Responses to Significant Comments on the 

2007 Proposed Rule on the 

National Ambient Air Quality Standards 

for Ozone 

(July 11, 2007; 72 FR 37818)

Docket Number OAR-2005-0172

U.S. Environmental Protection Agency 

March 2008 
ii

Table of Contents 

List of Acronyms 

Frequently Cited Documents 

I. INTRODUCTION .................................................................................................................. 1 

II. RESPONSES TO SIGNIFICANT COMMENTS ON PROPOSED O3 STANDARDS........ 2 

A. Primary O3 Standards.......................................................................................................... 2 

1. General Comments on Proposed Primary O3 standard ................................................... 2 

a. Support for Revising the Current Standard................................................................. 2 

b. Support for Retaining the Current Standard ............................................................... 5 

2. Specific Comments on Proposed Primary O3 Standards................................................. 9 

a. Averaging Time .......................................................................................................... 9 

b. Form of the Standard ................................................................................................ 10 

c. Level ......................................................................................................................... 11 

i. Comments on Health Evidence Considerations.................................................... 12 

ii. Comments on Exposure and Risk Considerations................................................ 16 

3. Specific Comments on the Interpretation of Scientific Evidence................................. 20 

a. Evidence from Controlled Human Exposure Studies ............................................... 20 

b. Evidence from Epidemiological Studies................................................................... 28 

c. Evidence Pertaining to At-Risk Subgroups for O3-Related Effects.......................... 56 

d. Adversity of Health Effects ...................................................................................... 61 

e. Comments on Role of Ground-Level O3 in Solar Radiation-Related Health Effects66 

4. Specific Comments on the Population Exposure Analyses .......................................... 68 

5. Specific Comments on the Health Risk Assessment .................................................... 73 

6. Specific Comments Related to Communication of Public Health Information.......... 101 

B. Secondary O3 Standards.................................................................................................. 104 

1. General Comments on Proposed Alternative Secondary O3 Standards ...................... 104 

a. Support for Distinct Cumulative, Seasonal Secondary Standard............................ 105 

b. Support for Secondary Identical to Current or Revised 8-Hour Standard.............. 106 

2. Specific Comments on Proposed Alternative Secondary O3 Standards ..................... 108 

a. Form........................................................................................................................ 108 

b. Averaging Times..................................................................................................... 113 

iii. Seasonal Window............................................................................................ 113 

iv. Diurnal Window.............................................................................................. 114 

v. Annual vs. Three Year Average.......................................................................... 115 

c. Level ....................................................................................................................... 116 

3. Specific Comments on the Interpretation of Scientific Evidence............................... 120 

4. Specific Comments on the Vegetation Exposure and Risk Assessments................... 128 

C. Specific Comments Related to Data Handling (Appendix P)......................................... 134 

1. Specific Comments on Data Handling Related to the 8-hour Standard...................... 135 

2. Specific Comments Related to Non-identical Secondary Standard Provisions of 

Appendix P.......................................................................................................................... 140 

D. Comments Related to Monitoring................................................................................... 141 
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1. Specific Comments Related to Monitoring and the Primary Standard....................... 142 

2. Specific Comments Related to Monitoring and the Secondary Standard................... 144 

III. RESPONSES TO LEGAL, ADMINISTRATIVE, AND PROCEDURAL ISSUES AND 

MISPLACED COMMENTS ...................................................................................................... 146 

A. Legal, Administrative and Procedural Issues.................................................................. 146 

B. Misplaced Comments...................................................................................................... 164 

References................................................................................................................................... 169 

Appendix - Provisional Consideration of Recent Studies 
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List of Acronyms

The following acronyms have been used for the sake of brevity in this document: 

Act Clean Air Act 

AAM Alliance of Automobile Manufacturers 

AAP American Academy of Pediatrics 

ACC American Chemistry Council 

ACCP American College of Chest Physicians 

AHA American Heart Association 

ALA American Lung Association 

AMA American Medical Association 

ANA American Nurses Association 

APHA American Public Health Association 

API American Petroleum Institute 

AQI Air Quality Index 

AQS Air Quality System 

ARMs Approved Regional Methods 

ATS American Thoracic Society 

CAA Clean Air Act 

CARB California Air Resources Board 

CASAC Clean Air Scientific Advisory Committee 

CASTNET Clean Air Status and Trends Network 

CDC Centers for Disease Control 

CFR Code of Federal Regulations 

CHPAC Children’s Health Protection Advisory Committee 

CI Confidence interval 

CO Carbon monoxide 

COPD Chronic obstructive pulmonary disease 

EPA Environmental Protection Agency 

FEM Federal Equivalent Method 

FEV1 Forced Expiratory Volume for 1 second 

FRM Federal Reference Method 

GAM Generalized additive model 

GLM Generalized linear model 

HEI Health Effects Institute 

HML Highest measured level 

IQG Information Quality Guidelines 

LML Lowest measured level 

MSA Metropolitan Statistical Area 

NACAA National Association of Clean Air Agencies 

NACCHO National Association of County and City Health Officials 

NAAQS National ambient air quality standards 

NAM National Association of Manufacturers 

NESCAUM Northeast States Coordinated Air Use Management 

NMMAPS National Morbidity, Mortality, and Air Pollution Study 
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NO2 Nitrogen Dioxide 

NPS National Park Service 

NRC National Research Council 

NRDC Natural Resources Defense Council 

NTAA National Tribal Air Association 

O3 Ozone 

OAP Office of Atmospheric Programs 

OR Odds ratio 

OTC Ozone Transport Commission 

PAMS Photochemical Assessment Monitoring Stations 

PEFR Peak Expiratory Flow Rate 

ppm Parts per million 

ppb Parts per billion 

PM Particulate matter 

PM2.5 Particles generally less than or equal to 2.5 μm in diameter 

PM10 Particles generally less than or equal to 10 micrometers (μm) in diameter 

PRB Policy relevant background 

QA Quality assurance 

RIA Regulatory Impact Analysis 

RR Relative risk 

SAB Science Advisory Board 

SO2 Sulfur Dioxide 

TSD Technical support document 

UARG Utility Air Regulatory Group 

USDA U.S. Department of Agriculture 

US PIRG U.S. Public Interest Research Group 

WHO World Health Organization 
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Frequently Cited Documents

The following documents are frequently cited throughout EPA=s response to comments, often by 

means of the short names listed below: 

Criteria Document: Environmental Protection Agency (2006) Air Quality Criteria for Ozone 

and Related Photochemical Oxidants (Final). Washington, DC, 

EPA/600/R-05/004aB-cB. Available online at: 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923. 

Preamble to the final rule: 

 Preamble to the Final Rule on the Review of the National Ambient Air 

Quality Standards for Ozone; to be published in the Federal Register in 

March 2008. 

Proposal notice: National Ambient Air Quality Standards for Ozone: Proposed Rule. 72 

FR 37818, July 11, 2007. 

Staff Paper: Environmental Protection Agency (2007a) Review of the national ambient 

air quality standards for ozone: assessment of scientific and technical 

information. OAQPS staff paper. (Final) July 2007. Research Triangle 

Park, NC: Office of Air Quality Planning and Standards; EPA report no. 

EPA-452/R-07-003. Available online at: 

http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html. 

Health Risk TSD: Abt Associates Inc. (2007a) Ozone Health Risk Assessment for Selected 

Urban Areas. Prepared for Office of Air Quality Planning and Standards, 

U.S. Environmental Protection Agency, Research Triangle Park, NC. July 

2007. Available electronically on the internet at: 

http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. 

Human Exposure TSD: 

Environmental Protection Agency (2007b) Ozone Population Exposure 

Analysis for Selected Urban Areas. Office of Air Quality Planning and 

Standards, Research Triangle Park, NC. (Final) July 2007. Available 

online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. 

Vegetation Risk TSD: Abt Associates Inc. (2007b) Technical Report on Ozone Exposure, Risk, 

and Impacts Assessments for Vegetation: Final Report. Prepared for 

Office of Air Quality Planning and Standards, U.S. Environmental 

Protection Agency, Research Triangle Park, NC. January 2007. Available 

online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. 
1

Responses to Significant Comments on the 2007 Proposed Rule on 

the National Ambient Air Quality Standards for Ozone 

I. INTRODUCTION 

This document, together with the preamble to the final rule on the review of the national 

ambient air quality standards (NAAQS) for ozone (O3), presents the responses of the 

Environmental Protection Agency (EPA) to some of the thousands of public comments received 

on the 2007 O3 NAAQS proposal notice (72 FR 37818). All significant issues raised in the 

public comments have been addressed. 

Due to the large number of comments that addressed similar issues, as well as the sheer 

volume of the comments received, this response-to-comments document does not generally 

cross-reference each response to the commenter(s) who raised the particular issue involved, 

although commenters are identified in some cases where they provided particularly detailed 

comments that were used to frame the overall response on an issue. 

 

 The responses presented in this document are intended to augment the responses to 

comments that appear in the preamble to the final rule or to address comments not discussed in 

the preamble to the final rule. Although portions of the preamble to the final rule are 

paraphrased in this document where useful to add clarity to responses, the preamble itself 

remains the definitive statement of the rationale for the revisions to the standards adopted in the 

final rule. 

 In many instances, particular responses presented in this document include cross 

references to responses on related issues that are located either in the preamble to the O3 NAAQS 

final rule, or in this Response to Comments document. All issues on which the Administrator is 

taking final action in the O3 NAAQS final rule are addressed in the O3 NAAQS rulemaking 

record. Issues on which the Administrator is taking final action in the monitoring final rule are 

addressed in that rulemaking record. 

 Accordingly, this Response to Comments document, together with the preamble to the O3

NAAQS final rule and the information contained in the Criteria Document (EPA, 2006) and the 

Staff Paper (EPA, 2007), should be considered collectively as EPA’s response to all of the 

significant comments submitted on EPA’s 2007 O3 NAAQS proposed rule. This document 

incorporates directly or by reference the significant public comments addressed in the preamble 

to the O3 NAAQS final rule as well as other significant public comments that were submitted on 

the proposed rule. 

 Various commenters have referred to and discussed a number of “new” scientific studies 

on the health and welfare effects of O3 that had been published recently and therefore were not 
2

included in the Criteria Document.1

 EPA has provisionally considered any significant “new” 

studies, including those submitted during the public comment period. The purpose of this effort 

was to ensure that the Administrator was fully aware of the “new” science before making a final 

decision on whether to revise the current O3 NAAQS. EPA provisionally considered these 

studies to place their results in the context of the findings of the Criteria Document. EPA’s 

provisional consideration of “new” studies is included as an Appendix to this document and is 

referred to throughout this document with regard to specific comments related to “new” studies. 

EPA concludes that, taken in context, the “new” information and findings do not materially 

change any of the broad scientific conclusions regarding the health effects of O3 exposure made 

in the Criteria Document. 

 Consistent with the final decisions presented in the notice of final rulemaking, comments 

on the primary O3 standard are addressed in section II.A. Comments on the secondary O3 

standard are addressed below in section II.B. Comments on data handling procedures are 

addressed in II.C. Comments on monitoring related issues are addressed in section II.D. Section 

III includes responses to legal, administrative, procedural, or misplaced comments. 

II. RESPONSES TO SIGNIFICANT COMMENTS ON PROPOSED O3 STANDARDS 

A. Primary O3 Standards 

1. General Comments on Proposed Primary O3 standard 

 General comments based on relevant factors that either support or oppose any change to 

the current O3 primary standard are addressed in this section. The responses to these comments 

are also discussed in section II.B.2 of the preamble to the final rule. Specific comments on the 

proposed primary standard, including comments on the indicator, averaging time, form and level 

are addressed in sections II.C in the preamble to the final rule and discussed more fully below in 

section II.A.2. Specific comments about the health effects evidence and the results of the human 

exposure and health risk assessments are addressed in sections II.B.2 in the preamble to the final 

rule and discussed in sections II.A.3 through II.A.5 below. Incorporating responses contained in 

sections II.B of the preamble to the final rule, EPA provides the following responses to general 

comments related to the need to revise the O3 standard. 

a. Support for Revising the Current Standard 

 1

 For ease of reference, these studies will be referred to as “new” studies or “new” 

science, using quotation marks around the word new. Referring to studies that were published 

too recently to have been included in the 2004 Criteria Document as “new” studies is intended to 

clearly differentiate such studies from those that have been published since the last review and 

are included in the 2004 Criteria Document (these studies are sometimes referred to as new 

(without quotation marks) or more recent studies, to indicate that they were not included in the 

1996 Criteria Document and thus are newly available in this review. 
3

 Many public comments received on the proposal asserted that, based on the available 

scientific information, the current O3 standard is insufficient to protect public health with an 

adequate margin of safety and revisions to the standard are appropriate. Among those calling for 

revisions to the current standards are medical groups, including the American Thoracic Society 

(and other health organizations, including American Medical Association (AMA), American 

College of Chest Physicians (ACCP), American College of Preventive Medicine, American 

Association of Cardiovascular and Pulmonary Rehabilitation, American College of Occupational 

and Environmental Medicine, National Association for the Medical Direction of Respiratory 

Care) (ATS et al.), and the American Academy of Pediatrics (AAP), as well as medical doctors 

and academic researchers. Similar conclusions were also submitted in comments from many 

national, state, and local public health organizations, including, for example, the American Lung 

Association (and other environmental organizations, including Environmental Defense, Sierra 

Club, Earthjustice) (ALA et al.), the American Heart Association (and other health organizations, 

including, National Association of County and City Health Officials (NACCHO), American 

Lung Association, American Nurses Association (ANA), American Public Health Association 

(APHA), Physicians for Social Responsibility) (AHA et al.), and the American Nurses 

Association (ANA), as well as in letters to the Administrator from EPA’s Children’s Health 

Protection Advisory Committee (CHPAC) (Marty, 2007a, 2007b). Environmental groups also 

commented in support of revising the standard, including the Sierra Club, Environmental 

Defense, the Natural Resources Defense Council (NRDC), Earthjustice, and the US Public 

Interest Research Group (US PIRG). All of these medical, public health and environmental 

commenters stated that the current O3 standard needs to be revised and that an even more 

protective standard than proposed by EPA is needed to protect the health of sensitive population 

groups. Many individual commenters also expressed such views. 

 The majority of State and local air pollution control authorities who commented on the 

O3 standard supported revision of the current O3 standard, as did the National Tribal Air 

Association (NTAA). Environmental agencies that supported revising the standard include 

agencies from: Arkansas; California; Delaware; Iowa; Illinois; Michigan; North Carolina; New 

Mexico; New York; Oklahoma; Oregon; Pennsylvania; Utah; Wisconsin; and Washington, DC. 

State organizations, including the National Association of Clean Air Agencies (NACAA), 

Northeast States for Coordinated Air Use Management (NESCAUM), and the Ozone Transport 

Commission (OTC) urged that EPA revise the O3 standard. All of these commenters supported 

revisions to the current standard, with most supporting a standard consistent with CASAC’s 

recommendations. 

 

Comment: Many public comments received on the proposal asserted that the current O3

standard is insufficient to protect public health, especially the health of sensitive groups, 

with an adequate margin of safety and revisions to the standard are appropriate. For 

example, the ATS stated: 

We believe that the Administrator has correctly stated that, beyond any degree of 

scientific uncertainty, convincing and compelling evidence has demonstrated that 

exposure to ozone at levels below the current standard is responsible for 

measurable and significant adverse health effects, both in terms of morbidity and 

mortality. ........... The known respiratory, cardiac and perinatal effects of ozone 
4

pollution are each in their own right major public health issues. In combination 

they provide immediate, actionable information and require a meaningful public 

health policy response from the EPA. (ATS et al., pp. 1, 11) 

All of these commenters supported revisions to the current standard, with most 

supporting a standard consistent with CASAC’s recommendations. In general, the 

commenters noted above primarily based their views on the body of evidence assessed in 

the Criteria Document as articulated in sections II.A and II.C of the preamble to proposal, 

finding it to be stronger and more compelling than in the last review. Some specifically 

agreed with the weight of evidence approach taken by the Criteria Document. These 

commenters generally placed much weight on CASAC’s interpretation of the body of 

available evidence and the results of EPA’s exposure and risk assessments, both of which 

formed the basis for CASAC’s recommendation to revise the O3 standard to provide 

increased public health protection. 

These commenters also noted that in recent years, a broad scientific consensus has 

emerged that EPA's current air quality standards for ozone are not sufficient to protect 

public health, and that the levels and form must be greatly tightened. This consensus is 

evidenced by the strong unanimous comments of the CASAC, which was backed by the 

endorsement of over 100 leading independent air quality scientists, EPA's Children's 

Health Protection Advisory Committee, and many others. In the face of this strong 

scientific consensus, one commenter stated that it is untenable to cite "uncertainty" as a 

rationale for failing to propose tighter standards. [ALA et al., p. 15] 

Medical and public health commenters also expressed the view that EPA must not use 

uncertainty in the scientific evidence as justification for retaining the current O3 standard. 

For example, the ATS stated: 

We note with concern that throughout the standard setting process, senior EPA 

officials have take a very conservative approach to reviewing the scientific 

literature on the health effects of ozone. We find the science on the health effects 

of ozone to be robust and compelling. (ATS et al., p. 11) 

Response: EPA generally agrees with these commenters’ conclusion regarding the need 

to revise the O3 primary standard. The scientific evidence noted by these commenters 

was generally the same as that assessed in the Criteria Document and the Staff Paper, and 

EPA agrees that this evidence provides a basis for concluding that the current O3 standard 

is not sufficient to protect public health with an adequate margin of safety. However, for 

reasons discussed in section II.B of the preamble to the final rule and in sections II.A.2 

and II.A.3 below, EPA disagrees with aspects of these commenters’ views on the level of 

protection that is appropriate and supported by the available scientific information. The 

Administrator’s overall conclusions about the need for revisions to the primary O3

standard, which include consideration of these general comments, are presented in the 

response to comment (1) in section II.A.1.b below. 
5

b. Support for Retaining the Current Standard 

 Another group of commenters representing industry associations and businesses opposed 

revising the current primary O3 standard. These views were extensively presented in comments 

from the Utility Air Regulatory Group (UARG), representing a group of electric generating 

companies and organizations and several national trade associations, and in comments from 

other industry and business associations including, for example: Exxon Mobil Corporation; the 

Alliance of Automobile Manufacturers (AAM); the National Association of Manufacturers 

(NAM), and the American Petroleum Institute (API). The API sponsored a workshop at the 

University of Rochester in June 2007 to review the scientific information and health risk 

assessment considered by EPA during the review of the O3 NAAQS. Although the report 

(hereafter, “Rochester Report”) from this workshop does not offer judgments on the specific 

elements of the current or proposed standard, it has been cited in a number of public comments 

that opposed revision of the current 8-hour standard. The Annapolis Center for Science-Based 

Public Policy issued a report (hereafter, “Annapolis Center”) on the science and health effects of 

O3, which explicitly opposed revising the current O3 primary standard. Several State 

environmental agencies also opposed revising the current O3 primary standard, including 

agencies from: Georgia; Indiana; Kentucky; Louisiana; Nevada; and Texas. 

 As discussed more fully below in sections dealing with specific comments, these and 

other commenters in this group generally mentioned many of the same studies that were cited by 

the commenters noted above who supported revising the standard, as well as other studies, but 

highlighted different aspects of these studies in reaching 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. 

Comment: These commenters generally expressed the view that the current standard 

provides the requisite degree of public health protection. In so doing, they considered 

whether the evidence that has become available since the last review has established a 

more certain risk or a risk of effects that are significantly different in character to those 

that provided a basis for the current standard, or whether the evidence demonstrates that 

the risk to public health upon attainment of the current standard would be greater than 

was understood when EPA established the current standard in 1997. 

In supporting their view that the present primary O3 standard continues to provide the 

requisite public health protection and should not be revised, UARG and others generally 

stated that: 

• the effects of concern have not changed significantly since 1997 

• the uncertainties in the underlying health science are as great or greater than in 

 1997 

• the estimated risk upon attainment of the current O3 standard has decreased since 

 1997 

• “new” studies not included in the Criteria Document continue to increase 

 uncertainty about possible health risks associated with exposure to O3. 
6

Response: As noted in the response to comment (1) in section II.A.1.a above, EPA, 

believes, contrary to the view fo the commenters, that the available information provides 

a basis for concluding that the current O3 standard does not protect public health with an 

adequate margin of safety. EPA has responded to the specific points noted above as well 

as additional specific issues raised by those contending that the current 8-hour primary 

standard should not be revised in sections II.A.3 through II.A.5 below and in the 

Appendix to this document. 

More generally, the rationale for EPA’s position regarding the need for revision of the 

current primary O3 standard is necessarily based upon consideration of all the comments, 

including the specific comments that are presented in sections II.A.3 through II.A.5. The 

Administrator’s overall conclusions about the need for revisions to the primary O3

standard, which include consideration of these general comments, are presented below.

Having carefully considered all of the public comments related to the need for revision of 

the current O3 primary standard, the Administrator believes the fundamental scientific 

conclusions on the effects of O3 reached in the Criteria Document and Staff Paper, briefly 

summarized below in section II.A.2 and discussed more fully in section II.A of the 

proposal, remain valid. In considering whether the primary O3 standard should be 

revised, the Administrator places primary consideration on the body of scientific 

evidence available in this review on the health effects associated with O3 exposure, as 

summarized in section II.B.1 of the preamble to the final rule,. The Administrator notes 

that there is much new evidence that has become available since the last review, 

including an especially large number of new epidemiological studies. The Administrator 

believes that this body of scientific evidence is very robust, recognizing that it includes 

large numbers of various types of studies, including toxicological studies, controlled 

human exposure studies, field panel studies, and community epidemiological studies, that 

provide consistent and coherent evidence of an array of O3-related respiratory morbidity 

effects and possibly cardiovascular-related morbidity as well as total nonaccidental and 

cardiorespiratory mortality. The Administrator observes that (1) the evidence of a range 

of respiratory-related morbidity effects seen in the last review has been considerably 

strengthened, both through toxicological and controlled human exposure studies as well 

as through many new panel and epidemiological studies; (2) newly available evidence 

from controlled human exposure and epidemiological studies identifies people with 

asthma as an important susceptible population for which estimates of respiratory effects 

in the general population likely underestimate the magnitude or importance of these 

effects; (3) newly available evidence about mechanisms of toxicity more completely 

explains the biological plausibility of O3-induced respiratory effects and is beginning to 

suggest mechanisms that may link O3 exposure to cardiovascular effects; and (4) there is 

now relatively strong evidence for associations between O3 and total nonaccidental and 

cardiopulmonary mortality, even after adjustment for the influence of season and PM. 

The Administrator believes that this very robust body of evidence, taken together, 

enhances our understanding of O3-related effects relative to what was known at the time 

of the last review. Further, he believes that the available evidence provides increased 

confidence that respiratory morbidity effects such as lung function decrements and 

respiratory symptoms are causally related to O3 exposures, that indicators of respiratory 
7

morbidity such as emergency department visits and hospital admissions are causally 

related to O3 exposures, and that the evidence is highly suggestive that O3 exposures 

during the warm O3 season contribute to premature mortality. 

Further, the Administrator judges that there is important new evidence demonstrating that 

exposures to O3 at levels below the level of the current standard are associated with a 

broad array of adverse health effects. This is especially true in at-risk populations that 

include people with asthma or other lung diseases, who are likely to experience more 

serious effects from exposure to O3, children, and older adults with increased 

susceptibility, as well as those who are likely to be vulnerable as a result of spending a lot 

of time outdoors engaged in physical activity, especially active children and outdoor 

workers. The Administrator notes that this important new evidence demonstrates O3-

induced lung function effects and respiratory symptoms in some healthy individuals 

down to the previously observed exposure level of 0.080 ppm, as well as very limited 

new evidence at exposure levels well below the level of the current standard. In addition, 

the Administrator notes that (1) there is now epidemiological evidence of statistically 

significant O3-related associations with lung function and respiratory symptom effects, 

respiratory-related emergency department visits and hospital admissions, and increased 

mortality, in areas that likely would have met the current standard; (2) there are also 

many epidemiological studies done in areas that likely would not have met the current 

standard but which nonetheless report statistically significant associations that generally 

extend down to ambient O3 concentrations that are below the level of the current 

standard; (3) there are a few studies that have examined subsets of data that include only 

days with ambient O3 concentrations below the level of the current standard, or below 

even much lower O3 concentrations, and continue to report statistically significant 

associations with respiratory morbidity outcomes and mortality; and (4) the evidence 

from controlled human exposure studies, together with animal toxicological studies, 

provides considerable support for the biological plausibility of the respiratory morbidity 

associations observed in the epidemiological studies and for concluding that the 

associations extend below the level of the current standard. 

Based on the available evidence, the Administrator agrees with the CASAC Panel and the 

majority of public commenters that the current standard is not requisite to protect public 

health with an adequate margin of safety because it is does not provide sufficient 

protection and that revision of the current O3 standard is needed to provide increased 

public health protection. The Administrator notes that extensive critical review of this 

body of evidence and related uncertainties during the criteria and standard review 

process, including review by the CASAC Panel and the public of the basis for EPA’s 

proposed decision to revise the primary O3 standard, has identified a number of issues 

about which different reviewers disagree and for which additional research is warranted. 

Nonetheless, on balance, the Administrator believes that the remaining uncertainties in 

the available evidence do not diminish confidence in the causal relationships between O3

exposures and indicators of serious respiratory morbidity effects, or the highly suggestive 

evidence of associations between O3 exposures and premature mortality, nor do they 

diminish confidence in the conclusion that the associations extend below the level of the 

current standard. 
8

Beyond a primary consideration of the available evidence, the Administrator has also 

taken into consideration the Agency’s exposure and risk assessments to help inform his 

evaluation of the adequacy of the current standard. As at the time of proposal, the 

Administrator believes the results of those assessments inform his judgment on the 

adequacy of the current standard to protect against health effects of concern. In 

considering the exposure analysis results at this time, the Administrator recognizes that 

there is a risk of confusion in the term “exposure of concern” that was used at the time of 

proposal, as it could be read to imply a determination that a certain benchmark level of 

exposure has been shown to be causally associated with adverse health effects. As a 

consequence, the Administrator believes that it is more appropriate to consider such 

exposure estimates in the context of a continuum rather than focusing on any one discrete 

benchmark level, as was done at the time of proposal, since the Administrator does not 

believe that the underlying scientific evidence is certain enough to support a focus on any 

bright-line benchmark level. In so doing, the Administrator recognizes that associations 

between O3 exposures and health effects of concern become increasingly uncertain at 

lower O3 exposure levels. Thus, the Administrator has taken into consideration the 

pattern of such exposure estimates across the range of discrete benchmark levels 

considered in EPA’s exposure assessment to provide some indication of the potential 

magnitude of the incidence of health outcomes that could not be evaluated in the 

Agency’s quantitative risk assessment but which have been demonstrated to occur in 

healthy people at O3 exposures as low as 0.080 ppm, the lowest level at which such 

health outcomes have been tested.2

More specifically, the Administrator has considered the pattern of reductions in such 

exposures across the benchmark levels of 0.080, 0.070, and 0.060 ppm, which span the 

level at which there is strong evidence of effects in healthy people down to a level at 

which the Administrator judges the evidence of effects to be very limited. The 

Administrator observes that based on the aggregated exposure estimates for the 2002 

simulation for the 12 urban areas included in the exposure analysis, upon just meeting the 

current standard, the percentages of asthmatic or all school age children likely to 

experience one of more exposures at and above these benchmark levels of 0.080, 0.070, 

and 0.060 ppm (while at moderate or greater exertion) are approximately 4%, 20%, and 

45%, respectively. As noted at the time of proposal, the Administrator recognizes that 

there is substantial year-to-year and city-to-city variability in these estimates and that it is 

important to recognize this variability in considering these estimates. For example, for 

the 0.080, 0.070, and 0.060 ppm benchmark levels, these percentages are estimated to 

range from approximately 1 to 10%, 1 to 40%, and 7 to 65%, respectively, across each of 

 2

 As noted above, such health outcomes include increased airway responsiveness, 

increased pulmonary inflammation, increased cellular permeability, and decreased pulmonary 

defense mechanisms, which have been associated with aggravation of asthma, increased 

medication use, increased school and work absences, increased susceptibility to respiratory 

infection, increased visits to doctors’ offices and emergency departments, increased admissions 

to hospitals, and possibly to cardiovascular system effects and chronic effects such as chronic 

bronchitis or long-term damage to the lungs that can lead to reduced quality of life.
9

the 12 urban areas based on the 2002 simulation, and from approximately 0 to 1%, 0 to 

7%, and 1 to 25%, respectively, based on the 2004 simulation. 

 

With regard to the results of the risk assessment, the Administrator again considered the 

risks estimated to remain upon just meeting the current standard. The Administrator 

takes note of the estimated magnitudes of such risks, which are presented in section 

II.B.1.c of the preamble to the final rule for a range of health effects including moderate 

and large lung function decrements (including percentages of children and number of 

occurrences), respiratory symptom days, respiratory-related hospital admissions, and 

nonaccidental and cardiorespiratory mortality, as well as year-to-year and city-to-city 

variability, and the uncertainties in these estimates. Further, the Administrator recognizes 

that these estimated risks for the specific health effects that could be analyzed in the 

Agency’s risk assessment are indicative of a much broader array of O3-related health 

endpoints that are part of a “pyramid of effects” that include various indicators of 

morbidity that could not be included in the risk assessment (e.g., school absences, 

increased medication use, emergency department visits) and which primarily affect 

members of at-risk groups. 

 

In considering these quantitative exposure and risk estimates, as well as the broader array 

of O3-related health endpoints that could not be quantified, the Administrator believes 

that they are important from a public health perspective and indicative of potential 

exposures and risks to at-risk groups. The Administrator thus finds that the exposure and 

risk estimates provide additional support to the evidence-based conclusion, reached 

above, that the current standard needs to be revised. Based on these considerations, and 

consistent with CASAC Panel’s unanimous conclusion that there is no scientific 

justification for retaining the current standard, the Administrator concludes that the 

current primary O3 standard is not sufficient and thus not requisite to protect public health 

with an adequate margin of safety, and that revision is needed to provide increased public 

health protection. It is important to note that this conclusion, and the reasoning on which 

it is based, do not address the question of what specific revisions are appropriate. That 

requires looking specifically at the current indicator, averaging time, form, and level of 

the O3 standard, and evaluating the evidence relevant to determining whether and to what 

extent any of these elements should be revised. Comments on the proposed elements of 

the primary standard are addressed below in section II.A.2. 

2. Specific Comments on Proposed Primary O3 Standards 

a. Averaging Time 

 The EPA received limited public comments on the issue of averaging time for the O3

primary standard. In addition to the discussion contained in section II.C.2 of the preamble to the 

final rule, EPA provides the following response to a specific issue related to the averaging time 

for O3. 

Comment: A few comments specifically supported keeping only the 8-hour averaging 

time. However, there were other comments in support of setting a separate 1-hour 
10

standard along with am 8-hour standard to better protect against peak exposures 

(California EPA, ALA et al.). 

Response: EPA has conducted extensive air quality analyses to determine the extent to 

which meeting the 8-hour standard provides protection from 1-hour and longer-term 

ambient air concentrations of O3. It was concluded from these analyses that adequate 

protection from both 1-hour and longer-term ambient O3 concentrations would be 

provided in areas meeting the 8-hour primary standard. 

 

b. Form of the Standard 

The EPA received a limited number of public comments on the appropriate form for the 

O3 standard. Incorporating responses contained in sections II.C.3 of the preamble to the final 

rule, EPA provides the following responses to specific comments related to the form of the 8-

hour O3 standard. 

(1) Comment: Some public commenters that expressed the view that the current primary O3

standard is not adequate also submitted comments that supported a more healthprotective form of the standard than the current form (e.g., a second- or third-highest 

daily maximum form)(e.g., ALA et al.). Most commenters who expressed the view that 

the current standard should not be revised did not provide any views on alternative forms 

that would be appropriate for consideration should the Administrator consider revisions 

to the standard. A few industry association and business commenters supported changing 

to a 5th highest form (e.g., Dow Chemical, AAM). One commenter (Oklahoma 

Department of Transportation) suggested the use of a 6th or 7th highest daily maximum 

form.

Response: There is not a clear health-based threshold for selecting a particular nthhighest daily maximum form of the standard from among the ones analyzed in the Staff 

Paper, recognizing that the 4th-highest daily maximum, 8-hour average concentration 

form of the standard provides a stable target for implementing programs to improve air 

quality. The principal advantage of the concentration-based form is that it is more directly 

related to the ambient O3 concentrations that are associated with the health effects. With 

a concentration-based form, days on which higher O3 concentrations occur would weigh 

proportionally more than days with lower concentrations, since the actual concentrations 

are used in determining whether the standard is attained. That is, given that there is a 

continuum of effects associated with exposures to varying levels of O3, the extent to 

which public health is affected by exposure to ambient O3 is related to the actual 

magnitude of the O3 concentration, not just whether the concentration is above a specified 

level. EPA also believes that the adequacy of the public health protection provided by 

the combination of the level and form is a foremost consideration. Based on this, EPA 

detemined that the form of the current standard, 4th-highest daily maximum 8-hour 

average concentration, averaged over 3 years, should be retained, recognizing that the 

public health protection that would be provided by this standard is based on combining 
11

this form with the increased health protection provided by the lower level of the standard 

discussed in the section below. 

 

(2) Comment: While the CASAC Panel unanimously supported specifying the level of the 

standard to a three decimal places (i.e., ppb) degree of precision, public comments were 

mixed. Environmental organizations (e.g., ALA et al.) and some State/regional agencies 

(e.g., NESCAUM, PA Department of Environmental Protection) supported the proposed 

increased precision but did not support truncating to the third decimal. However, several 

industry associations (e.g., API, EMA, AAM) suggested that there is not sufficient 

evidence to modify the 1997 decision to round to two decimal places.

Response: EPA concludes that the level of the standard should be specified to the 

thousandth ppm (three decimal places), based on the staff’s analysis and conclusions 

discussed in the Staff Paper that current monitoring technology allows accurate 

measurement of O3 to support specifying the 8-hour standard to this degree of precision, 

and on the CASAC Panel’s reasoning and recommendation with respect to this aspect of 

the standard. A discussion of the issue of truncating vs. rounding can be found in section 

II.C.1 of this Response to Comments document. 

c. Level 

 A large number of comments on the proposed range of levels for the primary O3 standard 

basically expressed one of two substantively different views: (1) support for a more health 

protective standard at or below the range of levels proposed by EPA or (2) opposition to any 

modification of the current O3 standard. Many of these commenters simply expressed their 

views without stating any rationale, while others gave general reasons for their views but without 

reference to the factual evidence or rationale presented in the proposal notice as a basis for the 

Agency’s proposed decision regarding the level of the primary O3 standard. 

With regard to the evaluation and consideration of the health effects evidence and how 

such information should be considered in the decision on the standard level, EPA notes that the 

commenters fell into the same two groups discussed in section II.B.2 of the preamble to the final 

rule. The two groups often cited the same studies and evidence, but they reached sharply 

divergent conclusions as to what standard level is supported by the health effects evidence. The 

general views of both groups on the interpretation and use of the health effects evidence are 

presented in section II.B.2.a of the preamble, with most comments from one group arguing that 

this evidence supports a decision to revise the 8-hour standard to 0.060 ppm or below, and the 

other group arguing that it supports a decision not to revise the current 8-hour standard. 

A number of commenters, including many States and Tribes, who supported selecting a 

standard in the range 0.060 to 0.070 ppm generally placed great weight on the recommendation 

of CASAC. Section II.C.4 of the preamble to the final rule presents the Agency’s response to 

these very general views. In addition to the discussion contained in that section, EPA provides 

the following responses to specific issues related to the level for the primary O3 standard. The 

first section below addresses comments on health evidence considerations, and the next section 
12

addresses comments on exposure and risk considerations related to consideration of the level for 

the primary standard. Additional specific comments on the exposure analysis and health risk 

assessment are included in sections II.A.4 and II.A.5 below. 

i. Comments on Health Evidence Considerations 

(1) Comment: With regard to the evidence from controlled human exposure studies, 

commenters that included public health and environmental groups who supported 

revising the current standard expressed the view that the large body of evidence available 

at the time of the last review, demonstrating an array of adverse health effects (i.e., 

reduced lung function, respiratory symptoms, increased airway responsiveness, 

inflammation, and increased susceptibility to respiratory infection), at concentrations of 

0.080 ppm O3, indicated that the standard should have been set at a lower level. These 

commenters noted that standards must be set below the level shown to cause effects in 

healthy subjects in order to protect sensitive populations with an adequate margin of 

safety. As discussed in section II.B.2.a above, these commenters focused on the results 

of the Adams studies (2002, 2006) as evidence that exposure to 0.060 ppm O3 will result 

in a significant proportion (i.e., 7%) of the adult population who do not have asthma or 

other lung diseases experiencing notable lung function decrements (FEV1 decrement ≥

10%), and furthermore that larger decrements in FEV1 would be expected in more 

susceptible populations. This evidence caused these commenters to reject EPA’s 

proposed range: 

Clearly, EPA’s proposed standard of 0.070 to 0.075 ppm cannot be considered 

protective of public health in light of experimental evidence demonstrating 

adverse respiratory effects in healthy individuals exposed to 0.060 ppm, and the 

legal requirements to protect sensitive populations with an adequate margin of 

safety. (ALA et al., p. 51) 

 The second group of commenters, who opposed revision of the standard, expressed the 

view that the group mean changes reported in the Adams studies (2002, 2006) were 

small, that such decrements should not be considered to be adverse, and that the 

individuals who experienced larger responses were too few to serve as a basis for a 

revised O3 standard. This group included virtually all commenters representing industry 

associations and businesses. These general comments are also addressed in section 

II.B.2.a in the preamble to the final rule. 

Response: In considering comments received on controlled human exposure studies, and 

how these studies support a focus on particular standard levels, the Administrator 

observes that in general the comments support his original view that these studies provide 

the most certain evidence of adverse health effects, and that the large bulk of evidence 

derives from studies of exposures at levels of 0.080 ppm and above. The Administrator 

notes that since the last review important new evidence includes demonstration of O3-

induced lung function effects and respiratory symptoms in some healthy adults down to 

the previously observed exposure level of 0.080 ppm, as well as very limited new 

evidence of the same effects at exposure levels well below the level of the current 
13

standard (Adams, 2002, 2006). Based on careful consideration of the comments, the 

Administrator again concludes that while the Adams studies provide evidence that some 

healthy individuals will experience lung function decrements and respiratory symptoms 

at the 0.060 ppm exposure level, this evidence is too limited to support a primary focus at 

this level. Moreover, the Administrator notes that while the CASAC panel supported a 

level of 0.060 ppm, they also supported a level above 0.060, indicating that they disagree 

with the commenters view that the results of Adams studies mean that the level of the 

standard has to be set at 0.060 ppm. 

(2) Comment: With regard to the information from epidemiological studies, commenters 

representing public health, environmental, and medical organizations generally asserted 

that the large body of new epidemiological studies provides evidence of causal 

associations between O3 exposures and a wide array of respiratory and cardiovascular 

morbidity effects, including emergency department visits and hospital admissions. They 

expressed the view that a significant body of strong, consistent evidence links short-term 

exposures to premature mortality and noted that this evidence is supported by new 

research that provides biological plausibility for such effects. These commenters noted 

that various approaches, including air quality assessments which show that statistically 

significant associations occurred in areas that likely would have met the current standard, 

or statistical approaches that examined subsets of the data which indicate that statistically 

significant associations remain down to very low ambient O3 levels, show effects well 

below the level of the current standard. Moreover they identified particular studies, 

including some “new” studies not considered in the Criteria Document, that indicated 

there are additional sub-populations that are likely to be sensitive to O3, including infants, 

women, and African-Americans, that should be considered in deciding the requisite level 

of protection. They asserted that this information supports a standard set at a level no 

higher than 0.060 ppm O3. 

 With regard to the information from epidemiological studies, the second group of 

commenters focused strongly on EPA’s interpretation of the epidemiological evidence 

and the uncertainties they saw in this evidence as a basis for concluding that no change to 

the current level of the 8-hour O3 standard is warranted. In commenting on the proposed 

range of levels, these commenters generally relied on the same arguments presented 

above in section II.A.1.b as to why they believed it would be inappropriate for EPA to 

make any revisions to the primary O3 standard. That is, they asserted that the health 

effects of concern associated with short-term or prolonged exposures to O3 have not 

changed significantly since 1997; that the inconsistencies and uncertainties inherent in 

these studies as a whole should preclude any reliance on them as justification for a more 

stringent standard; and that “new” science not included in the Criteria Document 

continues to increase uncertainty about possible health risks associated with exposure to 

O3. Specific methodological issues cited as additional support for their conclusions 

included: adequacy of exposure data; potential confounding by copollutants; model 

selection; inconsistent evidence relating O3 exposure to mortality, and “new” studies that 

provide additional evidence of inconsistencies. These general comments are also 

addressed in section II.B.2.a of the preamble to the final rule. 
14

 Response: In considering these comments on the epidemiological evidence with regard 

to the interpretation of the epidemiological evidence and methodological issues, the 

Administrator notes that in general, most of the issues and concerns raised by those who 

do not support any revisions to the primary O3 standard with regard to the interpretation 

of the epidemiological evidence and methodological issues, are essentially restatements if 

issues raised during the review of the Criteria Document and Staff Paper. The same is 

true of the views of commenters who supported a level of the standard no higher than 

0.060 ppm O3. EPA presented and the CASAC Panel reviewed the interpretation of the 

epidemiological evidence in the Criteria Document and the integration of the evidence 

with policy considerations in the development of the policy options presented in the Staff 

Paper for consideration by the Administrator. CASAC reviewed the scientific content of 

both the Criteria Document and Staff Paper and advised the Administrator that these 

documents provided an appropriate basis for use in regulatory decision making. 

Therefore, these comments do not provide a basis for the Administrator to reach 

fundamentally different conclusions than he reached at the time of proposal. 

 Moreover, the Administrator notes that epidemiological evidence is most appropriately 

evaluated in the context of all available evidence, including evidence from controlled 

human exposure and toxicological studies. The Administrator agrees with the weight of 

evidence approach used in the Criteria Document and believes that this body of scientific 

evidence is very robust, recognizing that it includes a large number of various types of 

studies that provide consistent and coherent evidence of an array of O3-related respiratory 

morbidity effects and possibly cardiovascular-related morbidity as well as total 

nonaccidental and cardiorespiratory mortality. Therefore, the Administrator judges that 

the body of epidemiological evidence indicating associations with a wide range of serious 

health effects, including respiratory emergency department visits and hospital admissions 

and premature mortality, at and below 0.080 ppm supports revising the current standard 

to protect public health. While the great majority of evidence concerning effects below 

0.080 ppm was from epidemiological studies, the epidemiological studies do not identify 

any bright-line threshold level for effects. At the same time, the epidemiological studies 

are not themselves direct evidence of a causal link between exposure to O3 and the 

occurrence of the effects. Therefore, Administrator has considered these studies in the 

context of all the other available evidence in evaluating the degree of certainty that O3-

related adverse health effects would occur at various ambient levels below 0.080 ppm. In 

that context, there is only quite limited evidence from controlled human exposure studies 

at exposure levels below 0.080 ppm O3. The Administrator recognizes that in the body of 

epidemiological evidence, many studies reported positive and statistically significant 

associations, while others reported positive results that were not statistically significant, 

and a few did not report any positive O3-related associations. In addition, the 

Administrator judged that evidence of a causal relationship between adverse health 

outcomes and O3 exposures became increasingly uncertain at lower levels of exposure. 

Based on this the Administrator continues to believe that the body of epidemiological 

evidence does not support setting a standard as low as 0.060 as suggested by some 

commenters. 
15

 The Administrator also notes the many epidemiological studies done in areas that likely 

would not have met the current standard but which nonetheless report statistically 

significant associations that generally extend down to ambient O3 concentrations that 

were below the level of the current standard. Further, there were a few studies that have 

examined subsets of data that include only days with ambient O3 concentrations below 

the level of the current standard, or below even much lower O3 concentrations, and 

continued to report statistically significant associations with respiratory morbidity 

outcomes and mortality. In the context of the strong clinical evidence of adverse effect in 

healthy adults at 0.080, the Administrator finds that the body of epidemiological evidence 

does not support retaining a standard of 0.08, as suggested by commenters. 

(3) Comment: Both groups of commenters also considered evidence from controlled human 

exposure and epidemiological studies of increased susceptibility in people with lung 

disease, especially people with asthma, but they reached sharply divergent conclusions 

about what standard level is supported by this evidence. As discussed above in section 

II.B.2.a, medical organizations and public health and environmental groups agreed with 

EPA that, based on evidence from controlled human exposure and epidemiological 

studies, people with asthma, especially children, are likely to have greater lung function 

decrements and respiratory symptoms in response to O3 exposure than people who do not 

have asthma, and are likely to respond at lower levels. Furthermore, these commenters 

noted that epidemiological studies have identified other potentially sensitive 

subpopulations, including for example, infants, women and African-Americans, and that 

effects in these groups should be part of the consideration in providing an adequate 

margin of safety. These commenters concluded that the appropriate level for the primary 

O3 standard is 0.060 ppm, to provide protection for members of sensitive groups, 

especially people with asthma, who are likely to have more serious responses and to 

respond at lower levels that healthy people. They also contend that a standard set at this 

level also would provide protection against anticipated, but as yet unproven effects in the 

additional groups cited. 

 Response: The Administrator agrees with these commenters that important new evidence 

shows that asthmatics have more serious responses, and are more likely to respond at 

lower O3 levels, than healthy individuals. Moreover, he agrees that this evidence 

supports a standard set at a level below 0.080 ppm O3, based on the strong evidence from 

human clinical studies in healthy adults at this level. However, for the reasons described 

in preamble to the final rule and in the response to comment number (2) above, he does 

not agree that the controlled human exposure and epidemiological evidence provide 

support for a standard set at 0.060 ppm. 

(4) Comment: Industry association and business commenters asserted that EPA is wrong to 

claim that new evidence indicates that the current standard does not provide adequate 

health public health protection for people with asthma. In support of this position, these 

commenters made the following major comments: (1) the lung function decrements and 

respiratory symptoms observed in clinical studies of asthmatics are not clinically 

important; (2) EPA postulates that asthmatics would likely experience more serious 

responses and responses at lower levels than the subjects of controlled human exposure 
16

experiments, but that hypothesis is not supported by scientific evidence; and, (3) EPA 

recognized asthmatics as a sensitive subpopulation in 1997, and new information does 

not suggest greater susceptibility than was previously believed. 

 Response: EPA has specifically responded to these comments in the response to 

comment (2) in section II.3.c below. After careful consideration of these comments and 

based on the response given below, the Administrator continues to judge that there is 

important new evidence demonstrating that exposures to O3 at levels below the level of 

the current standard are associated with a broad array of adverse health effects, especially 

in at-risk populations that include people with asthma or other lung diseases who are 

likely to experience more serious effects from exposure to O3, as well as children and 

older adults with increased susceptibility, and those who are likely to be vulnerable as a 

result of spending a lot of time outdoors engaged in physical activity, especially active 

children and outdoor workers. 

ii. Comments on Exposure and Risk Considerations 

(1) Comment: With regard to considering how the quantitative exposure and health risk 

assessments should factor into a decision on the standard level, EPA notes that the 

comments generally fell into two groups that reached sharply divergent conclusions as to 

what standard level is supported by these assessments. The general views of both groups 

on the implications of the exposure and risk assessment are presented in the preamble to 

the final rule (section II.B.2.b), with one group arguing that it supports a decision to 

revise the 8-hour standard to 0.060 ppm or below, and the other group arguing that it 

supports a decision not to revise the current 8-hour standard. 

A joint set of comments from ALA and several environmental groups expressed the view 

that EPA cannot use exposures of concern to justify a standard in the range of 0.070 to 

0.075 ppm. These commenters contend that standards in the proposed range would 

continue to expose too many asthmatic children, as well as other at risk groups such as 

outdoor workers and preschool children, to “demonstrably unhealthy levels of ozone 

pollution” in only 12 cities which does not represent a national estimate (ALA et al., p. 

106). These same commenters asserted that if EPA were to consider exposures of 

concern, then the benchmark level must be defined as 0.060 ppm based on the 

considerable evidence of adverse health effects occurring at this level. They also cited 

various reasons why the exposure estimates were underestimated, including: only 12 

cities were included in the assessment, various at risk groups including outdoor workers 

and preschool children were not included in the assessment, and EPA’s exposure 

assessment underestimated exposures since it considers average children, not active 

children who spend more time outdoors and repeated exposures also were 

underestimated. 

In contrast, industry association and business group commenters expressed the view that 

the concept of exposures of concern should not be considered as a basis for revising the 

level of the standard because it provided no indication of the probability that individuals 

would actually experience an adverse health effect. These same commenters also 
17

provided various reasons why the exposure estimates were overestimated based on 

specific methodological choices made by EPA including, for example, O3 measurements 

at fixed-site monitors can be higher than other locations where individuals are exposed, 

the exposure estimates do not account for O3 avoidance behaviors, and the exposure 

model overestimates elevated breathing rates. Finally, these commenters also contend 

that the estimates of exposures of concern associated with just meeting the current 

standard, using the 0.080 ppm benchmark levels, have not appreciably changed since the 

prior review and, thus provide no support for revising the current standard. 

Response: EPA has responded below to the criticisms from both groups of commenters 

related to concerns that the exposure estimates are either underestimated or overestimated 

in sections II.A.4 and II.A.5 of this document. EPA also has addressed the issues raised 

by both groups of commenters concerning the appropriateness of considering exposures 

at and above various benchmark levels as an element in the decision on the level of the 

standard in the preamble to the final rule (section II.C.4) and in the response to comment 

(2) below. 

