropriate for the Administrator to place any weight on this O3 effect in determining the adequacy of the current standard. As an initial matter, the EPA agrees with the comment that the current evidence does not include an approach for relating visible foliar injury to growth suppression,[195] as recognized in section IV.A.1.b above. Further, we note that, similar to decisions in past O3 reviews, the Administrator's proposed decision in this review recognized the “complexities and limitations in the evidence base regarding characterizing air quality conditions with respect to the magnitude and extent of risk for visible foliar injury” and the “challenges of associated judgments with regard to adversity of such effects to public welfare” (79 FR 75336; December 17, 2014). Contrary to the implications of the commenters, although the Administrator took into consideration the potential for adverse effects on public welfare from visible foliar injury, she placed weight primarily on growth-related effects of O3, both in her proposed decision on adequacy and with regard to proposed judgments on what revisions would be appropriate. Although visible foliar injury may impact the public welfare and accordingly has the potential to be adverse to the public welfare (as noted in section IV.B.2 of the proposal), the Administrator placed less weight on visible foliar injury considerations in identifying what revisions to the standard would be appropriate to propose. In considering these effects for this purpose, she recognized “significant challenges” in light of “the variability and the lack of clear quantitative relationship with other effects on vegetation, as well as the lack of established criteria or objectives that might inform consideration of potential public welfare impacts related to this vegetation effect” (79 FR 75349; December 17, 2014). As summarized in section IV.A.1.a above, the evidence demonstrates a causal relationship of O3 with visible foliar injury. Accordingly, we note that the uncertainty associated with visible foliar injury is not with regard to whether O3 causes visible foliar injury. Rather, the uncertainty is, as discussed in sections IV.A.1.b and IV.A.3 above, with the lack of established, quantitative exposure-response functions that document visible foliar injury severity and incidence under varying air quality and environmental conditions and information to support associated judgments on the significance of such responses with regard to associated public welfare impacts. As with the Administrator's proposed decisions on the standard, such considerations also informed her final decisions, described in sections IV.B.3 and IV.C.3 below.

In support of their view that the current standard should be retained, some commenters note the WREA finding for the current standard scenario of no U.S. counties with RYL estimates at or above 5%, the RYL value emphasized by CASAC and state that policy reasons provide support for not focusing on crops in the decision; other commenters state that additional studies on crops and air quality are needed. As Start Printed Page 65389described previously in this section, and in section IV.A.2 above, an aspect of uncertainties associated with the WREA air quality scenarios, including the current standard scenario, is underestimation of the highest W126 index values, contributing to underestimates in the effects associated with the current standard scenario. The EPA agrees with commenters that additional studies on crops and air quality will be useful to future reviews. Additionally, however, as noted above, the Administrator's proposed conclusion on adequacy of the current standard, as well as her final decision described in section IV.B.3 below, gives less weight to consideration of effects on agricultural crops in recognition of the complicating role of heavy management in that area.

Lastly, we note that many commenters cited the costs of compliance as supporting their view that the standard should not be revised, although as we have described in section I.B above, the EPA may not consider the costs of compliance in determining what standard is requisite to protect public welfare from known or anticipated adverse effects.

3. Administrator's Conclusions on the Need for Revision

Having carefully considered the advice from CASAC and public comments, as discussed above, the Administrator believes that the fundamental scientific conclusions on the welfare effects of O3 in ambient air reached in the ISA and summarized in the PA and in section IV.B of the proposal remain valid. Additionally, the Administrator believes the judgments she reached in the proposal (section IV.D.3) with regard to consideration of the evidence and quantitative assessments and advice from CASAC remain appropriate. Thus, as described below, the Administrator concludes that the current secondary standard is not requisite to protect public welfare from known and anticipated adverse effects associated with the presence of O3 in the ambient air and that revision is needed to provide additional protection.