(2) Comment: Environmental and public health group comments expressed the view that if 

exposures of concern were considered, then the Administrator should focus only on the 

0.060 ppm benchmark based on the contention that adverse health effects had been 

demonstrated down to this level. These commenters generally argued that significant 

exposure reductions could be achieved by setting the standard level at 0.060 ppm or 

lower. In contrast, other commenters, primarily industry and business groups focused on 

comparisons of the exposures of concern at the 0.080 ppm benchmark level based on 

their view that there was no convincing evidence demonstrating adverse health effects at 

levels below this benchmark. 

Response: In view of the comments received related to the definition and use of the term 

“exposure of concern” at the time of proposal, the Administrator recognizes that that 

there is a risk of confusion, as it could be read to imply a determination that a certain 

benchmark level of exposure has been shown to be causally associated with adverse 

health effects. As a consequence, the Administrator believes that it is more appropriate to 

consider such exposure estimates in the context of a continuum rather than focusing on 

any one discrete benchmark level, as was done at the time of proposal, since the 

Administrator does not believe that the underlying scientific evidence is certain enough to 

support a focus on any single bright-line benchmark level. Thus, the Administrator 

believes it is appropriate to consider a range of benchmark levels from 0.080 down to 

0.060 ppm, recognizing that concentrations at and above specified benchmark levels 

while at elevated exertion must be considered in the context of a continuum of the 

potential for health effects of concern, and their severity, with increasing uncertainty 

associated with the likelihood of such effects at lower O3 exposure levels. 

EPA recognizes that the 0.080 ppm benchmark level represents a level at which several 

health outcomes including lung inflammation, increased airway responsiveness, and 

decreased resistance to infection have been shown to occur in health adults. The 

Administrator places relatively great weight on the public health significance of 
18

exposures exceeding this benchmark level given the greater certainty that these adverse 

health responses are likely to be observed in a significant fraction of the at-risk 

population. With respect to his decision on the level of the 8-hour standard, the 

Administrator notes that upon just meeting a standard within the range of 0.070 to 0.075 

ppm based on the 2002 simulation, the number of school age asthmatic children likely to 

experience exposures at and above the 0.080 ppm benchmark level in aggregate (for the 

12 cities in the assessment) is estimated to range from 0.1 to 0.4 percent of asthmatic 

school age children. Based on the 2004 simulation, the estimates are even lower, with no 

asthmatic children estimated to experience exposures at and above the 0.080 ppm 

benchmark level. Similar patterns are observed for all school age children. Recognizing 

the uncertainties inherent in the exposure assessment, the Administrator concludes that 

the exposure assessment suggests that exposures at and above the 0.080 ppm level, where 

several health effects have been shown to occur in healthy individuals, are eliminated or 

nearly eliminated depending on the modeling year. 

However, the Administrator does not agree with those commenters who would only 

consider this single benchmark level. While the Administrator places less weight on 

exposures exceeding the 0.070 pm benchmark level, given the increased uncertainty 

about the fraction of the population and severity of the health responses that might occur 

associated with exposures above this level, he believes that it is appropriate to consider 

exposures at this benchmark as well in judging what level will protect public health with 

an adequate margin of safety. Consideration of the 0.070 ppm benchmark level 

recognizes that the effects observed at 0.080 ppm were in healthy adult subjects and 

sensitive population groups, such as asthmatics, are expected to respond at lower O3

levels than healthy individuals. The Administrator notes that upon just meeting a 

standard within the range of 0.070 to 0.075 ppm based on the 2002 simulation, the 

number of asthmatic school age children likely to experience exposures at and above the 

0.070 ppm benchmark level in aggregate (for the 12 cities in the assessment) is estimated 

to range from about 2 to 5 percent of asthmatic school age children. Based on the 2004 

simulation, the estimates are substantially lower, with 0 to 0.6 percent of asthmatic 

children estimated to experience exposures at and above the 0.070 ppm benchmark level. 

The Administrator considered but placed very little weight on exposures at and above the 

0.060 ppm benchmark given the very limited scientific evidence supporting a conclusion 

that O3 is causally related to various health outcomes at this exposure level. 

Considering the uncertainties associated with the exposure assessment, the Administrator 

concludes that the exposure estimates associated with each of the benchmark levels are 

not appreciably different, between a 0.070 or 0.075 ppm standard, and therefore, the 

exposure assessment does not provide a clear enough basis for choosing a specific level 

within the proposed range. 

(3) Comment: With regard to considering how the quantitative risk assessment should factor 

into a decision on the standard level, both groups of commenters generally considered the 

risk assessment in their comments on the standard level, but they reached sharply 
19

divergent conclusions as to what standard level is supported by the risk assessment. 

More specifically, the environmental, public health, most medical organizations, and 

some State and regional air pollution agencies (e.g., California, NESCAUM) contend that 

EPA’s proposed range of 0.070 to 0.075 ppm would result in significant residual public 

health risks. As articulated most fully in the joint set of comments from ALA and several 

environmental organizations, these commenters expressed the view that EPA’s risk 

assessment clearly demonstrates that a more stringent 8-hour O3 standard of 0.065 ppm, 

the most stringent standard analyzed by EPA, would significantly decrease O3-related 

lung function decrements, respiratory symptoms, hospital admissions, and mortality and 

that “EPA must adopt a more stringent ozone standard of 0.060 ppm or below – a level 

that incorporates a more adequate margin of safety” (ALA et al., p. 108). These same 

commenters also cited various reasons for asserting that the risk assessment likely 

underestimates health risks to a substantial degree, including the limited nature of the 

assessment with respect to number of cities, populations covered, and health endpoints 

analyzed. 

Response: EPA has responded to the comments concerning the scope of the risk 

assessment and assertion that health risks are likely underestimated both in the preamble 

to the final rule (section II.B.2.b) and in more detail in section II.A.5 of this document. 

While the Administrator places less weight on the results of the risk assessment, he notes 

that the results indicate that a standard set within the proposed range would likely reduce 

risks to at-risk groups from the O3-related health effects considered in the assessment, 

and by inference across the much broader array of O3-related health effects that can only 

be considered qualitatively, relative to the level of protection afforded by the current 

standard. Moreover, he notes that the results of the assessment suggest a gradual 

reduction in risks with no clear breakpoint as increasingly lower standard levels are 

considered. However, in light of the important uncertainties inherent in the assessment 

discussed above and in the proposal, the Administrator concludes that the risk assessment 

does not provide a basis for choosing a level within the proposed 0.075 to 0.070 ppm 

range. 

(4) Comment: Industry association and business group commenters who supported not 

revising the level of the current 8-hour standard generally asserted the following points: 

(1) that risk estimates have not changed significantly since the prior review in 1997; (2) 

that uncertainties and limitations underlying the risk assessments make them too 

speculative to be used in supporting a decision to revise the standard; (3) that EPA should 

have defined PRB differently and that EPA underestimated PRB levels which results in 

health risk reductions associated with more stringent standards being overestimated; and 

(4) that health risks are overestimated based on specific methodological choices made by 

EPA including, for example, selection of inappropriate effect estimates from health effect 

studies, EPA’s approach to addressing the shape of exposure-response relationships, and 

whether or not to incorporate thresholds into its models for the various health effects 

analyzed. 
20

Response: EPA has responded to the comments concerning the scope of the risk 

assessment and assertion that health risks are likely underestimated both in the preamble 

to the final rule (section II.B.2.b) and in more detail in section II.A.5 of this document. 

3. Specific Comments on the Interpretation of Scientific Evidence 

 More specific comments on the EPA’s interetation of the scientific evidence and EPA's 

responses are discussed below. The summary of comments and responses follows the discussion 

of these topics in the preamble to the final rule. The first section below contains comments on 

evidence from controlled human exposure studies (preamble section II.B.2.a.i); the second 

section below contains comments on evidence from epidemiological studies, including 

interpretation of the evidence and specific methodological issues (preamble section II.B.2.a.ii); 

the third section below contains comments on evidence pertaining to at-risk subgroups for O3-

related effects (preamble section II.B.2.a.iii). A fourth section contains comments on the 

adversity of health effects, a topic that was discussed generally in the preamble and also as part 

of some responses to comments on at-risk subgroups for O3-related effects and the fifth section 

below contains comments on the role of ground-level O3 in solar radiation-related health effects. 

 EPA notes here that most of the issues and concerns raised by commenters concerning 

the health effects evidence, including both the interpretation of the evidence and specific 

technical or methodological issues, were essentially restatements of issues raised during the 

review of the Criteria Document and the Staff Paper. Most of these issues were highlighted and 

thoroughly discussed during the review of these documents by the CASAC. Incorporating 

responses contained in section II.B.2.a of the preamble to the final rule, EPA provides the 

following responses to specific issues related to the need to revise the O3 standard. 

a. Evidence from Controlled Human Exposure Studies 

(1) Comment: NAM contended that EPA did not disclose critical studies and analyses 

(NAM, p. 17). This commenter stated that a noticeable instance of bias is EPA’s failure 

to disclose at least one critical collection of information within its control: its reanalysis 

of the data obtained by Adams (2006a). NAM contends that this reanalysis (Brown 2007, 

"Brown Memorandum") is a crucial element of Agency staff policy recommendations 

and that EPA did not disclose enough information to make it reproducible. NAM 

contends that it reaches conclusions opposite of the researcher, such that it is equivalent 

to a new study inserted into the record in a discriminatory fashion. 

Response: EPA has disclosed all critical studies and analyses. As an initial matter, the 

Brown Memorandum is not a crucial element of the staff’s policy recommendations, as it 

was prepared after completion of the Staff Paper, or the Administrator’s final decision. 

The Brown Memorandum represents a logical progression in the interpretation of a study, 

not published until 2006, that was included in the final Criteria Document in February 

2006. In Chapter 8 of the Criteria Document, it was noted that the FEV1 responses 

during exposure to 0.06 ppm ozone appeared to diverge away from the responses of 
21

filtered air and 0.04 ppm ozone after about 5.6 hr. Subsequently, in the Staff Paper, it 

was noted that a statistically significant difference in FEV1 responses was suggested by a 

lack of overlap in the standard error of the responses following 6.6 hours of exposure to 

0.06 ppm ozone versus filtered air. That interpretation of the data was supported by 

CASAC review. In late February 2007, public comments were submitted by a Dr. 

Richard Smith. In his comments, he provided a table comparing changes in FEV1

following all of the six exposure protocols utilized by Adams (2006) and the data for 0.04 

ppm O3 (corrected for filtered air responses) from Adams (2002). His table specifically 

indicated that the FEV1 responses, in the Adams (2006) study, following the two 0.06 

ppm O3 exposures were statistically different from the FEV1 responses following filtered 

air exposures using a paired t test. The Brown Memorandum presents these same 

comparisons. The table provided in the Brown Memorandum discloses all information 

necessary to reproduce the standard statistical paired t test which was utilized. Thus, it 

was a public commenter that first placed the analysis of FEV1 responses following 

exposure to 0.06 ppm O3 versus filtered air in the public rulemaking docket. In short, the 

Brown Memorandum confirms Dr. Smith’s analyses, frames the analysis in terms of the 

analysis performed by Dr. Adams versus prior O3 studies, and discusses the biological 

significance of FEV1 responses. 

(2) Comment: NAM also contends that the Brown Memorandum itself exemplifies multiple 

types of violations of the information quality standard of objectivity (pp. 18-19). First, 

NAM contends that it is a post hoc statistical analysis conducted on data whose initial 

analysis did not support the declared policy preferences of Agency staff. Second, NAM 

contends that it was prompted by a low-quality analytic review (“visual comparison” and 

“cursory evaluation,” p. 3). Ioannidis (2005) shows that positive results are usually false 

even when researchers exercise normal restraint with respect to Type I error (rejecting the 

no-effect hypothesis when in fact it is true). NAM also contends that EPA has included 

or excluded data or studies based on the extent to which they support stated or unstated 

risk management objectives (NAM, p. 19). In the proposal notice, NAM contends that 

EPA acknowledges implicitly that Agency staff used the Adams data for purposes that 

were never intended by the study design. It is reported that two of the 30 healthy adult 

subjects experienced exercise-adjusted FEV1 decrements exceeding 10% at 0.060 ppm 

using one of the two exposure patterns examined (but not the other) (72 FR 37828, n. 16). 

It is inappropriate to obtain a sample, subject its members to a well designed test, learn 

that the sample does not yield hoped-for outcome, and in response, abandon the sample in 

favor of focusing on selected individuals within it. Federal information quality 

guidelines require transparency. When, as in this case, the disclosed portion of 

information shows the hallmarks of purposeful bias, the only responsible default 

inference is that the reanalysis does not meet applicable information quality standards. 

Unless EPA can show otherwise, the reanalysis should not be disseminated and the 

Brown Memorandum should be withdrawn. 

Response: EPA rejects NAM’s contention that the Brown Memorandum exemplifies any 

violation of the information quality standard of objectivity. The API, which funded the 

Adams (2006) study, asked that the data from that study be included in the EPA risk 

assessment. Dr. Adams then provided his data to the EPA. Thus, the funding 
22

organization and the author provided their data for the express purpose that it be included 

in EPA’s analyses. Reporting that two of 30 subjects in the Adams (2006) study 

experienced exercise-adjusted FEV1 decrements exceeding 10% at 0.060 ppm is merely a 

statement of fact by EPA. Adams (2002) reported that 6 of 30 subjects exposed to 0.06 

ppm had greater than a 10% decrement in FEV1. API has refused to provide Dr. Adams 

technical report describing that data. In the reference cited by NAM, Ioannidis (2005) 

notes “... that true research findings may occasionally be annulled because of reverse 

bias. For example, with large measurement errors relationships are lost in noise [12], or 

investigators use data inefficiently or fail to notice statistically significant relationships, 

or there may be conflicts of interest that tend to “bury” significant findings [13].” 

The Brown Memorandum confirms analyses completed by Dr. Smith who was funded by 

API to perform his analyses and to provide comments to CASAC. In the Brown 

Memorandum EPA used the same statistical approach as used by Dr. Smith. In both Dr. 

Brown’s and Dr. Smith’s analyses a standard statistical test was used which is appropriate 

for the type of comparison made. EPA rejects NAM’s contention that this approach has 

the “peculiar quality of dramatically increasing Type I error.” Thus, EPA has not 

included or excluded data that has a stated policy purpose. 

 

The Brown Memorandum objectively describes the FEV1 responses following exposure 

to 0.06 ppm ozone relative to filtered air in terms of both statistical and biological 

significance. The Brown Memorandum discusses relevant public and CASAC 

comments. The table provided in the Brown Memorandum discloses all information 

necessary to reproduce the standard statistical paired t test which was utilized. In EPA’s 

judgment, its weight-of-the-evidence approach looks at all of the available evidence and 

the Brown Memorandum is transparent and without purposeful bias. 

(3) Comment: NAM contends that EPA draws inferences from a study that are not supported 

by the data and analysis reported (NAM, p. 27). Five clinical studies have been 

performed since the last review, but only three involved exposures below the current 

standard level (Adams 2002, 2003b, 2006a). EPA’s interpretation of Adams’ work 

diverges, and is inconsistent with, that of the author (Adams 2007). Adams reports no 

statistically significant effects from O3 at 0.040 ppm, but EPA finds them in its 

reanalysis. This poses special information quality issues. EPA’s interpretation of Adams’ 

work does not enjoy a rebuttable presumption of objectivity. Moreover, to utilize 

Adams’ work in contrary ways, the Agency must first rebut the presumption of 

objectivity that attaches to these studies. Furthermore, EPA’s reanalysis of Adams’ data 

in the final Staff Paper and Brown Memorandum is neither transparent nor capable of 

being substantially reproduced. This is an essential prerequisite for adherence to the 

objectivity standard and inconsistent with EPA’s information quality guidelines. 

Response: EPA did not draw inferences that were not supported by the data and the 

reported analysis as NAM contends. The Adams (2007) teleconference comments to 

CASAC concerned the description of his 2006 publication in the Staff Paper. CASAC 

heard Dr. Adams comments and did not object to the discussion of the Adams (2006) 
23

publication in the Staff Paper. With regard to the effects of O3 at 0.040 ppm, NAM is 

incorrect. Neither the Adams (2006) publication nor EPA describe statistically 

significant effects of exposure to 0.04 ppm O3 on lung function. As already discussed, 

the table provided in the Brown Memorandum discloses all information necessary to 

reproduce the standard statistical paired t test which was utilized. 

(4) Comment: NAM also contends (NAM, p. 29) that EPA’s analysis of clinical data on 

cardiac effects is problematic with respect to information quality standards. In the 

proposed rule, NAM contends that EPA emphasizes the increase in AaPO2 and interprets 

it as evidence that O3 exposure “result[s] in an overall increase in myocardial work and 

impairment in pulmonary gas exchange” (72 FR 38734). EPA says nothing about the 

relevance of the exposure level, which was 0.3 ppm -- 3.75 times greater than the current 

NAAQS, or the uncertainties implied by extrapolating to the population clinical data 

obtained from a sample of 16. 

Response: proposal notice. The quote provided by NAM, which appeared in the Staff 

Paper and proposal notice was based on the conclusion of Dr. Henry Gong stated in the 

original article. Dr. Gong was a physician and first author of the study in question. The 

details of his study were provided in Chapter 6 and Annex 6 of the Criteria Document. 

Furthermore, in the paragraph to which NAM has referred (72 FR 38734), the EPA 

specifically states, "Since then, a very limited body of evidence from animal, controlled 

human exposure and epidemiologic studies has emerged that provides evidence for some 

potential plausible mechanisms for how O3 exposures might exert cardiovascular system 

effects, however much needs to be done to substantiate these potential mechanisms” 

(emphasis added). Absent evidence to the contrary, there is no reason to believe that 

there would be a threshold O3 concentration for such effects. Additionally, the Gong et 

al. (1998) study was ethically restricted to patients with mild hypertension and could not 

examine these effects in individuals more severely affected by cardiovascular disease. 

EPA explicitly stated that mechanistic data was limited and needed to be substantiated. 

In that context, no further discussion of limitations or extrapolations was warranted 

(5) Comment: Some commenters cited the discussion of the controlled human exposure 

studies in the Rochester Report as supporting their views that the current standard should 

be retained. The following passages from the Rochester Report summarize the points 

made in that report: 

Adams (2006a), seeking differences in patterns of response among the different 

exposures, utilized a Scheffe post hoc test for controlling study-wide level of 

alpha while making multiple comparisons among the many data points. This test 

(which is not particularly powerful for detecting specific differences in the 

context of large numbers of comparisons) did not identify the response of the 0.06 

ppm exposure as statistically different from that of the FA exposure. However, 

alternative statistical tests suggest that the observed small group mean response in 

FEV1 induced by exposure to 0.06 ppm compared to FA is not the result of 

chance alone. The mean difference in the FEV1 decrements between the two 

exposures at 6.6 hours was approximately 2.9% which was statistically different 
24

(p<0.001) from zero when tested using a t-statistic without correction for multiple 

comparisons. 

 Further examination of the post-exposure FEV data and mean data at other time 

points and concentrations also suggest a pattern of response at 0.06 ppm that is 

consistent with a dose-response rather than random variability. For example, the 

response at 5.6 hours was similar to that of the post-exposure 6.6 hour response 

and appeared to also differ from the FA response. The volunteers in this study 

did not appear to be more responsive to ozone than volunteers in previous studies 

as the observed response at 0.08 ppm in this study was similar to that of previous 

studies. Although of much smaller magnitude, the temporal pattern of the 0.06 

ppm response was generally consistent with the temporal patterns of response to 

higher concentrations of ozone in this and other studies. Responses below 0.08 

ppm ozone have not previously been observed, but this finding is not totally 

unexpected because the previously observed FEV responses to 0.08 ppm were in 

the range of 6-9% suggesting that exposure to lower concentrations of ozone 

would result in smaller, but real FEV decrements. The EPA re-analysis and reinterpretation of the studies of Adams has been questioned by Adams (2007) and 

by Smith (2007) in presentations to the Clean Air Scientific Advisory Committee. 

Thus, the public health significance of responses at 0.06 ppm ozone is still being 

debated. The Panel recognizes that uncertainty necessarily surrounds a secondary 

analysis and the integration of results from a single study in one laboratory with 

0.06 ozone exposures and results obtained in studies at higher concentrations by 

other investigators. Resolution of this uncertainty will require that further 

research be conducted to clarify the issue. (Rochester Report, pp. 56-57) 

Response: The EPA generally agrees with the Rochester Report’s evaluation of the 

Adams (2006) study and the interpretation of the EPA’s secondary analysis of the data. 

EPA agrees that there is a small group mean response in FEV1 induced by exposure to 

0.060 ppm ozone compared to FA and that the observed response is not the result of 

chance alone. Furthermore, EPA agrees that the pattern of response at 0.060 ppm ozone 

is consistent with a dose-response curve rather than random variability. Given that the 

0.060 ozone exposures and results have not been replicated, some uncertainty exists and 

EPA agrees that further research is needed to clarify the issue. 

(6) Comment: One commenter submitted a statistical analysis and evaluation (Exxon 

Mobil) of the Adams (2006) study and data by Dr. Nicolich. Dr. Nicolich reached four 

conclusions from his analysis: 

1) Based on the additional statistical analyses detailed in this report, we have shown that 

the basic results of Adams (2006) ozone chamber study were replicated. 

2) Based on analyses of the response pattern over the 6.6 hours of experimentation, the 

only percent changes in FEV1 responses that are statistically significantly different from 

the first period fresh air exposures were the 0.08 ppm triangle exposure at hours 4.6, 5.6 

and 6.6 hours and the 0.08 ppm square wave exposure at 6.6 hours. 

3) The analysis of only the 6.6 hour readings indicated the 0.08 ppm square wave and 

0.08 ppm triangle wave exposures were different from the fresh air exposure. 
25

4) The magnitude of the estimated changes for all individuals in all exposure groups are 

less than the 15 percent decrement considered to be of clinicall significance by the 

American Thoracic Society. 

Response: Dr. Nicolich conducted a statistical reanalysis of the Adams (2006) data. To 

correct for the multiple comparisons, the significance level was adjusted by the Dunnett’s 

test which “is not as conservative as Scheffé’s test or as extreme as individual t-tests.” It 

should be recognized that Dr. Nicolich ran multiple comparisons and had to correct for 

these multiple comparisons in order to avoid type 1 error (falsely rejecting the null 

hypothesis when there is no effect). Thus, the probability of type 2 error (falsely 

accepting the null hypothesis when a real effect exists) was increased just as in the case 

of Dr. Adams’ analysis. Furthermore, Dr. Nicolich did not provide estimates of the 

power of his statistical analysis to detect an effect. Therefore, the lack of being able to 

find a statistically significant effect at 0.060 ppm ozone does not mean that no effect 

exists. On page A-3, Dr. Nicolich states “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.” Later on page A-5, Dr. 

Nicolich states that his “results are essentially correct, but the significance levels may not 

be exactly correct.” Regarding the analysis of responses at 6.6 hours, Dr. Nicolich again 

stated that the “significance levels may not be exact because of the failure to meet the 

normality assumption.” Therefore, given that the underlying statistical assumptions 

required for his analysis were not met and that significance levels are questionable, in 

EPA’s judgment the analyses presented by Dr. Nicolich are ambiguous. 

On page A-5 of his comments, Dr. Nicolich states that “The model predicted response for 

individuals in Figure 3 shows that none of the predicted points shows more than about a 6 

percent decrement and the lower confidence intervals (not shown) are all greater than 10 

percent and, therefore, do not include the 15 percent decrement considered to be of 

clinical significance by the ATS (Wang and Petsonk 2004).” On inspection of the Adams 

(2006) data for the 0.080 ppm exposures, a greater than 15% ozone-induced decrement in 

FEV1 is seen in 2 individuals for the square-wave exposure protocol and in 3 individuals 

for the triangular exposure protocol. It is unclear why Dr. Nicolich would utilize a 

statistical model that violates basic statistical assumptions to support his assertion. The 

commenter does not accurately characterize the cited ATS guidelines on the magnitude of 

lung function (FEV1) change. The cited guidelines were not defining the magnitude of 

lung function (FEV1) change that can be considered to be clinically adverse. The cited 

guidelines were established to help determine whether a change in lung function, between 

two tests made a year or more apart, is “real” or only the result of test variability (ATS 

1991). The guideline goes on to note that all lung function measurements tend to be 

more variable when made weeks to months apart than when repeated at the same test 

session or even daily. EPA’s discussion of adversity in the Staff Paper, NPRM, preamble 

to the final rule and this Response to Comments document appropriately characterizes the 

ATS adversity guidelines (ATS, 2000). Therefore, Dr. Nicolich’s comment regarding 

clinical significance of FEV1 responses in the Adams (2006) study is without merit. 
26

(7) Comment: Dr. Adams in his October 2007 comments states that the FEV1 response in 

healthy young adults to 6.6 h exposure to 0.060 ppm O3 in his study (Adams, 2006a) do 

not demonstrate a significant mean effect by ordinarily acceptable statistical analysis and 

then references the analysis of Dr. Mark Nicolich in support of this assertion. He 

considers the response to be in somewhat of a gray area, both in terms of a biologically 

meaningful response and a statistically significant response. Further, he feels that more 

studies of human pulmonary function (and measurements of related physiological 

mechanisms) should be conducted in prolonged 0.060 ppm O3 exposures as soon as 

possible. 

Response: Both Dr. Adams and Dr. Nicolich ran multiple comparisons which increases 

probability of type 2 error (falsely accepting the null hypothesis when a true effect exists) 

when evaluating the simple issue of whether post-exposure lung function was decreased 

in subjects exposed to 0.060 ppm ozone versus filtered air in the Adams (2006) study. 

The two-factor analysis of variance and Scheffé method cited by Adams (2006) assumes 

that data are normally distributed and that variances are equal within cells. From 

previous studies of higher O3 exposures, we know that FEV1 responses become skewed 

and variance increases (McDonnell 1996). This increase in variance is clearly apparent 

in the Adams (2006) data with the standard deviation of FEV1 responses increasing from 

2.98% for filtered air to 4.24% for exposures at 0.060 ppm O3 to 8.65% for exposures at 

0.080 ppm. Dr. Nicolich’s analysis also found that the underlying statistical assumptions 

of data normality required for Dr. Adams’ analysis were violated. Thus, it is very 

possible that the wide range in variances among the cells could have resulted in wider 

confidence levels and inaccuracies of the reported p-values for a subset of the 

comparisons. Dr. Nicolich even stated that “significance levels may not be exact because 

of the failure to meet the normality assumption.” Therefore, as addressed in response to 

Dr. Nicolich’s comments, not finding a statistically significant effect at 0.06 ppm ozone 

does not mean that no effect exist. 

Dr. Adams contends that, “it appears that paired t tests were applied to my data without 

an initial ANOVA to examine whether there was statistical significance in pre- versus 

post-exposure FEV1 response across multiple exposure conditions. If this were done, it 

would necessitate a post-hoc correction of the paired t test results that might or might not 

result in the statistical significance for the FEV1 response reported in the memorandum. 

Statistical texts (e.g., Neter et al., 1996) routinely recommend that ANOVA is preferable 

because the t-test is too extreme (non-conservative)” (Adams, 2007, p. 2). Dr. Adams is 

not accurate with regard to the analysis presented in the Brown Memorandum. The 

effects of other exposure protocols (0.040 and 0.080 ppm) were not considered. The goal 

of the memorandum was to address whether there was a pre- to postexposure change in 

the lung function of individuals exposed to 0.060 ppm ozone versus filtered air. A 

repeated measures ANOVA of the change in FEV1 following exposure to 0.060 ppm 

ozone versus filtered air provides the same result as the paired t test which was utilized in 

the Brown Memorandum, i.e., a relatively small but statistically significant decrease in 

group mean FEV1 responses following 6.6 h of exposure to 0.060 ppm ozone compared 

to filtered air. Dr. Adams’ comments (page 2) regarding the magnitude of lung function 

decrements due to exposure to 0.080 ppm versus 0.060 ppm ozone or other ozone 
27

exposure protocols are not relevant other than to establish that a trend in responses exists. 

Therefore, there was no need for an initial repeated measures ANOVA of all the exposure 

protocols in the Adams (2006) study to discern if ozone effected post-exposure lung 

function at 0.060 ppm versus filtered air. 

As presented in the Brown Memorandum, paired t test were conducted for the two 0.060 

ppm exposure protocols versus filtered air responses. The reported two-tailed 

significance levels were 0.009 and 0.001 for the triangular and square-wave exposure 

protocols, respectively. Dr. Adams contends (Adams, 2007, p. 3) that “no correction for 

post hoc application is used (which would result in their increase by 5 times)” and 

thereby lead to a critical p-value of 0.01 (i.e., 0.05/5). However, it should be noted that in 

actuality, only two comparisons were made in the Brown Memorandum. Clearly, the 

significance levels reported in the Brown Memorandum which were <0.01 should remain 

statistically significant following any reasonable multiple comparison correction. Dr. 

Adams also generally objected to the use of a t test for evaluating the significance of 

results from his study. However, Dr. Richard Smith (a statistician at the University of 

North Carolina) also utilized t tests to evaluate the statistical significance of the Adams 

data in his public comments to CASAC (March 5, 2007). Therefore, we conclude that 

ordinarily acceptable statistical analyses such as presented in the Brown Memorandum 

show that exposure to 0.060 ppm O3 causes a relatively small but statistically significant 

decrease in group mean FEV1 responses compared to filtered air. 

Dr. Adams agrees in his October 2007 comments (p. 3) that pre- to postexposure 

responses may be an acceptable means of evaluating effects on lung function for the 

square-wave exposure protocols. He does not, however, consider it appropriate for 

analysis of triangular exposure protocols. Dr. Adams’ concern arises because during 

triangular exposures to 0.080 and 0.120 ppm ozone, subjects have been observed to 

experience their maximal pulmonary function decrements at one to two hours before the 

end of the exposure. Hence, by examining only pre- to postexposure pulmonary function 

changes, the maximal effects would be missed. However, as noted by Dr. Adams 

(Adams, 2007, p. 2) “no such tendency is apparent for FEV1 response with time in the 

two 0.06 ppm exposures in Fig. 1 of the memorandum. Rather, there is a nonsignificantly greater drop from 4.6 h to 5.6 h for the 0.06 ppm square-wave exposure than 

for the 0.06 ppm triangular exposure.” Therefore, for the 0.060 ppm ozone protocols, it 

appears that the use of pre- to postexposure responses are an acceptable means of 

evaluating effects on lung function for the square-wave and triangular exposure 

protocols. 

 Dr. Adams did correctly note, contrary to what is stated in the Brown Memorandum, that 

Horstman et al. (1995) used an ANOVA for a split-plot design to test the hypothesis that 

pre- minus post-exposure differences in FEV1 for the air and O3 exposures were the same 

for a group of asthmatics as for a group of nonasthmatics. The t tests were used in the 

Horstman et al. (1995) study to evaluate the differences between an aerosol test of small 

airways function, not FEV1, between the asthmatics and nonasthmatics. 
28

Overall, there appears to be general agreement among Dr. Adams, the Rochester Report, 

and the EPA that the effects on pulmonary function at 0.060 ppm O3 appear to be 

consistent with the trend in FEV1 responses observed for exposures ranging from to 0.04 

ppm to 0.08 ppm O3 and that further studies below 0.08 ppm are warranted. 

b. Evidence from Epidemiological Studies 

 This section contains comments on EPA’s assessment of epidemiological studies in the 

proposal and the Agency’s general responses to those comments. Comments on EPA’s 

interpretation and assessment of the body of epidemiological evidence are discussed first and 

then comments on methodological issues and particular study designs are discussed. EPA notes 

here that most of the issues and concerns raised by commenters on the interpretation of the 

epidemiological evidence and methodological issues are essentially restatements of issues raised 

during the review of the Criteria Document and Staff Paper. EPA presented and the CASAC 

Panel reviewed the interpretation of the epidemiological evidence in the Criteria Document and 

the integration of the evidence with policy considerations in the development of the policy 

options presented in the Staff Paper for consideration by the Administrator. CASAC reviewed 

both the Criteria Document and Staff Paper and approved of the scientific content and accuracy 

of both documents. The CASAC chairman sent to the Administrator one letter (Henderson, 

2006a) for the Criteria Document and another letter for the Staff Paper (Henderson, 2006c) 

indicating that these documents provided an appropriate basis for use in regulatory decision 

making regarding the O3 NAAQS. 

 As with evidence from controlled human exposure studies, comments on the evidence 

from epidemiological studies, including EPA’s interpretation of the evidence, were highly 

polarized. One group of commenters from medical, public health and environmental 

organizations, in general, supported EPA’s interpretation of the epidemiological evidence (72 FR 

37838, sections II.a.3.a-c) with regard to whether the evidence for associations is consistent and 

coherent and whether there is biological plausibility for judging whether exposure to O3 is 

causally related to respiratory and cardiovascular morbidity and mortality effects. 

(1) Comment: Comments of public health and environmental groups, including a joint set of 

comments from ALA and several environmental groups (ALA et al.), note that more than 

250 new epidemiological studies, published from 1996 to 2005, were included in the 

Criteria Document and point to a figure from the Staff Paper and proposal (72 FR 37842, 

Figure 1) of short-term O3 exposures and respiratory health outcome showing consistency 

in an array of positive effects estimates and health endpoints observed in multiple 

locations in Canada and the U.S. 

 Medical commenters, including ATS and AMA, stated that these “real world” studies 

support the findings of chamber studies to show adverse respiratory health effects at 

levels below the current 8-hour O3 standard. These commenters generally expressed 

agreement with the weight of evidence approach taken by the Criteria Document and the 

conclusions reached, which were reviewed by CASAC, that the effects of O3 on 

respiratory symptoms, lung function changes, emergency department visits for 

respiratory and cardiovascular effects, and hospital admissions can be considered causal. 
29

 However, in contrast with EPA, these commenters assert that the causal associations 

extend down to the lowest ambient O3 concentrations reported in these studies. These 

commenters also expressed the view that the respiratory and cardiovascular system 

effects are well-supported by the Hill criteria3 of judging causality: strength of 

association, consistency between studies, coherence among studies, and biological 

plausibility (ALA et al., pp. 51-52). Medical commenters, including ATS and AMA, 

state that these “real world” studies support the findings of chamber studies to show 

adverse respiratory health effects at levels below the current 8-hour O3 standard. They 

also note that recent studies provide compelling evidence that exposure to O3 results in 

adverse cardiovascular health effects (ATS, pp. 6-7). 

Response: EPA generally agrees with this interpretation of the epidemiological evidence. 

The Criteria Document concludes that positive and robust associations were found 

between ambient O3 concentrations and various respiratory disease hospitalization 

outcomes and emergency department visits for asthma, when focusing particularly on 

results of warm-season analyses. These positive and robust associations are supported by 

the human clinical, animal toxicological, and epidemiological evidence for lung function 

decrements, increased respiratory symptoms, airway inflammation, and increased airway 

responsiveness. Taken together, the overall evidence supports a causal relationship 

between acute ambient O3 exposures and increased respiratory morbidity outcomes 

resulting in increased emergency department visits and hospitalizations during the warm 

season (Criteria Document, p. 8-77). 

 However, EPA disagrees with the assertion of these commenters that the causal 

associations extend down to the low ambient O3 concentrations reported in these studies. 

The biological plausibility of the epidemiological associations is generally supported by 

controlled human exposure and toxicological evidence of respiratory morbidity effects 

for levels at and below 0.080 ppm, but that biological plausibility becomes increasingly 

uncertain especially below 0.060 ppm, the lowest level at which effects were observed in 

controlled human exposure studies. Further, at lower levels, it becomes increasingly 

uncertain as to whether the reported associations are related to O3 alone rather than to the 

broader mix of air pollutants present in the ambient air. EPA notes that the multi-city 

times series studies evaluated in this review do not resolve this issue. It also becomes 

increasingly uncertain as to whether effect thresholds exist but can not be clearly 

discerned by statistical analyses. Thus, when considering the epidemiological evidence 

in light of the other available information, it is reasonable to judge that at some point the 

epidemiological associations can not be interpreted with confidence as providing 

evidence that the observed health effects can be attributed to O3 alone. For a fuller 

discussion of EPA’s approach to making judgments about causal relationships see 

response to comment 6 below. 

 

3 The Hill criteria, published by Sir Bradford Hill (1965), are commonly used criteria for 

reaching judgments about causality from observed associations, and these criteria were the basis 

for the critical assessment of the epidemiological evidence presented in the Criteria Document 

(pp. 7-3 – 7-4). 
30

 With regard to cardiovascular health outcomes, the Criteria Document concludes that the 

generally limited body of evidence from animal toxicology, human controlled exposure, 

and epidemiologic studies is suggestive that O3 can directly and/or indirectly contribute 

to cardiovascular-related morbidity, and that for cardiovascular mortality the Criteria 

Document suggests that effects estimates are more consistently positive and statistically 

significant in warm season analyses but that additional research is needed to more fully 

establish the underlying mechanisms by which such mortality effects occur (EPA, 2006a, 

pp. 8-77-78). 

 The second group of commenters, mostly representing industry associations and some 

businesses opposed to revising the primary O3 standard, disagreed with EPA’s interpretation of 

the epidemiological evidence. 

(2) Comment: These commenters expressed the view that while many new epidemiological 

studies have been published since the current primary O3 standard was promulgated, the 

inconsistencies and uncertainties inherent in these studies as a whole should preclude any 

reliance on them as justification for a more stringent primary O3 NAAQS. They contend 

that the purported consistency is the result of inappropriate selectivity in focusing on 

specific studies and specific results within those studies (UARG, p. 15). With regard to 

daily mortality, the proposal emphasizes the multi-city studies, suggesting that they have 

the statistical power to allow the authors to reliably distinguish even weak relationships 

from the null hypothesis with statistical confidence. However, these commenters note 

that these studies are not consistent, with regard to the findings concerning individual 

cities analyzed in the multi-city analyses. One commenter asserted that each of the multicity studies and meta-analyses cited by EPA involves cities for which the city-specific 

estimates of O3 effects have been observed to vary over a wide range that includes 

negative [i.e., beneficial] effects (API, p. 15). To illustrate this point, many commenters 

point to EPA’s use of the study by Bell et al., 2004. They note that in focusing on the 

national estimate from Bell of the association between 24-hour average O3 levels and 

daily mortality, the Administrator overlooks the very significant and heterogeneous 

information of the individual analyses of the 95 cities used to produce the national 

estimate and, based on this inconsistency, question whether what is being seen is actually 

an O3 mortality association at all (UARG, p. 16). 

Response: EPA has accurately characterized the inconsistencies and uncertainties in the 

epidemiological evidence and strongly denies that it has inappropriately focused on 

specific positive studies or specific positive results within those studies. EPA’s 

assessment of the health effects evidence in the Criteria Document has been reviewed by 

the CASAC Panel. EPA has appropriately characterized the heterogeneity in O3 health 

effects in assessing the results of the single-city and multi-city studies and the metaanalyses, as discussed in section 7.6.6 of the Criteria Document In general, the 

Administrator recognizes that in the body of epidemiological evidence, many studies 

reported positive and statistically significant associations, while others reported positive 

results that were not statistically significant, and a few did not report any positive O3-

related associations. In addition, the Administrator judges that evidence of a causal 
31

relationship between adverse health outcomes and O3 exposures became increasingly 

uncertain at lower levels of exposure. 

 More specifically, the Bell et al. (2004) study observed a statistically significant, positive 

association between short-term O3 concentrations (24-hour average) and all-cause 

mortality using data from 95 U.S. National Morbidity, Mortality, and Air Pollution Study 

(NMMAPS) communities. The objective of the NMMAPS was to develop an overall 

national effect estimate using multi-city time-series analyses, by drawing on information 

from all of the individual cities. The strength of this approach is the use of a uniform 

analytic methodology, avoidance of selection bias, and larger statistical power. 

Significant intercity heterogeneity was noted in the Bell et al. and other multi-city 

studies, probably due to many factors, including city-specific differences in pollution 

characteristics, the use of air conditioning, time spent indoors versus outdoors, and 

socioeconomic factors. Levy et al. (2005) found suggestive evidence that air 

conditioning prevalence was a predictor of heterogeneity in O3 effect estimates in their 

meta-analysis. 

(3) Comment: NAM contends that EPA has not considered publication bias in the 

presentation of reported results (NAM, pp. 11-13). 

 Response: Nam’s contention is not true, since EPA recognized the potential impact of 

publication bias on the conclusions that may be drawn from a body of studies, as 

indicated in section 7.1.3.6 of the Criteria Document. NAM describes the theoretical 

basis for publication bias, but EPA was able to draw upon the findings of several studies 

that assessed the potential for publication bias for O3-related health effects studies. As 

described in section 7.4.4 of the Criteria Document, two meta-analyses investigating the 

association between short-term exposure to O3 and mortality also examined the evidence 

for publication bias in the available literature. Bell et al. (2005) concluded that the results 

provided strong evidence of an association between O3 and mortality that was not 

sensitive to adjustment for PM or for model specifications. However, they suggested that, 

based on comparisons between the meta-analysis results and NMMAPS results from 95 

U.S. communities (Bell et al., 2004), there was evidence of publication bias (1.75% [95% 

CI: 1.10, 2.37] per 20 ppb increase in 24-h avg O3 for meta-analysis versus 0.50% [95% 

CI: 0.24, 0.78] for NMMAPS 0-day lag results). Ito et al. (2005) also observed a 

statistically significant association between O3 and mortality that was generally robust to 

adjustment for PM. They found suggestive evidence of publication bias (a significant 

asymmetry in the funnel plot), but adjusting for the asymmetry reduced the combined 

estimate only slightly (from 1.6% [95% CI: 1.1, 2.0] to 1.4% [95% CI: 0.9, 1.9] per 20 

ppb increase in 24-h avg O3). The extent of potential bias implicated in this study 

differed compared to that reported by Bell et al. (2005). The source of this difference is 

not clear, but Ito et al. stated that sensitivity analyses comparing estimates from 

commonly used weather model specifications suggest that the stringent weather model 

used in NMMAPS may tend to yield smaller risk estimates than those used in other 

studies. 
32

NAM also contends that EPA should, for each critical study, determine the extent to 

which nonpositive outcomes were not reported and include that information in its 

presentation. EPA rejects NAM’s contention that it should determine the extent to which 

nonpositive outcomes were not reported and include that information in its presentation 

of each critical study. First, there is no evidence to show that researchers are not 

reporting all results. Second, EPA can not include in its assessment results that were not 

reported. Third, EPA uses a weight of evidence approach to evaluate evidence that does 

not depend on a few critical studies. 

 Specifically, NAM (p. 13) cites three studies of respiratory symptoms (Gent et al., 2003; 

Korrick et al., 1998; Mortimer et al., 2002) as example of studies that “report only the 

most statistically significant results.” This is clearly not the case, as Gent et al. (2003), 

for example, reported that while effects were observed in asthmatic children using 

maintenance medication, no effects were observed among asthmatics not using 

maintenance medication. In the Criteria Document, EPA recognized the post-hoc nature 

of the population stratification by medication use as one of the limitations of this study. 

 NAM contends that Gent et al. (2003) exaggerates their findings in their conclusions 

regarding the susceptibility of asthmatic children using maintenance medication. NAM 

states “Peak ozone exposures, which logically drive the results observed, exceeded 

current standards” (NAM, p. 13). However, there is no reason to believe that the peak O3

concentrations drive the findings of this study. The Mortimer et al. (2002) study 

observed that excluding days when 8-h avg O3 levels were greater than 80 ppb provided 

effect estimates that were similar to those when all days were included in the analysis, 

indicating that the negative effect of O3 on morning PEF were not driven by the peak O3

concentrations. 

 NAM also contends that Mortimer et al. (2002) selectively reported study results, by 

focusing on specific average lag periods for the various pollutants. However, as 

discussed in section 7.2.3.2 of the Criteria Document, Mortimer et al. examined the 

association between O3 and respiratory effects using single day lags from lag day 1 to lag 

day 6. Small morning effects were observed at 1- and 2-day lags. The effect of O3 on 

morning outcomes increased over several days. Examination of these single lag day 

effects led to the consideration of a multiday lag period of 1 to 5 days in the case of PEF 

and 1 to 4 days in the case of respiratory symptoms to estimate the cumulative effect of 

O3. The different multiday lag periods used for the various pollutants likely reflects the 

different relationship between the individual pollutant and the health effects. 

 NAM further states that the odds ratios in the Mortimer et al. (2002) study were “barely 

statistically significant” and it cannot be discerned whether any of these ratios would 

have retained statistical significance or declined in magnitude in a multipollutant model. 

In fact, Mortimer et al. does report multipollutant model results, as presented in section 

7.2.4 of the Criteria Document. The odds ratios for the incidence of symptoms per 30 

ppb increase in 8-h avg O3 were 1.23 (95% CI: 0.94, 1.61) with SO2 and 1.14 (95% CI: 

0.85, 1.59) with NO2. In the three urban areas with PM10 data, the odds ratios were 1.21 

(95% CI: 0.61, 2.40) in the O3-only model and 1.08 (95% CI: 0.41, 2.40) when PM10 also 
33

was included in the model. Though the O3 effect was shown to be slightly diminished 

and did not retain statistically significance in multipollutant models, there was 

considerable overlap in the 95% confidence intervals between the single-pollutant and 

multipollutant model results, leading EPA to conclude that the association was generally 

robust. 

 Finally, NAM contends that EPA did not recognize the fundamental data quality 

problems with self-reported respiratory testing found by Kamps et al. (2001). In section 

7.2.3 of the Criteria Document, EPA does in fact state that PEF measurements have been 

shown to be more variable than FEV1 in some studies (Vaughan et al., 1989; Cross and 

Nelson, 1991) and can have an element of uncertain reliability when self-administered by 

study subjects. However, Lippmann and Spektor (1998) state that PEF measurements 

from small inexpensive flow meters, which are more feasible to use in field studies, can 

produce similar results to PEF measured spirometrically. 

 In conclusion, EPA does not agree that reported associations between O3 and health 

effects are an artifact of publication bias. The EPA acknowledges that publication bias 

can result in potential overestimation of the estimated risk in a body of literature. 

However, for an individual study, factors such as exposure error or selection of results 

from an individual lag period from among several positive associations can result in 

underestimation of an effect estimate. 

(4) Comment: NAM contends that EPA inappropriately assumes confidence intervals 

adequately describe variability and uncertainty (NAM, p. 49). 

Response: EPA does not inappropriately assume that confidence intervals fully describe 

variability and uncertainty. As an initial matter, EPA notes that while statistical 

significance (i.e., confidence intervals) is considered in the evaluation of the scientific 

evidence, EPA has emphasized the importance of examining the pattern of results across 

various studies and not focusing solely on statistical significance as a criterion (discussed 

in further detail in response to comments below and in section II.A.2 of the preamble to 

the proposed decision). Second, the point that the uncertainty ranges reported in the risk 

assessment do not reflect all of the uncertainty in the risk estimates is explicitly discussed 

in the Staff Paper (section 5.3.2.5). 

 NAM contends that epidemiologists tend to use convenience samples and other nonrandom research designs, which result in reported confidence intervals representing “best 

case” conditions. EPA disagrees that most of the epidemiologic literature evaluated in 

the O3 Criteria Document is based on non-random research designs. Not all 

epidemiologic studies evaluated in the O3 Criteria Document use study populations that 

are generalizable to the entire population, but this does not mean that the study 

population was non-random. In fact, these epidemiologic studies tend to randomly select 

subjects into their study based on the study selection criteria. The study selection criteria 

would limit the generalizability of the study results, for example, results from a study of 

asthmatic children are likely not generalizable to healthy children or asthmatic adults, but 

this does not imply a lack of randomization. In time-series studies that use population-
34

level data, randomization is also not an issue as the available data on the entire population 

(or within certain age groups of the population) in the specified location are utilized. 

(5) Comment: Several commenters argued that EPA overstates the probability of causal 

links between health effects and exposure to O3, especially at the lower concentrations 

examined, and that the statistical associations found in the cited epidemiological studies 

do not automatically imply that a causal relationship exists. These commenters expressed 

the view that the correlation between health effects and O3 exposure must be rigorously 

evaluated according to a standard set of criteria before concluding that there is a causal 

link and that EPA fails to articulate and follow the weight of the evidence or established 

causality criteria for evaluating epidemiological studies in drawing conclusion regarding 

causality (Exxon Mobil, pp. 10-11). 

Response: In the proposal, EPA explicitly stated that epidemiological studies are not 

themselves direct evidence of a causal link between exposure to O3 and the occurrence of 

effects (72 FR 37879). Throughout the O3 review, a standard set of criteria have been 

used to evaluate evidence of a causal link. The critical assessment of epidemiological 

evidence presented in the Criteria Document was conceptually based upon consideration 

of salient aspects of the evidence of associations so as to reach fundamental judgments as 

to the likely causal significance of the observed associations in accordance with the Hill 

criteria (Criteria Document, pp. 7-3 - 7-4). Moreover, consistent with the proposal the 

Administrator has specifically considered evidence from epidemiological studies in the 

context of all the other available evidence in evaluating the degree of certainty that O3-

related adverse health effects occur at various levels at and below 0.080 ppm, including 

the strong evidence from controlled human exposure studies and the toxicological studies 

that demonstrate biological plausibility and mechanisms for effects. More detailed 

discussion of the criteria used to evaluate evidence with regard to judgments about 

causality can be found in section d. below. 

(6) Comment: NAM contends that EPA uses policy judgment, rather than scientific 

judgment in assessing causality (NAM, pp. 37-39). 

Response: EPA strongly disagrees with this comment by NAM that EPA’s approach to 

judging causality is “unambiguously and transparently policy directed” (NAM, p. 38) 

EPA’s approach to assessing the epidemiologic evidence is presented in section 7.1.2 of 

the Criteria Document. The critical assessment of epidemiologic evidence presented in 

the Criteria Document is conceptually based upon consideration of salient aspects of the 

evidence of associations so as to reach fundamental judgments as to the likely causal 

significance of the observed associations, as described by Hill (1965). 

 NAM further alleges that EPA’s analysis and presentation of the scientific evidence does 

not follow a “plausibly objective analysis.” (p. 38) In developing an integrated 

assessment of the health effects evidence for O3, EPA has emphasized the importance of 

examining the pattern of results across various studies, and not focusing solely on 

statistical significance as a criterion. In doing so, EPA recognizes the distinction between 

evaluation of individual study results and integration of a body of evidence. Individual 
35

studies are discussed and evaluated to assess their relative scientific quality. Statistical 

significance is an indicator of the precision of that study’s results, which is influenced by 

the size of the study, as well as exposure and measurement error and other such factors. 

It is important not to focus the on results of statistical tests to the exclusion of other 

information. As observed by Rothman (1998): 

 Many data analysts appear to remain oblivious to the qualitative nature of 

significance testing. Although calculations based on mountains of valuable 

quantitative information may go into it, statistical significance is itself only a 

dichotomous indicator. As it has only two values, significant or not significant, it 

cannot convey much useful information. . . . Nevertheless, P-values still 

confound effect size with study size, the two components of estimation that we 

believe need to be reported separately. Therefore, we prefer that P-values be 

omitted altogether, provided that point and interval estimates, or some equivalent, 

are available. (Rothman, 1998, p. 334) 

 The concepts underlying EPA’s approach to integrated assessment of statistical 

associations have been discussed in numerous publications, including a recent report by 

the U.S. Surgeon General on the health consequences of smoking (Centers for Disease 

Control and Prevention, 2004). This report also cautions against over-reliance on 

statistical significance in evaluating the overall evidence for an exposure-response 

relationship. 

 Hill made a point of commenting on the value, or lack thereof, of statistical testing in the 

determination of cause: “No formal tests of significance can answer those [causal] 

questions. Such tests can, and should, remind us of the effects the play of chance can 

create, and they will instruct us in the likely magnitude of those effects. Beyond that, 

they contribute nothing to the ‘proof’ of our hypothesis” (Hill, 1965, p. 299). 

 Hill’s warning was in some ways prescient, as the reliance on statistically significant 

testing as a substitute for judgment in causal inference remains today (Savitz et al., 1994; 

Holman et al., 2001; Poole 2001). To understand the basis for this warning, it is critical 

to recognize the difference between inductive inferences about the truth of underlying 

hypotheses, and deductive statistical calculations that are relevant to those inferences, but 

that are not inductive statements themselves. The latter include p values, confidence 

intervals, and hypothesis tests (Greenland 1998; Goodman 1999). The dominant 

approach to statistical inference today, which employs those statistical measures, 

obscures this important distinction between deductive and inductive inferences (Royall 

1997), and has produced the mistaken view that inferences flow directly and inevitably 

from data. There is no mathematic formula that can transform data into a probabilistic 

statement about the truth of an association without introducing some formal 

quantification of external knowledge, such as in Bayesian approaches to inference 

(Goodman 1993; Howson and Urbach 1993). Significance testing and the 

complementary estimation of confidence intervals remain useful for characterizing the 

role of chance in producing the association in hand (CDC, pp. 23-24). 
36

 Accordingly, the statistical significance of individual study findings has played an 

important role in EPA’s evaluation of the study’s results, and EPA has placed greater 

emphasis on studies reporting statistically significant results. However, in the broader 

evaluation of the evidence from many epidemiologic studies, EPA has also emphasized 

the pattern of results for drawing conclusions on the relationship between air pollutants 

and health outcomes, as well as consideration of the integration of epidemiologic 

evidence with findings of laboratory studies. 

 It is also important to reiterate that the EPA’s evaluation of the scientific evidence was 

reviewed in detail by CASAC and the public. Two drafts of the Criteria Document were 

released for CASAC and public review at public meetings, and an additional 

teleconference meeting was held with CASAC for review of Chapter 8. Evidence related 

to the substantive issues raised by the commenters were evaluated in the Criteria 

Document drafts, and discussed at length in public CASAC meetings. This process 

ensured that overemphasis or underemphasis on any study or group of studies was 

addressed. 

(7) Comment: Several commenters made the point that the results of the new 

epidemiological studies included in this review are not coherent. They state that although 

EPA notes that estimates of risk from cardiovascular mortality are higher than those for 

total mortality and indicates that these findings are highly suggestive that short-term O3

exposure directly or indirectly contributes to cardiovascular mortality, the Agency fails to 

contrast the mortality studies to studies of hospital admissions for cardiovascular causes. 

Most studies of cardiovascular causes have not found statistically significant associations 

with O3 exposures (UARG, pp. 16-17). 

Response: EPA strongly disagrees that it has failed to appropriately characterize the 

association between O3 exposure and potential cardiovascular morbidity and mortality 

effects. As noted above, the Criteria Document characterizes the overall body of 

evidence as limited, but highly suggestive, and concludes that much needs to be done to 

more fully integrate links between ambient O3 exposures and adverse cardiovascular 

outcomes (Criteria Document, p. 8-77). Some field/panel studies that examined 

associations between O3 and various cardiac physiologic endpoints have yielded limited 

epidemiological evidence suggestive of a potential association between acute O3

exposure and altered HRV, ventricular arrhythmias, and incidence of myocardial 

infarction (Criteria Document, section 7.2.7). In addition, there were approximately 20 

single-city studies of emergency department visits and hospital admissions for all 

cardiovascular diseases or specific diseases (i.e., myocardial infarction, congestive heart 

failure, ischemic heart disease, dysrhythmias). In the studies using all year data, many 

showed positive results but few were statistically significant. Given the strong seasonal 

variations in O3 concentrations and the changing relationship between O3 and other 

copollutants by season, inadequate adjustment for seasonal effects might have masked or 

underestimated the associations. In the limited number of studies that analyzed data by 

season (6 studies), statistically significant associations were observed in all but one study 

(Criteria Document, section 7.3.4). Newly available animal toxicology data provide 

some plausibility for the observed associations between O3 and cardiovascular outcomes. 
37

EPA believes that its characterization of the evidence for O3-related cardiovascular 

system effects is appropriate. It is clear that coherence is stronger in the much larger 

body of evidence of O3-related respiratory morbidity and mortality effects. 

 Many commenters who did not support revising the current O3 primary standard also 

submitted comments on specific methodological issues related to the epidemiological evidence, 

including: the adequacy of exposure data; confounding by copollutants; model selection; 

evidence of mortality; and, new studies not included in the Criteria Document. The comments 

on methodological issues raised by these commenters are discussed below. 

(8) Comment: Many commenters, mostly representing industry associations and some 

businesses opposed to revising the primary O3 standard, expressed concern about the 

adequacy of exposure data both for time-series and panel studies. These commenters 

argued that almost all of the epidemiological studies on which EPA relies in 

recommending a more stringent O3 standard are based on data from ambient monitors for 

which there is a poor correlation with the actual personal exposure subjects receive 

during their daily activities. They questioned the Administrator's conclusion that in the 

absence of available data on personal O3 exposure, the use of routinely monitored 

ambient O3 concentrations as a surrogate for personal exposures is not generally expected 

to change the principal conclusions from epidemiological studies. These commenters 

also note that, in its June 2006 letter, the CASAC Panel raised the issue of exposure error, 

concluding that it called into question whether observed associations could be attributed 

to O3 alone (API, p. 17). One of these commenters cited studies (e.g., Sarnat et al., 2001; 

Sarnat et al., 2005) that show a lack of correlation between personal exposures and 

ambient concentrations (NAM, p. 22). Another cited studies (Sarnat et al., 2001, 2005, 

and 2006; and Koutrakis et al., 2005) that have found that the ability of ambient gas 

monitors to represent personal exposure to such gases is similarly quite limited, 

including: (1) most personal exposures are so low as to be not detectable at a level of 5 

parts per billion (ppb), resulting in very low correlation between concentrations reported 

from central ambient monitors and personal monitors; (2) O3 measurements from ambient 

monitors are a better surrogate for personal exposure to PM2.5 than to O3; and (3) 

populations expected to be potentially susceptible to O3, including children, the elderly, 

and those with COPD, are at the low end of the population exposure distribution (Exxon 

Mobil, pp. 15-16). These commenters contended that without such a correlation there is 

no legitimate way for EPA to conclude that O3 exposure has caused the reported health 

effects, or to conclude that use of routinely monitored ambient O3 concentrations as a 

surrogate for personal exposures is adequate. Some of these commenters also contended 

that EPA incorrectly concludes that the exposure error in epidemiological studies results 

in an underestimate of risk (Exxon Mobil, p. 20). 

Response: With regard to the views on exposure measurement error expressed by 

CASAC, while the commenter is correct that the CASAC Panel raised the question of 

exposure error and whether observed associations could be attributed to O3 alone, the 

commenter failed to note that CASAC’s comment was focused on the association 

between O3 and mortality, at very low O3 concentrations and in the group of people most 

susceptible to premature mortality. The CASAC Panel stated: 
38

 The population that would be expected to be potentially susceptible to dying from 

exposure to ozone is likely to have ozone exposures that are at the lower end of 

the ozone population distribution, in which case the population would be exposed 

to very low ozone concentrations, and especially so in winter. Therefore it seems 

unlikely that the observed associations between short-term ozone concentrations 

and daily mortality are due solely to ozone itself. (Henderson 2006b, pp. 3-4) 

 This section of the quote, which was not addressed in the comment submitted by API, 

together with the conclusions in the final CASAC letter (Henderson, 2007), leads EPA to 

conclude that contrary to the commenters’ assertion, the CASAC Panel was not calling 

into question the association between O3 exposure and the full range of morbidity effects 

found in panel or time-series studies that rely on ambient monitoring data as a surrogate 

for personal exposure data. It is important to note that EPA agrees that the evidence is 

only highly suggestive that O3 directly or indirectly contributes to mortality, as compared 

to the stronger evidence of causality for respiratory morbidity effects. 

 EPA agrees that exposure measurement error may result from the use of stationary 

ambient monitors as an indicator of personal exposure in population studies. There is a 

full discussion of measurement error and its effect on the estimates of relative risk in 

section 7.1.3.1 of the Criteria Document. However, the possibility of measurement error 

does not preclude the use of ambient monitoring data as a surrogate for personal exposure 

data in time-series or panel studies. It simply means that in some situations where the 

likelihood of measurement error is greatest, effects estimates must be evaluated carefully 

and that caution must be used in interpreting the results from these studies. Throughout 

this review, EPA has recognized this concern. The Criteria Document states that there is 

supportive evidence that ambient O3 concentrations from central monitors may serve as 

valid surrogate measures for mean personal O3 exposures experienced by the population, 

which is of most relevance to time-series studies, in which individual variations in factors 

affecting exposure tend to average out across the study population. This is especially true 

for respiratory hospital admission studies for which much of the response is attributable 

to O3 effects on asthmatics. In children, for whom asthma is more prevalent than adults, 

ambient monitors are more likely to correlate reasonably well with personal exposure to 

O3 of ambient origin because children tend to spend more time outdoors than adults in the 

warm season. EPA does not agree that the correlation between personal exposure and 

ambient monitoring data is necessarily poor, especially in children. Moreover, the 

CASAC Panel supported this view as they noted that “[p]ersonal exposures most likely 

correlate better with central site values for those subpopulations that spend a good deal of 

time outdoors, which coincides, for example, with children actively engaged in outdoor 

activities, and which happens to be a group that the ozone risk assessment focuses upon.” 

(Henderson, 2006c. p. 10). However, the Criteria Document notes that there is some 

concern in considering certain mortality and hospitalization time-series studies regarding 

the extent to which ambient O3 concentrations are representative of personal O3

exposures in another particularly susceptible group of individuals, the debilitated elderly, 

as the correlation between the two measurements has not been examined in this 

population. A better understanding of the relationship between ambient concentrations 

and personal exposures, as well as of the factors that affect the relationship, will improve 
39

the interpretation of observed associations between ambient concentration and population 

health response. 

 With regard to the specific comments that reference the findings of studies by Sarnat et 

al. (2001, 2005, 2006) and Koutrakis et al. (2005), the fact that personal exposure 

monitors cannot detect O3 levels of 5 ppb and below may in part explain why there was a 

poor correlation between personal exposure measurements and ambient monitoring data 

in the winter relative to the correlation in the warm season, along with differences in 

activity patterns and building ventilation. In one study conducted in Baltimore, Sarnat et 

al. (2001) observed that ambient O3 concentrations showed stronger associations with 

personal exposure to PM2.5 than to O3; however, in a later study conducted in Boston 

(Sarnat et al., 2005), ambient O3 concentrations and personal O3 exposures were found to 

be significantly associated in the summer. Another study cited by the commenter, but not 

included in the Criteria Document, conducted in Steubenville (Sarnat et al., 2006), also 

observed significant associations between ambient O3 concentrations and personal O3. 

The authors noted that the city-specific discrepancy in the results may be attributable to 

differences in ventilation. Though the studies by Sarnat et al. (2001, 2005, and 2006) 

included senior citizens, the study selection criteria required them to be nonsmoking and 

physically healthy. EPA is not relying on studies that are not in the Criteria Document, 

such as Sarnat et al. (2006), to refute the commenters. However, EPA notes that Sarnat et 

al. (2006) does not support the conclusion drawn by the commenters that this study 

shows very limited associations between ambient O3 concentrations and personal 

exposures. 

 Existing epidemiologic models may not fully take into consideration all the biologically 

relevant exposure history or reflect the complexities of all the underlying biological 

processes. Using ambient concentrations to determine exposure generally overestimates 

true personal O3 exposures (by approximately 2- to 4- fold in the various studies 

described in the Criteria Document, section 3.9), which assuming the relationship is 

causal, would result in biased descriptions of underlying concentration-response 

relationships (i.e., in attenuated effect estimates). From this perspective, the implication 

is that the effects being estimated in relationship to ambient levels occur at fairly low 

personal exposures and the potency of O3 is greater than these effect estimates indicate. 

On the other hand, as very few studies evaluating O3 health effects with personal O3

exposure measurements exist in the literature, effect estimates determined from ambient 

O3 concentrations must be evaluated and used with caution to assess the health risks of

O3 (Criteria Document, pp. 7-8 to 7-10). Nonetheless, as noted in section II.C.3 of the 

proposal, the use of routinely monitored ambient O3 concentrations as a surrogate for 

personal exposures is not generally expected to change the principal conclusions from O3

epidemiologic studies. Therefore, population risk estimates derived using ambient O3

concentrations from currently available observational studies, with appropriate caveats 

about personal exposure considerations, remain useful. (72 FR 37839) 

(9) Comment: NAM contends that EPA characterizes a study as reporting something when it 

reports the opposite, specifically referring to the work by Sarnat and colleagues (2001, 

2005) (NAM, pp. 22-23) NAM states that in Sarnat et al. (2001), “the authors concluded 
40

that ambient concentrations did not provide a surrogate for personal exposures, and in 

2005 they reconfirmed that result” (NAM, p. 22). NAM then contends that EPA has “the 

study sites reversed and the results reported incorrectly” (NAM, p. 23). 

 Response: EPA has correctly characterized the conclusions of Sarnat et al. (2001) while 

NAM has the study sites reversed. Sarnat et al. (2001) was conducted in Baltimore, MD 

while the 2005 study was conducted in Boston, MA. As reported in the Criteria 

Document, in the study conducted in Baltimore, Sarnat et al. (2001) observed no 

relationship between ambient O3 concentrations and personal O3 exposures in both the 

summer and winter. The ambient O3 concentrations showed stronger associations with 

personal exposure to PM2.5 than to O3; thus authors noted that “ambient concentrations of 

gaseous pollutants cannot be considered as surrogates for their respective personal 

exposure without site-specific evidence to support that assumption.” They also noted, 

however, that a limitation of their study was that it was only conducted in one city. In the 

later study conducted in Boston (Sarnat et al., 2005), ambient O3 concentrations and 

personal O3 exposures were found to be significantly associated in the summer. From 

this they noted that these results suggest that “there may be differences, by location in the 

strength of the personal-ambient association for the gases.” and that “it is incorrect to 

assume that ambient gas measurements are consistent surrogates for PM exposures.” 

(10) Comment: Many commenters, mostly representing industry associations and some 

businesses opposed to revising the primary O3 standard, argued that known confounders 

are inadequately controlled in the epidemiological studies of O3 and various health 

outcomes and that the health effects of O3 are often not statistically significant when 

epidemiological studies consider the effects of confounding air pollutants (e.g., PM2.5, 

CO, nitrogen dioxide (NO2) in multi-pollutant models. Many commenters cited 

Mortimer et al. (2002), a large multi-city asthma panel study as an example, and 

indicated that it found that when other pollutants, i.e., sulfur dioxide (SO2), NO2, and 

particles with an aerodynamic diameter less than or equal to a nominal 10 micrometers 

(PM10), were placed in a multi-pollutant model with O3, the O3-related associations with 

respiratory symptoms and lung function became non-significant. 

Response: EPA has thoroughly reviewed issues related to confounding and the evidence 

of potential confounding by copollutants in sections 7.1.3 and 7.6.4 of the Criteria 

Document. EPA recognizes that a major methodological issue affecting O3 

epidemiologic studies concerns the evaluation of the extent to which other air pollutants 

may confound or modify O3-related effect estimates, and that the changing relationship 

between O3 and copollutants across seasons further complicates the issue. The use of 

multipollutant regression models is the prevailing approach for controlling potential 

confounding by copollutants in O3 health effects studies (Criteria Document, p. 7-24). In 

section 7.6.4.2, the Criteria Document reviews the evidence from studies that use 

multipollutant models to evaluate confounding by copollutants for effects ranging from 

mortality and respiratory hospitalizations to lung function measures and symptoms. It 

concluded that multipollutant regression analyses indicated that O3 risk estimates, in 

general, were not sensitive to the inclusion of copollutants, including PM2.5 and sulfate. 

As can be seen in the Figure 1 below (Figure 7-22 from the Criteria Document) the ozone 
41

effect estimates for mortality are generally unchanged upon inclusion of PM in the 

models. These results suggest that the effect of O3 on respiratory health outcomes 

appears to be robust and independent of the effects of other copollutants (Criteria 

Document, p. 7-154). 

Figure 1. All-cause (nonaccidental) O3 excess mortality risk estimates (95% CI) with 

adjustment for PM indices for all-year analyses per standardized increment (see Section 

7.1.3.2). Analyses include all ages unless otherwise noted. 

 The National Cooperative Inner-City Asthma Study (Mortimer et al., 2002) evaluated air 

pollution health effects in 846 asthmatic children in 8 urban areas. The pollutants 

evaluated included O3, PM10, SO2, and NO2. Three effects were evaluated: (1) daily 

percent change in lung function, measured as peak expiratory flow rate (PEFR); (2) 

incidence of ≥ 10% reduction in lung function (PEFR); and, (3) incidence of symptoms 
42

(i.e., cough, chest tightness, and wheeze). EPA notes that in this study, O3 was the only 

pollutant associated with reduction in lung function. Nitrogen dioxide had the strongest 

effect on morning symptoms, and the authors concluded it "...may be a better marker for 

the summer-pollutant mix in these cities” but had no association with morning lung 

function. In a two-pollutant model with NO2, the O3 effect on morning symptoms 

remained relatively unchanged. Sulfur dioxide had statistically significant effects on 

morning symptoms but no association with morning lung function. Particulate matter 

(PM10), which was measured daily in 3 cities, had no statistically significant effect on 

morning lung function. In a two-pollutant model with O3, the PM10 estimate for morning 

symptoms was slightly reduced and there was a larger reduction in the O3 estimate, which 

remained positive but not statistically significant. 

(11) Comment: NAM contends that EPA did not consider non-air pollutant confounders that 

are not adequately controlled in the literature (NAM, pp. 32-33). NAM cites a number of 

factors that have been reported to be associated with asthma, and argues that failure to 

control for all of these factors “yields upwardly biased estimates of risk.” (NAM, p. 32). 

 Response: Contrary to NAM’s contention, EPA thoroughly reviewed the issues related 

to confounding and the evidence of potential confounding in the Criteria Document. A 

number of the factors listed by NAM would not appropriately be identified as potential 

confounders for a relationship between O3 and health outcomes. For example, the NAM 

comment discusses cockroach and house dust mite allergens and exercise, none of which 

would be likely to confound a relationship with O3 in a time-series study. To be a 

confounder, the variable must be correlated with both the health outcome and the 

exposure under study. In a time-series analysis, only variables that are temporally 

correlated with O3 can truly confound an O3-health outcome relationship. It is highly 

unlikely that exercise behaviors are correlated with O3 concentrations – that people 

choose to exercise when O3 concentrations are highest. It is known that house dust mite 

and cockroach allergen concentrations in a home do not vary from day to day as do 

ambient O3 concentrations. Thus, these factors may be independently associated with 

exacerbation of asthma, but would not be confounders in a relationship between ozone 

and asthma exacerbation. 

 NAM also observes that control for meteorological variables is important. EPA agrees, 

and carefully evaluated the potential for confounding by temperature and humidity, as 

discussed in section 7.1.3.4 and further in section 7.6.3 of the Criteria Document. EPA 

concluded that O3 risk estimates were generally more sensitive to alternative weather 

models than to varying degrees of freedom for temporal trend adjustment. In addition, 

careful consideration was given to whether studies had considered seasonality, as many 

epidemiologic studies observed differences in O3-related health effects in the warm 

versus cool season. Seasonality influences the relationship between O3 and health 

outcomes, as it may serve as an indicator for time-varying factors, such as temperature, 

copollutant concentrations, infiltration, and human activity patterns. Given the 

potentially significant influence of season, EPA noted that season-specific analyses were 

more informative in assessing O3-related health risks and only estimated health risks for 

the O3 warm season in its health risk assessment. 
43

 The Administrator acknowledges that uncertainties concerning other potential 

confounders may be an important source of uncertainty affecting the specific risk 

estimates included in EPA’s risk assessment and that these quantitative risk estimates 

must be used with appropriate caution, keeping in mind these important uncertainties. As 

discussed in the preamble to the final rule, the Administrator is not relying on any 

specific quantitative effect estimates from the time-series studies or any risk estimates 

based on the time-series studies in reaching his judgment about the need to revise the 

current 8-hour O3 standard. 

(12) Comment: Commenters who did not support revision of the primary O3 standard raised 

issues regarding the adequacy of model specification including control of temporal and 

weather variables in the time-series epidemiological studies that EPA has claimed 

support the finding of O3-related morbidity and mortality health outcomes. Specifically, 

concerns were expressed regarding the following issues: (1) commenters noted that 

recent meta-analyses have confirmed the important effects of model selection in the 

results of the time-series studies, including the choice of models to address weather and 

the degree of smoothing, in direct contradiction of the Staff Paper’s conclusion on the 

robustness of the models used in the O3 time-series studies (Exxon Mobil, p. 41); (2) 

commenters contended that there were no criteria for how confounders such as 

temperature or other factors were to be addressed, resulting in arbitrary model selection 

potentially impacting the resulting effect estimates; and (3) commenters expressed the 

view that to appropriately address concerns about model selection in the O3 time-series 

studies, EPA should rely on an alternative statistical approach, Bayesian model 

averaging, that incorporates a range of models addressing confounding variables, 

pollutants, and lags rather than a single model. 

Response: In response to the first issue, EPA agrees that the results of the meta-analyses 

do support the conclusion that there are important effects of model selection and that, for 

example, alternative models to address weather might make a difference of a factor of 

two in the effect estimates. However, as noted in the Criteria Document, one of the metaanalyses (Ito et al., 2005) suggested that the stringent weather model used in the Bell et 

al. (2004) NMMAPS study may tend to yield smaller effect estimates than those used in 

other studies (Criteria Document, p. 7-96), and, thus concerns about appropriate choice of 

models could result in either higher or lower effect estimates than reported. In addressing 

this issue, the Criteria Document concluded, 

 Considering the wide variability in possible study designs and statistical model 

specification choices, the reported O3 risk estimates for the various health 

outcomes are in reasonably good agreement. In the case of O3-mortality timeseries studies, combinations of choices in model specifications ... alone may 

explain the extent of difference in O3 risk estimates across studies. (Criteria 

Document, p. 7-174) 

 Second, the issues surrounding sensitivity to model specifications were thoroughly 

discussed in the Criteria Document (see section 7.1.3.6) and evaluated in some of the 
44

meta-analyses reviewed in the Criteria Document and Staff Paper. As stated in the 

Criteria Document, O3 effect estimates “were generally more sensitive to alternative 

weather models than to varying degrees of freedom for temporal trend adjustment” 

(Criteria Document, p. 7-176). The Criteria Document also concluded that “although 

there is some concern regarding the use of multipollutant models ... results generally 

suggest that the inclusion of copollutants into the models do not substantially affect O3

risk estimates” and the results of the time-series studies are “robust and independent of 

the effects of other copollutants” (Criteria Document, p. 7-177). Overall, EPA continues 

to believe that based on its integrated assessment, the time-series studies provide strong 

support for concluding there are O3-related morbidity effects, including respiratoryrelated hospital admissions and emergency department visits during the warm season and 

that the time-series studies provide findings that are highly suggestive that short-term O3

exposure directly or indirectly contributes to non-accidental and cardiorespiratory-related 

mortality. The Administrator acknowledges that uncertainties concerning appropriate 

model selection are an important source of uncertainty affecting the specific risk 

estimates included in EPA’s risk assessment and that these quantitative risk estimates 

must be used with appropriate caution, keeping in mind these important uncertainties. As 

discussed in the preamble to the final rule, the Administrator is not relying on any 

specific quantitative effect estimates from the time-series studies or any risk estimates 

based on the time-series studies in reaching his judgment about the need to revise the 

current 8-hour O3 standard or on the appropriate level of the standard. 

 Third, in response to commenters who suggested that EPA adopt an alternative statistical 

approach, i.e., Bayesian model averaging, to address concerns about potential arbitrary 

selection of models, the Criteria Document evaluated the strengths and weaknesses of 

such methods in the context of air pollution epidemiology. The Criteria Document noted 

several limitations, especially where there are many interaction terms and meteorological 

variables and where variables are highly correlated, as is the case for air pollution studies, 

which makes it very difficult to interpret the results using this alternative approach. EPA 

believes further research is needed to address concerns about model selection and to 

develop appropriate methods addressing these concerns. 

 

(13) Comment: NAM asserts that EPA selected models known to yield upwardly biased risk 

estimates, such as single-pollutant models and models that do not control for known 

confounders (NAM, pp. 31-32, 34). NAM also criticizes the use of single-pollutant 

model results in EPA’s risk assessment, which is addressed in comment numbers (7) and 

(9) in section II.A.5. 

Response: EPA rejects NAM’s assertion that it selected models known to yield upwardly 

biased risk estimates, such as single-pollutant models and models that do not correct for 

confounders in the Criteria Document, Staff Paper, or risk assessment. EPA’s approach 

in all of these documents was to include and discuss results from both single- and multipollutant models when available. EPA’s Criteria Document rigorously and thoroughly 

evaluated the potential for confounding in O3 epidemiological studies. EPA discussed 

the merits and issues with both single- and multipollutant models in section 7.1.3.5 of the 

Criteria Document. EPA further evaluated the potential confounding of the association 
45

between O3 and various health outcomes by copollutants in section 7.6.4 of the Criteria 

Document. EPA stated that although there was some concern regarding the use of 

multipollutant models given the varying concurvity across pollutants, results generally 

suggested that the inclusion of copollutants into the models did not substantially affect O3

risk estimates. From these findings, EPA concluded that effects of O3 on various health 

outcomes were robust and independent of the effects of other copollutants. Additional 

response to this comment with respect to the issue of alleged upward bias in the context 

of the health risk assessment is addressed in the response to comment number (7) and 

number (9) in section II.A.5 of this document. 

(14) Comment: NAM also contends that EPA disseminates results from models known to 

yield risk estimates that are upwardly biased and more uncertain, such as Generalized 

Additive Models conducted with insufficient convergence criteria (NAM, pp. 36-37). 

Response: NAM incorrectly states “For years EPA has relied on studies utilizing 

Generalized Additive Models (GAMs) and software (S-PLUS) that yielded estimates of 

health effects from air pollution that were upwardly biased and excessively uncertain.” 

(p. 36). In fact, that has not been the case in recent years. NAM cites results from the 

Special Report prepared by the Health Effects Institute (HEI, 2003); in fact EPA has been 

a leader in examining this issue. Upon first learning of the questions surrounding the use 

of GAM, EPA funded a special workshop and supported the HEI in a project to reanalyze 

dozens of studies to fully investigate this issue. EPA has always carefully evaluated the 

methodology used in epidemiologic studies in the process of its scientific assessments. 

EPA discusses the issue of GAM and other methodologies in section 7.1.3.7 of the 

Criteria Document. The Criteria Document generally only includes results from studies 

that used methods other than GAM or the newly developed convergence criteria that 

addressed the issues found with the initial use of GAM in SPlus. Thus EPA’s Criteria 

Document and the risk assessment do not rely on studies that are impacted by the “GAM 

issues.” 

(15) Comment: NAM contends (NAM, pp. 34-35) that for lags to be biologically plausible, at 

least three critical biological principles must be respected: (1) all health effects must 

occur after exposure; (2) for each health effect, the gradient of risk must be biologically 

appropriate; and (3) more severe health effects must occur subsequent to minor effects. 

NAM contends that the time-series studies EPA relies upon do not respect these 

fundamental biological requirements. NAM specifically notes that biologically 

implausible lags are reported by Mortimer et al. (2002). 

Response: EPA disagrees with NAM’s charge that lags for specific health effects have 

been selected based on statistical strength without regard for the underlying biology. All 

the epidemiologic studies included in the Criteria Document examined O3 health effects 

associated with exposure from the same day or previous days; thus, in these studies the 

health effect did not precede the exposure. In section 7.1.3.3 of the Criteria Document, 

EPA recognized that analyzing a large number of lags and simply choosing the largest 

and most significant results may bias the air pollution risk estimates away from the null. 

However, most time-series analyses have shown that O3 has a fairly consistent, 
46

immediate effect on emergency department visits, hospitalizations, and mortality. For the 

respiratory and cardiovascular outcomes investigated, the “most significant” lags were 

generally 0- or 1-day lags, suggesting that the majority of the single-day associations 

were immediate, not a random pattern in which associations could be observed on any of 

the lags examined with equal probabilities. 

EPA further recognized that effects can occur acutely with exposure on the same or 

previous day, cumulatively over several days, or after a delayed period of a few days. 

Several studies also observed significant O3 effects over longer cumulative lag periods, 

suggesting that in addition to single-day lags, multiday lags should be investigated to 

fully capture a delayed O3 effect on health outcomes. Due to these findings, in the 

Criteria Document, discussion largely focused on effect estimates from same day and 

previous day exposures, with some consideration of cumulative, multiday lag effects. 

NAM specifically uses Mortimer et al. (2002) as an example to note that multiple lag 

times are used without biological justification. As discussed briefly in response to a 

previous comment #(7), Mortimer et al. examined the association between O3 and 

respiratory effects using single day lags from lag day 1 to lag day 6. Small morning 

effects were observed at a 1-day lag. The effect of O3 on morning outcomes increased 

over several days. A single-day lag model calculates a risk estimate that assumes 

dependence only on exposure from the specified day. In contrast, a multiday lag model 

provides an estimate that is a summary measure of the cumulative lag effect from all 

included lag days. The effect estimates were not all statistically significant for each 

single-day lag, but the pattern of the effect estimates was generally consistent with 

considerable overlap in the confidence intervals for the multiple days considered, 

suggesting that the gradient of risk was, in general, biologically appropriate. 

Examination of these single lag day effects led to the consideration of a multiday lag 

period of 1 to 5 days in the case of PEF and 1 to 4 days in the case of respiratory 

symptoms to estimate the cumulative effect of O3. The selected cumulative lag period 

was biologically plausible and consistent with previous findings that asthma exacerbation 

is generally associated with pollutant exposures over a several day period. The 

observation of greater effects in the morning and the change in effects following 

adjustment for copollutants were addressed in responses to previous comments (see 

comments #(16) and #(10) in this section). 

NAM also comments that more severe health effects must occur subsequent to more 

minor effects for a lag to be biologically plausible. NAM notes that respiratory 

symptoms should occur before emergency department visits and hospital admissions. 

Though not specified in the comments, NAM seems to be implying that the longer 

cumulative lag observed for respiratory symptoms in the Mortimer et al. study compared 

to the shorter, more immediate lags observed in the time-series analyses of emergency 

department visits and hospital admissions indicate that the observed association between 

respiratory health outcomes and O3 is biologically implausible. EPA disagrees that a 

direct comparison can be made in the exposure lags between these two very different 

types of studies. Mortimer et al. is a panel study of asthmatic children, in which 

individual-level health outcome data is linked with ambient O3 concentrations for a 
47

limited number of subjects. In contrast, time-series analyses link daily community-level 

health outcome data (i.e., counts of emergency department visits or hospitalizations) with 

ambient concentrations. By design, a population with a much wider variability in 

susceptibility is considered in these time-series analyses. It is important to note that 

while several studies consistently observed associations between O3 and respiratory 

emergency department visits and hospitalizations at lag 0- or 1-day, strong associations 

were also observed in studies that examined longer multiday, cumulative exposures. In 

addition, it should be noted that there are potentially different mechanisms between the 

different endpoints described above. For example, asthmatics may experience severe 

acute exacerbations that result in emergency department visits, or they may have 

inflammatory responses that develop over a longer period of time. It is well known that 

asthma is a complex disease likely to have multiple etiologic pathways for health 

responses. 

(16) Comment: NAM contends that methodological errors, e.g., repeated statistical tests, 

biologically implausible lags, and inadequate control for confounders, have not been 

properly considered by EPA in the evaluation of the evidence for O3 health effects 

(NAM, pp. 14-16). 

Response: In the Criteria Document, EPA conducted a rigorous assessment of potential 

methodological error in epidemiologic analyses, as can be seen in section 7.1.3. Issues 

such as those cited by NAM, including control for copollutants and other potential 

confounders, consideration of exposure lag periods, and measurement error, were 

evaluated by EPA in its assessment of the scientific evidence. EPA does not agree that 

methodological errors exist in these studies that are “so severe that they have a material 

effect on utility, particularly for regulatory decision-making.” (p. 14). 

 With regard to NAM’s statement that repeated statistical tests are performed without 

apparent regard for the resulting increase in the rate of false positive, EPA discusses the 

issue of multiple hypothesis testing in Section 7.1.3.6 of the Criteria Document. In 

particular, EPA notes that multiple hypotheses may need to be developed for researchers 

to explore more thoroughly potential associations for an O3-related health effect. NAM 

specifically cites Korrick et al. (1998) and Mortimer et al. (2002) in reference to this 

comment. In Korrick et al. (1998), though multiple hypotheses are tested, these 

hypotheses can be divided into confirmatory vs exploratory hypotheses. The main 

confirmatory hypothesis is whether O3 concentrations are associated with pulmonary 

function. In their models adjusting for multiple covariates, they observe a clear inverse 

association between O3 and FEV1 and FVC. In their sensitivity or exploratory analyses, 

they observe that the O3 effect estimate is generally robust to adjustment for PM2.5 and 

acidity. They further observed that the effect of O3 may be modified by asthma status, 

but not by smoking status, gender, or age. In Mortimer et al. (2002) the issue pertains to 

the examination of multiple lags. As discussed above, the examination of multiple lags 

may be viewed as the testing of exploratory hypotheses. As noted in the response to 

comment (15) above, in section 7.1.3.3 of the Criteria Document, EPA recognized that 

analyzing a large number of lags and simply choosing the largest and most significant 

results may bias the air pollution risk estimates away from the null. In the response 
48

above and in the response to comment (3) the issue of lags is further discussed 

specifically with regard to Mortimer et al. (2002) 

 Other methodological errors that NAM mention include the reliability of selfadministered PEF testing (Mortimer et al., 2002), selective use of data from different 

times of day (Mortimer et al., 2002), reliance on subjective symptoms rather than 

objective signs (Gent et al., 2003), and the use of a nonstandard measure of incremental 

change (Korrick et al., 1998). 

 One issue that NAM discusses in some detail in this section is the error related to selfreported peak expiratory flow data. NAM presents the results of Kamps et al. (2001) 

which found that compliance and reliability of self-reported data was less than optimal. 

EPA recognizes that PEF measurements have been shown to be more variable than FEV1

in some studies (Vaughan et al., 1989; Cross and Nelson, 1991) and can have an element 

of uncertain reliability when self-administered by study subjects. As increased variability 

in the PEF measurement will add noise to the relationship between O3 and PEF, it will 

likely lead to bias towards the null rather than a spurious significant association. 

Furthermore, the observed association between O3 and PEF concur with the strong 

associations found between O3 and measures of spirometry, which is a more consistent 

test of lung function and typically conducted by a trained individual. 

 NAM also comments on the selective use of data from different times of day. In 

Mortimer et al. (2002), while associations were found between O3 and morning PEF and 

respiratory symptoms, no associations were observed with evening PEF or respiratory 

symptoms. The fact that associations were more evident with asthma symptoms 

measured in the morning is consistent with the understanding that the development of 

asthma exacerbation through an inflammatory mechanism would occur over time, with 

symptoms manifested hours after the exposure period. Mortimer et al. further explain 

that the most severe bronchoconstriction occurs in the morning, when measurable 

differences between and within individuals may be greatest. Therefore, there are 

biologically plausible reasons as to why associations would be observed at different times 

of day. 

 The NAM statement that Gent et al. (2003) relied on a subjective measure of symptoms 

rather than an objective measure is incorrect. In addition to respiratory symptoms, Gent 

et al. also observed an association between O3 and rescue medication use, which is an 

objective measure. Regardless, EPA deems respiratory symptoms to be a valuable health 

outcome, which considered in conjunction with various other more “objective” measures, 

allows a more complete depiction of the potential respiratory health effects of pollutants. 

 NAM further contends that Korrick et al. (1998) uses a nonstandard measure of 

incremental change (% per 50-100 ppb O3) that is too large to have any practical utility 

for making policy decisions over small exposure ranges. EPA disagrees with this 

contention as these effect estimates can be standardized to any incremental change based 

on the linear concentration-response function. Discussion of this approach can be found 

in section 7.1.3.2 of the Criteria Document (Criteria Document, p. 7-10). 
49

(17) Comment: With regard to evidence of O3-related mortality, many commenters, including 

those that argued for revising the current O3 standard as well as those that argued against 

revisions, focused on the new evidence from multi-city time-series analyses and metaanalyses linking O3 exposure with mortality. Again, sharply divergent comments were 

received. One group of commenters, including medical, public health, and environmental 

organizations argued that recent published research has provided more robust, consistent 

evidence linking O3 to cardiovascular and respiratory mortality. The ATS, AMA, and 

others stated that data from single-city studies, multiple-city studies, and meta-analyses 

show a consistent relationship between O3 exposure and mortality from respiratory and 

cardiovascular causes. These commenters noted that this effect was observed after 

controlling for co-pollutants and seasonal impacts. These commenters stated that 

research has demonstrated that exposure to O3 pollution is causing premature deaths, and 

has also provided clues on the possible mechanisms that lead to premature mortality 

(ATS, p. 4). These commenters noted that people may die from O3 exposure even when 

the concentrations are well below the current standard. They pointed to a study (Bell et 

al., 2006) in which the authors followed up on their 2004 multi-city study to estimate the 

exposure-response curve for O3 and the risk of mortality and to evaluate whether a 

threshold exists below which there is no effect. The authors applied several statistical 

models to data on air pollution, weather, and mortality for 98 U.S. urban communities for 

the period 1987 to 2000. The study reported that O3 and mortality results did not appear 

to be confounded by temperature or PM and showed that any threshold, if it existed, 

would have to be at very low concentrations, far below the current standard (ALA et al., 

p. 74). Another approach also indicated that the mortality effect is unlikely to be 

confounded by temperature. A case-crossover study (Schwartz 2005) of over one million 

deaths in 14 U.S. cities, designed to control for the effect of temperature on daily deaths 

attributable to O3, found that the association between O3 and mortality risk reported in the 

multi-city studies is unlikely to be due to confounding by temperature (ALA et al., p. 76). 

These commenters argue that meta-analyses also provide compelling evidence that the 

O3-mortality findings are consistent. They point to three independent analyses conducted 

by separate research groups at Johns Hopkins University, Harvard University and New 

York University, using their own methods and study criteria, which reported a 

remarkably consistent link between daily O3 levels and total mortality. 

Response: In response, EPA notes that the Criteria Document states that the results from 

the U.S. multi-city time-series studies provide the strongest evidence to date for O3

effects on acute mortality. Recent meta-analyses also indicate positive risk estimates that 

are unlikely to be confounded by PM; however, future work is needed to better 

understand the influence of model specifications on the risk coefficient (EPA, 2006a, p. 

7-175). The Criteria Document concludes that these findings are highly suggestive that 

short-term O3 exposure directly or indirectly contributes to non-accidental and 

cardiorespiratory-related mortality but that additional research is needed to more fully 

establish the underlying mechanisms by which such effects occur (72 FR 37836). Thus 

while EPA generally agrees with the direction of the comment, EPA believes the 

evidence supports a view as noted above. In addition, it must be noted that the 

Administrator did not focus on mortality as a basis for proposing that the current O3
50

standard was not adequate or on determining the appropriate level of the standard. In the 

proposal, the Administrator focused on the very strong evidence of respiratory morbidity 

effects in healthy people at the 0.080 ppm exposure level and new evidence that people 

with asthma are likely to experience larger and more serious effects than healthy people 

at the same level of exposure and evidence that epidemiological studies indicated an 

association with health effects at the current level of the standard (72 FR 37870). With 

regard to the ambient concentrations at which O3-related mortality effects may be 

occurring, EPA recognized in the proposal that evidence of a causal relationship between 

adverse health effects and O3 exposures becomes increasingly uncertain at lower levels of 

exposure (72 FR 37880). This is discussed more fully in other sections. 

(18) Comment: Another group of commenters, including several industry organizations 

argued against placing any reliance on the time-series epidemiological studies, especially 

those studies related to mortality effects. The Annapolis Center (p. 46) makes the point 

that although there may be somewhat more positive associations than negative 

associations, there is so much noise or variability in the data that identifying which 

positive associations may be real health effects and which are not is beyond the capability 

of current methods. They cite the view that the CASAC Panel expressed in a June 2006 

letter (Henderson, 2006b), noting that “Because results of time-series studies implicate all 

of the criteria pollutants, findings of mortality time-series studies do not seem to allow us 

to confidently attribute observed effects specifically to individual pollutants.” 

 Several of these commenters focused on the O3 mortality multi-city studies in particular, 

arguing that, although these studies have the statistical power to distinguish weak 

relationships between daily O3 and mortality, they do not provide reliable or consistent 

evidence implicating O3 exposures as a cause of mortality. Several reasons were given, 

including: (a) the multi-city studies cited by EPA involve a wide range of city-specific 

effects estimates, including some large cities that have very slight or negligible effects 

(e.g., Los Angeles) (Bell et al., 2004), thus causing several commenters to question the 

relevance of a “national” effect of O3 on mortality and argue that a single national O3

concentration-mortality coefficient should be used and interpreted with caution 

(Rochester Report p. 4); (b) the multi-city mortality studies did not sufficiently account 

for other pollutants, for example, Bell et al. (2004) adjusted for PM10 but did not have the 

necessary air quality data to adequately adjust for PM2.5, which EPA has concluded also 

causes mortality and is correlated with O3, especially in the summer months (Annapolis 

Center, p. 42); and (c) these studies contain several findings that are inconsistent or 

implausible, such as premature mortality reported at such low levels as to imply that O3-

related mortality is occurring at levels well within natural background, which is not 

biologically plausible (Annapolis Center, p. 42). 

Response: Evidence supporting an association between short-term O3 exposure and 

premature mortality is not limited to multi-city time-series studies. Most single-city 

studies show elevated risk of total, non-accidental mortality, cardiorespiratory, and 

respiratory mortality (> 20 studies), including one study in an area that would have met 

current standard (Vedal et al., 2003). Three large meta-analyses, which pool data from 

many single-city studies to increase statistical power, reported statistically significant 

associations and examined sources of heterogeneity in those associations (Bell et al., 
51

2005; Ito et al., 2005; Levy et al. 2005). These studies found: (1) larger and more 

significant effects in the warm season than in the cool season or all year; (2) no strong 

evidence of confounding by PM; and (3) suggestive evidence of publication bias, but 

significant associations remain even after adjustment for the publication bias. 

 In the letter cited, the CASAC Panel did raise the issue of the utility of time-series studies 

in the standard setting process with regard to time-series mortality studies. Nevertheless, 

in a subsequent letter to the Administrator, CASAC noted these mortality studies as 

evidence to support a recommendation to revise the current primary O3 standard. 

“Several new single-city studies and large multi-city studies designed specifically to 

examine the effects of ozone and other pollutants on both morbidity and mortality have 

provided more evidence for adverse health effects at concentrations lower than the 

current standard (Henderson, 2006c, p. 3).” 

 With regard to the specific issues raised in the comments as to why the times-series 

mortality studies do not provide reliable or consistent evidence implicating O3 exposure 

as a cause of mortality, EPA has the following responses: 

 (1) The purpose of the NMMAPS approach is not to single out individual city results but 

rather to estimate the overall effect from the 95 communities. It was designed to provide 

a general, nationwide estimate. With regard to the very slight or negligible effects 

estimates for some large cities (e.g., Los Angeles), an important factor to consider is that 

the Bell et al. (2004) study used all available data in their analyses. Bell et al. reported 

that the effect estimate for all available (including 55 cities with all year data) and warm 

season (April-October) analyses for the 95 U.S. cities were similar in magnitude; 

however, in most other studies, larger excess mortality risks were reported in the summer 

season (generally June-August when O3 concentrations are the highest) compared to all 

year or the cold season. Though the effect estimate for Los Angeles is small compared to 

some of the other communities, it should be noted that all year data (combined warm and 

cool seasons) was used in the analyses for this city, which likely resulted in a smaller 

effect estimate. Because all year data was used for Los Angeles, the median O3 

concentration for Los Angeles is fairly low compared to the other communities, ranked 

23rd out of 95 communities. The median 24-hour average O3 concentration for Los 

Angeles in this dataset was 22 ppb, with a 10th percentile of 8 ppb to a 90th percentile of 

38 ppb. The importance of seasonal differences in O3-related health outcomes has been 

well documented. 

 (2) In section 7.4.6, O3 mortality risk estimates adjusting for PM exposure, the Criteria 

Document states that the main confounders of interest for O3, especially for the northeast 

U.S., are “summer haze-type” pollutants such as acid aerosols and sulfates. Since very 

few studies included these chemical measurements, PM (especially PM2.5) data, may 

serve as surrogates. However, due to the expected high correlation among the 

constituents of the “summer haze mix,” multipollutant models including these pollutants 

may result in unstable coefficients; and, therefore, interpretation of such results requires 

some caution. 
52

 In section 7.4.6 of the Criteria Document, Figure 7-22 shows the O3 risk estimates with 

and without adjustment for PM indices using all-year data in studies that conducted twopollutant analyses. Approximately half of the O3 risk estimates increased slightly, 

whereas the other half decreased slightly with the inclusion of PM in the models. In 

general, the O3 mortality risk estimates were robust to adjustment for PM in the models. 

 The U.S. 95 communities study by Bell et al. (2004) examined the sensitivity of acute O3-

mortality effects to potential confounding by PM10. Restricting analysis to days when 

both O3 and PM10 data were available, the community-specific O3-mortality effect 

estimates as well as the national average results indicated that O3 was robust to 

adjustment for PM10 (Bell et al., 2004). As commenters noted, there were insufficient 

data available to examine potential confounding by PM2.5. One study (Lipfert et al., 

2000) reported O3 risk estimates with and without adjustment for sulfate, a component of 

PM2.5. Lipfert et al. (2000a) calculated O3 risk estimates based on mean (45 ppb) less 

background (not stated) levels of 1-hour max O3 in seven counties in Pennsylvania and 

New Jersey. The O3 risk estimate was not substantially affected by the addition of sulfate 

in the model (3.2% versus 3.0% with sulfate) and remained statistically significant. 

 Several O3 mortality studies examined the effect of confounding by PM indices in 

different seasons (Figure 7-23, section 7.4.6, Criteria Document). In analyses using allyear data and warm-season only data, O3 risk estimates were once again fairly robust to 

adjustment for PM indices, with values showing both slight increases and decreases with 

the inclusion of PM in the model. In the analyses using cool season data only, the O3 risk 

estimates all increased slightly with the adjustment of PM indices, although none reached 

statistical significance. 

 The three recent meta-analyses (Bell et al., 2005; Ito et al., 2005; Levy et al. 2005) all 

examined the influence of PM on O3 risk estimates. No substantial influence was 

observed in any of these studies. In the analysis by Bell et al. (2005), the combined 

estimate without PM adjustment was 1.75% (95% PI: 1.10, 2.37) from 41 estimates, and 

the combined estimate with PM adjustment was 1.95% (95% PI: -0.06, 4.00) from 11 

estimates per 20 ppb increase in 24-hour average O3. In the meta-analysis of 15 cities by 

Ito et al. (2005), the combined estimate was 1.6% (95% CI: 1.1, 2.2) and 1.5% (95% CI: 

0.8, 2.2) per 20 ppb in 24-hour average O3 without and with PM adjustment, respectively. 

The additional time-series analysis of six cities by Ito et al. found that the influence of 

PM by season varied across alternative weather models but was never substantial. Levy 

et al. (2005) examined the regression relationships between O3 and PM indices (PM10 and 

PM2.5) with O3-mortality effect estimates for all year and by season. Positive slopes, 

which might indicate potential confounding, were observed for PM2.5 on O3 risk 

estimates in the summer and all-year periods, but the relationships were weak. The effect 

of one causal variable (i.e., O3) is expected to be overestimated when a second causal 

variable (e.g., PM) is excluded from the analysis, if the two variables are positively 

correlated and act in the same direction. However, EPA notes that the results from these 

meta-analyses, as well as several single- and multiple-city studies, indicate that 

copollutants, including PM, generally do not appear to substantially confound the 

association between O3 and mortality. 
53

 (3) Moreover, EPA asserts that the biological plausibility of the epidemiological 

mortality associations is generally supported by controlled human exposure and 

toxicological evidence of respiratory morbidity effects for levels at and below 0.080 ppm, 

but that biological plausibility becomes increasingly uncertain especially below 0.060 

ppm, the lowest level at which effects were observed in controlled human exposure 

studies. Further, at lower levels, it becomes increasingly uncertain as to whether the 

reported associations are related to O3 alone rather than to the broader mix of air 

pollutants present in the ambient air. EPA notes that the multi-city times series studies 

evaluated in this review can not resolve this issue. It also becomes increasingly uncertain 

as to whether effect thresholds exist but can not be clearly discerned by statistical 

analyses. Thus, when considering the epidemiological evidence in light of the other 

available information, it is reasonable to judge that at some point the epidemiological 

associations can not be interpreted with confidence as providing evidence that the 

observed health effects can be attributed to O3 alone. 