In considering the adequacy of the current secondary O3 standard, the Administrator has carefully considered the available evidence, analyses and conclusions contained in the ISA, including information newly available in this review; the information, quantitative assessments, considerations and conclusions presented in the PA; the advice and recommendations from CASAC; and public comments. The Administrator gives primary consideration to the evidence of growth effects in well-studied tree species and information, presented in the PA and represented with a narrower focus in section IV.B.2 above, on cumulative exposures occurring in Class I areas when the current standard is met. This information indicates the occurrence of exposures associated with Class I areas during periods when the current standard is met for which associated estimates of growth effects, in terms of the tree seedling RBL in the median species for which E-R functions have been established, extend above a magnitude considered to be “unacceptably high” by CASAC. This analysis estimated such cumulative exposures occurring under the current standard for nearly a dozen areas, distributed across two NOAA climatic regions of the U.S. The Administrator gives particular weight to this analysis, given its focus in Class I areas. Such an emphasis on lands afforded special government protections, such as national parks and forests, wildlife refuges, and wilderness areas, some of which are designated Class I areas under the CAA, is consistent with such emphasis in the 2008 revision of the secondary standard (73 FR 16485, March 27, 2008). As noted in section IV.A above, Congress has set such lands aside for specific uses that are intended to provide benefits to the public welfare, including lands that are to be protected so as to conserve the scenic value and the natural vegetation and wildlife within such areas, and to leave them unimpaired for the enjoyment of future generations. The Administrator additionally recognizes that states, tribes and public interest groups also set aside areas that are intended to provide similar benefits to the public welfare for residents on those lands, as well as for visitors to those areas.

As noted in prior reviews, judgments regarding effects that are adverse to public welfare consider the intended use of the ecological receptors, resources and ecosystems affected. Thus, the Administrator recognizes that the median RBL estimate for the studied species is a quantitative tool within a larger framework of considerations pertaining to the public welfare significance of O3 effects on the public welfare. Such considerations include effects that are associated with effects on growth and that the ISA has determined to be causally or likely causally related to O3 in ambient air, yet for which there are greater uncertainties affecting our estimates of impacts on public welfare. These other effects include reduced productivity in terrestrial ecosystems, reduced carbon sequestration in terrestrial ecosystems, alteration of terrestrial community composition, alteration of below-grown biogeochemical cycles, and alteration of terrestrial ecosystem water cycles, as summarized in section IV.A.1. Thus, in her attention to CASAC's characterization of a 6% estimate for tree seedling RBL in the median studied species as “unacceptably high”, the Administrator, while mindful of uncertainties with regard to the magnitude of growth impact that might be expected in mature trees, is also mindful of related, broader, ecosystem-level effects for which our tools for quantitative estimates are more uncertain and those for which the policy foundation for consideration of public welfare impacts is less well established. She finds her consideration of tree growth effects consistent with CASAC advice regarding consideration of O3-related biomass loss as a surrogate for the broader array of O3 effects at the plant and ecosystem levels.

The Administrator also recognizes that O3-related effects on sensitive vegetation can occur in other areas that have not been afforded special federal protections, including effects on vegetation growing in managed city parks and residential or commercial settings, such as ornamentals used in urban/suburban landscaping or vegetation grown in land use categories that are heavily managed for commercial production of commodities such as timber. In her consideration of the evidence and quantitative information of O3 effects on crops, the Administrator recognizes the complexity of considering adverse O3 impacts to public welfare due to the heavy management common for achieving optimum yields and market factors that influence associated services. In so doing, she notes that her judgments that place emphasis on the protection of forested ecosystems inherently also recognize a level of protection for crops. Additionally, for vegetation used for residential or commercial ornamental purposes, the Administrator believes that there is not adequate information specific to vegetation used for those purposes, but notes that a secondary standard revised to provide protection for sensitive natural vegetation and ecosystems would likely also provide some degree of protection for such vegetation.