(19) Comment: NAM contends that EPA assumes that associations observed in time-series 

studies are significant but the absence of associations in long-term cohort studies is not. 

NAM states that EPA arrives at the conclusion that “ozone causes premature mortality in 

the short-term that cannot be observed over the long-term” by “leap of faith, not scientific 

inference” (NAM, p.50) 

Response: EPA rejects NAM’s contention that it has reached inappropriate conclusions 

about associations between O3 exposure and premature mortality. In the Criteria 

Document, EPA presented numerous recent epidemiologic studies conducted in the 

United States and abroad which have investigated the association between short-term 

exposure to O3 and mortality. Results from several large U.S. multicity studies as well as 

several single-city studies indicated a positive association between increases in ambient 

O3 levels and excess risk of all-cause (nonaccidental) daily mortality. Newly available 

experimental data from both animal and human studies provide evidence suggestive of 

plausible pathways by which risk of respiratory or cardiovascular morbidity and mortality 

could be increased by ambient O3 either acting alone or in combination with copollutants 

in ambient air mixes. These overall findings led EPA to conclude that there is highly 

suggestive evidence that O3 directly or indirectly contributes to non-accidental and 

cardiopulmonary-related mortality, but additional research is needed to more fully 

establish underlying mechanisms by which such effects occur. As few epidemiologic 

studies were available on long-term exposure to O3 and mortality, and the results from 

these studies were not consistent, EPA further concluded that there was insufficient 

evidence to suggest a causal relationship between long-term O3 exposure and increased 

risk for mortality in humans. 

 Kunzli et al. (2001) state that air pollution may play a role both in increasing the 

decedent’s underlying susceptibility or frailty and in triggering the event. In another 

case, the underlying frailty may be related to long term air pollution, but the event or the 

occurrence of death itself is unrelated to the levels of air pollution shortly before death. 

In the third case, reduced health status or frailty is not related to air pollution, but ambient 
54

air pollution experienced before death may trigger the terminal event. Thus, mortality 

from long-term exposure to a pollutant is not simply the accumulation of mortality from 

short-term exposures. Different mechanisms are at play for mortality associated with 

short-term versus long-term exposures; therefore, the inability to assess causality of the 

effect of long-term O3 exposure on mortality does not have bearing on the EPA’s finding 

that there is highly suggestive evidence that short-term exposure to O3 contributes to 

mortality. 

 Further, in a letter to the Administrator, CASAC noted these mortality studies as 

evidence to support a recommendation to revise the current primary O3 standard. 

“Several new single-city studies and large multi-city studies designed specifically to 

examine the effects of ozone and other pollutants on both morbidity and mortality have 

provided more evidence for adverse health effects at concentrations lower than the 

current standard” (Henderson, 2006c, p. 3). 

(20) Comment: NAM contends that EPA characterizes in the proposal notice that results from 

“numerous” multi-city and single-city studies show that the association between O3 and 

mortality do not appear to be changed in multipollutant models including PM10 or PM2.5 

(72 FR 37839). NAM contends that these studies are NMMAPS studies, none of which 

has daily PM2.5 data. These associations “do not appear to be changed” because they only 

measure PM10 (NAM, pp. 21). 

Response: EPA disagrees with NAM’s characterization of the basis for the statements 

made in the proposal notice with respect to what the scientific evidence shows with 

respect to the influence of PM in affecting the relationship observed between O3 and 

mortality. NAM mistakenly states that the conclusion in the proposal notice was solely 

based on results of the NMMAPS; in fact, it is based on the results of many other studies 

as presented in Figures 7-22 and 7-23 in section 7.4.6 of the Criteria Document. The 

studies used different PM indices, including PM2.5, PM10, BS, as well as TSP, to adjust 

for potential confounding by PM of the O3 relationship with mortality. Furthermore, 

while not relying on “new” studies published since completion of the Criteria Document, 

EPA notes that specifically in response to the use of PM10 by NMMAPS, a recently 

published study (not included in the Criteria Document) by Bell et al. (2007) reported 

that the national and community-specific effect estimates of the short-term effects of O3

on mortality were robust to inclusion of PM10 or PM2.5 in time-series models. 

(21) Comment: NAM contends that EPA has misinterpreted two epidemiologic studies by 

Moolgavkar and colleagues (1995; 2000) in EPA’s risk assessment and that EPA’s 

interpretation is different than that of the primary author and states that “EPA represents 

the results of these studies in ways that the corresponding author says are says are 

incorrect (Moolgavkar 2007, 4-5)” (NAM, p.21). 

Response: EPA disagrees with NAM’s contention that it has interpreted the two cited 

studies by Moolgavkar differently than the primary author. Moolgavkar (2007) on pages 

4 and 5 states that EPA included the positive association that he reported in his 1995 

Philadelphia paper but that EPA failed to cite his 2000 study in Los Angeles. EPA notes 
55

that there is nothing on pp. 4-5 of Moolgavkar that supports NAM’s contention that EPA 

has interpreted these two studies in a way different than the primary author. Furthermore, 

there is no discussion of EPA’s risk assessment or the use of Moolgavkar’s studies in the 

risk assessment on pp.4-5 of the Moolgavkar (2007) document. 

(22) Comment: Many commenters identified “new” studies that were not included in the 

Criteria Document that they stated support arguments both for and against the revision of 

the current O3 standard. Commenters who supported revising the current O3 standard 

identified new studies that generally supported EPA’s conclusions about the associations 

between O3 exposure and a range of respiratory and cardiovascular health outcomes. 

These commenters also identified new studies that provide evidence for associations with 

health outcomes that EPA has not linked to O3 exposure, such as cancer, and populations 

that EPA has not identified as being susceptible or vulnerable to O3 exposure, including 

African-American and women. Commenters who did not support revision of the current 

O3 standard often submitted the same “new” studies, but focused on different aspects of 

the findings. Commenters who did not support revision of the current O3 standard stated 

that these “new” studies provide inconsistent and sometimes conflicting findings that do 

little to resolve uncertainties regarding whether O3 has a causal role in the reported 

associations with adverse health outcomes, including premature mortality and various 

morbidity outcomes. 

Response: To the extent that these commenters included “new” scientific studies, studies 

that were published too late to be considered in the Criteria Document, in support of their 

arguments for revising or not revising the standards, EPA notes, as discussed in section II 

of the preamble to the final rule, that as in past NAAQS reviews, it 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 and will consider newly 

published studies for purposes of decision making in the next O3 NAAQS review. In 

provisionally evaluating commenters’ arguments, EPA notes that its provisional 

consideration of “new” science found that such studies did not materially change the 

conclusions in the Criteria Document. For more information about this provisional 

consideration see the Appendix. 

(23) Comment: NAM contends that EPA displays a systematic preference for studies that 

show positive associations even among studies that have important information quality 

limitations (NAM, pp. 30-31). NAM asserts that it has been unable to identify any 

epidemiological studies that EPA has identified as dispositive but which did not find a 

positive association. NAM claims that EPA “consistently selects studies that show 

positive associations with ozone (e.g., Gent et al., 2003; Mortimer et al., 2002) over 

studies that do not (e.g., Schildcrout et al., 2006) but does not establish an information 

quality basis for its selections” (NAM, p. 30). 

Responses: EPA rejects NAM’s contention that it displays a systematic preference for 

studies that show positive associations. EPA has clearly presented the results of 

Mortimer et al. (2002) and Gent et al. (2003), including results that were not positive. 

EPA has described studies that do not report positive or statistically significant results. 
56

The reason that NAM is unable to find any epidemiological studies that EPA has 

identified as dispositive but which did not find a positive association is that there is no 

single study or group of studies that is “dispositive.” EPA asserts that this would be an 

inappropriate way to represent the entire body of evidence. EPA uses a weight of 

evidence approach that integrates evidence from different types of studies including: 

animal toxicology; controlled human exposure; and epidemiological studies. 

Schildcrout et al. (2006) is not included in the Criteria Document as it was published after 

the date specified for inclusion (new studies accepted for publication by December 2004). 

In fact, it was published on-line in June of 2006, after the Criteria Document had been 

finalized. As noted above, 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 and will consider the newly published studies for purposes of 

decision making in the next O3 NAAQS review. This study has not been relied upon as it 

is one of the “new” studies that have been published since the cutoff date. 

 NAM cites only the Schildcrout study to support its claim that “EPA’s risk assessment 

for ozone includes a large measure of study selection bias” (NAM, p. 31). In fact, clearly 

the converse is true. EPA’s evaluation of the scientific evidence has been rigorous and 

thorough, and the process for selection of studies for inclusion in the assessment has been 

transparent and subject to review by the CASAC and the public. 

c. Evidence Pertaining to At-Risk Subgroups for O3-Related Effects 

 This section contains major comments on EPA’s assessment of the body of evidence, 

including controlled human exposure and epidemiological studies, related to the effects of O3

exposure on sensitive subpopulations. Since new information about the increased responsiveness 

of people with lung disease, especially children and adults with asthma, was an important 

consideration in the Administrator’s proposed decision that the current O3 standard is not 

adequate, many of the comments focused on this information and the conclusions drawn from it. 

There were also comments on other sensitive groups identified by EPA, as well as comments 

suggesting that additional groups should be considered at increased risk from O3 exposure. As 

with the comments on controlled human exposure and epidemiological studies, upon which 

judgments about sensitive subpopulations were based, the comments about EPA’s delineation of 

these groups were highly polarized. 

(1) Comment: In general, one group of commenters who supported revising the current O3

primary standard, including medical associations, public health and environmental 

groups, agreed in part with EPA’s assessment of the subpopulations that are at increased 

risk from O3 exposure, but commented that there are additional groups that need to be 

considered. A comment from ATS, AMA and other medical associations noted: 

Within this population exists a number of individuals uniquely at much higher 

risk for adverse health effects from ozone exposures, including children, people 
57

with respiratory illness, the elderly, outdoor workers and healthy children and 

adults who exercise outdoors. (ATS, p. 2) 

 These commenters agreed with EPA that, based on evidence from controlled human 

exposure and epidemiology studies, people with asthma, especially children, are likely to 

have greater lung function decrements and respiratory symptoms in response to O3

exposure than people who do not have asthma, and are likely to respond at lower levels. 

Because of this, these commenters make the point that controlled human exposure studies 

that employ healthy subjects will underestimate the effects of O3 exposures in people 

with asthma. 

 These commenters also agreed with EPA’s assessment that epidemiological studies 

provide evidence of increased morbidity effects, including lung function decrements, 

respiratory symptoms, emergency department visits and hospital admissions, in people 

with asthma and that controlled human exposure studies provide biological plausibility 

for these morbidity outcomes. Further, the Rochester Report evaluated some of the same 

the studies that EPA did and found similar results with regard to the increased 

inflammatory responses and increased airway responsiveness of people with asthma 

when exposed to O3. The Rochester Report reached the same conclusion that EPA did, 

that this increased responsiveness provides biological plausibility for the respiratory 

morbidity effects found in epidemiological studies. 

 

Several new studies have demonstrated that exposure of individuals with atopic 

asthma to sufficient levels of ozone produces an increase in specific airway 

responsiveness to inhaled allergens.........These findings, in combination with 

previously observed effects of ozone on nonspecific airway responsiveness and 

airway inflammation, supports the idea that ambient ozone exposure could result 

in exacerbation of asthma several days following exposure, and provides 

biological plausibility for the epidemiologic studies in which ambient ozone 

concentration has been associated with increased asthma symptoms, medication 

use, emergency room visits, and hospitalizations for asthma. (Rochester Report, 

pp. 57-58) 

 

 Commenters also often mentioned the increased susceptibility of people with COPD and 

in this case cited “new” studies not considered in the Criteria Document. 

 They identify that one potentially susceptible subpopulation that EPA did not focus on in 

the proposal is infants. Commenters from medical associations, and environmental and 

public health groups expressed the view that O3 exposure can have important effects on 

infants, including reduced birth weight, pre-term birth, and increased respiratory 

morbidity effects in infants. Exposure to O3 during pregnancy, especially during the 

second and third trimesters, was associated with reduced birth weight in full-term infants. 

Although this effect was noted at relatively low O3 exposure levels, the ATS notes that, 

“...the reduced birth weight in infants in the highest ozone exposures communities 

equaled the reduced birth weight observed in pregnant women who smoke” (ATS, p. 7). 
58

 Response: In general, EPA agrees with comments that there is very strong evidence from 

controlled human exposure and epidemiological studies that people with lung disease, 

especially children and adults with asthma, are susceptible to O3 exposure and are likely 

to experience more serious effects than those people who do not have lung disease. This 

means that controlled human exposure studies that employ subjects who do not have lung 

disease will likely underestimate effects in those people that do have asthma or other lung 

diseases. 

 In summarizing the epidemiological evidence related to birth-related health outcomes, the 

Criteria Document (p. 7-133) concludes that O3 was not an important predictor of several 

birth-related outcomes including premature births and low birth weight. Birth-related 

outcomes generally appeared to be associated with air pollutants that tend to peak in the 

winter and are possibly traffic-related. However, given that most of these studies did not 

analyze the data by season, seasonal confounding may have therefore influenced the 

reported associations. One study reported some results suggestive of associations 

between exposures to O3 in the second month of pregnancy and birth defects, but further 

evaluation of such potential associations is needed. With regard to comments about 

effect in infants, EPA notes that some of the studies cited by commenters were “new” 

studies too late for inclusion in the Criteria Document and thus were not considered in the 

Criteria Document. 

(2) Comment: The second group of commenters, mostly representing industry associations 

and some businesses opposed to revising the primary O3 standard, asserted that EPA is 

wrong to claim that new evidence indicates that the current standard does not provide 

adequate health public health protection for people with asthma. In support of this 

position, these commenters made the following major comments: (1) lung function 

decrements and respiratory symptoms observed in controlled human exposure studies of 

asthmatics are not clinically important; (2) EPA postulates that asthmatics would likely 

experience more serious responses and responses at lower levels than the subjects of 

controlled human exposure experiments, but that hypothesis is not supported by scientific 

evidence; and, (3) EPA recognized asthmatics as a sensitive subpopulation in 1997, and 

new information does not suggest greater susceptibility than was previously believed. 

 With regard to the first point, these commenters expressed the view that asthmatics are 

not likely to experience medically significant lung function changes or respiratory 

symptoms at ambient O3 concentrations at or even above the level of the current standard. 

Many of these commenters cited the opinion of one physician who was asked on behalf 

of a group of trade associations and companies to provide his views on the health 

significance for asthmatics of the types of responses that have been reported in controlled 

human exposure studies of O3. This commenter (McFadden) reviewed controlled human 

exposure studies of asthmatics from the last review as well as the recent controlled 

human exposure studies of healthy individuals (Adams 2002, 2003, and 2006) at 0.12, 

0.08, 0.06, and 0.04 ppm and expressed the view that “...these studies on asthmatics 

indicate that ozone exposures at ~ 0.12 ppm do not produce medically significant 

functional changes and are right around the inflection point where one begins to see an 

increase in symptoms; however, that increase is small” (McFadden, p. 3). This 
59

commenter went on to express the view that responses to O3 exposure at levels < 0 .08 

ppm would be even less and that the available data are not sufficiently robust to indicate 

that such exposures would present a significant health concern even to sensitive people 

like asthmatics. 

 With regard to the third point, commenters note that there is no significant new evidence 

establishing greater risk to asthmatics than was accepted in 1997, when EPA concluded 

that the existing NAAQS was sufficiently stringent to protect public health – including 

asthmatics – with and adequate margin of safety (UARG, pp. 22-23). To support this 

view, these commenters note the points made above, that the effects of O3 at and below 

0.080 ppm are not clinically significant and that asthmatics do not have more serious 

responses and responses at lower levels. They also express the view that epidemiological 

studies of asthmatics that provide new evidence of respiratory symptoms and medication 

use in asthmatic children are subject to the limitations of epidemiological studies 

discussed above (e.g., confounding by co-pollutants, and heterogeneity of results). In 

addition, these commenters identified a new, large multi-city panel study not included in 

the Criteria Document, by Schildcrout et al. (2006), which reported no association 

between O3 concentrations and exacerbation of asthma. 

Response: With regard to the first point, EPA notes that this commenter based his 

comment on the group mean functional and respiratory symptom changes in the studies 

he reviewed. EPA agrees that group mean changes at these levels are relatively small and 

has described them as such in both the previous review and this one (72 FR 37828). The 

importance of group mean changes is to evaluate the statistical significance of the 

association between the exposures and the observed effects, to try to determine if the 

observed effects are likely due to O3 exposure rather than chance. In the previous review 

as well as in this one, EPA has also focused on the fact that some individuals experience 

more severe effects that may be clinically significant. With regard to the significance of 

individual responses, this commenter (McFadden, p. 2) states “...transient decreases in 

FEV1 of 10-20% are not by themselves significant or meaningful to asthmatics.... It has 

been my experience from examining and studying thousands of patients for both clinical 

and research purposes that asthmatics typically will not begin to sense 

bronchoconstriction until their FEV1 falls about 50% from normal.” EPA strongly 

disagrees with this assessment. As stated in the Criteria Document (Table 8-3, p. 8-68) 

for people with lung disease, even moderate functional responses (e.g., FEV1 decrements 

≥ 10% but < 20%) would likely interfere with normal activities for many individuals, and 

would likely result in more frequent medication use. EPA notes that in the context of 

standard setting, CASAC indicated (Henderson, 2006c) that a focus on the lower end of 

the range of moderate functional responses (e.g., FEV1 decrements ≥ 10%) is most 

appropriate for estimating potentially adverse lung function decrements in people with 

lung disease. 

 With regard to the second point, whether asthmatics would likely experience more 

serious responses and responses at lower levels than the subjects of controlled human 

exposure experiments and EPA’s discussion of the relationship of increased airway 

responsiveness and inflammation experienced by asthmatics to exacerbation of asthma, 
60

this commenter stated that “there simply are no data to support the sequence described” 

and that “the assumption that these responses would lead to clinical manifestations in 

terms of exacerbations of asthma or other adverse health effects remains unproven 

theory”(McFadden, p. 3). In the proposal (72 FR 37826, and 37846-37847), EPA 

describes the evidence that people with asthma are as sensitive as, if not more sensitive 

than, normal subjects in manifesting O3-induced pulmonary function decrements. 

Controlled human exposure studies show that asthmatics present a differential response 

profile for cellular, molecular, and biochemical parameters that are altered in response to 

acute O3 exposure. Asthmatics have greater O3-induced inflammatory responses and 

increased O3-induced airway responsiveness (both incidence and duration) that could 

have important clinical implications. 

 There are two ways to interpret these comments. One way to interpret them is that 

because these controlled human exposure studies have not produced exacerbations of 

asthma in study subjects resulting in the need for medical attention, there are no data to 

support the clinical significance of the results. EPA rejects this interpretation because it 

would be unethical to knowingly conduct a controlled human exposure study that would 

lead to exacerbation of asthma. Controlled human exposure studies are specifically 

designed to avoid these types of responses. The other interpretation is that the 

commenter does not agree that the differences in lung function, inflammation and 

increased airway responsiveness found in these controlled human exposure studies 

support the inference that asthmatics are likely to have more serious responses than 

healthy subjects, and that these responses could have important clinical implications. 

EPA rejects this interpretation as well. EPA did not base its increased concern for 

asthmatics solely on the results of the controlled human exposure studies, but has 

appropriately used a weight of evidence approach, integrating evidence from animal 

toxicological, controlled human exposure and epidemiological studies as a basis for this 

concern. The Criteria Document evaluated a number of epidemiological studies that have 

been conducted using asthmatic study populations (72 FR 37847). These studies suggest 

that O3 exposure may be associated with increased respiratory symptoms and medication 

use in children with asthma, and also respiratory symptoms, lung function decrements, 

emergency department visits and hospital admissions for respiratory causes and 

respiratory mortality. The Criteria Document concludes that the positive and robust 

epidemiological associations between O3 exposure and emergency department visits and 

hospitalizations in the warm season are supported by the human clinical, animal 

toxicological and epidemiological evidence for lung function decrements, increased 

respiratory symptoms, airway inflammation, and increased airway responsiveness (72 FR 

37832). The CASAC Panel itself expressed the view that people with asthma, especially 

children, have been found to be more sensitive to O3 exposure, and indicated that EPA 

should place more weight on inflammatory responses and serious morbidity effects, such 

as increased respiratory-related emergency department visits and hospitalizations 

(Henderson, p. 4). Moreover, the Rochester Report, cited above, reaches essentially the 

same conclusions as EPA did, that the evidence from controlled human exposure studies 

provides biological plausibility for the epidemiological studies in which ambient O3

concentrations have been associated with increased asthma symptoms, medication use, 

emergency room visits, and hospitalizations for asthma. Therefore, EPA continues to 
61

assert that there is strong evidence that asthmatics likely have more serious responses to 

O3 exposure than people without asthma, and that these responses have the potential to 

lead to exacerbation of asthma as indicated by the serious morbidity effects, such as 

increased respiratory-related emergency department visits and hospitalizations found in 

epidemiological studies. 

 With regard to the third point, at the time of the last review EPA concluded that people 

with asthma were at greater risk because the impact of O3-induced responses on alreadycompromised respiratory systems would noticeably impair an individual's ability to 

engage in normal activity or would be more likely to result in increased self-medication 

or medical treatment. At that time there was little evidence that people with pre-existing 

disease were more responsive than healthy individuals in terms of the magnitude of 

pulmonary function decrements or symptomatic responses. The new results from 

controlled exposure and epidemiologic studies indicate that individuals with preexisting 

lung disease, especially people with asthma, are likely to have more serious responses 

than people who do not have lung disease and therefore are at greater risk for O3 health 

effects than previously judged in the 1997 review. EPA notes that comments on the 

limitations of epidemiological studies and the evidence from “new” studies (not in the 

Criteria Document) have been addressed above. 

d. Adversity of Health Effects 

 This section contains comments on EPA’s assessment of the body of evidence 

particularly related to judgments about the adversity of the health effects associated with O3

exposure, primarily estimates of moderate lung function decrements (FEV1 decrements ≥ 10%) 

from controlled human exposure studies. 

(1) Comment: NAM contends that there is no consensus concerning where to draw the line 

distinguishing adverse from non-adverse effects, such as effects that are transient and 

reversible over short periods of time. 

NAM contends that EPA increasingly treats as adverse mere exposure and that when 

exposure cannot be detected, EPA increasingly looks for biomarkers of exposure - 

irrespective of whether they are associated with symptoms or signs; their selectivity with 

respect to the hazard of concern; or the capacity to detect them without complex analytic 

techniques. As an example of this, the commenter points to the definition of a “key 

event” in EPA’s Guidelines of Carcinogenic Risk Assessment. A “key event” is an 

empirically observable precursor step that is itself a necessary element of the mode of 

action or is a biologically based marker for such an element. The term “mode of action” 

is defined as a sequence of key events and processes, starting with interaction of an agent 

with a cell, proceeding through operational and anatomical changes, and resulting in 

cancer formation. The scientific task is a very limited one, consisting only of the 

assignment of phenomena into categories defined by policy. Commenter notes that 

information quality guidelines require that the Agency be transparent in its scientific 

description of these phenomena and the available data. 
62

NAM contends that this same problem infects EPA’s description of effects to asthmatics. 

Transient and reversible effects, such as chest tightness or wheezing, have a dozen 

reported triggers, including laughter. How similar are the effects of O3 to the effects 

caused by exposure to humor? (NAM, p. 42) 

 Response: EPA strongly rejects NAM’s assertion that there is no consensus in 

distinguishing adverse from non-adverse effects, with regard to the Administrator’s 

judgments as to when O3-related effects become regarded as adverse to the health of 

individuals. Evaluating the adversity of health effects in individuals and the resulting 

impacts on public health is a main focus of all NAAQS reviews. The issue of adversity 

was clearly addressed in this review and the judgments about adversity are consistent 

with the previous review. In this review, as in the 1997 review of the O3 standard, the 

Administrator has looked to guidelines published by ATS and the advice of the CASAC 

panel. While recognizing that perceptions of “medical significance” and “normal 

activity” may differ among physicians, lung physiologists and experimental subjects, the 

ATS (1985)4

 defined adverse respiratory health effects as “medically significant 

physiologic changes generally evidenced by one or more of the following: (1) 

interference with the normal activity of the affected person or persons, (2) episodic 

respiratory illness, (3) incapacitating illness, (4) permanent respiratory injury, and/or (5) 

progressive respiratory dysfunction.” During the 1997 review, it was concluded that 

there was evidence of causal associations from controlled human exposure studies for 

effects in the first of these five ATS-defined categories, evidence of statistically 

significant associations from epidemiological studies for effects in the second and third 

categories, and evidence from animal toxicology studies, which could be extrapolated to 

humans only with a significant degree of uncertainty, for the last two categories. 

For ethical reasons, clear causal evidence from controlled human exposure studies still 

covers only effects in the first category. However, for this review there are results from 

epidemiological studies, upon which to base judgments about adversity, for effects in all 

of the categories. Statistically significant and robust associations have been reported in 

epidemiology studies falling into the second and third categories. These more serious 

effects include respiratory events (e.g., triggering asthma attacks) that may require 

medication (e.g., asthma), but not necessarily hospitalization, as well as respiratory 

hospital admissions and emergency department visits for respiratory causes. 

Less conclusive, but still positive associations have been reported for school absences 

and cardiovascular hospital admissions. Human health effects for which associations 

have been suggested through evidence from epidemiological and animal toxicology 

 

4

 In 2000, the American Thoracic Society (ATS) published an official statement on “What 

Constitutes an Adverse Health Effect of Air Pollution?” (ATS, 2000), which updated its earlier 

guidance (ATS, 1985). Overall, the new guidance does not fundamentally change the approach 

previously taken to define adversity, nor does it suggest a need at this time to change the 

structure or content of the tables describing gradation of severity and adversity of effects 

described below.
63

studies, but have not been conclusively demonstrated still fall primarily into the last two 

categories. In the last review of the O3 standard, evidence for these more serious effects 

came from studies of effects in laboratory animals. Evidence from animal studies 

evaluated in this Criteria Document strongly suggests that O3 is capable of damaging the 

distal airways and proximal alveoli, resulting in lung tissue remodeling leading to 

apparently irreversible changes. Recent advancements of dosimetry modeling also 

provide a better basis for extrapolation from animals to humans. Information from 

epidemiological studies provides supporting, but limited evidence of irreversible 

respiratory effects in humans than was available in the prior review. Moreover, the 

findings from single-city and multi-city time-series epidemiology studies and metaanalyses of these epidemiology studies are highly suggestive of an association between 

short-term O3 exposure and mortality particularly in the warm season. 

While O3 has been associated with effects that are clearly adverse, application of these 

guidelines, in particular to the least serious category of effects related to ambient O3

exposures, involves judgments about which medical experts on the CASAC panel and 

public commenters have expressed diverse views in the past. It is these effects that are 

the focus of this comment, and have been an important focus in the current and the 1997 

review of the primary O3 standard. To help frame such judgments, EPA staff have 

defined specific ranges of 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, that have been used in previous NAAQS reviews. These 

ranges of pulmonary responses and their associated potential impacts are summarized in 

Tables 3-2 and 3-3 of the Staff Paper (EPA, 2007). 

For active healthy people, moderate levels of functional responses (e.g., FEV1

decrements of > 10% but < 20%, lasting up to 24 hours) and/or moderate symptomatic 

responses (e.g., frequent spontaneous cough, marked discomfort on exercise or deep 

breath, lasting up to 24 hours) would likely interfere with normal activity for relatively 

few responsive individuals. On the other hand, EPA staff determined that large 

functional responses (e.g., FEV1 decrements > 20%, lasting longer than 24 hours) and/or 

severe symptomatic responses (e.g., persistent uncontrollable cough, severe discomfort 

on exercise or deep breath, lasting longer than 24 hours) would likely interfere with 

normal activities for many responsive individuals. EPA staff determined that these 

would be considered adverse under ATS guidelines. In the context of standard setting, 

CASAC indicated that a focus on the mid to upper end of the range of moderate levels of 

functional responses (e.g., FEV1 decrements ≥ 15% but < 20%) is appropriate for 

estimating potentially adverse lung function decrements in active healthy people. 

However, for people with lung disease, even moderate functional (e.g., FEV1 decrements 

> 10% but < 20%, lasting up to 24 hours) or symptomatic responses (e.g., frequent 

spontaneous cough, marked discomfort on exercise or with deep breath, wheeze 

accompanied by shortness of breath, lasting up to 24 hours) would likely interfere with 

normal activity for many individuals, and would likely result in more frequent use of 

medication. For people with lung disease, large functional responses (e.g., FEV1

decrements > 20%, lasting longer than 24 hours) and/or severe symptomatic responses 
64

(e.g., persistent uncontrollable cough, severe discomfort on exercise or deep breath, 

persistent wheeze accompanied by shortness of breath, lasting longer than 24 hours) 

would likely interfere with normal activity for most individuals and would increase the 

likelihood that these individuals would seek medical treatment. In the context of standard 

setting, the CASAC indicated (Henderson, 2006c) that a focus on the lower end of the 

range of moderate levels of functional responses (e.g., FEV1 decrements ≥ 10%) is most 

appropriate for estimating potentially adverse lung function decrements in people with 

lung disease. There is more discussion of the focus on the lower end of moderate levels 

of functional responses (e.g., FEV1 decrements ≥ 10%) in the next comment below. 

In judging the extent to which these impacts represent effects that should be regarded as 

adverse to the health status of individuals, an additional factor that has been considered in 

previous NAAQS reviews is whether such effects are experienced repeatedly during the 

course of a year or only on a single occasion. While some experts would judge single 

occurrences of moderate responses to be a “nuisance,” especially for healthy individuals, 

a more general consensus view of the adversity of such moderate responses emerges as 

the frequency of occurrence increases. This is the reason that EPA focuses not only on 

single, but also on repeated occurrences of moderate lung function decrements in schoolage children. 

As indicated by the discussion above and the additional discussions of adversity in the 

rationale for finding that the current standard needs revision and rationale for the level of 

the standard that is appropriate, EPA has clearly addressed the issue of the adversity of 

the transient and reversible effects attributable to O3 exposure, specifically respiratory 

symptoms and lung function decrements, in both healthy people and people who have 

asthma. Moreover, EPA has evaluated the adversity of these effects in the context of 

daily activities. Its evaluation has been subjected to peer-review and supported by the 

CASAC in both the 1997 and current reviews of the O3 standard. In this review of the O3

standard EPA has not evaluated the adversity of any biomarkers of exposure, so with 

regard to the discussion of biomarkers the comment is not accurate. 

(2) Comment: NAM contends that the 10% threshold for FEV1 decrements is a post hoc 

threshold apparently chosen for compatibility with EPA staff policy recommendations in 

the Staff Paper. This threshold differs significantly from the clinical thresholds 

recommended by the ATS (15%) and CASAC (15-20%). While EPA says CASAC 

agrees with its 10% threshold, there is “strong evidence suggesting that any such 

agreement was at best a minority view based on policy considerations not science” 

(NAM, p.19). An individual CASAC panel member stated: 

While most attributions to CASAC are correct, I don’t believe it was a written 

opinion of CASAC that “more emphasis should be placed on numbers of subjects 

in controlled human exposure studies with FEV1 decrements greater than 10%, 

which can be clinically significant, rather than on the relatively small decrements” 

(p. 6-43). While this may have merit in some (or even many) situation, for 

example when noting that 26% of individuals had > 10% FEV1 decrements at 

0.08 ppm ..., in other cases, such as the specific case of 0.060 or 0.040 ppm 

exposures, this approach amounts to attempting to find effects in a very few 
65

individuals when the statistical tests are not significant, which is a dangerous 

precedent – especially in this case where we are looking at small effects in 3 of 30 

vs. 1 of 30, a pitiful number on which to attempt to base policy ... (CASAC, 

2007, C-30) (NAM, pp. 19-20) 

NAM states that EPA did not correct the misstatement in the final Staff Paper on p.6-43. 

Response: The focus on FEV1 decrements ≥ 10% came up in the context of evaluation of 

the adversity of transient and reversible effects, as discussed in the comment above. 

There was an extensive discussion of this topic at the August 24, 2006 meeting of the 

CASAC O3 Panel in Research Triangle Park, NC (see transcript p. 142-150). During the 

discussion of Chapter 3 of the Staff Paper, one of the CASAC Panel members noted that 

in Chapter 6 of the Staff Paper, EPA staff focused on the lower end of the moderate range 

(i.e., FEV1 decrements ≥ 10%) as an indicator of adverse effects in people with asthma, 

given the new evidence that people with asthma have more serious responses to O3

exposure than healthy people. The CASAC panel, including Dr. Vedal the author of the 

opinion cited in the comment above, agreed that this focus on a 10% reduction in FEV1

was an appropriate one and should also be included in the discussion of adversity in 

Chapter 3 of the Staff Paper. Clearly the CASAC Panel agreed that more weight should 

be placed on lung function decrements (FEV1 decrements ≥ 10%) as an indictor of 

adversity for people with asthma. Since FEV1 is measured primarily in controlled human 

exposure studies, EPA asserts that this statement “more emphasis should be placed on 

numbers of subjects in controlled human exposure studies with FEV1 decrements greater 

than 10%, which can be clinically significant,” is appropriately attributed to the CASAC 

Panel. 

The commenter also incorrectly asserts that ATS has recommended a clinical threshold of 

a 15% decrement in FEV1. In fact, ATS has not done this. The ATS guidelines indicate 

that a reduction in FEV1 or FVC associated with clinical symptoms is adverse. The 

guidelines also indicate that a small but significant reduction in a population mean FEV1

is probably medically significant: 

Exposure could also enhance risk for a population to an unacceptable degree, 

perhaps without shifting the risks of any particular individuals to an unacceptable 

level. Effects on persons with asthma are illustrative. A population of children 

with asthma could have a distribution of lung function such that no individual 

child has a level associated with significant impairment. Exposure to air pollution 

could shift the distribution toward lower levels without bringing any individual 

child to a level that is associated with clinically relevant consequences. 

Individuals within the population would, however, have diminished reserve 

function and are at potentially increased risk if affected by another agent, e.g., a 

viral infection. Assuming that the relationship between the risk factor and the 

disease is causal, the committee considered that such 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, 2000) 
66

 ATS also defines as adverse increased exacerbations of disease (i.e., shortness of breath) 

in people with chronic lung disease that could be reflected in a variety of ways, including 

for example, being less able to cope with daily activities. Clearly this is entirely 

consistent with EPA’s definition of adversity, as discussed above. 

e. Comments on Role of Ground-Level O3 in Solar Radiation-Related Health Effects 

Comment: A few commenters responded to EPA’s request for comments, including 

available studies or data that would be relevant to conducting a critical assessment with 

reasonable certainty of UV-induced health outcomes and how evidence of UV-induced 

health outcomes might inform the Agency’s review of the primary O3 standard potential 

preventative effect ground level ozone may have in reducing exposure to ultraviolet 

radiation. 

ATS, AMA and other medical organizations expressed the view that given the known 

adverse respiratory health effects of O3, it would appear more prudent to focus on current 

approaches to reducing ultraviolet radiation by preventing UV exposures, rather than 

permitting the harmful respiratory effects of O3. These commenters conclude that there is 

“no compelling evidence that should persuade the Administrator to consider this issue 

when setting the NAAQS O3 standard.” (ATS et al., p. 9) 

AAM and a few other commenters that did not support revising the current primary O3

standard expressed the opposite view that tropospheric O3 has a beneficial effect along 

with stratospheric O3 in protecting public health from solar UV radiation. A reduction in 

tropospheric O3 would act to increase UV exposures and UV-induced health effects, 

including both non-melanoma and melanoma skin cancer. These commenters noted that 

when EPA responded to a court’s remand (68 FR 614, Jan 2003) to consider UV-related 

effects of ground level O3 there was no disagreement with the fact that ground-level O3

has beneficial effects. The only disagreements centered on the magnitude of the effect or 

the certainty with which it can be estimated. 

Response: EPA asserts that it has appropriately assessed the UV-B shielding effects of 

tropospheric O3. The Criteria Document has assessed potential indirect effects related to 

the presence of O3 in the ambient air by considering the role of ground-level O3 in 

mediating human health effects that may be directly attributable to exposure to solar 

ultraviolet radiation (UV–B). The Criteria Document (chapter 10) focused this 

assessment on three key factors, including those factors that govern (1) UV–B radiation 

flux at the earth’s surface, (2) human exposure to UV–B radiation, and (3) human health 

effects due to UV–B radiation. In so doing, the Criteria Document provided a thorough 

analysis of the current understanding of the relationship between reducing ground-level 

O3 concentrations and the potential impact these reductions might have on increasing 

UV–B surface fluxes and indirectly contributing to UV–B related health effects.
67

There are many factors that influence UV–B radiation penetration to the earth’s surface, 

including latitude, altitude, cloud cover, surface albedo, PM concentration and 

composition, and gas phase pollution. Of these, only latitude and altitude can be defined 

with small uncertainty in any effort to assess the changes in UV–B flux that may be 

attributable to any changes in tropospheric O3 as a result of any revision to the O3

NAAQS. Such an assessment of UV–B related health effects would also need to take 

into account human habits, such as outdoor activities (including age- and occupationrelated exposure patterns), dress and skin care to adequately estimate UV–B exposure 

levels. However, little is known about the impact of these factors on individual exposure 

to UV–B. 

Moreover, detailed information does not exist regarding other factors that are relevant to 

assessing changes in disease incidence, including: Type (e.g., peak or cumulative) and 

time period (e.g., childhood, lifetime, current) of exposures related to various adverse 

health outcomes (e.g., damage to the skin, including skin cancer; damage to the eye, such 

as cataracts; and immune system suppression); wavelength dependency of biological 

responses; and interindividual variability in UV–B resistance to such health outcomes. 

Beyond these well recognized adverse health effects associated with various wavelengths 

of UV radiation, the Criteria Document (section 10.2.3.6) also discusses protective 

effects of UV–B radiation. Recent reports indicate the necessity of UV–B in producing 

vitamin D, and that vitamin D deficiency can cause metabolic bone disease among 

children and adults, and may also increase the risk of many common chronic diseases 

(e.g., type I diabetes and rheumatoid arthritis) as well as the risk of various types of 

cancers. Thus, the Criteria Document concludes that any assessment that attempts to 

quantify the consequences of increased UV–B exposure on humans due to reduced 

ground-level O3 must include consideration of both negative and positive effects. 

However, as with other impacts of UV–B on human health, this beneficial effect of UV–

B radiation has not been studied in sufficient detail to allow for a credible health benefits 

or risk assessment. In conclusion, the effect of changes in surface-level O3

concentrations on UV-induced health outcomes cannot yet be critically assessed within 

reasonable uncertainty (Criteria Document, p. 10–36). 

The Agency last considered indirect effects of O3 in the ambient air in its 2003 final 

response to a remand of the Agency’s 1997 decision to revise the O3 NAAQS. In so 

doing, based on the available information in the last review, the Administrator 

determined that the information linking (1) Changes in patterns of ground-level O3

concentrations likely to occur as a result of programs implemented to attain the 1997 O3

NAAQS to (2) changes in relevant exposures to UV–B radiation of concern to public 

health was too uncertain at that time to warrant any relaxation in the level of public health 

protection previously determined to be requisite to protect against the demonstrated direct 

adverse respiratory effects of exposure to O3 in the ambient air (68 FR 614). At that 

time, the more recent information on protective effects of UV–B radiation was not 

available, such that only adverse UV–B-related effects could be considered. Taking into 

consideration the more recent information available in this review, the Criteria Document 

and Staff Paper conclude that the effect of changes in ground-level O3 concentrations, 

likely to occur as a result of revising the O3 NAAQS, on UV-induced health outcomes, 
68

including whether these changes would ultimately result in increased or decreased 

incidence of UV–B-related diseases, cannot yet be critically assessed. 

4. Specific Comments on the Population Exposure Analyses 

Comments related to the population exposure analyses conducted for O3 are addressed in 

this section. Incorporating responses contained in section II.B.2.b and II.C.4 of the preamble to 

the final rule, EPA provides the following responses to specific issues related to the exposure 

analyses. Comments related to the overall weight placed on the exposure analyses in reaching 

decisions on the need to revise the current standard and on an appropriate standard level are 

addressed in the preamble to the final rule and in section II.A.2.c.ii of this document. 

(1) Comment: Several commenters (e.g., UARG, API, AAM) contend that EPA has failed 

to adequately address the significant uncertainties with its exposure assessment, including 

those associated with EPA’s APEX exposure model. 

Response: As discussed in the proposal notice, EPA recognizes that the exposure 

assessment necessarily contains many sources of uncertainty including those noted by 

these commenters, and EPA has accounted for such uncertainties to the extent possible. 

EPA developed and presented an uncertainty analysis addressing the most significant 

uncertainties affecting the exposure estimates (Langstaff, 2007). The CASAC Panel 

reviewed in detail the approach used to assess exposure and the presentation of the results 

in the Staff Paper. EPA believes, and the CASAC Panel concurred, that the model used 

to estimate exposures represents a state-of-the-art approach and that “there is an explicit 

discussion of the limitations of the APEX model in terms of variability and quality of the 

input data, which is appropriate and fine” (Henderson, 2006c, p. 11). Although EPA 

agrees that important limitations and uncertainties remain, and that future research 

directed toward addressing these uncertainties is warranted, EPA believes that overall 

uncertainties of short-term O3 population exposure assessment have diminished since the 

last review. The Administrator has carefully considered the limitations and uncertainties 

associated with these quantitative assessments but continues to believe that they provide 

general support for concluding that exposures and health risks associated with meeting 

the current 8-hour standard are important from a public health perspective and that the 8-

hour standard needs to be revised to provide additional protection in order to protect 

public health with an adequate margin of safety. 

(2) Comment: One commenter (AAM) stated that O3 monitors are often sited so as to 

capture the highest O3 concentrations expected in an area. Since downwind sites are 

usually the design value sites, they will dominate the upper tail of the O3 distribution and 

yet may not reflect the overall outdoor exposures in the area. This phenomenon will tend 

to bias the modeled exposures high. 

Response: EPA agrees that O3 concentrations can vary spatially across an urban area. In 

the exposure modeling conducted, EPA used several O3 monitors in each area to take into 

account the spatial variations of O3 concentrations. The geographic variation of O3
69

concentration is accounted for by using measurements from the closest O3 monitor to 

represent concentrations in a neighborhood and the measurements at downwind monitors 

are applied only to the downwind areas. Therefore this is not a source of bias in the 

modeled exposures. 

(3) Comment: One commenter (AAM) stated that O3 concentrations are lower at person’s 

breathing height compared to measurement height. (Wisbeth et al. measured the 

increment between O3 at 2 and 10 meters and reported an average 13 percent difference.) 

 This phenomenon will tend to bias the modeled exposures high. 

Response: EPA recognizes that there can be differences in O3 concentrations between 

breathing and monitor heights and that this will result in some uncertainty in the modeled 

exposures, with some exposures underestimated and some overestimated as a result. 

However, as discussed in the exposure uncertainty analysis, data were not available to 

quantify the potential biases of differences between O3 concentrations at a person’s 

breathing height compared to the heights of nearby monitors. EPA believes that these 

biases, to the extent that they exist, are relatively small during warm summer afternoons 

when the atmosphere is well-mixed and O3 concentrations tend to be higher. 

(4) Comment: One commenter (AAM) stated that if people spend time outdoors in closer 

proximity to streets or in areas with more surface area (buildings, etc.) to quench O3, their 

exposures will be below that measured at the monitor. This commenter contends that the 

APEX model assumes that whatever O3 is interpolated from the monitor measurement is 

the actual O3 exposure in the outdoor microenvironment, which will tend to bias the 

modeled exposures high. 

Response: This statement about APEX is not true. The reduction in O3 concentrations 

near roadways due to titration of O3 from automobile emissions of NO is accounted for 

and explicitly modeled in APEX and thus does not bias estimates of exposures. This 

phenomenon was modeled through the use of “proximity factors,” which adjust the 

monitored concentrations to account for the titration of O3 by NO emissions (the 

monitored concentrations are multiplied by the proximity factors). Three proximity 

factor distributions were developed, one for local roads, one for urban roads, and one for 

interstates, with mean factors of 0.75, 0.75, and 0.36 respectively (section 3.10.2, Human 

Exposure TSD). Furthermore, the uncertainty of these proximity factor distributions was 

included in the exposure uncertainty analysis. 

(5) Comment: Some commenters (API, AAM) noted that the upper tail of the distribution of 

breathing rates (equivalent ventilation rates (EVR)) is particularly important because it is 

a critical factor in determining the number of exposures of concern. These commenters 

contend that the APEX model predicts more elevated ventilation rate occurrences than 

observed in real world data. They argue that this results in an overestimation of the 

number of exposures of concern and of the risk estimates. 

Response: EPA does not agree that the APEX model overestimates the number of 

exposures at specified exertion levels across all age groups. EPA did a comparison 
70

(Langstaff, 2007) of ventilation rates predicted by APEX to measurements which showed 

APEX over-predicting ventilation rates for ages 5 to 10, under-predicting ventilation rates 

for ages 11 to 29 and greater than 39, and in close agreement for ages 30 to 39. The 

overall agreement was judged favorable, and the errors of the predicted ventilation rates 

were partially incorporated into the overall uncertainty analysis as part of the 

uncertainties of the metabolic equivalents (MET), which are the primary drivers of 

ventilation rates. 

(6) Comment: One set of comments (ALA et al., pp. 104-105) contends that school 

absences, increased use of asthma medication, emergency room visits, and hospital 

admissions are not accurately reflected in EPA’s use of “exposures of concern.” 

Contrary to EPA’s assertion, the exposure estimates cannot be generalized beyond the 

effects studied in the controlled human exposure studies -- that is, primarily lung function 

decrements and respiratory symptoms. Other health endpoints, such as school absences, 

increased use of asthma medications, long-term deficits in lung function and associated 

risk of illness, emergency room visits, hospital admissions, and premature deaths, have 

been characterized principally in epidemiological studies, where increased risks are a 

function of the ambient concentrations. The exposure analysis, which relies on activity 

profiles to minimize assumed population exposures, is not relevant to the estimation of 

those health endpoints which have been reported in epidemiological studies. This 

limitation contradicts EPA’s desired use of the exposure assessment to “provide some 

perspective on the public health impacts of health effects that we cannot currently 

evaluate in quantitative risk assessments.” 72 FR 37853. (ALA et al., pp. 104-105) 

Response: The exposure analysis is not intended to be used to characterize potential 

health risks for health endpoints which have been reported in epidemiological studies. It 

also is not true that the exposure modeling “relies on activity profiles to minimize 

assumed population exposures” (ALA, p. 105). In discussing exposures at specified 

exertion levels EPA has referred to evidence of inflammation, increased airway 

responsiveness, and changes in host defenses in healthy people exposed to 0.080 ppm O3 

in controlled human exposure studies. 

(7) Comment: EPA’s exposure model underestimates repeated outdoor exposures. As EPA 

acknowledges, CHAD underestimates the frequency of occurrences of “repeated routine 

behavior.” This results in underestimates of exposures to children who spend large 

portions of their summers playing outside or in summer camps. The “exposures of 

concern” assessment does not include outdoor workers or outdoor recreation enthusiasts 

who receive higher inhaled doses of O3 due to their increased ventilation rates. Outdoor 

workers experience more frequent exposure to O3 than the general population, due to the 

time spent outdoors, and the increased breathing rate under physical exertion. Several 

studies have examined the association between O3 exposure and health outcomes in 

outdoor workers, including farm workers, mail carriers, and others. The Exposure 

Assessment and Risk Assessment completely ignore health risks to outdoor workers, a 

population that is exposed to ambient O3 while under exertion. In the United States, this 

population constitutes more than 9 million people. Outdoor workers include a diverse set 

of occupations, ranging from construction workers to farm workers. (ALA et al., p. 105) 
71

Response: This is discussed in the assessment of uncertainty of the exposure analysis. 

While EPA has not conducted an exposure analysis for outdoor workers since it was 

judged that school aged children presented the greatest likelihood of being outdoors and 

exposed under moderate exertion averaged over an 8-hour period based on the exposure 

analyses conducted for outdoor workers and children in the prior O3 NAAQS review. 

EPA has recognized in the Staff Paper and in the final notice that outdoor workers would 

also be potentially affected by O3 exposure. The Administrator has concluded that the 

revised standard will protect this population as well with an adequate margin of safety. 

(8) Comment: One set of comments (ALA et al., p.105) contends that the exposure 

assessment focuses on the average child rather than the highly exposed and that active 

children are not well characterized. The exposure and risk assessments do not adequately 

capture risks to active children. EPA had initially profiled exposures of “active” children 

as a separate subpopulation, but subsequently dropped this category, and considers only 

exposures to average children. This analytical approach is then used to argue against 

adequate protection for those active children or adults that spend a lot of time outdoors. 

Because EPA averages the activity patterns of active and sedentary people, standards 

may not protect the most exposed individuals. (ALA et al., p. 105) 

Response: This assertion is incorrect; all types of individuals are modeled, not the 

“average child.” The exposure modeling does not average activity patterns. Active 

children are a subset of all children, which are modeled. 

(9) Comment: The exposure analysis does not consider the effect of O3 avoidance behavior 

on activity profiles. People living in the 12 cities examined experience frequent O3 alerts 

warning them of unhealthy air quality and the need to avoid exercising outdoors. Schools, 

day cares and day camps routinely confine children indoors on code red days. The 

analysis fails to consider the extent to which O3 avoidance behavior has diminished the 

estimates of outdoor exercise in children. (ALA et al., p. 105) 

Response: EPA concurs that behavior changes in response to O3 pollution or in response 

to AQI notification alerts (“avoidance behavior”) were not explicitly taken into account 

in the exposure modeling. EPA recognizes that this is a limitation of the exposure 

analysis and discusses this in the exposure uncertainty analysis. There is not much 

information about the extent to which people currently modify their activities in response 

to O3 alerts; in particular the activity data (CHAD) used in the analysis does not have 

sufficient information to allow avoidance behavior to be modeled. However, under the 

scenarios modeled for just meeting alternative standards, O3 alerts would be infrequent 

relative to the number of alerts that currently occur in the nonattainment areas modeled. 

Consequently, EPA does not feel that this is an influential factor in the estimation of 

exposure for the scenarios simulating just meeting the current or proposed standards. 

(10) Comment: Babies, toddlers, and preschoolers, an important segment of the population 

that spends lots of time playing outdoors, are not factored into the analysis. Only schoolaged children are included in EPA’s estimates. (ALA et al., p. 105) 
72

Response: The exposure analysis focused on school age children and adults due to the 

lack of health effects evidence explicitly addressing O3-related respiratory effects in preschool age children. In addition, there is a paucity of data for human activity data for 

infants and toddlers that would make any exposure analysis applied to these populations 

very uncertain. The Administrator has taken into consideration that additional 

populations, including pre-school age children, are potentially at risk for the O3-related 

respiratory effects observed in school-age children. 

(11) Comment: Several commenters (e.g., ALA et al., p. 106) noted that most of the country 

is excluded from the analysis. The geographic scope of EPA’s analysis is limited to just 

12 metropolitan areas. 

Response: See response to comment (1) in section II.A.5. 

(12) Comment: One set of comments (ALA et al., p. 106) noted that the exposure assessment 

does not account for exposures and health impacts that result from O3 transported from 

the 12 MSAs analyzed, which can actually result in people downwind being exposed to 

higher concentrations. 

Response: The urban areas modeled are CSAs, not MSAs, and are large geographically 

(e.g., the Boston CSA extends into New Hampshire). However, the increase in O3

downwind may extend beyond the CSA for some of the areas modeled, and this is not 

captured in the analysis. The design of the exposure analysis intentionally focused on 12 

urban areas. 

(13) Comment: O3 concentrations vary from year to year with different weather conditions. 

Estimates of “exposures of concern” are subject to great variability depending on whether 

the baseline year for comparison is 2002, a relatively dirty year, or 2004, a relatively 

clean year. The risk and exposure analysis must focus on 2002 as a baseline year. Use of 

a year with favorable meteorology as the baseline year distorts exposure estimates. (ALA 

et al., p. 106) 

Response: EPA accounted for this variability by analyzing all three years (2002-2004) 

with a focus on the year with higher exposures, 2002. 

(14) Comment: One commenter (API) contends that “while EPA conducted an analysis of 

alternative adjustment procedures before choosing the quadratic over a linear one ... their 

two-parameter quadratic rollback procedure is still suspect” (API, p.27). API expressed 

concern that the quadratic method was developed from data spanning only six to eight 

years which would mean that ozone differences could have been caused more by extreme 

meteorologic events than from actual reductions in ozone precursor emissions. Thus, it 

was stated that air quality data spanning ten to fifteen years should be used. The 

commenter also cited an alternative analysis which utilized ten to fifteen years worth of 

data and proposed alternative optimized adjustment procedures which better fit the ozone 

data in four cities. 
73

Response: Regarding the commenter's objection that EPA's approach was developed 

from data spanning only six to eight years, EPA believes this time span was long enough 

to reflect sizable emission reductions and thus was an appropriate period to use for 

developing the approach. Also, use of a longer time span would have introduced 

uncharacteristically high O3 concentrations from the early part of the examined period 

when compared to those seen in more recent years. Since the commenters analysis is 

based on a longer period, up to 15 years, its conclusions about ranking alternative air 

quality adjustment approaches may have introduced uncharacteristically high O3

concentrations from the early part of the examined period. Further, EPA notes that the 

commenter’s analysis offered no evidence or analysis that its proposed alternative air 

quality adjustment procedures would have made any meaningful difference in the 

exposure or risk estimates associated with just meeting the current or alternative 8-hour 

standards. 

5. Specific Comments on the Health Risk Assessment 

Comments related to the health risk assessment conducted for O3 are addressed in this 

section. Incorporating responses contained in section II.B.2.b and II.C.4 of the preamble to the 

final rule, EPA provides the following responses to specific issues related to the quantitative 

health risk assessment. Comments related to the overall weight placed on the health risk 

assessment in reaching decisions on the need to revise the current standard and on an appropriate 

standard level are addressed in the preamble and in sections II.A.2.a and II.A.2.d above. 

(1) Comment: Several commenters (ALA et al., NESCAUM) argued that EPA’s risk 

assessment understated the total health benefits of reducing the O3 standard. Reasons 

given included: 

• It considered only 12 metropolitan statistical areas (MSA), and didn’t consider benefits to 

adjacent areas beyond the MSA boundaries, that are likely because of the regional 

character of O3; 

• It didn’t include all relevant health outcomes and populations; among the health 

outcomes and populations that were omitted are: lung function decrements and 

respiratory symptoms in adults; school absences for respiratory illness among children; 

asthma-related ER visits and increased medication usage among asthmatics; doctor visits, 

lung inflammation, and decreased resistance to infection among children and adults. 

• A number of the health effects that EPA omitted in its risk assessment have been 

quantified in other analyses, including EPA’s RIA, and in the benefits assessment 

conducted by California for the review of the state ambient air quality standard for O3, 

both of which used EPA’s BenMAP model. They concluded that the methodology for 

quantitatively assessing these other health endpoints is well established. 

• EPA’s risk assessment excluded vulnerable subpopulations that are either more 

susceptible to O3 health effects, experience greater exposure, or both. Specific 

populations they identified that are not quantitatively assessed include children under five 

years old, active children, outdoor workers, and senior citizens. 
74

• One commenter expressed the concern that EPA’s risk assessment, being focused on 12 

U.S. cities, may have underestimated O3 impacts since it has been shown that O3

concentrations downwind of an urban area are often higher than within a city. (Minister 

of the Environment, Province of Ontario, Canada) 

Response: EPA agrees that the exposure and health risk assessments are limited to 

certain urban areas and do not capture all of the populations at risk for O3-related effects, 

and that the risk assessment does not include all potential O3-related health effects. The 

criteria and rationale for selecting the populations and health outcomes included in the 

quantitative assessments were presented in the draft Health Assessment Plan, Staff Paper, 

and technical support documents for the exposure and health risk assessments that were 

reviewed by the CASAC Panel and the public. The CASAC Panel indicated in its letter 

that the health outcomes included in the quantitative risk assessment were appropriate, 

while recognizing that other health outcomes such as emergency department visits, 

increased doctors’ visits should be addressed qualitatively (Henderson, 2006c). The Staff 

Paper (and the CASAC Panel) clearly recognized that the exposure and risk analyses 

could not provide a full picture of the O3 exposures and O3-related health risks posed 

nationally. The proposal notice made note of this important point and stated that 

“national-scale public health impacts of ambient O3 exposures are clearly much larger 

than the quantitative estimates of O3-related incidences of adverse health effects and the 

numbers of children likely to experience exposures of concern associated with recent air 

quality or air quality that just meets the current or alternative standards” (72 FR 37866). 

However, as stated in the proposal notice, EPA also recognizes that inter-individual 

variability in responsiveness to O3 shown in controlled human exposure studies for a 

variety of effects means that only a subset of individuals in any population group 

estimated to experience exposures exceeding a given benchmark exposure of concern 

level would actually be expected to experience such adverse health effects. The 

Administrator continues to recognize that there is a broader array of O3-related adverse 

health outcomes for which risk estimates could not be quantified (that are part of a 

broader “pyramid of effects”) and that the scope of the assessment was limited to just a 

sample of urban areas and to some but not all at-risk populations, leading to an 

incomplete estimation of public health impacts associated with O3 exposures across the 

country. The Administrator is fully mindful of these limitations, along with the 

uncertainties in these estimates, in reaching his conclusion that observations from the 

exposure and health risk assessments provide additional support for his judgment that the 

current 8-hour standard does not protect public health with an adequate margin of safety 

and must be revised. 

 In considering the level at which the primary O3 standard should be set, the Administrator 

continues to place primary consideration on the body of scientific evidence available in 

this review on the health effects associated with O3 exposure, as summarized in section 

II.C.4.a of the preamble to the final rule, while viewing the results of exposure and risk 

assessment, as providing information in support of his decision. While the Administrator 

places less weight on the results of the risk assessment, he notes that the results indicate 

that a standard set within the proposed range would likely reduce risks to at-risk groups 

from the O3-related health effects considered in the assessment, and by inference across 
75

the much broader array of O3-related health effects that can only be considered 

qualitatively, relative to the level of protection afforded by the current standard. 

Moreover, he notes that the results of the assessment suggest a gradual reduction in risks 

with no clear breakpoint as increasingly lower standard levels are considered. However, 

in light of the important uncertainties inherent in the assessment discussed in the 

preamble to the final rule and in the proposal notice, the Administrator concludes that the 

risk assessment does not provide a basis for choosing a level within the proposed range. 

To the extent the commenters suggest that EPA is legally bound to base quantitative 

features of the standards (such as levels) on the results of the risk assessment, or that the 

standards must be established at a lower level because the risk assessment quantifies 

morbidity and mortality effects below the levels the Administrator selected, the 

commenter is mistaken. See ATA III, 283 F. 3d at 373-74 (EPA not obliged to use the 

numerical results of the risk assessment to establish the 24-hour PM2.5 standard at a lower 

level when it provided a reasonable basis for not using the assessment). 

(2) Comment: A group of commenters mostly representing industry associations, businesses, 

and some State and local officials opposed to revising the 8-hour standard, and most 

extensively presented in comments from UARG, API, Exxon-Mobil, AAM, NAM, and 

the Annapolis Center raised the concern that exposures of concern and health risk 

estimates have not changed significantly since the prior review in 1997. 

Response: In asserting that the estimated exposures and risks associated with air quality 

just meeting the current standard have not appreciably changed since the prior review, 

comments from Exxon-Mobil, the Annapolis Center and others have compared results of 

EPA’s lung function risk assessment done in the last review with those from the 

Agency’s risk assessment done as part of this review and have concluded that lung 

function risks upon attainment of the current O3 standard are below those that were 

predicted in 1997 and that uncertainties about other health effects based on 

epidemiological studies remain the same. These commenters used this conclusion as the 

basis for a claim that there is no reason to depart from the Administrator’s 1997 decision 

that the current 8-hour standard is requisite to protect public health. 

EPA believes that this claim is fundamentally flawed for three reasons, as discussed in 

turn below: (1) it is factually inappropriate to compare the quantitative risks estimated in 

1997 with those estimated in the current rulemaking; (2) it fails to take into account that 

with similar risks, increased certainty in the risks presented by O3 implies greater concern 

than in the last review, and (3) it fails to recognize that the Administrator has used these 

estimates in a supportive role, in light of significant uncertainties in the exposure and risk 

estimates, to inform the conclusions drawn primarily from integrative assessment of the 

controlled human exposure and epidemiological evidence on whether ambient O3 levels 

allowed under the current standard present a serious public health problem warranting 

revision of the O3 standard. 

With respect to the first point, the 1997 risk estimates, or any comparison of the 1997 risk 

estimates to the current estimates, are irrelevant for the purpose of judging the adequacy 
76

of the current 8-hour standard, as the 1997 estimates reflect outdated analyses that have 

been updated in this review to reflect the current science. Just comparing the results for 

lung function decrements ignores these differences. In particular, as discussed in section 

4.6.1 of the Staff Paper, there have been significant improvements to the exposure model 

and the model inputs since the last review that make comparisons inappropriate between 

the prior and current review. For example, the geographic areas modeled are larger than 

in the previous review and when modeling a larger area, extending well beyond the urban 

core, there will be more people exposed, but a smaller percentage of the modeled 

population will be exposed at high levels, if O3 concentrations are lower in the extended 

areas. In the prior review, only typical years, in terms of O3 air quality were modeled, 

while the current review used the most recent three year period (i.e., 2002-2004). Also, 

the prior review estimated exposures for children who spent more time outdoors, while 

the assessment for the current review included all school age and all asthmatic school age 

children. Therefore, the population groups examined in the exposure assessment are 

different between those considered in the 1997 and current review, making comparison of 

the resulting estimates inappropriate. Another important difference making comparison 

between the 1997 health risk assessment and the current assessment inappropriate is that 

a number of additional health effects were included in the current review (e.g., respiratory 

symptoms in moderate/severe asthmatic children, non-accidental and cardiorespiratory 

mortality) based on health effects observed in epidemiological studies that were not 

included in the risk assessment for the prior review. These commenters only compare the 

risk estimates with respect to lung function decrement and fail to account for differences 

in additional and more severe health endpoints not covered in the 1997 assessment, as 

well as the fact that there are somewhat different and more urban areas included in the 

current assessment. 

Second, it is important to take into account EPA’s increased level of confidence in the 

associations between short-term O3 exposures and morbidity and mortality effects. In 

comparing the scientific understanding of the risk presented by exposure to O3 between 

the last and current reviews, one must examine not only the quantitative estimate of risk 

from those exposures (e.g. the numbers of increased hospital admissions at various 

levels) but also the degree of confidence that the Agency has that the observed health 

effects are causally linked to O3 exposure at those levels. As documented in the Criteria 

Document and the recommendations and conclusions of CASAC, EPA recognizes 

significant advances in our understanding of the health effects of O3 based on new 

epidemiological studies, new human and animal studies documenting effects, new 

laboratory studies identifying and investigating biological mechanisms of O3 toxicity, and 

new studies addressing the utility of using ambient monitors to assess population 

exposures to ambient O3. As a result of these advances, EPA is now more certain that 

ambient O3, alone or in combination with other pollutants, presents a significant risk to 

public health at levels at or above the range of levels that the Agency had considered for 

these standards in 1997. From this more comprehensive perspective, since the risks 

presented by O3 are more certain and the current quantitative risk estimates include 

additional important health effects, O3-related risks for a wider range of health effects are 

now of greater concern at the current level of the standard than in the last review. 
77

Third, quantitative risk estimates were not the only basis for EPA’s decision in setting a 

level for the O3 standard in 1997, and they do not set any quantified “benchmark” for the 

Agency’s decision to revise the O3 standard at this time. While EPA believes that 

confidence in the causal relationships between short-term exposures to O3 and various 

health effects reported in epidemiological studies has increased markedly since 1997, the 

Administrator also recognizes that the risk estimates for these effects must be considered 

in the light of uncertainties about whether or not these O3-related effects occur at very 

low O3 concentrations. The Administrator continues to believe that the exposure and risk 

estimates associated with just meeting the current standard discussed in the Staff Paper 

and summarized in the proposal notice are important from a public health perspective and 

are indicative of potential exposures and risks to at-risk groups. In considering the 

exposure and risk estimates, the Administrator has considered the year-to-year and cityto-city variability in both the exposure and risk estimates, the uncertainties in these 

estimates, and recognition that there is a broader array of O3-related adverse health 

outcomes for which risk estimates could not be quantified (that are part of a broader 

“pyramid of effects”) and that the scope of the assessment was limited to just a sample of 

urban areas and to some, but not all, at-risk populations, leading to an incomplete 

estimation of public health impacts associated with O3 exposures across the country. 

(3) Comment: Several commenters, mostly representing industry associations, businesses, 

and some State and local officials opposed to revising the 8-hour standard (e.g., UARG, 

API, Exxon-Mobil, AAM), contend that, given the uncertainties and limitations 

underlying the risk assessments, the health risk estimates are too speculative to support 

lowering the primary standard level. Specific uncertainties and limitations cited include: 

• uncertainties in the exposure estimates; 

• uncertainties about the concentration-response relationship (and especially the 

assumption of a linear non-threshold relationship between O3 exposures and effects) 

particularly at levels below 0.08 ppm, so that the extrapolations assumed in the risk 

assessment may not be valid; 

• uncertainties related to the use of single pollutant models rather than multi-pollutant 

models to estimate O3-related health risks; 

• the risk estimates based on lung function decrements use a benchmark of FEV1 

declines of ≥ 15% for healthy individuals and ≥ 10% for asthmatics; these types of 

changes are transient, routinely experienced and well-tolerated, and not of adverse 

health consequence for either healthy or asthmatic individuals; 

• the estimated risks of respiratory symptoms, hospital admissions, and non-accidental 

mortality are based on epidemiological studies, which do not reliably implicate O3, 

and certainly not O3 at any specific level, as the causal agent for the effects reported; 

• the evidence for a causal relationship is particularly uncertain at lower O3 levels; to 

the extent that the assumption of a causal link at lower O3 levels is invalid, estimated 

reductions in O3-related risk are artificially inflated; 

• the evidence from single-city epidemiological studies reporting relationships between 

O3 and cardiorespiratory mortality are too unreliable and mixed to be included in the 

health risk assessment. 
78

Response: EPA’s response concerning uncertainties in the exposure estimates is 

discussed in the previous section (II.A.4) on exposure analysis. EPA’s response to 

comments concerning the assumption of a linear non-threshold concentration-response 

relationship is addressed under comment number 5 in this section. EPA’s response to 

comments concerning the use of single vs. multi-pollutant models to estimate O3-related 

health risks is addressed under comment number (9) in this section. EPA’s response to 

comments asserting that the lung function decrement benchmarks included in the 

assessment do not represent adverse health consequences for either healthy or asthmatic 

individuals is addressed above in section II.A.3.d (comment number (2)). 

In response to the assertion that the results of time-series studies should not be used at all 

in quantitative risk assessments, EPA notes that the selection of specific studies and 

effect estimates was based on a careful evaluation of the evidence evaluated in the 

Criteria Document and that the criteria and rationale for selection of studies and effect 

estimates were presented and extensively reviewed and discussed by the CASAC Panel 

and in public comments presented to the CASAC Panel. EPA notes that the CASAC 

Panel judged the selection of the endpoints based on the epidemiological studies for 

inclusion in the quantitative risk assessment to be “appropriate” and that the risk 

assessment chapter of the Staff Paper and its accompanying risk assessment were “well 

done, balanced and reasonably communicated” (Henderson, 2006c, p. 12). 

In response to comments that O3-related risks for mortality and other endpoints based on 

the epidemiological evidence are artificially inflated due to the assumption of a causal 

relationship which is particularly uncertain at lower O3 levels, EPA has responded to 

comments related to EPA’s characterization of the weight-of-the-evidence with respect to 

judgments about causality in section II.A.3 above. The Administrator has carefully 

considered the epidemiological evidence and has taken into consideration the 

implications of the uncertainties regarding whether or not there is a causal relationship 

which extends to lower O3 levels, particularly below 0.075 ppm. As discussed in the 

preamble to the final rule, this concern is one of the principle reasons that the 

Administrator has not placed much weight on the results of the risk assessment in his 

decision on the final level of the O3 primary standard. 

In response to the comments that risk estimates from single-city time-series studies 

should not be used since they are highly heterogeneous and influenced by publication 

bias, EPA notes that while two of the meta-analyses, Bell et al. (2005) and Ito et al. 

(2005), provided suggestive evidence of publication bias, O3-mortality associations 

remained after accounting for that potential bias. The Criteria Document (p. 7-97) 

concludes that the “positive O3 effects estimates, along with the sensitivity analyses in 

these three meta-analyses, provide evidence of a robust association between ambient O3

and mortality.” Concerns about the heterogeneity of responses observed across different 

urban areas, particularly for O3-related mortality, are addressed above in section II.A.3.b 

(comment number (2)). 

As discussed in more detail in the Staff Paper (section 5.3.2.3), there are different 

advantages associated with use of single-city and multi-city effect estimates as the basis 
79

for estimating health risks in specific urban areas. Therefore, the risk assessment 

included estimates based on both types of effect estimates where such information was 

available. 

(4) Comment: One commenter (NAM, pp. 10-11 and p. 28) argued that the portions of the 

health risk assessment that EPA generated itself or sponsored are not sufficiently 

transparent, i.e., EPA does not provide enough information for these results to be 

replicated. 

Response: EPA strongly disagrees with this comment. EPA has carefully documented 

the health risk assessment methods in the Health Risk TSD and has made available, upon 

request, the models and data inputs, including the exposure-response data from the 

controlled human exposure studies, used to develop both the exposure and health risk 

assessments as indicated on EPA’s FERA website 

(http://www.epa.gov/ttn/fera/risk_ozone.html) which states: 

Program and input files used in the Health Risk Assessment: Because of the 

number and size of the program and data files, they are not available for 

interactive download. To receive a DVD containing all of the code and data files, 

contact Harvey Richmond via email at Richmond.harvey@epa.gov 

In fact, comments submitted from another industry group (UARG) indicating that it was 

able to closely replicate the risk assessment results reported in the Health Risk TSD 

(UARG, Attachment 3) clearly refute the claim made by NAM that the health risk 

assessment is not transparent enough to be replicated. 

(5) Comment: Some commenters (e.g., API, Lefohn) contend that EPA’s risk assessment 

assumes a linear concentration-response relationship but that there is ample evidence in 

the epidemiological literature that the relationship between ambient O3 levels and health 

effects is nonlinear. Similarly, one commenter contends, there is evidence that the 

relationship between O3 and health endpoints in the human clinical literature is also 

nonlinear and that EPA’s assumption of linearity in its risk assessment is therefore 

invalid, it was argued, and the resulting risk estimates are also invalid (API, p.23) NAM 

contends that EPA assumed a constant risk per unit of O3 for all levels of O3 exposure in 

its health risk assessment and that this assumption is not biologically plausible and that 

EPA offers no scientific evidence to support this proposition (NAM, p.40). 

Response: The portion of the risk assessment based on epidemiological studies used 

studies that satisfied selection criteria that were clearly laid out (see section 4.1.5 in the 

Health Risk TSD), and the form of the concentration-response function was not one of 

the selection criteria – i.e., the risk assessment did not make its own assumptions about 

the form of the relationship between ambient O3 levels and a given health endpoint but 

simply used the best epidemiological evidence available. The vast majority of O3

epidemiological studies estimated log-linear concentration-response functions. There is 

not “ample evidence” in the epidemiological literature of a non-linear relationship 

between ambient O3 levels and health effects (or, specifically, of a threshold in that 
80

relationship). In fact, as discussed in the Staff Paper (p. 6-15), one recent multi-city 

study (Bell et al., 2006) examined the threshold question for the O3-mortality 

concentration-response function using several different approaches and concluded that 

“all results indicate that any threshold would exist at very low concentrations, far below 

current U.S. and international regulations and nearing background levels.” 

 The portion of the risk assessment based on controlled human exposure studies also did 

not assume linearity in the relationship between personal exposure to O3 and lung 

function response. In this portion of the risk assessment, EPA fit two different models – 

a linear (hockeystick) model and a logistic model – to the data from the available 

controlled human exposure studies. The hockeystick model was derived by fitting a 

linear regression to the data but not constraining the intercept to be zero. Thus, if the 

regression line crossed the x-axis, the data “dictated” a threshold value – EPA set the 

response rate to zero for all O3 exposures less than or equal to the exposure at which the 

regression line crossed the x-axis in this model, forming a “hockeystick” model. The 

logistic model is also nonlinear, and would constitute a smooth approximation to the 

hockeystick model. Both models allow for decreasing (or zero) response rates at lower 

levels of exposure. Because of the uncertainty about the correct functional form, EPA 

derived exposure-response functions that were mixtures of the two models. One such 

mixture hypothesized that the exposure-response relationship is logistic with 90% 

probability and linear (hockeystick) with 10% probability. The other two mixtures were 

80%/20% and 50%/50%. Thus, even if the linear model was truly linear (i.e., even if it 

did not cross the x-axis), none of the final models used in this portion of the risk 

assessment were linear, because each assigned a substantial probability (90%, in the base 

case model) to the (nonlinear) logistic form of the relationship between personal 

exposure to O3 and lung function response. 

 In response to NAM’s comment, as indicated above, EPA did not assume a constant risk 

per unit of O3 for the lung function portion of the health risk assessment. For the health 

outcomes based on epidemiological studies, as discussed above, EPA did not make its 

own assumptions about the form of the relationship between ambient O3 levels and a 

given health endpoint but simply used the best epidemiological evidence available. The 

vast majority of O3 epidemiological studies estimated log-linear concentration-response 

functions and EPA did offer scientific evidence, the analysis by Bell et al. (2006) which 

found only a very small change in the size of the effect estimate down to very low O3

levels (i.e., 10 ppb). EPA did acknowledge the uncertainties about the shape of the 

concentration-response relationships for the health outcomes based on the 

epidemiological studies and stated in the Staff Paper that the risk estimates for these 

effects “must be considered in the light of uncertainties about whether or not these O3-

related effects occur in the population at very low concentrations” (Staff Paper, p.5-45). 

 

(6) Comment: Several commenters (e.g., ACC) noted that only a single coefficient used in 

the risk assessment is based on 8-hour O3 concentrations, the averaging time of the 

current and proposed NAAQS. They argued that therefore the calculated excess risks are 

likely not relevant to setting a NAAQS with an 8-hour averaging time. 
81

Response: As with many of the criteria air pollutants, health effects have been reported 

in studies using a variety of averaging times. In this review, as in other NAAQS reviews, 

EPA has assessed risks arising from exposure to the pollutant associated with 

concentrations or exposures for various averaging times resulting from air quality just 

meeting the current and alternative standards for a specified averaging time. There is no 

requirement or logical argument that the averaging time of the models used to estimate 

specific health effects must be the same as the averaging time for the standard. It has 

long been recognized that air quality associated with just meeting a NAAQS with a 

specific averaging time will also limit air quality and exposures for other averaging times 

as well. For example, in 1997 EPA and the CASAC clearly concluded that an 8-hour O3

standard set at an appropriate level would provide protection against both 1-hour and 8-

hour O3-related effects. Therefore, EPA does not agree the calculated excess risks for 

health effects based on averaging times other than 8-hours are irrelevant to the setting of 

an 8-hour averaging time standard. 

(7) Comment: One commenter (NAM, pp. 30-32) contends that both study selection bias 

(consistently selecting studies that show positive associations) and model selection bias 

(selecting models known to yield upwardly biased risk estimates, such as single-pollutant 

models that do not control for known confounders) can be found in EPA’s risk 

assessment. Several sources of bias were given, including 

• publication bias (the predominance of positive studies reported); 

• the choice of which study to emphasize (with preference given to those with larger 

risk coefficients); 

• inadequate control for confounders (leading to their effects being attributed to O3); 

• the choice of statistical methods (with some more likely to reject the no-effect 

hypothesis than others); and 

• the choice of which estimate from which reported model to rely upon. 

The result, they contend, is “a cascade of bias such that the resulting risk assessment is 

much higher than would have been obtained using objective methods.” 

Another comment (the Rochester Report) asserted that EPA ignored model uncertainty in 

its health risk assessment. 

 Response: EPA has addressed the issues of alleged publication bias, selection bias, 

control of confounders, and choice of statistical methods in section II.A.3 above and EPA 

does not agree with the conclusion that there is a “cascade of bias” resulting in higher risk 

estimates. EPA takes exception to the implication that it used methods with some known 

bias. As stated in EPA’s IQG (p.22), “if data are subjected to formal, independent, 

external peer review the information may generally be presumed to be of acceptable 

objectivity.” EPA’s risk assessment underwent extensive peer review by the CASAC O3

Panel, and in EPA’s judgment the commenter has not rebutted the presumed objectivity 

of the methods used. 

 With respect to the selection of studies included, it is important to recognize that EPA’s 

criteria for selection of studies and concentration-response relationships were described 

in the draft “Health Assessment Plan” (EPA, 2005) and in draft Health Risk TSD reports 

(Abt Associates, 2005; Abt Associates, 2006) and drafts of the Staff Paper that were 
82

reviewed by the CASAC and made available to the public for comment at several stages 

during the review. The CASAC O3 Panel did not express any concerns about EPA’s 

selection of studies to be included in the O3 risk assessment and in its October 2006 letter 

(Henderson, 2006c, p. 12)) to the EPA Administrator stated, “... the panel found Chapter 

5 [the chapter in the Staff Paper that discusses the risk assessment] and its accompanying 

risk assessment to be well done, balanced and reasonably communicated.” The CASAC 

O3 Panel (Henderson, 2006c, p. 12) also explicitly stated that it judged the selection of 

health outcomes “for inclusion in the quantitative risk assessment to be appropriate.” 

 Contrary to the statement in the Rochester Report, EPA did not ignore the issue of model 

uncertainty in its risk assessment. While we did not include a quantitative treatment of 

model uncertainty, EPA’s risk assessment and Staff Paper clearly discussed the potential 

impact of model uncertainty and the importance of considering this issue in interpreting 

the results of the risk assessment. In particular, EPA’s Staff Paper acknowledged that 

“other uncertainties, such as differences in study location, time period, and model 

uncertainties are not represented by confidence or credible intervals presented” (p.5-44, 

OAQPS Staff Paper). As discussed further in the Staff Paper, “Based on the CD’s 

conclusions, we judge that there is insufficient evidence to support use of potential 

threshold levels in the quantitative risk assessment [we note that CASAC supported this 

choice during its review of the scope and methods to be used in the risk assessment], but 

we do recognize that there is increasing uncertainty about the concentration-response 

relationship at lower concentrations that is not captured by the characterization of the 

statistical uncertainty due to sampling error. Therefore, ... the risk estimates for 

premature mortality, respiratory symptoms in moderate to severe asthmatic children, and 

respiratory-related hospital admissions associated with exposure to O3 must be 

considered in the light of uncertainties about whether or not these O3-related effects occur 

in the population at very low concentrations” (p. 5-45, OAQPS Staff Paper, emphasis 

added). 

 With respect to choice of models to rely upon in the risk assessment, EPA agrees that 

recent work on model sensitivity has raised new concerns and the Agency has given 

much attention to this issue. In so doing, EPA recognizes, as does HEI and other 

researchers, that there is no clear consensus at this time as to what constitutes appropriate 

control of weather and temporal trends in time-series studies, and that no single statistical 

modeling approach is likely to be most appropriate in all cases (EPA, 2004, p. 8-238). 

The recent time-series epidemiologic studies evaluated in the Criteria Document have 

included some degree of control for variations in weather and seasonal variables. 

However, as summarized in the HEI review panel commentary, selecting a level of 

control to adjust for time-varying factors, such as temperature, in time-series 

epidemiologic studies involves a trade-off. For example, if the model does not 

sufficiently adjust for the relationship between the health outcome and temperature, some 

effects of temperature could be falsely ascribed to the pollution variable. Conversely, if 

an overly aggressive approach is used to control for temperature, the result would 

possibly underestimate the pollution-related effect and compromise the ability to detect a 

small but true pollution effect (EPA, 2004, p. 8-236; HEI, 2003, p. 266). The selection of 
83

approaches to address such variables depends in part on prior knowledge and judgments 

made by the investigators, for example, about weather patterns in the study area and 

expected relationships between weather and other time-varying factors and health 

outcomes considered in the study. EPA is unaware of any information that supports the 

commenters’ contention that the models selected by the original investigators are biased. 

In considering these issues related to uncertainties in the underlying health science, on 

balance, EPA believes that the available evidence interpreted in light of these remaining 

uncertainties does provide increased confidence relative to the last review in the reported 

associations between short-term O3 exposures and mortality and morbidity effects, alone 

and in combination with other pollutants, and generally supports stronger inferences as to 

the causal nature of the associations. EPA also believes that this increased confidence, 

when taken in context of the entire body of available health effects evidence, adds 

support to its conclusion that the current 8-hourstandard needs to be revised to provide 

increased public health protection. 

(8) Comment: Several commenters contend that EPA inappropriately uses data from 

ambient monitors as proxies for personal exposures in studies estimating effects that are 

used in the risk assessment. These commenters noted that the literature consistently 

shows that personal O3 exposure is generally less than the values obtained from ambient 

monitors. Further, they stated that the only subpopulation for which ambient monitors 

may closely track personal exposure are outdoor workers during the O3 season and there 

is virtually no overlap between this subpopulation and the sensitive subpopulations. To 

adhere to the information quality substantive objectivity standard, one commenter (NAM, 

p.32) contends that, “EPA must provide unbiased estimates of exposure for each 

subpopulation of concern.” 

Response: Since the relationships used in the risk assessment for the health outcomes 

based on epidemiological studies are concentration-response relationships that relate 

ambient concentrations to a population response there is no bias introduced in the health 

risk estimates by not having an exposure assessment. The fact that ambient 

concentrations may overstate actual personal exposure does not imply that the risk 

estimates are biased. EPA does not agree that there is any requirement to provide 

unbiased estimates of exposure for each subpopulation group of concern before it can use 

concentration-response relationships in its risk assessments. 

(9) Comment: One commenter (NAM, p. 34) contends that EPA’s decision to disseminate 

risk estimates derived from single-pollutant models as estimates of risk, even when multipollutant models are available, is an unambiguous violation of the objectivity standard. 

NAM contends that EPA has utilized the study by Gent et al. (2003) in ways that 

systematically overstate risk estimates and that EPA assumes asthmatics are exposed at 

the same level as other children (NAM, p. 34). 

Response: EPA rejects NAM’s contention that disseminating risk estimates derived from 

single-pollutant models is a violation of the objectivity standard. As discussed in the 

Criteria Document and section 3.3.2.1 of the Staff Paper, O3 epidemiological studies have 
84

reported results based on both single and/or multi-pollutant models. As stated in the Staff 

Paper (p. 5-35), “To the extent that any of the co-polluants present in the ambient air may 

have contributed to the health effects attributed to O3 in single pollutant models, risks 

attributed to O3 might be overestimated where concentration-response functions are based 

on single pollutant models. However if co-pollutants are highly correlated with O3, their 

inclusion in an O3 health effects model can lead to misleading conclusions in identifying 

a specific causal pollutant. When collinearity exists, inclusion of multiple pollutants in 

models often produces unstable and statistically insignificant effect estimates for both O3

and the co-pollutants. Given that single and multi-pollutant models each have both 

potential advantages and disadvantages, with neither type clearly preferable over the 

other in all cases, risk estimates based on both single-and multiple-pollutant models have 

been included in the risk assessment where both are available.” The CASAC O3 Panel 

generally agreed with this approach in its review of the risk assessment scope and 

methods plan, Health Risk TSD, and final Staff Paper. Further, EPA notes that CASAC’s 

overall assessment of the risk assessment was that it was “well done, balanced and 

reasonably communicated” (Henderson, 2006c) which supports EPA’s view that the 

approach used did not violate the objectivity standard under the IQG. 

For the reasons discussed in the paragraph above, EPA does not agree that it has used the 

Gent et al. (2003) study in ways that systematically overstate risk estimates. Further, 

EPA did not make any assumption about the exposure of asthmatics relative to other 

children. EPA applied concentration-response relationships reported in this study, which 

are relationships between levels observed at ambient monitors and a given response, to 

ambient data in the Boston area. Thus, NAM is incorrect in stating that EPA assumed 

asthmatics had the same exposure as other children in the risk assessment. 

(10) Comment: Several commenters (e.g., AAM, NAM, p. 50) contend that, because EPA 

failed to show that the associations between O3 and health endpoints are causal, the risk 

assessment should include a probabilistic consideration that the associations may not be 

causal. They contend that, in contrast to the acute respiratory effects in clinical studies 

where we know the observed effects are due to the exposure of the pollutant being 

assessed, “the most important uncertainty is the extent to which the associations between 

O3 and the health endpoints included in the assessment actually reflect causal 

relationships” (AAM, citing Second Draft SP at 5-76). Noting the “biologically 

implausible” wide range of associations for mortality, one commenter questioned the 

practice of using Bayesian techniques to shrink the (highly heterogeneous) city-specific 

estimates towards the overall mean, especially when the heterogeneity includes both no 

effect and protective effects (AAM). They concluded that the risk assessment should 

include a probabilistic consideration that the associations may not be causal, pointing out 

that the Regulatory Impact Analysis (RIA) does evaluate the case assuming that O3

mortality associations are not causal. 

Response: EPA does not agree that it must include a probabilistic characterization of 

causality for the health effects included in the risk assessment. EPA’s characterization of 

likely causality for the various O3-related health endpoints included in the risk assessment 

is presented in the Criteria Document and Staff Paper (see section 3.7.5). As stated in the 
85

Staff Paper, EPA has only included health endpoints in the quantitative risk assessment 

for which there is, “at a minimum, a likely causal relationship with either short-term O3

exposure itself or with O3 serving as an indicator for itself and other components of the 

photochemical oxidant mix, especially during the warm O3 season” (p.5-42), EPA has 

not assigned a probability to causation. The Administrator has taken into consideration 

qualitatively uncertainties related to whether or not there is a causal relationship in 

general and particularly the extent to which there may or may not be a causal relationship 

at increasingly lower O3 levels. 

(11) Comment: One commenter (NAM) contends that EPA abandoned its commitment “to 

provide the best possible scientific characterization of risks based on a rigorous analysis 

of available information and knowledge” by declaring, in the following statement, that its 

practices were biased, and purposefully so: "EPA’s risk assessments are conducted in 

support of its mission to protect public health and the environment. Given the 

uncertainty, variability, and data gaps encountered when conducting any risk assessment, 

a key objective for EPA's risk assessments is that they avoid both underestimation of risk 

and gross overestimation of risk. ... EPA seeks to adequately protect public and 

environmental health by ensuring that risk is not likely to be underestimated.” (NAM, 

pp. 39-40) 

Response: Contrary to the claim made in the comment, EPA has not abandoned its 

commitment to provide the best possible scientific characterization of risks. As noted 

previously, EPA’s approach and analytical assumptions were carefully documented and 

subject to review by the CASAC O3 Panel and the public and were based on the 

scientifically peer-reviewed final Criteria Document. The CASAC O3 Panel clearly 

supported EPA’s view that the health risk assessment was not biased when it stated that 

the assessment was “well done, balanced, and reasonably communicated” and that the 

selection of health endpoints for inclusion in the quantitative risk assessment was 

appropriate (Henderson, 2006c). As the quoted passage in the comment indicates, EPA 

seeks to avoid both underestimation of risk and gross overestimation of risk. EPA notes 

that in conducting any health risk assessment, analytical choices have to be made and 

EPA has carefully discussed any known directional influences of these choices in the 

Health Risk TSD and Chapter 5 of the Staff Paper. 

(12) Comment: One commenter (NAM) contends that when EPA says that its estimates of 

risk from O3 (or a peer reviewed study on which it relies) has “controlled for PM,” it is 

not clear whether that control addressed only PM10 or PM2.5 as well. PM2.5 is correlated 

in space and time with O3; PM10 is not. Thus, controlling for PM10 is, in effect, 

functionally equivalent to no control at all (NAM, p. 41). 

Response: For each concentration-response function used in the risk assessment, the 

specifics of the function, including co-pollutants in the model, are listed in Table 4-2 of 

the Health Risk TSD. For those models that included a measure of PM, the exact 

measure used (i.e., PM2.5 or PM10) is given in Table 4-2, so there should be no lack of 

clarity about this. 
86

Moreover, there is some evidence that the influence of PM on the O3-mortality effect 

estimate may not be very substantial. One study, Levy et al. (2005), ran univariate 

regressions at a number of sites with O3 as the dependent variable and another criteria 

pollutant as the independent variable, for each of the other criteria pollutants, including 

PM10 and PM2.5. They then examined the extent to which the relationship (correlation) 

between O3 and the other pollutant at a site influenced the O3-mortality effect estimate at 

the site. They found only a weak relationship between the O3-PM2.5 correlation at a site 

and the O3-mortality effect estimate at the site. Further analysis of a possible PM2.5

impact on the O3-mortality effect estimate did not alter this finding (see Levy et al., 2005, 

p. 463). 

(13) Comment: Several commenters (e.g., NAM, Rochester Report, UARG) argued that EPA 

should conduct an “integrated uncertainty analysis” – or, as it was described in one 

comment quoting the National Research Council (NRC, 2002), “EPA should begin to 

move the assessment of uncertainties from its ancillary analyses into its primary analyses 

by conducting probabilistic, multiple source uncertainty analysis. This shift will require 

specification of probability distributions for major sources of uncertainty, which should 

be based on available data and expert judgment” (Rochester Report, p. 19; NAM, p.46) 

Such an “integrated uncertainty analysis” would include the effects of additional sources 

of uncertainty, “including model selection, non-linearity of the concentration response 

function at lower and lower concentrations, and the role of other pollutants” (UARG, p. 

28). Additional related comments included: 

• It was suggested that, the preponderant effect of all of the sources of uncertainty is to 

create an upward bias in EPA’s risk estimates. “Even when leaving aside the uncertainty 

about causality, analyses produced by other researchers have demonstrated that when an 

integrated uncertainty analysis is performed, the large majority of probability in the 

estimates falls far below the primary estimates that EPA reports (Rochester Report, p. 

75).” 

• EPA has presented the Administrator data and analyses that led him to be much more 

confident than is scientifically justified that O3 exposure below the current NAAQS poses 

actual human health risks. EPA’s risk estimates capture only statistical variability for the 

selected models, not scientific uncertainty about their validity and reliability as estimates 

of human health risk. Information about variability, which is small relative to the 

magnitude of variability and uncertainty combined, has no utility to the Administrator 

unless it is placed in proper context with information about uncertainty” (NAM, pp. 44-

45). 

• One group of commenters contends that EPA sometimes reports “confidence bounds” or 

“uncertainty intervals” for its primary estimates, but these ranges are based solely on the 

standard error of the single relative risk coefficient estimate. “In other words,” they 

contend, “EPA presents to the public a measure of variability as if it were a measure of 

uncertainty. This is highly misleading to the non-technical audience that may not take the 

time to learn all of the details of EPA’s analysis methods. Thus, this audience is easily 

swayed into believing that these ranges are a reasonably complete representation of the 

uncertainties about the level of risk. Given that some of these ranges are very wide (in 

many cases falling into the negative numbers) it would be quite understandable if people 
87

were to think these ranges present a comprehensive view of uncertainty, but they do not 

even start to do so” (Rochester Report, p. 73). 

Response: First, EPA notes that the 2002 NRC report cited by several commenters made 

recommendations with respect to EPA’s regulatory impact analyses which are required 

under E.O. 120266 and not EPA’s health risk assessments. Even in this separate context, 

the NRC recognized that it would require a transition over time to implement its 

recommendations to incorporate more probabilistic assessments in health benefits 

assessments. 

Second, the point that the uncertainty ranges reported in the risk assessment do not reflect 

all of the uncertainty in the risk estimates is explicitly discussed in the Staff Paper (EPA, 

2007, section 5.3.2.5). As indicated in the Staff Paper, statistical uncertainty surrounding 

the estimated O3 coefficients in the reported concentration-response functions is reflected 

in the confidence intervals and additional uncertainties “have been addressed 

quantitatively through sensitivity analyses and/or have been discussed throughout section 

5.3” (Staff Paper, p. 5-40). Given the existing data gaps in the scientific evidence and 

associated uncertainties, a more comprehensive integrated assessment of uncertainties, 

would have be desirable, but in the staff’s judgment would require use of techniques 

involving elicitation of probabilistic judgments from health scientists. While the Agency 

is currently developing these approaches, such comprehensive assessments of uncertainty 

are not available for the current O3 risk assessment for this NAAQS review. 

Third, EPA does not agree that the preponderant effect of all of the sources of uncertainty 

is to create an upward bias in EPA’s risk estimates and EPA does not agree that other 

researchers have presented a credible, balanced, peer-reviewed integrated uncertainty 

analysis that shows the large majority of probability in the estimates falls far below the 

primary estimates that EPA reported. The analysis conducted by A. Smith for UARG 

cited by the commenter only examined one health endpoint (i.e., premature mortality) 

and is based on the assumption that there is no O3-related response associated with levels 

below 0.070 ppm. As discussed in the Staff Paper (section 5.3.2.5) and section II.A.2 of 

the preamble to the final rule, there is no scientific basis to conclude that a population 

threshold exists at this level. 

Fourth, EPA has defined very carefully in the Staff Paper and Health Risk TSD (sections 

3.1.5 and 4.1.9) the concepts of uncertainty and variability and has extensively discussed 

important sources of both uncertainty and variability and their impact on the health risk 

assessment. 

(14) Comment: One commenter (NAM) contends that EPA has violated the fundamental risk 

assessment principle that double counting is not acceptable by attributing to O3 health 

risks that have been accounted for previously by EPA -- most prominently, premature 

mortality risks in its analysis of fine PM (NAM, pp. 51-52). 

Response: In discussing the selection of concentration-response functions to use in the 

portion of the O3 risk assessment based on epidemiological studies, EPA noted that, 
88

“single and multi-pollutant models each have both potential advantages and 

disadvantages, with neither type clearly preferable over the other in all cases...” and, as a 

result, EPA made the decision to “report risk estimates based on both single- and multipollutant models where both are available” (Health Risk TSD, p. 4-11). It is possible that 

a single pollutant model could falsely attribute some portion of mortality risk reduction 

(or avoided cases of mortality) to O3 that should instead be attributed to fine PM, and if 

those avoided cases of mortality were already attributed to fine PM in a PM2.5 analysis, 

then there would be some degree of double counting. However, the evidence that this is 

the case to any substantial degree for PM as the copollutant is weak. One study, Levy et 

al. (2005), ran univariate regressions at a number of sites with O3 as the dependent 

variable and another criteria pollutant as the independent variable, for each of the other 

criteria pollutants, including PM10 and PM2.5. They then examined the extent to which 

the relationship (correlation) between O3 and the other pollutant at a site influenced the 

O3-mortality effect estimate at the site. They found only a weak relationship between the 

O3-PM2.5 correlation at a site and the O3-mortality effect estimate at the site. Further 

analysis of a possible PM2.5 impact on the O3-mortality effect estimate did not alter this 

finding (see Levy et al., 2005, p. 463). This suggests that, if there is any “double 

counting” across EPA O3 and PM2.5 analyses, it will be fairly small. Given that there is a 

different price to be paid in using only multi-pollutant models (i.e., in reduced stability of 

the O3 coefficient estimate in such models), EPA continues to believe that the application 

of both single- and multi-pollutant models, where both were available, is an appropriate 

approach. 

(15) Comment: One commenter (UARG), “recognizing that the Administrator proposes to 

reject any possible standard level below 0.070 ppm because of the uncertainty about a 

causal effect of low levels of O3,” commissioned an analysis of the distribution of the risk 

in EPA’s risk assessment attributable to O3 exposures above and below 0.070 ppm. The 

analysis found that “very little of EPA’s estimated mortality and morbidity risk is 

attributable to days when the maximum 8-hour average level of O3 is more than 70 ppb” 

and that attainment of the existing NAAQS “would actually provide very significant 

protection against exposures to O3 right down to 70 ppb.” They concluded that there is no 

reason to believe that promulgation of a more stringent NAAQS would result in 

meaningful reduction in health risk. (UARG, pp. 24-25) 

Response: EPA had conducted its own analysis for non-accidental and cardiorespiratory 

mortality that partitioned the contribution to overall O3-related risk estimates from 

specified O3 concentration range intervals as displayed in figure 5-15 of the Staff Paper 

(p.5-79) and figures 4-14 and 4-15 of the Health Risk TSD (pp. 4-70 to 4-71). UARG’s 

analysis makes the assumption that there is population threshold at 0.070 ppm. The 

Administrator is very mindful of the uncertainties related to whether the observed 

associations between O3 concentrations at very low levels, well below 0.080 ppm, and the 

health outcomes reported in the epidemiological studies reflect actual causal relationships 

and has taken this into account in considering the risk assessment estimates in his 

decision. 
89

The Administrator does not agree with the commenter’s conclusion that a more stringent 

NAAQS would not result in meaningful reductions in health risk. The Administrator has 

taken into consideration the pattern of exposure estimates across the range of discrete 

benchmark levels considered in EPA’s exposure assessment to provide some indication 

of the potential magnitude of the incidence of health outcomes that could not be 

evaluated in the Agency’s quantitative risk assessment but which have been demonstrated 

to occur in healthy people at O3 exposures as low as 0.080 ppm, the lowest level at which 

such health outcomes have been tested.5 As discussed in the preamble to the final rule, 

the Administrator concludes that the exposure assessment suggests that exposures at 

above the 0.080 ppm benchmark level, where several health effects have been shown to 

occur in healthy individuals, are essentially eliminated for standards in the range 0.070 to 

0.075 ppm. He also concludes that at the 0.070 ppm benchmark level, the exposures are 

substantially reduced and eliminated for the vast majority of people in at-risk groups, and 

that the very low estimates of such exposures are not appreciably different, from a public 

health perspective, between those exposures associated with just meeting a standard set at 

0.070 ppm or 0.075 ppm. Further, the Administrator places relatively little weight on the 

exposures using the 0.060 ppm benchmark level given the very limited scientific 

evidence supporting a conclusion that O3 is causally related to health outcomes at this 

exposure level. Considering the uncertainties associated with the exposure assessment, 

the Administrator concludes that the exposure estimates associated with each of the 

benchmark levels are not appreciably different, between a 0.070 or 0.075 ppm standard, 

and therefore, the exposure assessment does not provide a basis for choosing a level 

within the proposed range. 

 

While the Administrator places less weight on the results of the risk assessment, he notes 

that the results indicate that a standard set within the proposed range would likely reduce 

risks to at-risk groups from the O3-related health effects considered in the assessment, 

and by inference across the much broader array of O3-related health effects that can only 

be considered qualitatively, relative to the level of protection afforded by the current 

standard. Moreover, he notes that the results of the assessment suggest a gradual 

reduction in risks with no clear breakpoint as increasingly lower standard levels are 

considered. However, in light of the important uncertainties inherent in the assessment 

discussed above and in the proposal, the Administrator concludes that the risk assessment 

does not provide a basis for choosing a level within the proposed range. 