The Administrator also takes note of the long-established evidence of consistent association of the presence of visible foliar injury with O3 exposure and the currently available information that indicates the occurrence of visible foliar injury in sensitive species of Start Printed Page 65390vegetation during recent air quality in public forests across the U.S. She additionally notes the PA conclusions regarding difficulties in quantitatively relating visible foliar injury symptoms to vegetation effects such as growth or related ecosystem effects. As at the time of the last review, the Administrator believes that the degree to which such effects should be considered to be adverse depends on the intended use of the vegetation and its significance. The Administrator also believes that the significance of O3-induced visible foliar injury depends on the extent and severity of the injury and takes note of studies in the evidence base documenting increased severity and/or prevalence with higher O3 exposures. However, the Administrator takes note of limitations in the available information with regard to judging the extent to which the extent and severity of visible foliar injury occurrence associated with conditions allowed by the current standard may be considered adverse to public welfare.

Based on these considerations, and taking into consideration the advice and recommendations of CASAC, the Administrator concludes that the protection afforded by the current secondary O3 standard is not sufficient and that the standard needs to be revised to provide additional protection from known and anticipated adverse effects to public welfare, related to effects on sensitive vegetation and ecosystems, most particularly those occurring in Class I areas. The Administrator additionally recognizes that states, tribes and public interest groups also set aside areas that are intended to provide similar benefits to the public welfare for residents on those lands, as well as for visitors to those areas. Given the clear public interest in and value of maintaining these areas in a condition that does not impair their intended use, and the fact that many of these areas contain O3-sensitive vegetation, the Administrator further concludes that it is appropriate to revise the secondary standard in part to provide increased protection against O3-caused impairment to vegetation and ecosystems in such areas, which have been specially protected to provide public welfare benefits. She further notes that a revised standard would provide increased protection for other growth-related effects, including for crop yield loss, reduced carbon storage and for areas for which it is more difficult to determine public welfare significance, as recognized in section IV.A.3 above, as well other welfare effects of O3, such as visible foliar injury.

C. Conclusions on Revision of the Secondary Standard

The elements of the standard—indicator, averaging time, form, and level—serve to define the standard and are considered collectively in evaluating the welfare protection afforded by the secondary standard. Section IV.C.1 below summarizes the basis for the proposed revision. Significant comments received from the public on the proposal are discussed in section IV.C.2 and the Administrator's final decision on revisions to the secondary standard is described in section IV.C.3.

1. Basis for Proposed Revision

At the time of proposal, in considering what revisions to the secondary standard would be appropriate, the Administrator considered the ISA conclusions regarding the weight of the evidence for a range of welfare effects associated with O3 in ambient air and associated areas of uncertainty; quantitative risk and exposure analyses in the WREA for different adjusted air quality scenarios and associated limitations and uncertainties; staff evaluations of the evidence, exposure/risk information and air quality information in the PA; additional air quality analyses of relationships between air quality metrics based on form and averaging time of the current standards and a cumulative seasonal exposure index; CASAC advice; and public comments received as of that date in the review. In the paragraphs below, we summarize the proposal presentation with regard to key aspects of the PA considerations, advice from the CASAC, air quality analyses of different air quality metrics and the Administrator's proposed conclusions, drawing from section IV.E of the proposal.

a. Considerations and Conclusions in the PA

As summarized in the proposal, in identifying alternative secondary standards appropriate to consider in this review, the PA focused on standards based on a cumulative, seasonal, concentration-weighted form consistent with the CASAC advice in the current and last review. Based on conclusions of the ISA, as also summarized in section IV.A above, the PA considered a cumulative, seasonal, concentration-weighted exposure index to provide the most scientifically defensible approach for characterizing vegetation response to ambient O3 and comparing study findings, as well as for defining indices for vegetation protection, as summarized in the proposal section IV.E.2.a. With regard to the appropriate index, the PA considered the evidence for a number of different such indices, as described in the proposal, and noted the ISA conclusion that the W126 index has some important advantages over other similarly weighted indices. The PA additionally considered the appropriate diurnal and seasonal exposure periods in a given year by which to define the seasonal W126 index and based on the evidence in the ISA and CASAC advice, as summarized in the proposal, decided on the 12-hour daylight window (8:00 a.m. to 8:00 p.m.) and the 3-consecutive-month period providing the maximum W126 index value.