(16) Comment: Several commenters (e.g., API, UARG, Rochester Report) contend that the 

approach EPA used to adjust hourly O3 concentrations to simulate just attaining an 

alternative standard, the quadratic rollback approach, may overstate the air quality 

 5

 Such health outcomes include increased airway responsiveness, increased pulmonary 

inflammation, increased cellular permeability, and decreased pulmonary defense mechanisms, 

which have been associated with aggravation of asthma, increased medication use, increased 

school and work absences, increased susceptibility to respiratory infection, increased visits to 

doctors’ offices and emergency departments, increased admissions to hospitals, and possibly to 

cardiovascular system effects and chronic effects such as chronic bronchitis or long-term damage 

to the lungs that can lead to reduced quality of life.
90

improvements resulting from emissions reductions and thus overstate the benefits of 

stricter standards. One commenter (API) stated that the quadratic air quality adjustment 

approach “was still suspect” (API, p. 27) and submitted an analysis examining alternative 

air quality adjustment procedures. In addition, there is uncertainty about whether the 

alternative standards in the proposed range are even attainable, given EPA’s focus on the 

mean background and failure to consider the extremes of background. One group of 

commenters contends that considerable uncertainty remains on the impact of reducing the 

8-hour O3 standard from the current level of 0.08 ppm to a lower level, because EPA has 

assumed for its analysis that shifts in the probability distribution of exposure to O3 will 

occur not just in the upper tail of the distribution (the days on which O3 levels will exceed 

the existing 8-hour standard of 0.08 ppm or proposed alternative standards of 0.060 to 

0.074 ppm), but also the lower and middle portions of this distribution, levels below 

0.060 ppm. It is these changes in the lower and middle portion of the distribution, they 

pointed out, that provide most of the calculated benefits in terms of reduced short termmortality and reduced hospital admissions associated with the more stringent alternative 

proposed standard (Rochester Report, p. 19). One commenter contends that EPA’s 

“proportional rollback” approach assumes that States will reduce O3 levels by a 

“proportionate amount throughout the distribution of 8-hour measurement periods” 

(NAM, p. 59). 

Response: First, with respect to the air quality adjustment approach used in the current 

review to simulate air quality just meeting the current and alternative O3 standards, as 

discussed in the Staff Paper (section 4.5.6) and in more detail in a staff memorandum 

(Rizzo, 2006), EPA concluded that the quadratic air quality adjustment approach 

generally best represented the pattern of reductions across the O3 air quality distribution 

observed over an 8-year period in areas implementing control programs designed to attain 

the O3 NAAQS. See the response to comment number (14) in section II.A.4 in this 

document for additional response to API’s analysis of alternative air quality adjustment 

procedures. While EPA recognizes that future changes in air quality distributions are 

area-specific, and will be affected by whatever specific control strategies are 

implemented in the future to attain a revised NAAQS, there is no empirical evidence to 

suggest that future reductions in ambient O3 will be significantly different from past 

reductions with respect to impacting the overall shape of the O3 distribution. 

Second, it is not permissible for EPA to consider whether or not a given alternative 

standard is or is not attainable under the provisions of section 109 of the Clean Air Act. 

Third, EPA believes that the commenters’ implied alternative approach of only reducing 

peak 8-hour daily maximum values that are at or near the standard level is unrealistic in 

that most O3-related air pollution control measures are continuous in nature and have an 

impact on the entire distribution of 8-hour O3 concentrations. In contrast, EPA’s use of a 

quadratic adjustment procedure that reduces not only the upper end of the distribution, 

but also to a lesser extent the middle and lower end of the distribution has been shown to 

match reductions observed in O3 concentrations over nearly a decade. 
91

Fourth, EPA rejects NAM’s contention that EPA used a “proportional rollback” approach 

and that the approach was not justified, when in fact, as described above, EPA used a 

quadratic air quality adjustment approach that reduced the upper end of the O3

distribution more than the middle or lower-end of the distribution. Further, as discussed 

above, EPA’s air quality adjustment approach was based on an analysis of historical 

changes in O3 concentrations and EPA’s approach is conistent with past changes in O3

concentrations resulting from a myriad set of national, state, and local control programs 

reducing O3 precursors. 

Finally, some commenters appear to interpret attainment of the standard using a single 

year. This is not consistent with the form of the current standard or the alternative 

standards that EPA analyzed. Thus, EPA does not agree that its approach assumed an 

arbitrary degree of further reduction, but rather EPA’s approach reflects that the 

reductions required are based on a three-year period, not just a single year. 

(17) Comment: One commenter contends that, because a number of areas -- including some 

of the cities involved in the risk assessment— will have difficulty in complying with the 

current 8-hour standard within the next decade, the full public health gains in these areas 

from a more stringent 8-hour standard are unlikely to be realized for a number of years. 

In light of this, this commenter questioned whether the Agency can or should consider 

these projected gains as a health-based criterion for its decision making (Dow Chemical). 

Another commenter states that “it is technically infeasible to eliminate all U.S. 

anthropogentic emissions” and that “it is also technically infeasible to achieve the revised 

ozone standards proposed” (NAM, p. 63). 

Response: EPA notes that the Administrator in reviewing and making decisions with 

respect to the NAAQS is prohibited from considering the ability of areas to attain the 

NAAQS. In addition, while cost and technological feasibility are taken into account in 

the implementation of the NAAQS – even if an area is delayed in meeting the standard 

due to cost or other implementation difficulties -- this does not reduce the benefits to 

public health that could be expected from full attainment of a new standard, which is the 

focus of EPA’s risk assessment. 

 (18) Comment: A group of environmental and health organizations contends that EPA “has 

illegally understated the health effects of O3 by basing its risk assessment solely on risks 

in excess of policy-related background levels. Section 109 of the [Clean Air] Act 

requires the primary NAAQS to be set at a level requisite to protect public health with an 

adequate margin of safety: it does not allow EPA to protect only against health risks 

presented by O3 attributable to anthropogenic sources. A person breathing the air is 

exposed to the total concentration of O3 in the air, including background, and the 

NAAQS must protect against that total exposure. There is nothing in the Act that allows 

EPA to ignore or discount the risk presented by the background component of such 

exposures.” (ALA et al., p. 110) 

Response: EPA does not agree that it is inappropriate or impermissible to assess risks 

that are in excess of PRB or that EPA must focus on total risks when using a risk 

assessment to inform decisions on the primary standard. Consistent with the approach 
92

used in the risk assessment for the prior O3 standard review and consistent with the 

approach used in risk assessments for other prior NAAQS reviews, estimating risks in 

excess of PRB is judged to be relevant to policy decisions regarding the ambient air 

quality standard as it provides useful information regarding the risks attributable to 

anthropogenic emissions. EPA also notes that with respect to the adequacy of the current 

standard taking total risks into account would not impact the Administrator’s decision as 

he judges that the current standard is not adequate even when risks in excess of PRB are 

considered. In addition, EPA notes that consideration of the evidence itself, as well as 

exposures at and above benchmark levels in the range of 0.060 to 0.080 ppm are not 

impacted at all by consideration of PRB. In this review, EPA’s use of PRB in the risk 

assessment had little impact on the Administrator’s determination regarding the level of 

the standard given the relative weight placed on the risk assessment and the range of PRB 

values compared to the standards under consideration. 

(19) Comment: While disagreeing with EPA’s approach of estimating risks only above PRB, 

ALA et al. supported the use of the GEOS-CHEM model as the “best tool available to 

derive background concentrations” should EPA continue to pursue this approach. 

Response: EPA agrees with this comment. 

(20) Comment: Many industry commenters argued that EPA’s (flawed) approach to 

estimating PRB concentrations has lead to underestimates of PRB and thus to an 

overestimation of the numbers of cases of health effects associated with O3

concentrations above PRB. Some commenters also pointed out that the major difference 

between this review and the previous one is the lower background level; others pointed 

out that if the same background level were used, almost all the health benefits would be 

reduced by up to 90% – or, as one commenter put it, “the choice of the PRB dominates 

EPA’s estimates of O3 health risks” (NAM, p. 62). These commenters expressed 

concerns that PRB levels were estimated by EPA solely by modeling using the GEOSCHEM model, which they argued underestimates PRB. Related arguments made related 

to the role of PRB in the risk assessment included: 

• A few commenters contend that EPA’s current PRB estimates inappropriately excluded 

certain emissions contributions that should be included – notably, anthropogenic 

precursor emissions from Canada and Mexico. They argued that this approach artificially 

inflates the risk estimates. 

• One commenter argued that, based on EPA’s limited sensitivity analysis to examine how 

sensitive the risk estimates are to differing assumptions about PRB, the understatement of 

PRB can result in substantial overstatements of risk. For example, assuming PRB was 

0.005 ppm higher than that predicted by the GEOS-CHEM model decreased estimates of 

nonaccidental mortality by 50% or more – and resulted in a 62% decrease in predicted 

incidence of nonaccidental mortality in Los Angeles upon attainment of the present 

standard when 2002 O3 air quality data were used (API). 

• One commenter contends that the risk estimates were “highly sensitive (in the downward 

direction) to any of several alternative possible assumptions on PRB. The commenter 

found that using the monitored air quality data from the Trinidad Head site, “believed by 

many to represent PRB better than do the results of the GEOS-CHEM modeling,” when 
93

estimating the risk remaining after attainment of the existing NAAQS reduced the 

average risk estimates by from 36% to 72% from the risk levels predicted in EPA’s 

analysis. For Sacramento and Los Angeles, the two cities considered in EPA’s risk 

assessment that are closest to the Trinidad Head site, the estimates of risk fell by 65% and 

72%, respectively. The commenter concluded that the absolute risk estimates are highly 

sensitive to alternative plausible PRB assumptions, preventing meaningful comparisons 

of health risks at alternative possible standard levels to that upon attainment of the 

existing NAAQS (UARG, pp. 25-27). 

• One commenter argued that the sensitivity to 0.005 ppm changes in background 

demonstrates that the bulk of estimated mortality comes from days with O3

concentrations that are very low. This commenter contends that this is not biologically 

plausible (AAM). 

• One commenter argued that EPA had ignored an important comment from the CASAC 

Panel which undermines the approach used in EPA’s risk assessment. Citing CASAC’s 

August teleconference, this commenter quoted the CASAC letter (Henderson, 2006b) 

which noted that PRB is highly problematic to calculate and is, in some sense, 

“unknowable.” CASAC went on to say, “One can avoid this problem, it was contended, 

by calculating the change in incidence of the health effect associated with a change in 

O3 from the current standard to some other specified concentration. This approach, it 

was argued, would allow focus on the question, ‘What is the difference in the expected 

number of health effects that will occur at various concentrations of O3, relative to the 

current standard of 0.08?’ A key advantage of this approach is that it does not depend on 

the choice of PRB, and thus is free of the uncertainties surrounding estimation of PRB” 

(NAM, p. 26). 

• One commenter argued that the sensitivity of clinical respiratory effects to background 

assumptions, while not as large as for other health effects, is still very important. Citing 

Tables 3-28 and 3-31 in the Health Risk TSD, this commenter noted that the numbers of 

occurrences of lung function response of healthy and asthmatic children are reduced 

with a 0.005 ppm increase in PRB almost as much as a lowering of the standard from 

0.084 to 0.074 ppm. The commenter concluded that, given the importance of the choice 

of background, the Agency should reevaluate its assumed background and then reevaluate the clinical risks (AAM). 

• One commenter contended that EPA had not considered one literature review 

(Vingarzan, 2004) and one research study (Ortmans et al., 2006) and that “both articles 

indicate that there is significant spatial and seasonal variability, with springtime peak” 

(NAM, p. 62). 

Response: First, the U.S. government has influence over emissions at our borders that 

affect ambient O3 concentrations entering the U.S. from Canada and Mexico through 

either regulations or international agreements, and therefore EPA does not agree that 

these emissions are uncontrollable. PRB is currently designed to identify O3 levels that 

result from emissions that are considered uncontrollable because the U.S. has little if any 

influence on their control, and in that context anthropogenic emissions from Mexico or 

Canada should be excluded from PRB. EPA has consistently defined PRB as excluding 

anthropogenic emissions from Canada and Mexico in NAAQS reviews over more than 

two decades and sees no basis in the comments to alter this current definition. 
94

Second, the criticisms raised concerning the use of a modeling approach (GEOS-CHEM) 

and the potential alternative approach of using remote monitoring data to estimate PRB 

were considered by EPA’s scientific staff and the CASAC Panel during the course of 

reviewing the Criteria Document. Both EPA’s experts and CASAC endorsed the use of 

the peer-reviewed, thoroughly evaluated modeling approach (GEOS-CHEM) described in 

the Criteria Document as the best approach for estimating PRB levels. The Criteria 

Document reviewed detailed evaluations of GEOS-CHEM with O3 observations at U.S. 

surface sites (Fiore et al., 2002, 2003) and comparisons of GEOS-CHEM predictions 

with observations at Trinidad Head, CA (Goldstein et al., 2004) and found no significant 

differences between the model predictions and observations for all conditions, including 

those given in the current PRB definition. The Criteria Document (p. 3-49) states that the 

current model estimates indicate that PRB in the U.S. is generally 0.015 to 0.035 ppm 

that declines from spring to summer and is generally < 0.025 ppm under conditions 

conducive to high O3 episodes. The Criteria Document acknowledges that PRB can be 

higher, especially at elevated sites in the spring due to stratospheric exchange. However, 

unusually high springtime O3 episodes tied to stratospheric intrusion are rare and 

generally occur at elevated locations and these can be readily identified and excluded 

under EPA’s exceptional events rule (72 FR 13560) to avoid any impact on 

attainment/non-attainment status of an area. 

 Third, many of the commenters who raised the concern that EPA’s current estimates of 

PRB were too low and had the impact of exaggerating the risks associated with the 

current standard ignored the fact that the risk assessment included a sensitivity analysis 

which showed the potential impact of both lower and higher estimates of PRB or only 

focused on the impact of higher estimates of PRB. The choices of lower and higher 

estimates of PRB included in the risk assessment sensitivity analyses were based on the 

peer-reviewed evaluation of the accuracy of GEOS-CHEM model. As discussed in the 

Staff Paper (p. 2-54), the Criteria Document refers to a number of GEOS-CHEM 

publications (Bey et al., 2001; Liu et al., 2002; Martin et al., 2002; Fusco and Logan, 

2003, Li et al., 2002; 2005), summarizing their conclusions as “results indicate no 

significant bias, and agreement to generally within 5 ppbv (parts per billion volume) for 

monthly mean concentrations at different altitudes”(Criteria Document, p. 3-51 to 3-53). 

The Criteria Document (p. 3-53) also states "in conclusion, we estimate that the PRB O3

values reported by Fiore et al. (2003) for afternoon surface air over the United States are 

likely 10 parts per billion by volume (ppbv) too high in the southeast in summer, and 

accurate within 5 ppbv in other regions and seasons." These error estimates are based on 

comparison of model output with observations for conditions which most nearly reflect 

those given in the PRB definition, i.e., at the lower end of the probability distribution. As 

discussed in the Criteria Document and Staff Paper, it can be seen that GEOS-CHEM 

overestimates O3 for the southeast and underestimates it by a small amount for the 

northeast. These commenters generally ignored the scientific conclusion presented in the 

Criteria Document that for some regions of the country the evidence suggests that the 

model actually overestimates PRB. Thus, the influence of alternative estimates of PRB 

on risks in excess of PRB associated with meeting the current standard can be to lower or 

increase the risk estimates. While the choice of estimates for PRB contributes to the 
95

uncertainty in the risk estimates, EPA does not agree that the approach currently used is 

biased since peer-reviewed evaluations of the model have shown relatively good 

agreement (i.e., generally within 5 ppb for most regions of the country). 

 

Fourth, with respect to commenters who pointed to the CASAC comment (Henderson, 

2006c, p. 12) that EPA could avoid problems about PRB by focusing on risk reductions 

relative to just meeting the current standard, EPA notes the following. An O3 risk 

assessment calculates the risk reductions associated with changing from O3

concentrations estimated to exist under one scenario to O3 concentrations estimated to 

exist under another scenario. For example, we can calculate 

• the risk reductions that would result from changing from “as is” (ambient) O3

concentrations to PRB O3 concentrations; or 

• the risk reductions that would result from changing from O3 concentrations under the 

current standard to PRB O3 concentrations; or 

• the risk reductions that would result from changing from O3 concentrations under the 

current standard to O3 concentrations under some more stringent standard. 

EPA can avoid using estimates of PRB in its calculations only if all O3 concentrations in 

both scenarios are above PRB. Since, by definition, we cannot get O3 concentrations to 

be less than PRB concentrations (i.e., we cannot get O3 concentrations to be lower than 

what they would be in the absence of human activity), we must know what PRB 

concentrations are (or have estimates of these concentrations) to know what the lower 

bound for feasibly reducing O3 concentrations is. 

The only way EPA could avoid using estimates of PRB concentrations in our risk 

assessment is if we were reasonably sure that all of the O3 concentrations in both 

scenarios (i.e., before reduction and after reduction) were above PRB concentrations – 

i.e., even if we don’t know the PRB concentrations, our estimated O3 concentrations are 

sufficiently high that we can be reasonably sure they are not below whatever PRB 

concentrations are. However, in practice, this doesn’t happen – i.e., we typically have O3

concentrations that are sufficiently low that we cannot be sure they are above PRB. 

EPA believes that some commenters have misread the CASAC Panel concern “that the 

current approach to determining PRB is the best method to make this estimation” 

(Henderson, 2007, p. 2) as a criticism of the use of the GEOS-CHEM modeling approach 

and/or support for primary reliance on estimates based on remote monitoring sites. 

However, the CASAC Panel went on to state that one reason for its concern was that the 

contribution to PRB from beyond North America was uncontrollable by EPA and that “a 

better scientific understanding of intercontinental transport of air pollutants could serve 

as the basis for a more concerted effort to control its growth ...” (Henderson, 2007, p. 3). 

Hence, CASAC’s concern appeared to be more with defining what emissions to include 

in defining PRB, and the role that PRB should play, as compared to the technical 

question of the best way to estimate PRB levels. 
96

In addition, EPA notes that Dr. Armistead Russell, the atmospheric modeling expert on 

the CASAC O3 Panel, stated the following about EPA’s current use of PRB in his 

comments on the second draft Staff Paper: 

In regards to PRB, given the contentious nature of the issue, the use of the PRB 

should be discussed in Chapter 2, along with other measures. However, their 

current approach has been peer-reviewed, and is appropriate. They should, before 

the next analyses, continue to refine and evaluate their approach to setting the 

PRB, and how it is used in the assessments. For example, might they use the PRB 

in the roll-back formula? This could be done by analyzing CMAQ simulations 

where the boundary conditions are set to those conditions representative of PRB 

conditions (Henderson, 2006c, p. D-48). 

Dr. Russell clearly endorsed EPA’s current approach to PRB and was discussing 

potential improvements for the next review of the O3 NAAQS. EPA notes that much of 

the spatial variability in O3 concentrations is due to spatial variability in the distribution 

of anthropogenic sources of O3 precursors. This source of variability is not a factor in the 

PRB simulations using the GEOS-CHEM model. While Dr. Russell suggested that 

higher resolution models such as CMAQ might be needed, it is not clear that results will 

be significantly improved by going to the much higher spatial resolution used in regional 

scale air quality models given the good agreement of GEOS-CHEM estimates with 

observations. 

In conclusion, the model used, GEOS-CHEM has been extensively evaluated and is one 

of the key models used in major international assessments including the 

Intergovernmental Panel on Climate Change and Long-Range Transboundary Air 

Pollution Converntion assessments. As such it is highly suitable for gauging the influence 

of intercontinental transport on air quality in the U.S. Thus, its predictions reflect state of 

the science estimates of intercontinental transport. In reviewing the Staff Paper, the 

atmospheric modeling expert on the CASAC Panel in his comments on how PRB had 

been estimated using the GEOS-CHEM model concluded that the “current approach has 

been peer-reviewed, and is appropriate” (Henderson, 2006b, p. D-48). 

Finally, in response to the NAM comment that EPA had ignored two studies related to 

PRB, the first study (Vingarzan, 2004) was considered by EPA and is discussed in the 

Annex to the final Criteria Document (see p. AX3-136). The other study (Oltmans et al., 

2006 – NAM misspelled the author of this study in its comment) was published after 

completion of the Criteria Document. EPA has already discussed the fact that there is 

spatial and seasonal variability in PRB in the Criteria Document and Staff Paper and the 

GEOS-CHEM model runs also show this spatial and seasonal variability. 

(21) Comment: Some commenters (e.g., Lefohn, API) asserted that the EPA made an 

administrative (arbitrary) decision in its choice of methods for estimating PRB levels. 

Response: EPA extensively evaluated the usefulness of different methods for estimating 

PRB levels. The methodology for estimating PRB levels was explained in section AX3.9 
97

of the Criteria Document. EPA noted in the Criteria Document and Staff Paper that the 

GEOS-CHEM model has been extensively evaluated for O3 and other species. 

Simulations at a number of relatively remote sites have indicated no significant bias in 

the model predictions (See comment #20 above). Ozone is a regional pollutant and it is 

thus highly problematic to separate the regional pollution contribution from PRB. Even 

the Annapolis Report acknowledges this point – at least for the eastern U.S. However, the 

same considerations also apply to the western U.S. As noted in the Criteria Document, it 

is impossible to tell whether or not a given site is subject to regional or continental 

anthropogenic influence without ancillary measurements. These include measurements 

of O3 precursors from which photochemical production rates can be calculated or of 

tracers of transport from source regions in North America. Either the requisite analyses 

have not been performed or data are not available for the monitoring sites suggested in 

the comments. On the other hand, the GEOS-CHEM model has been evaluated with 

respect to O3 precursors in addition to O3 itself. 

(22) Comment: One commenter (NAM, p. 63) contends that “presentational objectivity 

requires that EPA accurately and clearly state the proportion of reduced health effects 

properly attributable to each of the following factors: (a) the increase in EPA’s estimate 

of unit health risks; (b) the proposed reduction in the allowable peak O3 level; (c) the 

rollback procedure; and (d) the lowering of the Policy Relevant Baseline.” Without such 

disaggregation, this commenter contends, policymakers and the public will be misled to 

believe that all or virtually all of the projected health benefits are attributable to the 

reduction in the standard. 

 

Response: Contrary to the commenter’s contention, there is no requirement that EPA has 

to partition its risk estimates with respect to the factors cited. It is not clear what the 

commenter is referring to with respect to “the increase in EPA’s estimate of unit health 

risks.” Most of the health effects based on epidemiological studies were not included in 

the 1997 risk assessment, so these are new quantitative estimates, not increased risk 

estimates. EPA has appropriately discussed the air quality adjustment procedure in the 

Health Risk TSD and Staff Paper. Similarly, EPA has discussed its new estimates for 

PRB, which are based on the best available science as discussed in Chapter 2 of the 

Criteria Document (section 3.7) and has presented the results of sensitivity analyses that 

show the impacts on the risk estimates of both lower and higher estimates for PRB in 

several of the risk assessment locations. 

 (23) Comment: One commenter (NAM, p. 29) contends that EPA has used the data from the 

Adams’ clinical studies (Adams 2002, 2003a, 2003b, 2006a, 2006b) for the purpose of 

estimating individual or population variability in response, which was not the original 

purpose of the authors. This commenter further asserted that under the IQG EPA must 

provide an analysis supporting use of data for a purpose other than the original one. 

Response: As in the 1997 risk assessment, EPA obtained individual data from several 

6.6-hour O3 controlled human exposure studies from the author. API, the funding 

sponsor of the Adams studies, urged EPA to use the data from these studies, particularly 

the most recent study by Dr. Adams in its health risk assessment in its comments on the 
98

draft Staff Paper and draft health risk assessment in January 2006 (API, 2006). EPA 

obtained the individual data used in the health risk assessment directly from the author 

and explained that the data would be combined with other individual data from the 

Horstman, Folinsbee, and McDonnell 6.6-hour O3 studies. The health risk assessment for 

lung function responses was reviewed by the CASAC O3 Panel and there were no 

objections expressed by CASAC panel members or by Dr. Adams in either his oral or 

written comments to EPA concerning EPA’s use of the Adams data as part of the basis 

for estimating the exposure-response relationships used in the health risk assessment. 

(24) Comment: One commenter (API) urged EPA to use a dynamic response model 

developed by McDonnell to estimate minute-by-minute FEV1 decrements in its health 

risk assessment based on all of the controlled human exposure study data. This 

commenter also urged EPA to break the wide range of EVR cutpoints used in the 

exposure modeling into a number of smaller bins to test the hypothesis that the use of 

such a wide EVR range biases the overall result. This commenter asserted that the 

sensitivity of the results to the use of the API model should be evaluated prior to the 

issuance of the final rule. 

Response: The recommendation to replace the lung function exposure-response 

relationships developed for EPA’s risk assessment was first made in August 2006 in a 

presentation to the CASAC O3 Panel. EPA does not agree that it is appropriate or 

necessary to change the lung function exposure-response model used in its health risk 

assessment for the following reasons: (1) the proposed alternative model had not been 

peer-reviewed or published at the time EPA’s assessment was completed; (2) while there 

are clearly described criteria about the relative adversity of lung function decrements 

associated with 1- to 8-hour lung function decrements as discussed in the Criteria 

Document and Staff Paper and in the previous O3 NAAQS review, there is no consensus 

about the adversity of 1-minute decrements in lung function response, and (3) CASAC 

reviewed two drafts of the Health Risk TSD and did not recommend that EPA adopt the 

alternative approach suggested by the commenter. In EPA’s judgment the alternative 

approach recommended by the commenter requires further examination and review and 

should be investigated for potential use in the next O3 NAAQS review. 

(25) Comment: EPA assumes that all exposures between 13 and 27 EVR respond as though 

they were at 20 EVR, substantially overestimating the risk since there are many more 8-

hour occurrences of ozone at 13 EVR than at 20 and many more at 20 EVR than at 27. 

This results in an overestimation of the number of exposures of concern and of the risk 

estimates. (API, AAM) 

Response: The commenter incorrectly asserts that EPA assumed that all exposures 

between 13 and 27 EVR respond as though they were at 20 EVR. As in the lung function 

risk assessment conducted in the prior O3 NAAQS review, EPA matched the exposureresponse relationships from controlled human exposure studies where the vast majority of 

subjects (>99% of subjects) had EVR’s in the range of 13 to 27 l-min-1m2 with 8-hour 

average exposures corresponding to averaged EVR’s in this same range. The individuals 

in the 6.6-hour controlled human exposure studies did not all have the same EVR and in 
99

fact there were individuals throughout the range from 13 to 27 l-min-1m

2

. In EPA’s 

judgment there is not adequate data from 6 to 8-hour exposure studies to justify 

specifying lung function decrements for a more detailed breakdown of EVRs. Therefore, 

EPA does not agree that there is necessarily an overestimation of the number of 

exposures at specified exertion levels or that the risk estimates are overstated. In 

addition, as noted in the response to comment number (23) above, CASAC reviewed two 

drafts of the Health Risk TSD and did not recommend changing the approach 

implemented by EPA in its risk assessment. 

(26) Comment: One commenter contends that information quality principles require that 

scientific information be presented “within a proper context” and that “a starting point for 

context would be to compare the severity of respiratory effects from ozone to effects 

associated with the most relevant of perhaps a dozen confounders” (NAM, p.51) 

Response: EPA believes it has provided sufficient context in its discussion of respiratory 

effects in the Criteria Document and Staff Paper and that there is no specific requirement 

to make the type of comparison suggested by the commenter. Further, EPA is unaware 

of scientific evidence that would allow it to present an equivalent difference in allergen 

exposure, exercise, temperature or humidity to a specified change in ozone levels. 

(27) Comment: One commenter contends that EPA characterized its risk estimates as 

“primary” or “secondary” and that EPA’s primary estimates were those that tend to 

support a policy preference for a more stringent NAAQS and its secondary estimates 

were those that did not. “To adhere to information quality requirements, EPA must 

accurately and clearly describe what distinguishes between these two classes of risk 

estimates” (NAM, p. 53). EPA’s treatment of alternative risk estimates also show defects 

in presentational objectivity by “failing to carry forward all risk estimates of similar 

likelihood – and in this case, giving greater presentational attention to risk estimates of 

lower likelihood” (NAM, p. 53). 

Response: NAM’s contention that EPA’s risk estimates are characterized as “primary” or 

“secondary” in the Staff Paper or proposal notice is incorrect. EPA did use the term 

“base case” for its lung function risk estimates and provided its rationale for 

distinguishing between its base case and alternative assumptions about the shape of the 

exposure-response relationship in the proposal notice: 

EPA has chosen a model reflecting a 90 percent weighting on a logistic form and 

a 10 percent weighting on a linear form as the base case for the current risk 

assessment. The basis for this choice is that the logistic form provides a very 

good fit to the combined data set, but a linear model cannot be entirely ruled out 

since there are only very limited data (i.e., 30 subjects) at the two lowest exposure 

levels (i.e., 0.040 and 0.060 ppm). EPA has conducted a sensitivity analysis 

which examines the impact on the lung function risk estimates of two alternative 

choices, an 80 percent logistic/20 percent linear split and a 50 percent logistic/50 

percent linear split. (72 FR 37858) 
100

EPA strongly disagrees that its rationale for choosing its base case was influenced by a 

policy preference. As shown in Figures 5-17 and 5-18 in the Staff Paper (pp. 5-88 to 5-

91), the pattern and, in many cases, the actual percent reduction in lung function risk is 

very similar across the base case and alternative assumptions about the shape of the 

exposure-response relationship. 

With respect to the risk estimates for the health outcomes based on epidemiological 

studies, EPA presented its rationale for presenting certain risk estimates and noted where 

alternative estimates could be found in the Staff Paper and Risk Assessment TSD. For 

example, EPA stated in the proposal, 

EPA has focused on estimates based on multi-city studies where available. The 

advantages of relying more heavily on concentration-response functions based on 

multi-city studies include: (1) More precise effect estimates due to larger data 

sets, reducing the uncertainty around the estimated coefficient; (2) greater 

consistency in data handling and model specification that can eliminate city-tocity variation due to study design; and (3) less likelihood of publication bias or 

exclusion of reporting of negative or nonsignificant findings (72 FR 37859). 

In conclusion, EPA did not divide its risk estimates into “primary” and “secondary” 

categories: EPA clearly articulated its rationale for presenting some risk estimates over 

risk estimates in the proposal notice; its rationale was not influenced by any policy 

preference; and EPA discussed where alternative risk estimates could be found in its 

documents. Finally, the Administrator in his final decision focused on the overall pattern 

of the risk estimates, which is very similar between the base case estimates presented in 

the proposal notice and the alternative estimates more fully presented in the Staff Paper 

and Risk Assessment TSD. 

(28) Comment: One commenter contends that EPA characterized its risk estimates as 

“primary” or “secondary” and that EPA’s primary estimates were those that tend to 

support a policy preference for a more stringent NAAQS and its secondary estimates 

were those that did not. “To adhere to information quality requirements, EPA must 

accurately and clearly describe what distinguishes between these two classes of risk 

estimates” (NAM, p. 53). EPA’s treatment of alternative risk estimates also show defects 

in presentational objectivity by “failing to carry forward all risk estimates of similar 

likelihood – and in this case, giving greater presentational attention to risk estimates of 

lower likelihood” (NAM, p. 53). 

Response: EPA rejects NAM’s contention that EPA characterized its risk estimates as 

“primary” or “secondary” in the Staff Paper or proposal notice. EPA did use the term 

“base case” for its lung function risk estimates and provided its rationale for 

distinguishing between its base case and alternative assumptions about the shape of the 

exposure-response relationship in the proposal notice: 

EPA has chosen a model reflecting a 90 percent weighting on a logistic form and 

a 10 percent weighting on a linear form as the base case for the current risk 
101

assessment. The basis for this choice is that the logistic form provides a very 

good fit to the combined data set, but a linear model cannot be entirely ruled out 

since there are only very limited data (i.e., 30 subjects) at the two lowest exposure 

levels (i.e., 0.040 and 0.060 ppm). EPA has conducted a sensitivity analysis 

which examines the impact on the lung function risk estimates of two alternative 

choices, an 80 percent logistic/20 percent linear split and a 50 percent logistic/50 

percent linear split. (72 FR 37858) 

EPA strongly disagrees that its rationale for choosing its base case was influenced by a 

policy preference. As shown in Figures 5-17 and 5-18 in the Staff Paper (pp. 5-88 to 5-

91), the pattern and, in many cases, the actual percent reduction in lung function risk is 

very similar across the base case and alternative assumptions about the shape of the 

exposure-response relationship. 

With respect to the risk estimates for the health outcomes based on epidemiological 

studies, EPA presented its rationale for presenting certain risk estimates and noted where 

alternative estimates could be found in the Staff Paper and Risk Assessment TSD. For 

example, EPA stated in the proposal, 

EPA has focused on estimates based on multi-city studies where available. The 

advantages of relying more heavily on concentration-response functions based on 

multi-city studies include: (1) More precise effect estimates due to larger data 

sets, reducing the uncertainty around the estimated coefficient; (2) greater 

consistency in data handling and model specification that can eliminate city-tocity variation due to study design; and (3) less likelihood of publication bias or 

exclusion of reporting of negative or nonsignificant findings. (72 FR 37859) 

In conclusion, EPA did not divide its risk estimates into “primary” and 

“secondary” categories, EPA clearly articulated its rationale for presenting some 

risk estimates over over risk estimates in the proposal notice and its rationale was 

not influenced by any policy preference, and EPA discussed where alternative risk 

estimates could be found in its documents. Finally, the Administrator in his final 

decision focused on the overall pattern of the risk estimates, which is very similar 

between the base case estimates presented in the proposal notice and the 

alternative estimates more fully presented in the Staff Paper and Risk Assessment 

TSD. 

6. Specific Comments Related to Communication of Public Health Information 

 Information on the public health implications of ambient concentrations of criteria 

pollutants is currently made available primarily through EPA's Air Quality Index (AQI) program 

(40 CFR 58.50). The current Air Quality Index has been in use since its inception in 1999 (64 

FR 42530). It provides accurate, timely, and easily understandable information about daily 

levels of pollution. The Agency recognized the importance of revising the AQI in a timely 

manner to be consistent with any revisions to the NAAQS. Therefore, EPA proposed to finalize 

conforming changes to the AQI, in connection with the Agency's final decision on the O3
102

NAAQS if revisions to the primary standard were promulgated. This section responds to 

comments received on the proposed conforming changes to the AQI. 

Comment: EPA received relatively few comments on the proposed changes to the AQI. 

Three major 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 the AQI should be 

revised in conjunction with this rulemaking, or in a separate rulemaking; and, (3) whether 

an AQI value of 100 should be set equal to or lower than the level of the short-term 

primary O3 standard, and the other breakpoints adjusted accordingly. UARG asserted 

that EPA should not revise the AQI at all, even if EPA does revise the primary O3

standard. In support of this view, UARG noted that there is no requirement for EPA to 

set an AQI value of 100 equal to the level of the short-term standard, and cited the 1999 

decision to set the an AQI value of 100 for PM2.5 equal to 40 μg/m3, when the level of the 

short-term standard was then 65 μg/m3

. UARG also expressed the view that lowering the 

ambient concentrations associated with different AQI values would confuse and mislead 

the public about actual trends in air quality, which UARG asserted are improving. ALA 

and other environmental groups in a joint set of comments did not support revising the 

AQI in conjunction with this rulemaking. ALA et al. expressed the view that since EPA 

did not propose specific breakpoints in its proposed revisions to the AQI, EPA should 

conduct a separate rulemaking, specifying the proposed breakpoints to allow the public 

an opportunity to comment on them. Several State agencies, including agencies from 

Pennsylvania, Wisconsin and Oklahoma, and State organizations, including NACAA and 

NESCAUM, supported revising the AQI at the same time that the standard is revised. 

NACAA expressed the view that: “The effectiveness of the AQI as a public health tool 

will be undermined if EPA undertakes regulatory changes to the ozone NAAQS without 

simultaneously revising the AQI.” (NACAA, p. 5) The Wisconsin Department of 

Natural Resources (WI DNR) further noted that: 

“...when the 24-hour PM2.5 standard was revised, EPA missed an opportunity to 

adopt conforming changes to the AQI. The Administrator signed the Federal 

Register notice promulgating a revised fine-particle standard in September 2006, 

but EPA still has not changed the AQI to reflect the revised standard. We 

recommend that the AQI be amended to be consistent with the revised ozone and 

PM2.5 standards.” (WI DNR, p. 3) 

 Finally, ALA et al. and NESCAUM expressed the view that an AQI value of 100 should 

be set at an ambient concentration below the range for the proposed primary standard. 

These commenters cited the health evidence showing adverse health effects below the 

proposed range of the standard, the recommended range of CASAC, and also cited the 

1999 decision to set an AQI value of 100 for PM2.5 equal to 40μg/m3 when the level of 

the short-term standard was 65 μg/m3, as support for this view. Most other State 

commenters supported setting an AQI value of 100 equal to the level of the primary O3

standard. 

Response: Recognizing the importance of the AQI as a communication tool that allows 

the public to take exposure reduction measures when air quality may pose health risks, 
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EPA agrees with State agencies and organizations that favored revising the AQI at the 

same time as the primary standard. EPA also agrees with State agency commenters that 

its historical approach of setting an AQI value of 100 equal to the level of the revised 

primary standard is appropriate, both from a public health and a communication 

perspective. 

 Both UARG and ALA et al. cite the 1999 AQI rulemaking, which set an AQI value of 

100 for PM2.5 equal to 40 μg/m3

 a lower level than the level of the short-term PM2.5

standard, as support for their view that an AQI value of 100 does not need to be set at the 

level of the revised O3 standard. However, the sub-index for PM2.5 was developed using 

an approach that was conceptually consistent with past practice for selecting the air 

quality concentrations associated with the AQI breakpoints. The Agency’s historical 

approach to selecting index breakpoints had been to simply set the AQI value of 100 at 

the level of the short-term standard (e.g., 24 hours) for a pollutant. This method of 

structuring the index is appropriate in the case where a short-term standard is set to 

protect against the health effects associated with short-term exposures and/or an annual 

standard is set to protect against health effects associated with long-term exposures. In 

such cases, the short-term standard in effect defines a level of health protection provided 

against short-term risks and thus can be a useful benchmark against which to compare 

daily air quality concentrations. 

 In the case of the 1997 PM2.5 standards, EPA took a different approach to protecting 

against the health risks associated with short-term exposures. The intended level of 

protection against short-term risk was not defined by the 24-hour standard (set at a level 

of 65 μg/m3) but by the combination of the 24-hour and the annual standards working in 

concert. In fact, the annual standard (set at a level of 15 μg/m3

) was intended to serve as 

the principal vehicle for protecting against both long-term and short-term PM2.5

exposures by lowering the entire day-by-day distribution of PM2.5 concentrations in an 

area throughout the year. See generally 62 FR at 38668-70 (July 18, 1997). Because the 

24-hour standard served to provide additional protection against very high short-term 

concentrations, localized “hotspots,” or risks arising from seasonal emissions that would 

not be well-controlled by a national annual standard, EPA consequently concluded that it 

would be appropriate to caution members of sensitive groups exposed to concentrations 

below the level of the 24-hour standard. EPA also concluded that it would be 

inappropriate to compare daily air quality concentrations directly with the level of the 

annual standard by setting an AQI value of 100 at that level. EPA wanted to set the AQI 

value of 100 to reflect the general level of health protection against short-term risks 

offered by the annual and 24-hour standards combined, consistent with the underlying 

logic of the historical approach to establishing AQI 100 levels. Therefore EPA set the 

AQI value of 100 at the midpoint of the range between the annual and the 24-hour PM2.5

standards (i.e., 40 μg/m3) in order to reflect the combined role of the 24-hour and the 

annual PM2.5 standards in protecting against short-term risks. Therefore, this approach 

for defining and AQI value of 100 is conceptually consistent with the proposed decision 

to set an AQI value of 100 equal to the level of the primary O3 standard. 
104

 Therefore, EPA is revising the AQI for O3 by setting an AQI value of 100 equal to 0.075 

ppm, 8-hour average, the level of the revised O3 standard. EPA is also revising the 

following breakpoints: an AQI value of 50 is set at 0.059 ppm, an AQI value of 150 is set 

at 0.095 ppm; and an AQI value of 200 is set at 0.115 ppm. All these levels are averaged 

over 8 hours. As indicated in the proposal, these levels were developed by making 

proportional adjustments to the other AQI breakpoints (i.e., AQI values of 50, 150 and 

200). The proportional adjustments were modified slightly to allow for each category to 

span at least a 0.015 ppm range to allow for more accurate forecasting. So, for example, 

simply making a proportional adjustment to the level of an AQI value of 150 (0.104 ppm) 

would result in a level of about 0.092 ppm. Since most of these ranges are rounded to the 

nearest 5 thousandths of a ppm, that rounding would have resulted in a 0.014 ppm range 

(i.e., 0.076 to 0.090 ppm). So, the number was rounded upward to the nearest 5 

thousandths of a ppm, to allow for at least a 0.015 ppm range for forecasting. The same 

principle applies to the calculation of an AQI value for 200 (0.115 ppm). EPA believes 

that the finalized breakpoints provide a balance between proportional adjustments to 

reflect the revised O3 standard and providing category ranges that are large enough to be 

forecasted accurately, so that the new AQI for O3 can be implemented more easily in the 

public forum for which the AQI ultimately exists. 

B. Secondary O3 Standards 

Public comments on a range of issues related to the proposed secondary O3 standard 

options are addressed in the preamble to the final rule and/or in this document. In particular, 

general public comments related to whether or not the current secondary O3 standard should be 

revised are addressed in section IV.B of the preamble and below in section II.B.1. Specific 

comments addressing basic elements of the standard, including form, averaging times, and level, 

are addressed in section IV.C of the preamble and below in section II.B.2. Comments on the 

interpretation of the scientific evidence and EPA’s vegetation exposure and risk assessments for 

O3 are addressed in sections IV.B and IV.C of the preamble and below in sections II.B.3 and 

II.B.4. 

1. General Comments on Proposed Alternative Secondary O3 Standards 

A large number of comments on the proposed secondary standards for O3 were very 

general in nature, basically expressing one of two sharply divergent views: (1) support for 

revising the current secondary to provide additional protection for vegetation and ecosystems by 

establishing a separate and distinct cumulative, seasonal secondary standard with a biologically 

relevant form or (2) support for keeping the secondary standard identical to the 8-hour primary 

standard, either with revision as proposed, or without any revision. In general, commenters who 

supported a revised primary standard also supported adopting a distinct cumulative, seasonal 

secondary standard. Commenters who supported retaining the current primary standard 

generally also supported retaining the current secondary standard. Many of these commenters 

simply expressed their views without stating any rationale, while others gave general reasons for 
105

their views but without reference to the factual evidence or rationale presented in the proposal 

notice as a basis for the Agency’s proposed decision. 

 General comments based on relevant factors that either support or oppose any change to 

the current O3 secondary standard are addressed in this section. The biggest difference between 

the two main groups of commenters related to their views regarding the form of the standard; 

that is, whether a secondary standard with a form separate and distinct from that of the current or 

revised primary standard is appropriate, given the information available in this review. 

a. Support for Distinct Cumulative, Seasonal Secondary Standard

Many public comments received on the proposal asserted that, based on the available 

scientific information, the current secondary O3 standard is insufficient in both form and level to 

protect vegetation and ecosystems from known or anticipated adverse O3-induced effects and 

revisions to the standard are necessary and appropriate. Among those calling for revisions to the 

current secondary standard are national and local environmental organizations (e.g., 

Environmental Defense, Appalachian Mountain Club, Rocky Mountain Clean Air Action), 

individual States and State environmental/public health agencies, State and local air pollution 

control authorities, NESCAUM, NACAA, Tribal Associations, and the National Park Service 

(NPS). 

(1) Comment: These commenters stated that the available science clearly showed that O3-

induced vegetation and ecosystem effects are occurring at and below levels that meet the 

current 8-hour standard and, therefore, provides a strong basis and support for the 

conclusion that the current secondary standard is inadequate. 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 last review. These commenters 

pointed to the information and analyses in the Staff Paper and the conclusions and 

recommendations of CASAC as providing a clear basis for concluding that the current 

standard does not adequately protect vegetation from an array of O3-related effects. This 

group of commenters strongly supported revising the current standard, not only because 

in their view the available evidence conclusively demonstrates that the current standard is 

inadequate to protect sensitive vegetation, but also because the Staff Paper provides 

abundant evidence that it is appropriate to establish an alternative cumulative, seasonal 

secondary standard that is distinctly different in form from the current or revised primary 

standard. For example, NESCAUM states that “... the option of equating the ozone 

secondary NAAQS with the 8-hour primary is inappropriate and clearly not supported by 

the weight of scientific evidence.” 

Response: EPA agrees with these commenters that when evaluated as a whole, the 

information on vegetation and ecosystem effects available in this review supports the 

need to revise the current standard to provide increased protection from an array of O3-

related effects on sensitive vegetation and ecosystems. For reasons discussed below in 

sections II.B.2, however, EPA disagrees with these commenters’ views that use of a 
106

cumulative form and related averaging time(s) and level of such a standard is appropriate 

in light of all of the available scientific information. 

(2) Comment: These same commenters also presented new information for the 

Administrator’s consideration, including a number of “new” studies published after 

completion of the Criteria Document. These commenters encouraged the Administrator 

to consider these “new” studies in making his final decision. 

Response: EPA notes, as discussed in section I of the preamble to the final rule and in 

section I above, that as in past NAAQS reviews, it 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 and will consider newly published studies for 

purposes of decision making in the next O3 NAAQS review. In evaluating commenters’ 

arguments, as discussed below in section II.B.3, EPA notes that its provisional 

consideration of “new” science found that such studies did not materially change the 

conclusions in the Criteria Document (See further discussion in the Appendix.)

b. Support for Secondary Identical to Current or Revised 8-Hour Standard 

 The other main group of commenters, which included Exxon-Mobil, AAM, UARG, API, 

other industry groups, The Annapolis Center for Science Based Public Policy, individual States 

and other organizations representing local energy, agriculture or business interests, expressed the 

contrasting view that the limited number of studies published since the last review and 

addressed in the Criteria Document provided insufficient evidence to support a conclusion 

different than what was reached in the last review. In addition, these commenters also generally 

asserted that the evidence that has become available since the last review does not materially 

reduce the uncertainties that were present and cited by the Administrator in the last review as 

important factors in her decision to set the secondary standard identical to the revised primary 

standard. 

(1) Comment: These commenters asserted that the types of vegetation effects evaluated in 

the last review have not changed, and that the Criteria Document, Staff Paper, and 

CASAC have acknowledged that the information that has become available since the last 

review does not fundamentally change the conclusions reached in the last review. As a 

result, they argued that the currently available evidence fails to show that revision to the 

standard is requisite to provide additional protection from these effects. In particular, 

UARG states that “...the effects of interest now are for all practical purposes, identical to 

those that EPA considered in the last review” and “...furthermore, recent science has not 

significantly changed what is known quantitatively about these effects in association with 

O3.” Thus, UARG asserts that since “the record provides no new scientific insight 

concerning possible effects of O3 on vegetation, it supplies no information to call into 

question the Agency’s determination during the last review of the secondary O3 NAAQS 

that the existing standard provides the requisite protection to public welfare.”
107

Response: While EPA agrees with the above commenters that the array of known or 

anticipated vegetation effects evaluated in the last review is generally the same as in the 

current review, EPA strongly disagrees with the commenters’ assertion that the currently 

available evidence has not materially reduced key uncertainties present in the last review 

that factored into the Administrator’s decision. EPA notes that the information that has 

become available since the last review, though limited, strengthens the scientific basis 

supporting the need for revision to the secondary standard. The recent expansion of 

field-based evidence across a broad array of vegetation effects categories, as discussed in 

the Criteria Document, Staff Paper, and the preamble to the final rule, has significantly 

increased EPA’s confidence in extrapolating predictions based on chamber studies to the 

field. It was this uncertainty, e.g. applying chamber results to the field that in part, led 

the Administrator to conclude that it was not appropriate to go beyond the increased level 

of protection that would be expected to occur from an 8-hour revised primary and 

secondary in the 1997 review. There was not, as implied by the above comment, 

important uncertainties remaining with respect to the types of O3-induced effects on 

vegetation at the time of the last review, though significant uncertainties did and still do 

remain on the significance of these vegetation effects at the ecosystem level. This 

increased confidence in the likelihood that predicted effects based on open top chamber 

(OTC) data are and would continue to occur in the field at and below ambient levels was 

significant in forming EPA’s conclusion that revision to the secondary standard to 

provide increased protection to sensitive vegetation and associated ecosystems, is both 

necessary and appropriate at this time. 

A number of commenters also expressed the view that EPA has overstated conclusions 

that could be drawn from the vegetation data and in particular, questioned the Administrator’s 

conclusion that the vegetation effects that are occurring should be judged “adverse” to the public 

welfare. They assert that there remain considerable uncertainties about the degree to which and 

levels at which O3 produces adverse effects on the public welfare, as well as the extent to which 

the proposed revised secondary standard would protect the public welfare from such effects. 

These commenters make a number of specific points related to this issue of adversity, as 

described below. 

(2) Comment: One commenter stated “The extent to which the predicted effects on 

vegetation from ozone exposure at levels below the current standard would be adverse to 

the public welfare depends on the intended use of the vegetation and its significance to 

the public. These factors have not been adequately explored.” 

Response: EPA agrees that a judgment of adversity regarding any O3-induced 

vegetation effects takes into account the intended use of the vegetation and the 

significance of any O3-induced impairment of that use to the public (See following 

comment). However, EPA disagrees that these factors have not been adequately 

explored. EPA explicitly addressed the relationship between adversity and intended use 

with respect to the definition of adversity in section IV.A.3 of the proposal notice. EPA 

further considered in the Staff Paper and described in the proposal notice (72 FR 

37902/3) what information could be brought to bear to help inform judgments pertaining 

to the adversity of various O3-induced levels of crop yield loss to the public welfare. In 
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addition, EPA recognized in the proposal notice that “...the level selected is largely a 

policy judgment as to the requisite level of protection needed, ....and that it is appropriate 

to weigh the importance of the predicted risks of these effects in the overall context of 

public welfare protection.” Finally, EPA recognized in the proposal notice (72 FR 

37903) that “... the public welfare significance of O3-related effects can vary 

significantly, depending on the nature of the effect, the intended use of the plant, and/or 

the type of environment or location in which the plant grows. Any given O3-related effect 

on vegetation (e.g., biomass loss, or foliar injury) may be judged to have a different 

degree of impact on public welfare depending, for example, on whether that effect occurs 

in a Class I area, commercial cropland, or a city park.” 

(3) Comment: “The Administrator notes that ‘[T]he Staff Paper concludes that a 

determination of what constitutes an ‘adverse’ welfare effect in the context of the 

secondary NAAQS review’ can be viewed in the broader context of ‘linkages between 

stress-related effects ...at the species level and at higher levels with an ecosystem 

hierarchy.’ He does not, however, explicitly indicate that he is adopting this revised 

definition. Nor should he adopt it. The AQC [sic] is clear that we still lack sufficient 

scientific information to extrapolate meaningfully from effects on individual plants to 

ecosystem effects.” 

Response: EPA does not agree that it is inappropriate to expand considerations of 

adversity to include impacts on the intended use of ecosystems or the associated 

ecosystem goods and services. Such impacts, at sufficient levels, could clearly prove 

adverse to the public welfare. The preamble to the final rule states EPA “...believes it is 

appropriate to continue to rely on the definition of “adverse,” discussed in section IV.A.3 

of the proposal that imbeds the concept of “intended use” of the ecological receptors and 

resources that are affected, and applies that concept beyond the species level to the 

ecosystem level.” EPA further believes that such a broad definition is in keeping with the 

broad definition of welfare effects defined in section 302 (h) of the CAA, which includes 

effects on many interrelated components of ecosystems, (e.g., soils, water, wildlife, 

vegetation). Further, as stated in section IV.A.3 of the proposal notice, “...a recent 

publication ...(Young and Sanzone, 2002) provides additional support for expanding the 

consideration of adversity beyond the species level by making explicit the linkages 

between stress-related effects ...at the species level and at higher levels within an 

ecosystem hierarchy.” While EPA agrees that there still remains a high degree of 

uncertainty in assessing the linkages between O3 effects on vegetation and those at the 

ecosystem level, including ecosystem services, EPA believes such linkages have and 

continue to be made, and as such can reasonably be anticipated. 

2. Specific Comments on Proposed Alternative Secondary O3 Standards 

a. Form 

Comments received following proposal regarding the appropriate form for the secondary 

standard fell generally into two groups. One group expressed support for a new, cumulative 

seasonal form while the other group expressed support for retaining the current 8-hour form. 
109

These comments were similar to those raised prior to the proposal during earlier phases of the 

NAAQS review. Discussions of these comments are included in sections IV.B.2 and IV.C.2 of 

the preamble to the final rule, and in more detail below. 

(1) Comment: One group of commenters, including the National Park Service, 

Environmental Defense, NESCAUM, NACAA, individual States, Tribal Associations, 

and local environmental organizations, asserted that the weight of scientific evidence was 

unambiguous with regard to the need for a cumulative form, and specifically supported 

the proposed W126 exposure index. For example, New York State DEC explained that 

“...scientific research recognizes that exposure-based indices considering seasonal time 

period, exposure duration, diurnal dynamics, peak hourly ozone concentrations, and 

cumulative effects are important when assessing vegetation effects of ozone exposure 

(Musselman et al., 2006). The W126 exposure index has long been recognized as a 

biologically meaningful and useful way to summarize hourly ozone data as a measure of 

ozone exposure to vegetation (Lefohn et al., 1989).” Similarly, Environmental Defense 

stated “...[f]or reasons amply explained by CASAC and the Staff, neither the existing 

secondary standard for ozone nor the proposed primary standards are requisite to protect 

against adverse welfare effects on vegetation and forested ecosystems. CASAC and Staff 

further amply justified the need for a separate cumulative seasonal welfare standard to 

protect against these effects, rather than relying solely on the primary standards to 

provide such protection.” 

Response: For the reasons discussed in the preamble, EPA has determined that it is 

appropriate to adopt an 8-hour average secondary standard instead of a cumulative 

seasonal standard. 

(2) Comment: In addition to expressing strong support for the W126 cumulative seasonal 

form, commenters in this group also expressed serious concerns with EPA’s other 

proposed option of setting the secondary standard equal to a revised primary standard. 

For example, NPS agreed with CASAC that “retaining the current form of the 8-hour 

standard for the secondary NAAQS is inappropriate and inadequate for characterizing 

ozone exposures to vegetation.” NESCAUM stated “...we also strongly encourage EPA 

to avoid the flawed rationale employed in the previous 1997 ozone NAAQS review, i.e., 

that many of the benefits of a secondary NAAQS would be achieved if the primary 

NAAQS were attained. This rationale is flawed in at least two ways: first, ozone damage 

to vegetation persists in areas that attain the primary NAAQS; and second, the 

relationship between short-term 8-hour peak concentrations and longer-term seasonal 

aggregations is not constant, but varies over space and time...as EPA notes at 72 FR 

37904.... EPA should set a secondary NAAQS on its own independent merits based on 

adverse welfare effects. Real or perceived relationships between primary and secondary 

non-attainment areas are irrelevant to setting the appropriate form and level of the 

secondary NAAQS.” 

Response: For the reasons discussed in the preamble, EPA has determined that it is 

appropriate to adopt an 8-hour average secondary standard instead of a cumulative 

seasonal standard. 
110

(3) Comment: The other set of commenters, including UARG, API, Exxon-Mobil, The 

Annapolis Center, ASL and Associates, and AAM, did not support adopting an 

alternative, cumulative form for the secondary standard. Some of these commenters, 

while agreeing that “directionally a cumulative form of the standard may better match the 

underlying data,” believe that further work is needed to determine whether a cumulative 

exposure index for the form of the secondary standard is requisite to protect public 

welfare. 

Response: EPA agrees with the commenters who state that a cumulative form of the 

standard better matches the underlying data but for the reasons discussed in the preamble, 

EPA has determined that it is appropriate to adopt an 8-hour average secondary standard 

instead of a cumulative, seasonal standard. 

(4) Comment: These commenters also asserted that EPA’s analysis of the impact of the 

nation’s O3 control program for the 8-hour standard on W126 exposures is not 

scientifically sound due to the use of low estimates of PRB and an arbitrary rollback 

method that is uninformed by atmospheric chemistry from photochemical models. They 

argue that EPA must first realistically evaluate the total O3 reductions that would occur 

by using a state-of-the-art photochemical model and perform an analysis of the exposureresponse data to determine if effects are observed for exposures which do not exceed the 

8-hour standard. 

Response: EPA disagrees that the methods used are not scientifically sound and has 

provided a more detailed discussion under section IV.B.2 in the preamble to the final rule 

and in section II.A.4 of this Response to Comments document. Regarding the remaining 

uncertainties in the exposure and risk assessments and the reduction in uncertainties since 

the last review, these comments have already been addressed in section IV.B.2 of the 

preamble to the final rule and are further discussed in sections II.B.4 below. 

(5) Comment: These commenters also stated that without producing C-R functions for the 8-

hour form of the standard, EPA has failed to show that the current 8-hour standard would 

provide less than requisite protection. These commenters asserted that substantial 

uncertainties remain in this review, and that the benefits of changing to a W126 form are 

too uncertain to warrant revising the form of the standard at this time. 

Response: EPA emphasizes that the Criteria Document has reviewed hundreds of 

studies that support the conclusion that cumulative metrics, such as W126, are the most 

biologically relevant concentration-based metrics for vegetation available at this time 

(EPA 2006). EPA also notes that examples of crop concentration-response functions 

with the 8-hour form were provided (Staff Paper, Figure 7E-1 of Appendix 7E) and refers 

the reader to section II.B.3 below for a fuller discussion of this topic. For the reasons 

discussed in the preamble, EPA has determined that it is appropriate to adopt an 8-hour 

average secondary standard instead of a cumulative seasonal standard. 
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(6) Comment: This group of commenters also addressed perceived limitations associated 

with selection of the W126 cumulative form. Commenters asserted that: (a) the W126 

form lacks a biological basis, since it is merely a mathematical expression of exposure 

that has been fit to specific responses in OTC studies, such that its relevance for real 

world biological responses is unclear; (b) a flux-based model would be a better choice 

than a cumulative metric because it is an improvement over the many limitations and 

simplifications associated with the cumulative form; however, there is insufficient data to 

apply such a model at present; (c) the European experience with cumulative O3 metrics 

has been disappointing and now Europeans are working on their second level approach, 

which will be flux-based; and (d) the W126 form cannot provide nationally uniform 

protection, as the same value of an exposure index may relate to different vegetation 

responses; some commenters support adding a second index that reflects the 

accumulation of peaks at or above 0.10 ppm (called N100). These concerns are 

addressed in turn below. 

Response: (a) With respect to the comment that the W126 index lacks a biological basis, 

EPA disagrees. EPA concludes that the vegetation effects science provides evidence that 

exposures of concern to plants are not based on discrete 8-hour periods but on the 

repeated occurrence of elevated O3 levels throughout the plant’s growing season. The 

cumulative nature of the W126 is supported by the basic biological understanding of how 

most plants in the U.S. are most biologically active during the warm season and are 

exposed to ambient O3 throughout this biologically active period. In addition, it has been 

clearly shown in the scientific literature that, all else being equal, plants respond 

disproportionately more to higher concentrations, though there continues to be no 

evidence of an exposure threshold for vegetation effects. The W126 sigmoidal weighting 

function reflects both of these understandings, by not including a threshold below which 

concentrations are not included, and by differentially weighting concentrations to give 

greater weight to higher concentrations and less weight to lower ones. In addition, it has 

been clearly shown in the scientific literature that, all else being equal, plants respond 

more to higher concentrations, though there continues to be no evidence of an exposure 

threshold for vegetation effects. The W126 sigmoidal weighting function reflects both of 

these understandings, by not including a threshold below which concentrations are not 

included, and by differentially weighting concentrations to give greater weight to higher 

concentrations and less weight to lower ones. While recognizing that a cumulative, 

seasonal form is the most biologically relevant way to relate exposure to plant growth 

response, EPA’s reasons for adopting an 8-hour average standard instead of a cumulative 

seasonal standard are explained in the preamble. 

(b) With regard to the comment that a flux-based model would be a better choice, EPA 

acknowledges that flux models may produce a more accurate calculation of dose to a 

specific plant species in a specific area at a specific time, when detailed species-specific 

and site-specific information is known. However, flux calculations require large amounts 

of data on the physiology of each plant species and the local growing conditions for the 

growing range of each plant species. The EPA recognizes that the selection of an 

appropriate form of exposure index that can be nationally applied will necessarily 

represent a simplification of the multiple factors that can potentially affect specific plant 
112

response across the wide variety of species and ecosystems/conditions that occur within 

the U.S. 

 

(c) With regard to European dissatisfaction with the performance of a particular 

cumulative index in use in Europe6

 and growing interest in development of flux-based 

models, the Staff Paper (Appendix 7A) noted that “because of a lack of flux-response 

data, a cumulative, cutoff concentration-based (e.g., AOT40) exposure index will remain 

in use in Europe for the near future for most crops and for forests and seminatural 

herbaceous vegetation (Ashmore et al., 2004a).” 

 

(d) EPA disagrees with the comment that a W126 form, if it is to be used, must be 

coupled with a separate N100 index. EPA has found very little research on the N100 

index or a coupled approach. The Criteria Document did not evaluate this approach in 

the discussion of exposure indices (EPA 2006), and the CASAC, after reviewing all the 

information in the Criteria Document and the Staff Paper, did not recommend an 

additional N100 index for consideration. Therefore, the EPA has no basis at this time to 

judge the extent to which such a coupled W126-N100 form would be a better choice than 

the proposed W126 form. In addition, EPA notes that the W126 form already has built in 

a weighting scheme that places greater weight on increasing concentrations and gives 

every concentration of 0.10 ppm and above an equal weight of 1, which is the highest 

weight in this sigmoidal weighting function. As has already been discussed, there is no 

threshold of exposure that is considered adverse to all plants under all conditions. By 

putting such an emphasis on concentrations at or above 0.10 ppm, the commenters seem 

to imply that there is a sudden shift in importance between concentrations that fall just 

below and above 0.10 ppm. This has not been shown in the vegetation effects literature. 

In addition, in areas that typically have no occurrences of peaks above 0.10 ppm, yet still 

experience high cumulative exposures, it is not clear what purpose an N100 metric would 

serve, since it would not improve predictions of O3-induced effects. 

With respect to the related concern that foliar injury in not well correlated with the W126 

metric alone, EPA is aware that visible foliar injury can be caused by both acute and 

chronic exposures. The proposal notice states that “cellular injury can and often does 

become visible. Acute injury usually appears within 24 hours after exposure to O3 and, 

depending on species, can occur under a range of exposures and durations from 0.040 

ppm for a period of 4 hours to 0.410 ppm for 0.5 hours for crops and 0.060 ppm for 4 

hours to 0.510 ppm for 1 hour for trees and shrubs (Jacobson, 1977). Chronic injury may 

be mild to severe.” Clearly, with visible injury that occurs in response to an acute 

exposure, a 3-month cumulative value will have less meaning. However, as Jacobson, 

1977 makes clear, foliar injury effects can also occur under chronic low level exposure 

conditions. 

 6

 The AOT40 index used in Europe is a cumulative index that incorporates a threshold at 

0.04 ppm (40 ppb). This index is calculated as the area over the threshold (AOT) by subtracting 

40 ppb from the value of each hourly concentration above that threshold and then cumulating 

each hourly difference over a specified window. 
113

Several commenters, however, expressed the view that a W126 coupled with an N100 is 

necessary to better predict visible foliar injury in the field. EPA notes, however, that 

none of these commenters makes a recommendation as to what number of N100 is 

important to protect against different degrees of foliar injury so as to inform judgments 

concerning what constitutes requisite protection. One commenter, A.S.L. and Associates 

also mentions numerous other modifying factors that are important in accurately 

predicting levels of visible foliar injury observable in the field, including soil moisture, 

diurnal/nocturnal variation in stomatal conductance and detoxification potential. EPA 

was aware of these confounders. For example, the Criteria Document, Staff Paper, and 

proposal notice state that “a major confounding effect for O3 induced visible foliar injury 

is the amount of soil moisture (local rainfall) available to a plant during the year that the 

visible foliar injury is being assessed.” Given these complexities, it is not clear why this 

commenter concludes that adding the N100 alone will provide the stability this 

commenter asserts is needed to make the W126 a more appropriate form for predicting 

foliar injury. Lacking additional data to the contrary, and given the full discussion of 

these issues above, EPA disagrees that adding the N100 metric alone would significantly 

address the complexities and uncertainties that remain related to the relationship between 

available soil moisture, timing of peak O3 exposures and plant. 

b. Averaging Times

i. Seasonal Window 

(1) Comment: Only a few commenters specifically stated support for the 3-month seasonal 

window. In one example, the NPS stated that “...we agree that the maximum 

consecutive 3-month period within the ozone season is a reasonable averaging time for 

vegetation in many areas of the country.” Other commenters simply stated support for 

the recommendations of the Staff Paper and CASAC with regard to the W126 form 

which included a 3-month seasonal window. 

Response: For the reasons discussed in the preamble, EPA has determined that it is 

appropriate to adopt an 8-hour average secondary standard instead of a cumulative 

seasonal standard. 

(2) Comment: In contrast, other commenters recommended a longer seasonal averaging 

time. In particular, the Appalachian Mountain Club stated that “...the ozone season for 

the secondary standard should range from May to September to fully protect plant and 

ecosystem health” and further, that “...the standard should be based on the full growing 

season of a region and this should be re-evaluated over time. Growing seasons are 

expanding due to climate change.” 

Response: EPA agrees that many plants, including tree species, have growing seasons 

longer than three months and that the selection of any single seasonal exposure period for 

a national standard must necessarily represent a compromise, given the significant 
114

variability in growth patterns and lengths of growing seasons among the wide range of 

vegetation species occurring within the U.S. that may experience adverse effects 

associated with O3 exposures. For the reasons discussed in the preamble, EPA has 

determined that it is appropriate to adopt an 8-hour average secondary standard instead of 

a cumulative seasonal standard. 

ii. Diurnal Window 

(1) Comment: With respect to the 12-hour diurnal window, the NPS stated that “...for many 

areas of the country, the daytime 12-hour window is an appropriate period over which to 

cumulate diurnal ozone exposures. However, as the Staff Paper points out, there is 

evidence to suggest that in some species in some areas, ozone uptake occurs outside this 

12-hour window....Nevertheless, NPS agrees with EPA and CASAC that, for most areas 

and species, the 12-hour daytime period is sufficient and appropriate to characterize 

ozone uptake for the cumulative standard.” The NPS further noted that “...there may be 

specific areas (e.g., very dry, hot areas where stomates are primarily open at night) where 

a different window may better characterize ozone exposure. It may be appropriate to 

give States discretion, in these instances, to shift or extend the 12-hour window for 

calculating exposure in these areas.” 

Response: For the reasons discussed in the preamble, EPA has determined that it is 

appropriate to adopt an 8-hour average secondary standard instead of a cumulative 

seasonal standard. 

(2) Comment: Some commenters, however, including NESCAUM, NYSDEQ, AMC, and 

ADEQ, contended that the appropriate diurnal window for vegetation exposure is longer 

than 12 hours and typically recommend a 24-hour window. Some of these commenters 

provided additional air quality analyses and cited both published and unpublished sources 

of data that document the co-occurrence of sensitive species and elevated nighttime 

exposures. NESCAUM stated that it “...believes the literature on nighttime adverse 

ozone impacts is strong and can support an ozone secondary NAAQS that encompasses 

nighttime hours. This is important to the NESCAUM states as elevated nighttime ozone 

concentrations occur in many [high elevation] locations throughout the region.” 

NESCAUM also noted that the number of daylight hours during EPA’s presumed 3-

month growing season is greater than 12 hours at the latitudes of the NESCAUM region.” 

The Appalachian Mountain Club stated that “...we strongly disagree with the Staff and 

Administrator’s opinion that more evidence is needed ‘about the extent to which this cooccurrence of sensitive species and elevated nocturnal O3 exposure exists’ ...to warrant a 

24-hour standard.” AMC also provided four examples of National Parks and other 

federal lands where both elevated nighttime O3 exposure and sensitive species are 

present, some of which have been identified as showing nocturnal stomatal conductance 

in the review by Musselman and Minnick (2000). Arizona DEQ stated “...cacti and 

other desert succulents breathe at night when they lose less water. One of the impacts of 

ozone exposure identified in the literature is the inability of the guard cells to fully close 

stomata. If cacti and succulents cannot close stomata during the daytime, the resulting 

water loss may substantially weaken the plants or directly kill them. In addition, ozone 
115

damage could make stomata stay open overnight for most vegetative species, which 

exchange gases diurnally. Therefore, ADEQ supports a 24-hour time horizon for the 

Secondary Standard.” 

Response: For the reasons discussed in the preamble, EPA has determined that it is 

appropriate to adopt an 8-hour average secondary standard instead of a cumulative 

seasonal standard. 

iii. Annual vs. Three Year Average 

With respect to comments concerning the annual versus three-year averaging period for 

the cumulative form, comments are fairly evenly divided between support for an annual and 

support for a three year average. However, many of those commenters who agreed that a threeyear average could be appropriate only did so with the condition that the level of the standard 

selected should be lower to protect against adverse levels in one year. 

(1) Comment: Some commenters expressed support only for the annual averaging time in 

order to provide the appropriate degree of protection from effects occurring to vegetation 

on an annual basis. 

Response: EPA disagrees that only an annual form of the secondary standard could 

provide the appropriate degree of protection for annual plants. EPA recognizes and 

agrees that the adverse impact of some O3-induced vegetation effects are realized within 

an annual timeframe and are based on the cumulative O3 exposure that occurs in that 

same year. These effects can include growth and reproductive effects in annual species, 

crop yield loss, and foliar injury symptoms on both annuals and perennial species, 

including trees growing in protected national areas. EPA notes, however, that with 

regard to crop yield loss, foliar injury symptoms, and tree seedling biomass loss, 

determining what degree of vegetation impact is adverse, and, therefore, for which 

appropriate protection is required in any given year, is more uncertain. As discussed in 

the preamble, EPA believes that appropriate protection for vegetation can be achieved 

using a 3-year average of the 8-hour average form. 

(2) Comment: As stated above, many commenters, while preferring an annual standard, also 

gave conditional support to a three-year averaging time, on the condition that the level of 

the standard is lowered to achieve the same level of protection judged requisite on an 

annual basis. For example, NESCAUM stated that “...adverse vegetation damage occurs 

on an annual basis... If multi-year averaging is employed to promote a more ‘stable’ 

NAAQS (as opposed to more stable ecological health), the level should be set lower than 

what would otherwise have been set for an annual NAAQS. A reduction of the needed 

annual level by at least one-third can help assure that the intended threshold is not 

exceeded in individual years.”

Response: EPA agrees that the degree of protection provided by a standard is based on 

the combination of averaging time and level and thus should be considered together in 

establishing a standard that provides the requisite degree of protection. For the reasons 
116

discussed in the preamble, EPA has determined that it is appropriate to adopt an 8-hour 

average secondary standard instead of a cumulative seasonal standard.

(3) Comment: In contrast, several other commenters, including NC DFR, NC DAQ, MidOhio Regional Planning Commission, IDNR and IDPH, expressed the view that the 

cumulative, seasonal standard should be based on a 3-year average, rather than a 1-year 

average, regardless of level, due to concerns regarding the volatility of using a one-year 

averaging time with the W126 form. For example, Iowa DNR stated “...using only one 

year of monitoring data to compute the W126 makes it particularly volatile, as infrequent 

high hourly ozone spikes make it through the sigmoid filter and contribute to the three 

month sum but frequently occurring low ozone values do not.” 

Response: EPA agrees that stability in a standard is a desirable trait that confers benefit 

to the public welfare. Because EPA concluded that the appropriate degree of protection 

for vegetation can be achieved using a 3-year average form, EPA further concludes that a 

three year average form is both desirable and appropriate. 

c. Level 

(1) Comment: One group of commenters, which included the National Park Service, 

Environmental Defense, NESCAUM, NACAA, State, Tribal and local environmental 

groups, stated support for the CASAC range of 7- 15 ppm-hours. Many of these same 

commenters further emphasized the lower end of the proposed range as necessary to 

provide adequate protection for sensitive species. For example, the NPS “...strongly 

supports CASAC’s recommendation that the upper bound of the range for the standard 

should not exceed a W126 of 15 ppm-hours. Further, the NPS strongly recommends a 

value for the secondary standard that is representative of the low end of the range 

recommended by CASAC.” Similarly, NESCAUM states that it “...does not support a 

secondary NAAQS above 15 ppm-hrs...” and “...furthermore, based on observed ozone 

damage to forests in the NESCAUM region at current ozone levels, a secondary NAAQS 

of the W126 form towards the lower end of the CASAC-recommended range would 

provide better protection in the NESCAUM region.” The Appalachian Mountain Club 

stated “...we urge the more protective 7 ppm-hours level, proposed by EPA, be adopted 

for areas with known sensitive species and areas under special federal protection related 

to air quality. This protective approach should be used to ensure that Federal Land 

Managers are able, as directed by Congress, to protect the air quality related values in our 

National Parks and Forests and Wilderness areas for future generations.” 

These commenters who recommended a level at the mid- to lower end of the proposed 

range based their recommendation primarily on four sources of information: (a) fieldbased evidence of foliar injury occurring on sensitive species at air quality levels well 

below that of the current standard; (b) the 1996 consensus workshop recommendations 

for protective levels in terms of cumulative exposures for different vegetation types; (c) 

CASAC advice and recommendations; and (d) “new” studies published after the close of 
117

the 2006 CD that potentially point to a stronger link between species level impacts and 

ecosystem response. 

Response: EPA notes that in considering what standard is requisite to protect public 

welfare from known or anticipated adverse effects, judgment is required, based on an 

interpretation of the evidence and other information, that neither overstates or understates 

the strength and limitations of the evidence and information nor the appropriate 

inferences to be drawn. In light of significant remaining uncertainties, described by other 

commenters below, EPA disagrees that the appropriate level of protection for vegetation 

lies within the CASAC range. For the reasons discussed in the preamble, EPA has 

determined that it is appropriate to adopt an 8-hour average secondary standard instead of 

a cumulative seasonal standard. 

The other group of commenters, including Exxon-Mobil, the Annapolis Center, AAM, 

and State and local organizations, did not support revising the current secondary standard. While 

many of their comments regarding sources of uncertainties associated with the effects evidence 

and the exposure and risk assessments have been addressed in section IV.B.2 of the preamble 

and in sections II.B.3 and II.B.4 below, some of their comments also identify uncertainties 

regarding the sources of information relied upon by the first group of commenters as support for 

a level within the range of levels recommended by CASAC. 

(2) Comment: With regard to the usefulness of foliar injury evidence to inform selection of a 

level of protection, Exxon-Mobil stated “...EPA has not addressed potential confounders, 

such as soil moisture, or related the visible foliar injury symptoms to other vegetation 

effects.” Georgia DNR also identified uncertainties associated with visible foliar injury 

including “...a lack of linkage between visible foliar injury and other vegetation effects, 

and the inability to quantitatively assess the degree of visible foliar injury that should be 

judged adverse in all settings and across all species.” 

Response: In the proposal notice and preamble to the final rule, EPA concluded that 

foliar injury information available in this review provides compelling evidence that the 

current standard is inadequate to protect against this vegetation effect. However, EPA 

also concludes, given the many sources of uncertainty that have been raised regarding 

using the foliar injury data as a basis for determining an appropriate level of public 

welfare protection, that the foliar injury data available at this time is insufficient to 

specifically inform quantitative judgments regarding the selection of an appropriate 

standard and should only be considered qualitatively. 

(3) Comment: With regard to comments received stating concern with EPA’s and/or 

CASAC’s apparent reliance on the recommendations from the 1996 consensus workshop 

in selecting a range of levels, both the Annapolis Center and AAM state that “...[i]f the 

workshop recommendations are to be used for standard setting, then the studies 

underlying their basis, as well as the method for reaching the recommended values, 

should be stated in more detail than in the cited workshop summary. The basis for 

establishing a standard should be transparent and reproducible.” More specifically, 

Exxon-Mobil stated “...this workshop was by invitation only, and documentation is not 
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available to the public. The reference [sic] cited is short and provides consensus 

recommendations, but without details as to their basis. In particular, the basis for the 

recommendation to consider a 2 percent effect level to be significant is not provided. It is 

not clear how this effect level could be experimentally determined, if it is discernable 

from biological variability, or what references suggest the potential compounding effect 

over multiple years, ....” If available, a more detailed report of the consensus workshop 

should be released. If studies to support the recommendations cannot be provided, then 

the recommendations should be used with great caution.” 

Response: With regard to comments stating concern with EPA’s apparent reliance on the 

recommendations from the 1996 consensus workshop in selecting a range of levels, EPA 

agrees that though the workshop participants were asked to review, and thus were aware 

of, the scientific literature available at the time, as described in both the 1996 O3 Criteria 

Document and Staff Paper, the workshop discussion of ranges of levels recommended as 

protective of different vegetation types for different effects falls short of providing a 

scientific basis for determining at what level these effects become adverse to the public 

welfare. In addition, EPA agrees that the scientific basis for establishing a 2% level of 

biomass loss in tree seedlings as a benchmark of concern to take into account the 

possibility of compounding is unclear, though there was and continues to be, evidence of 

the potential for compounding effects to occur over multiple years. As the proposal 

states (72 FR 37885, 37886) with respect to potential compounding, there is important 

evidence that “...in perennial plant species, a reduction in carbohydrate storage in one 

year may result in the limitation of growth the following year (Andersen et al., 1997). 

Such ‘carry-over’ effects have been documented in the growth of tree seedlings (Hogsett 

et al., 1989; Sasek et al., 1991; Temple et al., 1993; EPA, 1996a) and in roots (Andersen 

et al., 1991; EPA, 1996a)”. However, EPA concludes that significant uncertainty 

remains as to what level of annual tree seedling biomass loss when compounded over 

multiple years should be judged adverse to the public welfare. Since tree seedling risk 

numbers were often compared to this level of biomass loss derived from expert judgment, 

EPA also notes that this issue adds additional uncertainty in judging the adversity of 

relative risks of tree seedling biomass loss predicted under different alternative air quality 

scenarios. 

(4) Comment: With regard to the strength of the scientific basis for CASAC’s views, the 

Annapolis Center and AAM stated that “...if ozone monitoring is continued under the 

current guidelines, the ranges for a seasonal secondary standard must be adjusted upward. 

Based on the reduction in ozone exposure at plant height of a factor of two compared to 

that at measurement height, the range should be increased by roughly a factor of two. 

Neither CASAC nor EPA took this into account in making their recommendations 

concerning the level of the secondary standard.” AAM also stated “...[i]t is now widely 

accepted that ozone concentrations at the ‘standard measurement height’ are not the same 

as the ozone exposures at plant height. When this factor was corrected in the vegetation 

risk assessment, the SUM06 and W126 exposures at plant height were approximately half 

those at measurement height.” 
119

Response: With regard to the uncertainty associated with monitor height gradients and 

its consideration by CASAC and EPA in making recommendations on an appropriate 

range of levels, EPA notes that the risk assessments conducted by EPA on both tree 

seedling biomass loss and crop yield loss included an exposure adjustment factor to better 

account for this issue. As a result, both EPA and the CASAC were fully aware of this 

issue when making recommendations on a range of levels for the Administrator’s 

consideration. However, the Staff Paper also “...recognizes that a 10% adjustment to 

hourly monitoring data across the country is a very simple method to deal with a 

complicated issue.” Thus, because there still remains significant uncertainty associated 

with selecting an appropriate adjustment method and because the impact of this issue on 

establishing the appropriate relationship between exposures measured at monitor height 

and predicted adverse levels of plant response for short vegetation (e.g., crops and tree 

seedlings) has not been fully evaluated, EPA believes caution should be used in selecting 

a level of air quality that would not be more protective than necessary in areas where the 

height of vegetation canopies are significantly lower than that of the monitor probe height 

(e.g., grasslands, croplands). 

EPA believes that this important uncertainty should be taken into account in establishing 

a standard that is not more protective than necessary. In so doing, EPA recognizes that 

the degree of protection afforded by a standard is determined by the combination of the 

various elements of a standard, including form, averaging time and level. Thus, EPA 

believes that this uncertainty can be addressed in part by coupling a standard level in the 

proposed range with a three year average standard, rather than an annual standard. 

(5) Comment: The Annapolis Center stated an additional concern that the CASAC made its 

recommendations based on the draft Staff Paper that contained errors overstating the 

magnitude of vegetation effects. In particular, the Annapolis Center states “...[t]here 

were major errors in the translation of the results of the vegetation risk assessment into 

the second draft Staff Paper, overstating the magnitude of crop loss from ozone....While 

this was corrected in the final SP, CASAC made its recommendations concerning the 

secondary standard based on the draft text that contained numerous errors overstating the 

magnitude of vegetation effects.” 

Response: EPA disagrees that this error factored significantly into CASAC’s 

recommendations. CASAC considered the entire body of information available during 

the review to inform its recommendations. In addition, CASAC reviewed the final Staff 

Paper and submitted an additional letter (Henderson, 2007) restating and in some cases 

elaborating on their earlier advice to the Administrator on the second draft Staff Paper 

(Henderson, 2006). Had the change in risk results significantly factored into their 

reasons for recommending a revised secondary, they would have revised their advice to 

the Administrator in their final letter following their review of the final Staff Paper to 

reflect this change. As they did not do so, it can be concluded that their final advice to 

the Administrator did not depend on the vegetation risk numbers. 
120

3. Specific Comments on the Interpretation of Scientific Evidence 

 

 Comments related to the interpretation of the vegetation and ecosystems effects evidence 

for O3 are addressed in this section. Incorporating responses contained in Section IV.B.2.a and 

IV.C.4 of the preamble to the final rule, EPA provides the following responses to specific issues 

related to the interpretation of the vegetation and ecosystems effects evidence. Comments 

related to the overall weight placed on the vegetation and ecosystem effects evidence in reaching 

decisions on the need to revise the current standard and on an appropriate standard level are 

addressed in the preamble and in Sections II.B.1 and II.B.2.c above. 

(1) Comment: A number of commenters reference information from “new” studies 

published after the close of the 2006 Criteria Document in support of their positions, both 

for and against revision of the secondary standard. 

Response: EPA notes that as in past NAAQS reviews, it 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 and will consider newly published 

studies for purposes of decision making in the next O3 NAAQS review. In evaluating 

commenters’ arguments, as discussed below in section II.B.3, EPA notes that its 

provisional consideration of “new” science found that such studies did not materially 

change the conclusions in the Criteria Document (See Appendix). 

(2) Comment: Several commenters questioned EPA’s basis for concluding that adverse 

effects on vegetation would be expected to occur under air quality that met or was below 

that of the current 8-hour secondary standard. In particular, Exxon-Mobil stated that 

“EPA is incorrect in concluding vegetation impacts at the current standard” and further 

that the “...newer field-based evidence EPA cites for ozone impacts on seedlings, 

saplings and mature trees indicates ozone impacts but at exposures that are likely in 

exceedence of the current secondary standard.” This commenter also asserted that 

“...the analysis is not transparent because different indices are not directly correlated, but 

the mean or seasonal ozone exposures provided appear to be sufficiently high that they 

would include multiple days with an 8-hour daily maximum average exceeding 80 ppb. 

Therefore, while these studies demonstrate ozone impact, they do not appear to provide 

additional evidence for adverse vegetation impacts under air quality scenarios meeting 

the current standard”. Exxon-Mobil also provided specific comment on a number of 

studies cited by EPA in the proposal, including: (a) King et al., 2005; (b) Gregg et al., 

2003; (c) Karnosky et al., 1999; and (d) Isebrand et al., 2001, and states that “...[w]hile 

these studies provide additional support for ozone impact on vegetation, including 

observance of ozone effects in field settings without chambers, they do not provide 

support for the conclusion that ambient levels in compliance with the current standard 

would result in significant ozone impact.” The specific comments on each study are 

presented individually below. The comment regarding transparency is addressed in a 

separate comment below. 

 (a) The commenter stated that King et al. (2005) “...provided ozone concentrations as 

seasonal daily averages (49-55 ppb) and total seasonal sums (81-97 ppm-hrs for 4.5 to 5 
121

months. Given expected daily fluctuations, it is likely that the current secondary standard 

was exceeded for the ozone levels specified, as would the W126 values. This study does 

not demonstrate impact from ozone levels at or below the current standard.” 

 (b) The commenter stated that “...the ambient areas where effects were reported had 

ozone concentrations that likely exceeded the current secondary standard....” However, 

“...[i]n Gregg et al. the ambient concentrations are NOT presented as exceedance of 8-

hour daily average or even as a cumulative metric, but rather as an annual seasonal 12-

hour mean ozone.... Whereas the data of Gregg et al. indicate that ambient levels of O3

are sufficient to produce biomass loss, it does not address if these ambient levels fall 

above or below the current standard.” 

 (c) The commenter stated that “Karnosky et al. (1999) reports foliar injury in two higher 

ozone ambient sites and no injury in one low ozone site. Symptoms were worse in FACE 

plots than in ambient gradient sites. Ozone exposure concentrations were: ambient 

higher ozone sites - seasonal sum over 12 hr/day = 47-70 ppm hr (5-43% leaves show 

injury); FACE exposures with symptoms – seasonal sum over 12 hr/day = 57-61 ppm hr, 

12 hr seasonal mean = 54-56 ppb, and 24 hr AOT40 = 27-31 ppm-hrs (11-55% leaves 

show injury); OTC exposures that produced symptoms – seasonal sum over 12 hr/day = 

50-60 ppm hr (50 percent leaves show injury of sensitive clones). These exposures are 

likely to include exceedances of the current secondary standard.” 

 (d) The commenter stated that “Isebrand et al. (2001) reports results for FACE plots of 

elevated ozone, although the levels in ozone addition treatments are indicated to be 

representative of current conditions in many areas surrounding midwestern [sic] cities. 

The exposures show episodic total seasonal exposures of 90 ppm-hr. The five clones 

studied showed significant variability in response to ozone, with one showing increased 

growth under elevated ozone. The results of this study support the potential of ozone to 

impact vegetation, but again the ozone exposure level is sufficiently high to indicate that 

there were likely multiple exceedances of the current secondary standard.” 

Response: The commenter is mistaken in its assertion that EPA is claiming that the 

above named studies, in and of themselves, demonstrate support for concluding that 

adverse O3-induced impacts on vegetation would occur at air quality levels that meet or 

are below the standard. Rather the conclusion reached by EPA regarding these field based 

studies, as the following excerpts from the proposal notice show, is that the new field 

based studies provided limited qualitative support to the use of the OTC derived C-R 

functions to describe plant response in the field. Specifically, the proposal notice states 

“One such study is of particular importance in that it documented growth effects from O3

exposure in the field without the use of chambers or other fumigation methods that were 

as great as those seen in OTC studies (Gregg et al., 2003).... Another recent set of 

studies employed a modified Free Air CO2 Enrichment (FACE) methodology to expose 

vegetation to elevated O3 without the use of chambers. Taking all of the above into 

account, results from the Wisconsin FACE site on quaking aspen appear to demonstrate 

that the detrimental effects of O3 exposure seen on tree growth and symptom expression 

in OTCs can be observed in the field using this exposure method (Karnosky et al., 1999; 
122

2005). The Staff Paper thus concluded that the combined evidence from the AspenFACE 

and Gregg et al. (2003) field studies provide compelling and important support for the 

appropriateness of continued use of the C-R functions derived using OTC from the 

NHEERL-WED studies to estimate risk to these tree seedlings under ambient field 

exposure conditions. These studies make a significant contribution to the coherence in 

the weight of evidence available in this review and provide additional evidence that O3-

induced effects observed in chambers also occur in the field” (72 FR 37886). As a result 

of this primary conclusion, the proposal then states “[o]n the basis of such key studies, 

the Staff Paper concludes that the expanded body of field-based evidence, in combination 

with the substantial corroborating evidence from OTC data, provides stronger evidence 

than that available in the last review that ambient levels of O3 are sufficient to produce 

visible foliar injury symptoms and biomass loss in sensitive vegetative species growing in 

natural environments” (72 FR 37897). In regard to comments on particular studies, EPA 

notes the following: 

(a) EPA agrees that the findings of King et al., 2005 do not demonstrate effects below 

the level of the current standard. However, the most important contribution of 

this study is not the level of exposures that produced the response, but that the 

response occurring in the field was comparable to that of previous OTC studies, 

thus strengthening the coherence across the available weight of evidence. 

(b) EPA agrees that Gregg et al., 2003 did not directly address whether the ambient 

concentrations experienced in the study fell above or below the current standard. 

However, EPA obtained the raw data from the authors in order to calculate the 

W126 values for those same ambient exposures (Figure 7-17 on page 7-57 of the 

Staff Paper). From this raw data, EPA observed that significant biomass loss was 

observed at O3 air quality ranging from the level of the current standard to 4th

highest daily maximum 8-hour averages well below (e.g., 0.072 ppm) the current 

8-hr standard. 

(c) EPA agrees that while not demonstrating effects below the level of the current 

standard, Karnosky et al. (1999) demonstrated that across FACE, gradient and 

OTC studies using the same tree species, the magnitude of O3-induced effects 

were similar, increasing EPA’s confidence in using OTC C-R functions and 

strengthening the coherence across the available weight of evidence. 

(d) EPA agrees that while not demonstrating effects below the level of the current 

standard Isebrand et al. (2001) further demonstrated that the response occurring in 

the field was comparable to that of previous OTC studies, thus strengthening the 

coherence across the available weight of evidence. 

(3) Comment: Exxon-Mobil asserted that the “...FACE and gradient studies show that 

ozone can impact tree species, but specific provision and/or comparison of the 

concentration-response functions from these studies with those from OTC studies is 

limited. Thus, these studies, while very informative, do not reduce the uncertainties in 

the OTC concentration-response functions.... EPA should develop concentrationresponse functions based upon the newer data in the same form as the existing ones, to 

allow direct comparison.”
123

Response: Because the C-R functions developed in OTC included multiple exposure 

levels including charcoal filtered air representing below ambient conditions, ambient and 

above ambient, it is not currently possible to create directly comparable C-R functions 

based on the FACE or gradient study data, since they cannot exclude ambient O3 

concentrations. However, in these field studies (e.g., the FACE studies) the observed 

vegetation response from O3 exposures at ambient or above was similar to that observed 

in OTC studies at similar levels of exposure. Though these studies are still limited in 

scope, it is nevertheless EPA’s conclusion that such field-based evidence reduces the 

uncertainties associated with the C-R functions generated in OTC studies that were noted 

by the Administrator in the last review. Thus, the current body of evidence increases 

EPA’s confidence in the results from the OTC studies which demonstrate O3-related 

effects at exposure levels below that of the current standard. 

(4) Comment: Exxon-Mobil stated that “[s]everal times in the proposed rule, EPA indicates 

the potential for a compounding effect of ozone exposures on perennial species, including 

studies that document carryover effects. (72 Fed. Reg. at 37,898). EPA fails to provide 

documentation that supports this claim. Neither the proposal nor the CD and SP 

reference studies that provide evidence of carry-over effects. The multiple-year studies 

on tree species cited by EPA do not demonstrate a carry-over or compounding effect, but 

rather that ozone resulted in a similar percent change across study years (Figure 4 in 

Isebrand et al. 2001; Figure 2 in King et al. 2005; ...). EPA should conduct analyses on 

other available data sets to determine if the results of the two studies cited above are 

generally representative. 

Response: The commenter is mistaken in asserting that EPA has not provided 

documentation for its claim of the possibility of carry-over effects. EPA directs the 

commenter to pp. 9-6 and 9-9 of the Criteria Document, 7-6 of the Staff Paper and pp. 72 

FR 37886, 37894, 37897, and 37898. For example, the proposal notice (72 FR 37886), in 

citing back to the Criteria Document states “Trees and other perennials, in addition to 

cumulating the effects of O3 exposures over the annual growing season, can also 

cumulate effects across multiple years. It has been reported that effects can “carry over” 

from one year to another (EPA, 2006a). Growth affected by a reduction in carbohydrate 

storage in one year may result in the limitation of growth in the following year 

(Andersen, et al., 1997). Carry-over effects have been documented in the growth of some 

tree seedlings (Hogsett et al. 1989; Simini et al., 1992; Temple et al., 1993) and in roots 

(Andersen et al., 1991; EPA, 1996a). On the basis of past and recent OTC and field 

study data, ambient O3 exposures that occur during the growing season in the United 

States are sufficient to potentially affect the annual growth of a number of sensitive 

seedling tree species. However, because most studies do not take into account the 

possibility of carry-over effects on growth in subsequent years, the true implication of 

these annual biomass losses may be missed. It is likely that under ambient exposure 

conditions, some sensitive trees and perennial plants could experience compounded 

impacts that result from multiple year exposures.”

(5) Comment: Exxon-Mobil stated that “[w]hile EPA is correct in stating that the field data 

indicate some level of visible ozone injury at ambient levels that meet the current 
124

secondary standard (Jacobson, 1977), EPA has not addressed potential confounders, such 

as soil moisture or related the visible foliar injury symptoms to other vegetation effects. 

EPA also indicates a major confounder for ozone induced visible foliar injury is soil 

moisture – with dry periods in local areas decreasing incidence and severity of visible 

foliar injury (p. 7-61). These same conditions would favor higher ozone levels. 

Furthermore, the W126 values for these sites are not provided, so it cannot be assessed if 

the proposed W126 standard would provide additional protection. EPA should provide 

the comparable W126 values and compare foliar injury at ‘non-background’ sites with 

‘background’ sites, to better understand the impact of ozone exposures above background 

levels.”

Response: EPA disagrees with the commenter that it has not addressed potential 

confounders such as soil moisture. EPA discusses this issue pg. 7-61 of the Staff Paper 

and clearly takes this into account in considering how much weight to put on foliar injury 

data (see also discussion under Form above). EPA further notes that it assessed incidence 

of visible foliar injury across a four year period (e.g., 2001-2004). Though not 

specifically evaluated, within that four year period it is likely that a variety of soil 

moisture conditions existed, both temporally and spatially. Even so, at no point in that 

four year period, did incidence of foliar injury drop below 21% for areas that met the 

level of 0.084 ppm (see Table 7-4, Staff Paper p. 7-64). At the time this analysis was 

conducted, EPA was still considering using the SUM06 form, so only SUM06 

comparisons are included in the table. However, EPA notes that a SUM06 of 25 ppm-hrs 

is approximately equivalent to a W126 of 21 ppm-hrs so that an approximate comparison 

could be made.

(6) Comment: Exxon-Mobil stated that “EPA also indicates that Morgan et al. 2003 show 

consistent deleterious effects of ozone exposures on soybean from 1973-2001.” The 

commenter goes on to assert however that “...the Morgan et al. 2003 meta-analysis is not 

presented by year and provides results by time, so it cannot be used to support the 

statement of consistent deleterious effects over time. Morgan et al. provide ranges of 

ozone impact for ozone concentrations in three average daily concentration categories: 

30-59 pb [sic], 60-79 ppb, 90-120 ppb. For the highest two categories and the upper 

range of the lowest category, it is likely that there were multiple exceedences of the 

current 8-hour secondary standard. EPA should follow its own recommendation included 

in footnote number 57 on page 37889 and develop new concentration-response functions 

for new studies that are updated to meet recent air quality conditions.” 

Response: The commenter is correct in that Morgan et al. (2003) does not list the studies 

by date. However, in Figure 2 of the paper O3 is shown to have a negative effect on 

nearly all the variables measured on soybean. Most importantly, seed yield was 

consistently lower under elevated O3 concentrations. This study was not cited to address 

whether effects were still occurring at the current standard level. It was cited to point out 

that across many cultivars in studies conducted over many years there is an apparent 

consistency of negative effects on soybean yield. 
125

(7) Comment: Several commenters argued that because the C-R functions used in this 

review were developed under the NCLAN program which used exposure regimes 

containing numerous hourly values greater than 100 ppm (Lefohn and Foley, 1992), a 

concentration response function should be developed that includes components for both 

the cumulative seasonal ozone exposure and frequency of hourly peaks. For example, 

Exxon-Mobil states that “Researchers have documented that the NCLAN studies contain 

numerous hourly values greater than 100 ppb (Lefohn and Foley, 1992). Failure to 

include these values known to be key determinants of plant effects in the exposureresponse function is a significant oversight for a proposed national standard. The number 

of hourly values greater than 100 ppb ...indicates that many of the NCLAN exposures 

would have multiple exceedences of an 8-hour standard of 80 ppb. Therefore, reliance on 

NCLAN data to support the conclusion that exposures below an 8-hour standard would 

result in ozone impact has significant limitations if the response function fails to consider 

these peak concentrations.

Response: EPA agrees with these commenters that a biologically relevant concentration 

response function should take into account both cumulative and peak exposures. 

However, EPA does not agree with the commenters that the W126 alone fails to do so. 

The W126 was designed to cumulate exposures while giving greater weight to peak 

concentrations. The Criteria Document and CASAC recommended a cumulative 

weighted metric (such as W126) as the most appropriate index and did not recommend 

the addition of N100 or any other modifications to W126. 

(8) Comment: Exxon-Mobil stated “Despite previous requests, EPA has not provided the 

concentration-response functions for the 8-hour form of the standard. Therefore, a 

comparative analysis of the relative protection afforded by an 8-hour form to that 

provided by the proposed W126 form cannot be completed... EPA has failed to show that 

the current 8-hour standard would provide less than requisite protection. EPA should 

develop concentration response relationships using the 8-hour form of the standard for 

the same datasets that form the basis for the proposed W126 standard. Frequency of peak 

occurrence should also be included in the analysis. This is the only meaningful way to 

compare the level of protection afforded by the different standards.” This commenter 

further stated that without such a comparison, EPA fails to show that the currently 

proposed W126 standard would result in additional protection than the current 8-hour 

secondary standard. 

Response: For the reasons discussed in the preamble, EPA has determined that it is 

appropriate to adopt an 8-hour average secondary standard instead of a cumulative 

seasonal standard. In response to the comment that EPA has failed to produce C-R 

functions in terms of the 8-hour form, EPA points the reader to Appendix 7E (Figure 7E1) of the Staff Paper that shows the NCLAN crop yield loss data recalculated in terms of 

the 8-hour form. This graph shows that a 4th highest maximum daily 8-hour average 

level that corresponds to the protection level used in the last review (e.g., no more than 

10% yield loss in 50% of the crop cases) would be close to 0.06 ppm. Therefore, the 

current 8-hour average secondary standard set at the current level (0.084 ppm) clearly 

does not provide the level of protection expected and judged to be requisite by the 
126

Administrator in the last review as expressed in terms of a SUM06 of 25 ppm-hrs 

(approximately equivalent to W126 of 21 ppm-hrs evaluated in this review). Field-based 

information that shows effects occurring in the field at ambient air quality levels at and 

below the level of the current 8-hour standard support this conclusion. For example, 

EPA staff obtained the raw hourly data that produced the results in Gregg, et al., 2003 in 

order to calculate the W126 values associated with the cottonwood tree seedling biomass 

loss as graphed in Figure 7-17 on page 7-57 of the Staff Paper. Though the 4th highest 

maximum daily 8-hour averages were not presented in the Staff Paper, the raw data to 

calculate this are available in the docket.7

 From this raw data, EPA observed that 

significant biomass loss was observed at O3 air quality ranging from the level of the 

current 8-hour standard to 4th highest daily maximum 8-hour averages well below (e.g., 

0.072 ppm) the current 8-hour standard. Taken together with the foliar injury data which 

occurred at areas meeting and/or below the level of the current 8-hour standard (see Staff 

Paper p. 7-61 to 7-64; Table 7-4), EPA concluded that significant vegetation effects can 

occur at air quality levels that meet or are below the level of the current 8-hour, 0.08 ppm 

secondary standard. 