Based on these considerations, the PA concluded it to be appropriate to retain the current indicator of O3 and to consider a secondary standard form that is an average of the seasonal W126 index values (derived as described in section IV.A.1.c above) across three consecutive years (U.S. EPA, 2014c, section 6.6). In so doing, the PA recognized that there is limited information to discern differences in the level of protection afforded for cumulative growth-related effects by potential alternative W126-based standards of a single-year form as compared to a 3-year form (U.S. EPA, 2014c, pp. 6-30). The PA concluded a 3-year form to be appropriate for a standard intended to provide the desired level of protection from longer-term effects, including those associated with potential compounding, and that such a form might be concluded to contribute to greater stability in air quality management programs, and thus, greater effectiveness in achieving the desired level of public welfare protection than might result from a single-year form. (U.S. EPA, 2014c, section 6.6).

As summarized in the proposal, the PA noted that, due to the variability in the importance of the associated ecosystem services provided by different species at different exposures and in different locations, as well as differences in associated uncertainties and limitations, it is essential to consider the species present and their public welfare significance, together with the magnitude of the ambient concentrations in drawing conclusions regarding the significance or magnitude of public welfare impacts. Therefore, in development of the PA conclusions, staff took note of the complexity of judgments to be made by the Administrator regarding the adversity of known and anticipated effects to the Start Printed Page 65391public welfare and recognized that the Administrator's ultimate judgments on the secondary standard will most appropriately reflect an interpretation of the available scientific evidence and exposure/risk information that neither overstates nor understates the strengths and limitations of that evidence and information. In considering an appropriate range of levels to consider for an alternative standard, the PA primarily considered tree growth, crop yield loss, and visible foliar injury, as well as impacts on the associated ecosystem services, while noting key uncertainties and limitations.

In specifically evaluating exposure levels, in terms of the W126 index, as to their appropriateness for consideration in this review with regard to providing the desired level of vegetation protection for a revised secondary standard, the PA focused particularly on RBL estimates for the median across the 11 tree species for which robust E-R functions are available. Table 4 below presents these estimates (U.S. EPA, 2014c, Appendix 5C, Table 5C-3; also summarized in Table 8 of the proposal). In so doing and recognizing the longstanding, strong evidence base supporting these relationships, the PA also noted uncertainties regarding inter-study variability for some species, as well as with regard to the extent to which tree seedling E-R functions can be used to represent mature trees. As summarized in the proposal, the PA conclusions on a range of W126 levels appropriate to consider are based on specific advice from CASAC with regard to median tree seedling RBL estimates that might be considered unacceptably high (6%), as well as its judgment on a RBL benchmark (2%) for identification of the lower end of a W126 index value range for consideration that might give more emphasis to the more sensitive tree seedlings (Frey, 2014c, p. 14).[196]

Table 4—Tree Seedling Biomass Loss and Crop Yield Loss Estimated for O3 Exposure Over a Season

W126 index value for exposure periodTree seedling biomass loss ACrop yield loss B
Median valueIndividual speciesMedian valueIndividual species
23 ppm-hrsMedian species w. 7.6% loss≤ 2% loss: 3/11 species ≤ 5% loss: 4/11 species ≤10% loss: 8/11 species ≤15% loss: 10/11 species >40% loss: 1/11 speciesMedian species w. 8.8% loss≤ 5% loss: 4/10 species >5,<10% loss: 1/10 species >10,<20% loss: 4/10 species >20: 1/10 species
22 ppm-hrsMedian species w. 7.2% loss≤ 2% loss: 3/11 species ≤ 5% loss: 4/11 species ≤10% loss: 7/11 species ≤15% loss: 10/11 species >40% loss: 1/11 speciesMedian species w. 8.2% loss≤ 5% loss: 4/10 species >5,<10% loss: 1/10 species >10,<20% loss: 4/10 species >20: 1/10 species
21 ppm-hrsMedian species w. 6.8% loss≤ 2% loss: 3/11 species ≤ 5% loss: 4/11 species ≤10% loss: 7/11 species ≤15% loss: 10/11 species >40% loss: 1/11 speciesMedian species w. 7.7% loss≤ 5% loss: 4/10 species >5,<10% loss: 3/10 species >10,<20% loss: 3/10 species
20 ppm-hrsMedian species w. 6.4% loss≤ 2% loss: 3/11 species ≤ 5% loss: 5/11 species ≤10% loss: 7/11 species ≤15% loss: 10/11 species >40% loss: 1/11 speciesMedian species w. 7.1% loss≤ 5% loss: 5/10 species >5,<10% loss: 3/10 species >10,<20% loss: 2/10 species
19 ppm-hrsMedian species w. 6.0% loss≤ 2% loss: 3/11 species ≤5% loss: 5/11 species ≤10% loss: 7/11 species ≤15% loss: 10/11 species >30% loss: 1/11 speciesMedian species w. 6.4% loss≤ 5% loss: 5/10 species >5, <10% loss: 3/10 species >10,<20% loss: 2/10 species
18 ppm-hrsMedian species w. 5.7% loss≤ 2% loss: 5/11 species ≤ 5% loss: 5/11 species ≤10% loss: 7/11 species ≤15% loss: 10/11 species >30% loss: 1/11 speciesMedian species w. 5.7% loss≤ 5% loss: 5/10 species >5,<10% loss: 3/10 species >10,<20% loss: 2/10 species
17 ppm-hrsMedian species w. 5.3% loss≤ 2% loss: 5/11 species ≤5% loss: 5/11 species ≤10% loss: 9/11 species ≤15% loss: 10/11 species >30% loss: 1/11 speciesMedian species w. 5.1% loss≤ 5% loss: 5/10 species >5, <10% loss: 3/10 species >10,<20% loss: 2/10 species
16 ppm-hrsMedian species w. 4.9% loss≤ 2% loss: 5/11 species ≤ 5% loss: 6/11 species ≤10% loss: 10/11 species >30% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: 5/10 species >5,<10% loss: 4/10 species >10,<20% loss: 1/10 species
15 ppm-hrsMedian species w. 4.5% loss≤ 2% loss: 5/11 species ≤5% loss: 6/11 species ≤10% loss: 10/11 species >30% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: 6/10 species >5, <10% loss: 4/10 species
14 ppm-hrsMedian species w. 4.2% loss≤ 2% loss: 5/11 species ≤ 5% loss: 6/11 species ≤10% loss: 10/11 species >30% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: 6/10 species >5,<10% loss: 4/10 species
13 ppm-hrsMedian species w. 3.8% loss≤ 2% loss: 5/11 species <5% loss: 7/11 species <10% loss: 10/11 species >20% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: 6/10 species >5, <10% loss: 4/10 species
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12 ppm-hrsMedian species w. 3.5% loss≤ 2% loss: 5/11 species ≤ 5% loss: 8/11 species ≤10% loss: 10/11 species >20% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: 8/10 species >5,<10% loss: 2/10 species
11 ppm-hrsMedian species w. 3.1% loss≤ 2% loss: 5/11 species ≤5% loss: 8/11 species ≤10% loss: 10/11 species >20% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: 9/10 species >5, <10% loss: 1/10 species
10 ppm-hrsMedian species w. 2.8% loss≤ 2% loss: 5/11 species ≤ 5% loss: 9/11 species <10% loss: 10/11 species >20% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: 9/10 species >5,<10% loss: 1/10 species
9 ppm-hrsMedian species w. 2.4% loss≤ 2% loss: 5/11 species 5% loss: 10/11 species >20% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: all species
8 ppm-hrsMedian species w. 2.0% loss≤ 2% loss: 5/11 species ≤ 5% loss: 10/11 species >15% loss: 1/11 speciesMedian species w. ≤5.0% loss≤ 5% loss: all species
7 ppm-hrsMedian species w. <2.0% loss≤ 2% loss: 7/11 species ≤5% loss: 10/11 species >15% loss: 1/11 species