(9) Comment: Exxon-Mobil stated that “[t]he basis for a regulatory standard should be 

transparent.” This commenter then identifies three areas where it alleges a lack of 

transparency: (a) “Inconsistent use and reporting of metrics and, in some cases, reference 

to unavailable information, result in a general lack of transparency in the science 

supporting a revised secondary standard. The studies presented differ in metrics and 

some studies fail to present all metrics. EPA has failed to conduct a re-evaluation of the 

studies in order to report results in a consistent format....EPA should provide re-analysis 

of data and reporting in common metrics as appropriate, particularly to support the key 

points of its rulemaking.” (b) “...EPA cites the recommendations of a consensus 

workshop (Heck and Cowling, 1997) several times. However, this workshop was by 

invitation only, and documentation is not available to the public. The reference [sic] 

cited is short and provides consensus recommendations, but without details as to their 

basis. In particular, the basis for the recommendation to consider a 2 percent effect level 

to be significant is not provided. It is not clear how this effect level could be 

experimentally determined, if it is discernible from biological variability, or what 

references suggest the potential compounding effect over multiple years, given the results 

of Isebrand et al. (2001) and King et al (2005) cited above.... If available, a more detailed 

report of the consensus workshop should be released. If studies to support the 

recommendations cannot be provided, then the recommendations should be used with 

great caution.” (c) “An additional reference cited in the SP (section 7.5.1) as the source 

of key information on crop and seedling concentration-response, Lee and Hogsett (1996), 

is not available. This document is an EPA report, and its release was requested in 

previous comments to EPA. However, it could not be found on a search of the EPA 

 7

 Data for Figure 7-17 on pg. 7-57 of the final ozone staff paper: The hourly ozone data in 

this file was used to calculate the 12-hr W126 ozone exposures for the cottonwood trees grown 

in the New York City area. Docket No. EPA-HQ-OAR-2005-0172-6753. November 29, 2007. 
127

website or a specific search of EPA publications....EPA should also make the Lee and 

Hogsett (1996) report available to the public” 

Response: (a) EPA agrees that different studies have used different metrics for reporting 

results and that this has resulted in a lack of direct comparability between these studies. 

However, in some of these studies, the authors have directly compared their results in the 

field to those from OTC studies and reported that results are similar between plant 

response in OTCs and in the field. It is this latter point of comparison that EPA felt was 

most informative in the context of this review. Thus, EPA does not agree that converting 

all exposure metrics to a common metric for comparability is a critical activity for the 

purpose of this review. 

(b) EPA agrees that insufficient information is available to judge the scientific basis for 

the consensus statements from the Heck and Cowling, 1997 consensus workshop. The 

preamble to the final rule states “With regard to comments stating concern with EPA’s 

apparent reliance on the recommendations from the 1996 consensus workshop in 

selecting a range of levels, EPA agrees that though the workshop participants were asked 

to review, and thus were aware of, the scientific literature available at the time, as 

described in both the 1996 O3 Criteria Document and Staff Paper, the workshop 

discussion of ranges of levels recommended as protective of different vegetation types for 

different effects falls short of providing a scientific basis for determining at what level 

these effects become adverse to the public welfare. In addition, EPA agrees that the 

scientific basis for establishing a 2% level of biomass loss in tree seedlings as a 

benchmark of concern to take into account the possibility of compounding is unclear, 

though there was and continues to be evidence of the potential for compounding effects 

to occur over multiple years (72 FR 37885, 37886). 

(c) EPA notes that the 1996 article by Lee and Hogsett is available in the docket (Docket 

No. EPA-HQ-OAR-2005-0172-0069. January 25, 2007.) 

(10) Comment: A number of commenters expressed concern that the possible impact of O3-

related reductions in plant productivity could result in a reduced capacity of vegetation to 

serve as a carbon sink to mitigate the impacts of rising CO2 in a changing climate, citing 

to a “new” study on that topic (Sitch et al., 2007). Many of these same commenters also 

cited to “new” field-based studies in the Great Smoky Mountain National Park that find a 

relationship between O3 exposure, tree stem growth loss, tree water use and stream flow 

as evidence that current ambient O3 levels can impact ecosystems and that ecosystems 

should be afforded protection from such potential effects. For example, some of these 

commenters note that “new” studies in the Great Smoky Mountain National Park 

(McLaughlin, et al., 2007a,b) have found that (1) ambient O3 caused substantial growth 

reductions in mature trees in a mixed deciduous forest, which was due in part to increased 

O3-induced water loss and led to seasonal losses in stem growth of 30 - 50 percent for 

most species in a high-ozone year; (2) increasing ambient O3 levels also resulted in 

depletion of soil moisture in the rooting zone and reduced late-season stream flow in the 

watershed; and (3) O3 may amplify the adverse effects of increasing temperature on 

forest growth and forest hydrology and may exacerbate the effects of drought on forest 
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growth and stream health. Other “new” research noted by these commenters as 

supporting EPA’s findings that current O3 exposures cause significant biomass losses in 

sensitive seedlings of various tree species include a study that predicted up to 31 percent 

growth loss in aspen in certain areas of its North American range in 2001-2003 (Percy, et 

al., 2007). 

Response: EPA agrees that O3 exposure can decrease the potential for plants to sequester 

carbon. This topic is discussed in the Criteria Document, Staff Paper and proposal 

notice. The proposal states (72 FR 37888/9) “Temperate forests of the northern 

hemisphere have been estimated to be a net sink of C per year (Goodale et al. 2002). 

Ozone interferes with photosynthesis, causes some plants to senesce leaves prematurely 

and in some cases, reduces allocation to stem and root tissue. Thus, O3 decreases the 

potential for C sequestration. In the presence of high O3 levels, the stimulatory effect of 

rising CO2 concentrations on forest productivity has been estimated to be reduced by 

more that 20 percent (Tingey et al., 2001; Ollinger et al. 2002; Karnosky et al., 2003). In 

summary, it would be anticipated that meeting lower O3 standards would increase the 

amount of CO2 uptake by many ecosystems in the U.S. However, the amount of this 

improvement would be heavily dependent on the species composition of those 

ecosystems. Many ecosystems in the U.S. do have O3 sensitive plants. For, example 

forest ecosystems with dominant species such as aspen or ponderosa pine would be 

expected to increase CO2 uptake more with lower O3 than forests with more O3 tolerant 

species. With regard to the other effects described in the “new” studies, EPA refers the 

reader to the Appendix. 

 

4. Specific Comments on the Vegetation Exposure and Risk Assessments 

 Comments related to the quantitative vegetation exposure and risk assessments conducted 

for O3 are addressed in this section. Incorporating responses contained in Section IV.B.2.b and 

IV.C.4 of the preamble to the final rule, EPA provides the following responses to specific issues 

related to these assessments. Most comments received on these assessments were from those 

commenters opposed to revising the current secondary standard, including Exxon-Mobil, UARG, 

the Annapolis Center, AAM, and some State agencies. Comments related to views regarding the 

appropriate weight to place on the vegetation exposure and risk assessments in reaching 

decisions on the need to revise the current standard and on an appropriate standard level are 

addressed in the preamble and in section II.B.2.a above. 

 

(1) Comment: In general, as stated by AAM, these commenters asserted that “there are 

problems, flaws and concerns with the Staff Paper analysis and vegetation risk 

assessment that precludes the establishment of a separate secondary standard to protect 

vegetation. 

Response: EPA agrees that there are uncertainties and limitations associated with the 

vegetation exposure and risk assessments. Comments regarding specific concerns will be 

addressed individually below. However, EPA disagrees that such limitations would 

necessarily “preclude the establishment of a separate secondary to protect vegetation.” 
129

(2) Comment: A number of commenters asserted that EPA used unrealistically low levels of 

PRB that resulted in an overestimate of risks and benefits associated with just meeting 

alternative standards. In particular, the Annapolis Center states that “...[t]he same 

analyses, arguments, and data that apply to consideration of background for the primary 

standard also apply to the secondary standard.” 

Response: EPA strongly disagrees with the assertion of these commenters that EPA 

used unrealistically low levels of PRB, for the reasons documented in section II.A.5 

above, and in the preamble to the final rule in section II.B.2.b, which addresses this and 

other comments related to EPA’s approach to estimating PRB and its role in exposure 

and risk assessments related to the primary standard. 

(3) Comment: The Annapolis Center and AAM state that “...the global model EPA relied on 

is not capable of resolving the phenomena that contribute to attainment or nonattainment 

of secondary ozone standards throughout the country. In fact, even a more refined, 

higher resolution model, the Community Multi-Scale Air Quality (CMAQ) modeling 

system... performed poorly in predicting the observed 2001 SUM06 and W126 in the 

west.... This means that the sources and processes that contribute to substantial levels of 

both SUM06 and W126 in rural and remote areas in the Western U.S. are not wellcaptured in state-of-the-art chemical transport models....” These commenters further 

state that “...[t]he map of ‘as is’ W127 levels included as Figure 7-6 of the SP shows 

W126 levels exceeding 7 ppm-hrs throughout many areas of the country...The overall 

pattern of W126 suggests both a contribution from U.S. man-made emissions and a 

background component that could involve biogenic emissions, agricultural emissions, 

long-range transport from non-U.S. sources, and a stratospheric component. In 

particular, W126 levels greater than 7 ppm-hr exist in many locations throughout the 

country, including many rural and remote Western sites well-removed from 

anthropogenic emission source areas. AAM further elaborates that “...[t]hese levels 

could be explained in part by NOx emissions from soils due to microbial processes. 

Jaegle, et al. [(2005)], using satellite observations of NO2 columns, found that soil NOx 

emissions were twice as high as assumed in the GEOSS-CHEM model. This will result 

in a misallocation of ozone between man-made and natural sources. The presence of a 

large soil NOx source in the Great Plains also may help explain the discrepancy between 

the locations of elevated SUM06 and W126 and the major populated areas of the country. 

Thus, “EPA and CASAC assume, incorrectly, based on the Fiore et al. 2003 global 

modeling analysis, that SUM06 or W126 is not confounded by background ozone. 

Response: EPA’s conclusions regarding the appropriateness of using the GEOSS-CHEM 

model predictions of PRB are discussed in detail in section II.A.5 above. Because PRB is 

defined as including those sources of ozone or ozone precursors that are uncontrollable 

by the U.S., the natural sources of O3 precursors such as soil NOx concentrations and 

stratospheric intrusions, as well as long-range transport from non-U.S. sources have 

already been included in these estimates. Based on the range of PRB values estimated in 

this review (e.g., 0.015 to 0.035 ppm), EPA calculated the maximum PRB background 

contribution that would be possible using the 3-month 12-hr W126 exposure index (see 
130

Staff Paper, p.7-22). Using a constant hourly O3 concentration of 0.035 ppm (the upper 

end of the PRB range), multiplied by the very low weight assigned by the W126 

weighting scheme and cumulated for 12 hours a day for 3 months (92 days), the PRB 

value is less than 1 ppm-hr. Thus, on this basis, EPA concludes that areas experiencing 

W126 values of 7 ppm-hrs or greater, as depicted in Figure 7-6 of the Staff Paper, likely 

have a very low contribution from PRB and a substantial contribution from non-PRB 

sources. It is unclear why the commenter views long-range transport of anthropogenic 

precursors of O3 or O3 itself from source regions within the U.S. improbable, since the 

possibility of long-range transport of these pollutants from non-U.S. sources in 

contributing to PRB has already been acknowledged. On a final note, the study cited by 

the commenter (e.g., Jaegle et al., 2005) was not evaluated in the Criteria Document or 

Staff Paper and is considered a “new” study (see discussion under II.B.3, above). 

The proposal notice further discusses considerations regarding the potential influence of 

PRB on the W126 value at high elevation sites and states “[t]he Criteria Document (EPA, 

2006a), discusses policy relevant background (PRB) levels for high elevation sites and 

makes the following observations: (1) PRB concentrations of 0.04 to 0.05 ppm occur 

occasionally at high-elevation sites (e.g., >1.5 km) in the spring due to the freetropospheric influence, including some limited contribution from hemispheric pollution 

(O3 produced from anthropogenic emissions outside North America); and (2) 

stratospheric intrusions might occasionally elevate O3 at high-altitude sites, however, 

these events are rare. Therefore, the Staff Paper concludes that springtime PRB levels in 

the range identified above and rare stratospheric intrusions of O3 are unlikely to influence 

3 month cumulative seasonal W126 values...” that are calculated for the maximum 3 

month period during the O3 season. 

(4) Comment: Another commenter disputed EPA’s calculation of the maximum PRB 

contribution to 3-month, 12-hour W126 values. Specifically, UARG asserts that “...[i]f, 

however, one takes monitored air quality at the remote Trinidad Head, California 

monitoring site as indicative of PRB, the contribution to the 3-month, 12-hour W126 

could be as much as 3.50 ppm-hour.” In a footnote to the comment, UARG explains that 

this value was arrived at by assuming that two-thirds of the 24-hour W126 value 

calculated for the 3-month period April to June 2003 would be equal to the 12 hour value. 

Response: As EPA has already stated in II.A.5, above, both EPA’s experts and CASAC 

endorsed the use of the peer-reviewed, thoroughly evaluated modeling approach (GEOSCHEM) described in the Criteria Document as the best approach for estimating PRB 

levels. The Criteria Document reviewed detailed evaluations of GEOS-CHEM with O3

observations at U.S. surface sites (Fiore et al., 2002, 2003) and comparisons of GEOSCHEM predictions with observations at Trinidad Head, CA (Goldstein et al., 2004) and 

found no significant differences between the model predictions and observations for all 

conditions, including those reflecting those given in the PRB definition. The Criteria 

Document (p. 3-49) states that the current model estimates indicate that PRB in the U.S. 

is generally 0.015 to 0.035 ppm that declines from spring to summer and is generally < 

0.025 ppm under conditions conducive to high O3 episodes. The Criteria Document 

acknowledges that PRB can be higher, especially at elevated sites in the spring due to 
131

stratospheric exchange. However, unusually high springtime O3 episodes tied to 

stratospheric intrusion are rare and generally occur at elevated locations and these can be 

readily identified and excluded under EPA’s exceptional events rule (72 FR 13560) to 

avoid any impact on attainment/non-attainment status of an area. Thus, EPA concludes 

that such a high PRB value would be extremely rare, and highly unlikely to occur during 

the maximum 3-month daytime period evaluated against the level of the W126 standard. 

If due to stratospheric exchange, this value would be excluded from consideration. 

(5) Comment: Many commenters also asserted that there was a lack of new information 

since the last review that would, in their judgment, materially reduce the uncertainties 

present in the assessments conducted for the last review. For example, the Annapolis 

Center asserted that “...[s]ome of the most important caveats and uncertainties 

concerning the exposure and risk assessments for crop yield that were listed in the [1996] 

proposal included (a) extrapolating from exposure-response functions generated in opentop chambers to ambient conditions; (b) the lack of a performance evaluation of the 

national air quality extrapolation; (c) the methodology to adjust modeled air quality to 

reflect attainment of various alternative standard options; and (d) inherent uncertainties in 

models to estimate economic values associated with attainment of alternative standard. . . 

. Because of the lack of new data or substantive improvements in the risk assessment, 

these same issues remain today, contributing a similar degree of uncertainty, as was the 

case in the prior review.” 

Response: While EPA recognizes that important uncertainties remain in estimates of 

vegetation exposure and O3-related risk to vegetation, especially with regard to O3-related 

effects on crop yields, EPA disagrees with comments that assert that the uncertainties in 

such assessments remain unchanged or generally have not been materially reduced since 

the last review. EPA discusses each of the uncertainties from the 1997 review identified 

by the commenters in turn below. 

(a) With regard to the uncertainties associated with using the OTC C-R functions, the 

Annapolis Center further stated that “CASAC characterized the estimates as rough 

estimates because the open-top chambers alter the ambient microclimate conditions 

introducing uncertainty. The concern was raised that in these studies, plant response to 

ozone has been optimized under conditions that do not reflect real-life field 

conditions....The Panel concluded that ‘five years from now, if we do not have the results 

of research coupling ozone air quality and plant biology under conditions more 

representative of ambient field conditions, then we will continue to be hampered by our 

inability to come to consensus on the levels of air quality that are protective of vegetation 

and ecosystems...’ ”. In addition, the Annapolis Center states that “...[t]en years have 

now elapsed, and the same concentration-response functions from the OTC studies of the 

1980’s are still the only viable data to use to estimate crop loss .... The 1996 CASAC 

Panel agreed that the estimates of crop loss at that time were highly uncertain. It raised 

specific issues concerning the procedures and noted that the background estimate of 

0.025 ppm was too low and would over-inflate the crop loss estimates.” 
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While EPA agrees that important uncertainties continue to be associated with the use of 

the C-R functions generated many years ago using OTC studies for crop yield loss, EPA 

does not agree that the new information available in this review has not reduced the 

uncertainties identified above and in the last review. EPA concludes that the 

uncertainties associated with continued use of the C-R functions derived from the 

NCLAN OTC studies have been materially reduced in three important ways by the recent 

information. First, and most importantly, as described above and in the Staff Paper and 

proposal, the results of significant new field based studies (e.g., AspenFACE, SoyFACE 

and gradient) show that the levels of vegetation response that have been observed in the 

field are of similar magnitude as those observed in OTC experiments, thus providing 

qualitative evidence that use of C-R functions generated in OTC would not be expected 

to overestimate risk to vegetation in the field. Second, the lower estimates of PRB in this 

review (e.g., 0.015 to 0.035 ppm) now bracket the 0.025 ppm level used as the lowest 

exposure level representing background in the OTC studies. This further reduces the 

concern that these C-R functions result in an overestimation of risks in the field. Third, 

limited information available in this review on the O3 sensitivities of some crop species 

(e.g., soybean, cotton) suggests that O3 sensitivity has not changed significantly in the 

intervening years. Taking all the above into account, EPA’s level of confidence in the 

applicability of the OTC generated C-R functions to represent ambient conditions in the 

field has materially increased. 

(b) With regard to the lack of a performance evaluation of the national air quality 

extrapolation, EPA disagrees and notes that there have been advancements in the tools 

and methods used for such extrapolations and the characterization of associated 

uncertainties since the last review. With respect to the generation of interpolated O3

exposure surfaces, EPA employed a different approach than that used in the last review 

and undertook a quantitative assessment of the uncertainties associated with the use of 

this method. This uncertainty assessment was accomplished by sequentially dropping out 

of the interpolation each monitoring site and then recalculating the exposure surface 

using the remaining monitoring sites. As discussed in the Staff Paper, this method of 

evaluation may result in a slight overestimation of error and bias for the exposure surface, 

since dropping out monitors loses information that the interpolation uses in that local 

area. As another point of comparison, EPA also examined the subset of rural CASTNET 

sites to illustrate how the interpolation technique predicted air quality in that rural 

monitoring network. For this subset, the evaluation indicated that in general, the 

interpolation technique slightly overestimated W126 exposures at relatively low levels 

and underestimated W126 exposure at relatively high levels. This aspect of the 

estimation method potentially resulted in an underestimation of the more important risks 

associated with higher cumulative exposures in some areas. Based on this evaluation, 

EPA reiterates the conclusion in the Staff Paper that “...the calculation of error and bias 

metrics for the interpolation represents a notable improvement over the 1996 assessment 

which did not have such an evaluation.” EPA further concludes that in general, the 

sources and likely direction of uncertainties associated with the exposure and risk 

assessments have been better accounted for and characterized than in the last review. 
133

(c) With regard to criticisms of the methodology used to adjust modeled air quality to 

reflect attainment of various alternative standard options, the Annapolis Center further 

states that “EPA’s analysis to date does not evaluate the impact of the nation’s ozone 

control program on W126 in a scientifically sound manner.” EPA strongly disagrees and 

notes that this issue has been raised in the context of both the primary and secondary 

standards. As noted above in section II.B.2.b, based on information in the Staff Paper 

(section 4.5.6) and in more detail in a staff memorandum (Rizzo, 2006), EPA concluded 

that the quadratic air quality adjustment approach used in this assessment generally best 

represented the pattern of reductions across the O3 air quality distribution observed over 

the last decade in areas implementing control programs designed to attain the O3

NAAQS. While EPA recognizes that future changes in air quality distributions are areaspecific and will be affected by whatever specific control strategies are implemented in 

the future to attain a revised NAAQS, there is no empirical evidence to suggest that 

future reductions in ambient O3 will be significantly different from past reductions with 

respect to impacting the overall shape of the O3 distribution. 

(d) With regard to comments that asserted that inherent uncertainties in models to 

estimate economic values of crop loss have not been reduced since the last review, EPA 

acknowledges that while an updated state of the art model, the AGSIM benefits model, 

was used in this review, substantial uncertainties remain in these estimates of economic 

crop loss. Further, EPA notes that these estimates were not relied on as a basis for 

reaching a decision on the need to revise the current standard. 

(6) Comment: Some commenters also asserted that the estimated exposures and risks 

associated with air quality just meeting the current standard have not appreciably changed 

since the last review. These commenters used this conclusion as the basis for a claim that 

there is no reason to depart from the Administrator’s 1997 decision that the current 

secondary standard is requisite to protect public welfare. 

Response: EPA believes that this claim is fundamentally flawed for three reasons, 

discussed in turn below: (a) it is factually inappropriate to compare quantitative 

vegetation risks estimated in 1997 with those estimated in the current rulemaking; (b) it 

fails to take into account that with similar risks, increased certainty in the risks presented 

by O3 implies greater concern than in the last review; and (c) it fails to recognize that the 

Administrator has used these estimates in a supportive role, in light of the significant 

uncertainties in the exposure and risk estimates, to inform the conclusions drawn 

primarily from the integrative assessment of the vegetation effects information on 

whether adverse O3-induced effects to vegetation observed under ambient O3 levels 

allowed under the current standard are sufficiently adverse to the public welfare to 

warrant a revision of the O3 standard. 

(a) The 1997 risk estimates, or any comparison of the 1997 risks estimates to the current 

estimates, are irrelevant for the purpose of judging the adequacy of the current 8-hour 

standard, as the 1997 estimates reflect outdated analyses that have been updated in this 

review to reflect the current science. In particular, as discussed in section 7 of the Staff 

Paper, there have been significant improvements to the exposure and risk methods used, 
134

incorporation of additional sources of information, more sophistication in application of 

approach and methods evaluation/uncertainty characterization that make comparisons 

inappropriate between the prior and current review. 

(b) It is important to take into account EPA’s increased level of confidence in use of 

OTC derived C-R functions to predict risks in the field based on important new field data 

and the lower estimates of PRB estimated in this review, since in judging the weight to 

place on quantitative risk estimates it is important to examine not only the magnitude of 

the estimated risks but also the degree of confidence in those estimates. 

(c) Quantitative vegetation risk estimates were not the main basis for EPA’s decision in 

setting a level for the secondary standard in 1997, and they do not set any quantified 

“benchmark” for the Agency’s decision to revise the current standard at this time. The 

proposal notice made clear that decisions about the need to revise the current standard are 

mainly based on an integrated evaluation of evidence available across a broad array of 

vegetation effects, while the more uncertain exposure, risk and benefits estimates were 

used in a supportive role. Both the Staff Paper and proposal clearly distinguished the 

roles that these different types of information played in informing the Administrator’s 

proposed decision. The proposal states that “...due to multiple sources of uncertainty, 

both known and unknown, that continue to be associated with these analyses, the Staff 

Paper put less weight on this information in drawing conclusions on the adequacy of the 

current standard. However, the Staff Paper also recognizes that some progress has been 

made since the last review in better characterizing some of these associated uncertainties 

and, therefore, concluded that the results of the exposure and risk assessments continue to 

provide information useful to informing judgments as to the relative changes in risks 

predicted to occur under exposure scenarios associated with the different standard 

alternatives considered.” In determining the requisite level of protection, the Staff Paper 

recognized that it is appropriate to weigh the importance of the predicted risks of these 

effects in the overall context of public welfare protection, along with a determination as 

to the appropriate weight to place on the associated uncertainties and limitations of this 

information. Thus, while EPA is fully mindful of the uncertainties associated with the 

estimates of exposure, risk and benefits, as discussed above, it judges that these estimates 

are still useful in providing additional support for his judgment that the current 8-hour 

secondary standard does not adequately protect sensitive vegetation. 

C. Specific Comments Related to Data Handling (Appendix P) 

 The primary and secondary ozone NAAQS are specified in terms of an indicator (i.e., the 

specific pollutant to be measured), a level that defines the highest ambient concentration for a 

monitoring site to be considered to be in attainment with the NAAQS, and a statistical form. To 

determine whether an ambient monitoring site violates the NAAQS, the relevant portion of the 

historical record of ambient concentrations of the indicator pollutant at the monitoring site must 

be selected, evaluated for suitability for making a determination, and if suitable summarized into 
135

a statistic appropriate for comparison to the adopted form and level of the NAAQS. An 

important aspect of the suitability evaluation is to determine whether the ozone monitoring data 

set is complete enough to represent the actual air quality situation well enough to allow any 

determination of current attainment or nonattainment to be made. These steps collectively are 

referred to as data handling. Precisely how these steps are performed affects the stringency of 

the NAAQS, so the detailed requirements for these steps are generally proposed and adopted at 

the same time as the NAAQS. In this case, they were proposed in the form of a new Appendix P 

to 40 CFR 50, and were discussed in the preamble to the notice of proposed rulemaking. 

 Appendix P as proposed was a modification of the existing Appendix I which applies to 

the ozone NAAQS adopted in 1997. The major modification consisted of conforming revisions 

to reflect that the proposed 3-decimal-places form of the proposed revised 8-hour primary 

standard simplifies the steps for comparing the monitoring data to the level of the NAAQS 

(because rounding is no longer needed). This issue is not fully separable from the choice of the 

level of the NAAQS. Comments on the level issue per se are addressed elsewhere in this 

document. The second set of modifications were new provisions for all aspects of data handling 

for the proposed secondary NAAQS using the cumulative peak weighted index (because the 

1997 primary and secondary NAAQS were identical and so no special provisions were needed 

for the secondary NAAQS). 

 In the preamble, EPA also invited comment on one particular issue related to data 

completeness, on possible objective criteria for considering ozone levels to have been low during 

a period of hours or days when ozone monitoring data was not successfully obtained. 

 Comments regarding data handling for the 8-hour NAAQS were mostly about the issue 

of using 3 decimal places in the level of the NAAQS. A majority of the comments this issue 

supported EPA’s proposal. Some of the favorable commenters noted that monitor precision 

allowed rounding to the third decimal place; others argued that the proposal would close an 

existing “loophole” that allowed communities to claim attainment at concentrations higher than 

the standard. Other commenters wrote that the standard should not be expressed to three decimal 

places. These commenters generally asserted, implicitly or explicitly, that ozone monitoring data 

has too much uncertainty to allow comparison to a pass/fail limit expressed with three decimal 

places. There were a few comments on other topics, which are included below. 

 Only a small number of comments were received on the portions of Appendix P that are 

relevant to a secondary standard non-identical to the primary standard. These generally 

concerned the proposed data completeness rules, including whether and how to compensate for 

an incomplete monitoring record. 

1. Specific Comments on Data Handling Related to the 8-hour Standard 

(1) Comment: Specifying the standard to the third decimal place implies a degree of 

precision in the underlying health effects data that does not exist. EPA recognized this 

when it adopted the current standard in 1997. It stated, at that time, that it was specifying 

the standard to two decimal places “in part to reflect uncertainties in the health effects 

evidence upon which the proposed standard is based,” including “the measurement 
136

uncertainty and representativeness inherent in the reported O3 concentrations used in field 

and epidemiological studies and the uncertainty in the exposure estimates upon which the 

quantitative risk estimates have been based” (62 FR 38886). Those uncertainties remain. 

EPA has not explained why those uncertainties should not lead to the same conclusion 

reached in 1997. 

Response: The body of scientific evidence supporting EPA’s current revision of the 

primary O3 NAAQS is different than the evidence considered in 1997, so EPA’s 

statements in 1997 cannot be taken to necessarily apply to the newer body of evidence 

and the new level of the NAAQS. The interpretation of that evidence is discussed in the 

final rule preamble. 

EPA notes that we are not asserting that monitoring precision in the field has broadly and 

substantially improved since 1997, although improvements have been made. We do not 

believe that major improvement is a precondition for the adoption of a NAAQS specified 

with three digits. 

EPA also notes that as a practical matter, given current O3 concentration measuring 

equipment and reporting practices, it is inevitable that three digits will be used in making 

comparisons to the NAAQS, effectively making the NAAQS have three significant digits 

even if nominally expressed with only two. Almost all States report hourly O3

concentrations with three digits. It is necessary, therefore, for the NAAQS rule to specify 

how those reported digits will be treated through all the steps leading up to and including 

the final comparison to the NAAQS. If the NAAQS were to be nominally expressed with 

only 2 digits, it would still be necessary to specify which final 3-year average values are 

considered to be in compliance. So, for example, a hypothetical NAAQS of 0.07 ppm 

functionally would be either 0.074 ppm (if the rule were to specify that the third digit of 

the final 3-year average value is rounded, as Appendix I specifies) or 0.079 ppm (if the 

third reported digit of the final 3-year average value were truncated)8. That is, the 

effective level of the NAAQS depends on the combination of the number of digits 

specified and the data handling and final comparison instructions. EPA believes that 

explicit use of three digits in the definition of the NAAQS is the more transparent 

approach, as well as the only approach that allows the NAAQS to be set so that 0.075 

ppm is treated as complying and 0.076 ppm is treated as noncomplying. 

(2) Comment: EPA’s ambient air monitoring reference methods specify a precision of two 

decimal places (0.01 ppm) for O3 concentrations (40 C.F.R. § 53.20, Table B-1). 

Response: The Table cited in CFR represents the minimum performance specifications 

and the 0.01 ppm precision is literally a pass/fail test to determine whether it is 

appropriate to employ a method in the field. Actual monitor precision is much better than 

the pass/fail limit (about 3 percent precision and about 0 percent bias). 

 

8

 In 1997, we considered establishing a NAAQS level of 0.08 ppm and data handling procedures that would result in 

any values above 0.080 ppm being considered a violation; in effect that would have been setting a NAAQS of 0.080 

ppm. 
137

(3) Comment: In 1997, EPA also stated its belief that “...expressing the proposed standard 

to the second decimal place is also consistent with the quality assurance guidelines that 

indicate the precision for such O3 measurements shall be within +15%....” Both of those 

concepts seem valid and appropriate. 

Response: The precision limit stated by quality assurance guidelines reflects a maximum 

limit of tolerance and does not at all represent what is occurring in the field. As of 2006, 

the precision limit for O3 has been lowered to 7% from the original 15% benchmark (40 

CFR Part 58, p.61304, section 2.3.1.2). 

(4) Comment: The Agency’s calculation of measurement uncertainty is at odds with research 

showing that instrument imprecision can represent 7-40% of the temporal variation in 

daily measurements for pollutants and that the population-weighted variation in daily 

ambient air pollutant levels can be as high as 20% for both instrument imprecision and 

spatial variability. 

Response: The statistics cited by the commenters were taken from an AWMA 

publication (Wade et al) and were not confined to O3 monitoring precision and variability 

but included many other pollutant gases and particulate species. A close examination of 

the Wade publication (Table 3) shows that the estimated “nugget” parameter for O3 was 

approximately 0.10 which the authors define to be the ratio of the standard deviation of 

the difference between two collocated monitors to the standard deviation of their mean. 

Since the ratio of the standard deviation of daily maximum 8-hour O3 to the mean 

concentration is approximately 0.3 in many urban areas, the nugget value reported by the 

authors (i.e. 0.10) translates into a coefficient of variation of approximately 3 percent for 

the mean difference between two collocated O3 monitors (0.10 X 0.30 about 0.03). The 

value of 3 percent is very close to the median precision associated with EPA’s assessment 

of the precision of O3 monitors nationally. The statistics cited that relate to the spatial 

variability of pollutant concentrations are not relevant to this issue. 

(5) Comment: The analysis cited by EPA in 1997 (Systems Analysis, International –SAI) 

concluded that “a conservative estimate for the typical error associated with an O3

concentration measurement in the real world is on the order of 4 ppb." It is unclear what 

has changed with respect to O3 monitor performance since the 1997 assessment. 

Moreover, questions have been raised about the recent analysis done by EPA staff and its 

applicability to the older monitors that make up much of the ambient monitoring network. 

The recent analysis should not, therefore, be taken as resolving the issue of whether to 

express the 8-hour NAAQS to the thousandth ppm. 

Response: EPA is not asserting that the national monitoring network is necessarily 

producing more accurate data now than in 1997. In fact, subsequent analysis (see 

comment below) confirms that theoretically derived O3 measurement error is still 

approximately 4 ppb, based on the analysis by Mikel (2006). 

(6) Comment: A number of commenters made reference to the analysis performed by SAI 

(1997) and a subsequent reanalysis (Mikel 2006) to estimate the “systematic error” 
138

involved in the collection of O3 data. Since each analysis concluded that “systematic 

error” for hourly O3 measurements is approximately 4 ppb, these commenters assumed 

the term “systematic error” meant that O3 measurements have an inherent error of 4 ppb 

for each hour measured during the O3 season. 

Response: The SAI (1997) and Dennis Mikel analysis (used in Cox and Camalier, 2006) 

independently assessed the potential for measurement uncertainty in the total monitoring 

system, which consists of combinations of error due to drift, detector non-linearity, 

precision and instrument calibration, and NIST standard calibration. The term 

“systematic error” is used in these documents to emphasize that the error estimate reflects 

all the components of the overall O3 monitoring system. It was not intended and does not 

mean that the O3 monitoring system always produces errors of 4 ppb (or larger). Rather, 

random errors are centered on zero, thus producing equally probable positive and 

negative errors, with most errors being less than 4 ppb. 

(7) Comment: Several commenters argued that EPA should not base its proposal on the Cox 

and Camalier (2006) analysis. The instrument bias shown has not been proved to be 

random. 

Response: With regard to the Cox and Camalier (2006) simulation analysis, the reference 

to “random bias”, was perhaps misleading and should have been referred to as “random 

error”. Bias connotes a constant deviation between truth and observation which certainly 

does not apply to O3 ambient monitors operating in the field. An assessment of the 

precision and bias of the reported data from the national network of O3 monitors has 

shown a median precision to be about 3 to 4% and bias to be about 0%. Since these 

statistics are based on individual hourly measurements, the precision and bias of an 

individual 8-hour daily maximum can be no larger and almost certainly smaller due to 

averaging of errors. Based on the national O3 performance statistics and additional 

information regarding the performance of individual O3 monitors, the simulation study 

assumed a “random error” of 0.004 ppm to be conservative (larger than necessary) but 

reasonably representative of an upper bound for a single individual daily maximum 8-

hour concentration. As demonstrated in the simulation study, this level of concentration 

uncertainty has a minimal impact (about 0.001 ppm) on the accuracy of the O3 design 

(8) Comment: EPA has access to considerable data on the site-specific precision and bias 

estimates, such as Langstaff, who reports bias estimates for individual Boston monitors 

varying between -7 and + 11 % in 2003 

Response: The values of precision and bias used in John Langstaff’s report were taken 

from a Quality Assurance assessment report which uses one-sided, upper confidence 

bound precision and bias indicators intended to trigger a quality assurance response by 

protecting against calibration issues and instrument malfunctions. While this 

conservatism may be useful to feed into the exposure models employed by Langstaff, the 

precision and bias results are overestimated and do not reflect the true uncertainty that is 

occurring at the particular monitor. Furthermore, the bias noted above by Langstaff 

represents the very high end of the bias values at individual sites across the country. Most 
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sites have bias values close to zero. Therefore, the Boston monitor example is 

unrepresentative of the performance of the network overall. 

(9) Comment: Regarding quality assurance procedures, one commenter wrote that, 

“Determination of O3 NAAQS attainment requires three years of data but of the more 

than 13,000 hourly observations taken over three years at a typical O3 monitoring site, 

less than 0.75% of the data receives significant scrutiny during the attainment 

determination process. Although statistical approaches utilizing all available precision 

and audit data are valuable for assessing overall O3 data quality EPA should seek and 

investigate concepts that focus on QA measures taken shortly before and after (e.g., 3-7 

days) peak 8-hour O3 concentrations are recorded. This approach would better assess the 

quality of O3 data in the higher concentration range which, ultimately, drives the 

attainment process.” 

Response: EPA appreciates the comment; however it is outside the scope of this 

rulemaking. 

(10) Comment: One commenter suggested that EPA add a site-specific “method detection 

level” (MDL) requirement to O3 measurement QA procedures: “this could be similar to 

the currently proposed MDL test for precursor trace gases11 in which SLT organizations 

challenge field-based monitors repeatedly with low concentration gases. The instrument’s 

MDL is calculated as the standard deviation of the average response multiplied by the 

Student’s t-test value for the number of test values. By performing this test under “as 

installed” conditions a more reliable gauge of an instrument’s sensitivity is generated. 

Additionally, monitoring organizations may discover and correct siting- or installationrelated problems while performing such tests and thus generate higher quality data.” 

Response: Although it is not a requirement, monitoring organizations do have the option 

to report their derived MDL or the vendor MDL to the Air Quality System (AQS). EPA 

appreciates the comment; however it is outside the scope of this rulemaking. 

(11) Comment: Regarding data completeness, one commenter generally supported EPA’s 

proposal and also urged EPA to allow State or local air pollution control agencies the 

flexibility to determine that certain days were not conducive to high O3 levels, should a 

monitor not be operational. They stated that the decisions may need to be made on a 

case-by-case basis, but listed the types of meteorological conditions that are generally not 

associated with high O3 levels: days with significant rain between 10 a.m. to 6 p.m.; days 

with cooler temperatures (< 60°F); days with north winds and frontal passages. 

Response: EPA recognizes the comment, however, EPA believes there are too many 

meteorological conditions to list; therefore, EPA will continue to handle this issue on a 

case-by-case basis as explained in Appendix P. 

(12) Comment: One commenter suggested that the rule allow for averaging the monitoring 

results among O3 monitors that are located in close proximity to each other in order to 

determine compliance. The commenter suggests that States have the option to average the 
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O3 measurements between monitors that are located within 20 miles of each other 

[suggested regulatory text included in comment]. 

Response: EPA disagrees with this comment since local O3 concentrations may be 

impacted by local NOx emissions from sources such as motor vehicles. Thus, local 

concentrations averaged together may not adequately characterize the true exposure to 

the local population. 

(13) Comment: One commenter wrote that the potential impact of stratospheric O3 intrusion 

needs to be thoroughly evaluated. 

Response: EPA’s Exceptional Event Rule handles the impact of stratospheric O3

intrusion. 

(14) Comment: In calculation of using raw data (such as computation of eight hour averages 

or design values) we recommend rounding the results of these calculations instead of 

truncating them, as truncation may result in low bias in the final design value. 

Response: EPA appreciates the comment. However, it has been standard practice since 

the 1997 NAAQS to report and handle O3 data by truncating. Consequently, our 

interpretation of the relationship between reported O3 concentrations and health effects in 

epidemiology studies inherently corrects for the small downward bias in multi-hour and 

multi-day average concentrations. In all or nearly all cases, data available to health 

effects researchers were truncated to three decimal places when submitted to AQS or 

stored in state monitoring agency or other data bases. Reports of prevailing multi-hour 

O3 concentrations in study areas were also made on the basis of truncated averages of 

hourly concentrations. Hence, the small downward bias in O3 statistics that will be 

compared to the NAAQS is the same as the small bias in nominal O3 concentrations 

examined in the assessment of the health studies and in the O3 risk assessment. The net 

effect should be nearly the same as if all O3 concentration averaging were done with 

rounding. 

2. Specific Comments Related to Non-identical Secondary Standard Provisions of 

Appendix P 

(1) Comment: Since the proposed W126 method "weights" certain hours more than others, 

not all missing hours would be of equal impact. The usual standard of 75% data 

completeness may therefore not be appropriate in this case. EPA should consider this 

further and address data completeness requirements in a conservative manner. 

Response: EPA appreciates the comment. Given the Administrator’s final decision to set 

the secondary standard identical to the primary standard, the comment is moot. 

(2) Comment: One commenter presented specific recommendations about missing data 

adjustment and data handling conventions: 
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In place of Equation 2, the commenter suggests the following missing data substitution 

scheme for all months with less than 100 percent completeness: 

1. For one or two hour missing data gaps, use a simple interpolation scheme. 

2. For three or more hour missing data gaps: 

-- Fill in using data from the closest representative monitoring site. 

“Representative” means that both sites measure O3 plumes from identical source 

regions; 

-- If data from a representative monitoring site are not available, then fill in using 

a technique approved by the administrator. 

Response: EPA appreciates the comment. Given the Administrator’s final decision to set 

the secondary standard identical to the primary standard, the comment is moot. 

(3) Comment: To be consistent with data handling conventions for the primary O3 NAAQS, 

NESCAUM recommends the following revisions to section 4.3 of Appendix P to Part 50: 

1. The secondary ambient O3 air quality standard is met when the annual maximum 

W126 value based on a consecutive 3-month period at an O3 air quality monitoring 

site is less than or equal to [7 to 15] ppm-hours. The number of significant figures in 

the level of the standard dictates the rounding convention for comparing the 

computed W126 value with the level of the standard. The first decimal place of the 

computed W126 value is rounded, with values equal to or greater than of 0.5 

rounding up. 

2. This requirement is met for the three month period at a monitoring site if O3

concentrations are available (before substituting for missing data) for at least 90% of 

the possible index hours with a minimum data completeness in any one month of at 

least 75% of the possible index hours. 

3. Months with W126 values greater than the level of the standard shall not be ignored 

on the ground that they have less than complete data. Thus, in computing the 3-month 

W126 value, months with less than 75% data completeness (before substituting for 

missing data) shall be included in the computation if the 3-month W126 value is 

greater than the level of the standard.” 

Response: EPA appreciates the comment. Given the Administrator’s final decision to set 

the secondary standard identical to the primary standard, the comment is moot. 

D. Comments Related to Monitoring 
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1. Specific Comments Related to Monitoring and the Primary Standard 

(1) Comment: Several commenters stated that EPA’s revision of the primary ozone NAAQS 

will be “seriously compromised” unless it is supported by accurate data establishing 

current ambient levels of ozone. For example, NACAA stated: “The proposed rule, 

however, ignores the needs that states and localities will have for additional monitors to 

measure ozone levels in currently under-monitored areas and, in particular, in 

unmonitored areas that have populations under 350,000. Unless this latter deficiency is 

corrected in the final rule, the health benefits of EPA’s ozone NAAQS revision will 

likely be limited to those living in MSAs with populations greater than 

350,000.”(NACAA, p. 9) 

Response: EPA recognizes that the issues raised by the commenters are important and 

will likely require changes in the monitoring requirements to address MSAs with a 

population lower than 350,000. As noted in section VI of the preamble to the final rule, 

EPA intends to address these issues as part of its proposed monitoring rule. EPA will 

likely consider proposed revisions to the minimum monitoring requirements that apply to 

smaller MSAs, as well as options for EPA Regional Administrators to consider in 

deviating from such revised minimum monitoring requirements, as is now permitted in 

certain sections of 40 CFR part 58, Appendix D. 

(2) Comment: Several commenters raised similar concerns, adding that the current 

breakpoint of 85 percent of the standard to determine if an ozone monitor is required in 

an MSA is “sorely inadequate.” They also questioned how EPA determines if an area is 

below the 85 percent threshold without monitoring. While one commenter supports the 

current breakpoint, they also contend that all areas, including rural areas that have the 

potential to exceed this breakpoint at least four times per year will need to have a large 

number of additional ozone monitors in order to demonstrate attainment with a new 

lower standard. 

Response: EPA notes that the current breakpoint of 85 percent of the standard (to require 

additional monitors in an MSA) provides a margin of safety by increasing minimum 

monitoring requirements as the design value for an MSA approaches any of the 

applicable NAAQS. This approach was adopted for O3 and PM2.5 minimum monitoring 

requirements on October 17, 2006 as part of a comprehensive review of ambient 

monitoring requirements for all criteria pollutants. (See 71 FR 61236). Specifically for 

O3, an 8-hour O3 design value of 0.068 ppm triggered increased minimum monitoring 

requirements for an MSA based on the pre-existing primary standard level of 0.08 ppm. 

With the decision to revise the 8-hour primary standard to a level of 0.075 ppm, the 8-

hour O3 design value that will trigger increased minimum monitoring requirements for an 

MSA has decreased from 0.068 ppm to 0.064 ppm. Therefore, MSAs with 8-hour 

design values between 0.064 ppm and 0.067 ppm are now required to increase the 

number of monitors operating to meet minimum requirements. EPA notes that in 

practice, however, virtually all of these areas already are operating at least as many 

monitors as the new requirements based on the revised primary standard, so the number 
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of monitors which would need to be initiated (or moved from a location of excess 

monitors) would be negligible. With regard to the specific comment about how EPA 

could determine if an area is below the 85 percent threshold without monitoring, EPA 

recognizes that current monitoring requirements do not require O3 monitors to be added 

in smaller MSAs in the absence of a O3 design value, and that this issue has become more 

important with the decision to revise the level of the primary standard to 0.075 ppm. As 

a result, EPA intends to issue a proposed monitoring rule in June 2008 and a final rule by 

March 2009, as stated in the preamble to the final rule, to deal with monitoring issues 

related to revisions of the primary and secondary standards. 

(3) Comment: Several commenters advocated for an expanded ozone monitoring network. 

They wrote that EPA needs to provide adequate funding for monitoring and the 

development of more appropriate ways to inform and display that data to the public and 

natural resource managers. One commenter contends that EPA must expand the national 

ozone monitoring network in areas with populations of less than 150,000 to identify 

natural background levels and the nature and patterns of domestic and international ozone 

transport. 

Response: As noted elsewhere in this Response to Comments document, EPA intends to 

issue a proposed monitoring rule in June 2008 and a final rule by March 2009 to deal 

with monitoring issues related to revisions of the primary and secondary standards. EPA 

notes that about 400 monitors are presently required in MSAs, but about 1100 are 

actually operating in MSAs because most States operate more than the minimum required 

number of monitors. Of these approximately 700 monitors that are operating in excess of 

minimum requirements, EPA expects that opportunities will exist for relocations of 

monitors to smaller MSAs that are presently unmonitored, allowing for more efficient use 

of existing O3-related resources without increasing the overall size of an already robust 

O3 network. EPA also expects to work with the Office of Atmospheric Programs (OAP) 

to finalize quality assurance upgrades to CASTNET monitors operating primarily in rural 

areas, to meet some of the objectives (monitoring background levels, transport patterns) 

noted by the commenter. 

(4) Comment: The New York State Department of Environmental Conservation noted that 

the proposed monitoring regulations essentially overlook the issue of the adequacy of the 

existing ozone monitoring network for determining compliance with the alternate 

proposed levels. They noted that in the section of the proposed regulations related to 

ambient monitoring, the EPA states that “The EPA does not intend to propose any 

changes to these requirements, because we believe these requirements would continue to 

be appropriate to support implementation of a revised O3 NAAQS.” This commenter 

noted that this statement is accurate only if the new primary standard remains at or near 

the current effective standard of 0.084 ppm or if the standard is dropped to as low as 

0.060 ppm. At levels in the range that the EPA is proposing, 0.070 - 0.075 ppm, the 

monitoring network becomes less than adequate.....” 
144

Response: As noted elsewhere in this Response to Comments document, EPA intends to 

issue a proposed monitoring rule in June 2008 and a final rule by March 2009 to deal 

with monitoring issues related to the revision of the primary and secondary standards, 

including the specific issue noted by this commenter. 

(5) Comment: Several comments were received on possible changes to the required O3

monitoring season if the primary standard is revised downward. For example, The New 

York State Department of Environmental Conservation stated: “The season for measuring 

Ozone is selected on a State by State basis on historical data and the standards that the 

data will be compared to. The season in New York (April through October) is appropriate 

if the proposed standard is set at a level at or near the current standard. If the standards 

are dropped to the low end of the proposed standards, it is likely that Ozone 

concentrations could be elevated in relation to the standards during periods prior to and 

following the currently designated Ozone season.” NESCAUM commented: “Moving to 

a primary ozone NAAQS of 0.070 ppm or lower may result in the need for additional 

sites to properly reflect non-urban population exposures. In addition, depending on the 

final NAAQS level, the ozone (and possibly the PAMS (photochemical assessment 

monitoring stations)) season may need to be extended. NESCAUM supports efforts that 

would better characterize public exposure to ozone, and urges that EPA be prepared to 

provide funding support for states to carry out such efforts.” 

Response: EPA agrees that the length of the required O3 monitoring should be reviewed 

in light of the Administrator’s decision to revise the level of the primary and secondary 

standard. EPA does not agree that the O3 season issue is linked to a primary standard 

level of 0.070 ppm or lower, and notes that the revision to a level of 0.075 ppm 

necessitates such a review as part of the proposed monitoring rule discussed elsewhere in 

this Response to Comments document. EPA has done a preliminary analysis of 2004-

2006 ambient data to address the issue of whether extensions of currently required O3

monitoring seasons are appropriate in light of the revised primary and secondary O3

standard level and the revised breakpoints for the AQI. The results of the analysis 

demonstrated that out-of-season exceedances of the revised primary standard level 

occurred in eight states during the study period. Additionally, the frequency of days with 

O3 concentrations that reached the revised Moderate AQI category (based on a breakpoint 

of 0.060 ppm) was much greater compared with the frequency of days with 

concentrations that reached the pre-existing Moderate AQI category (based on a 

breakpoint of 0.065 ppm). This increased frequency of days with Moderate AQI levels 

was noted to occur during periods before and after the currently required O3 seasons. 

Based on these preliminary analyses, EPA intends to consider changes to the length of 

the required O3 season for the coming monitoring rulemaking. Such changes could be 

based solely on the frequency of exceedances of the revised primary and secondary 

standards, or could also consider the frequency of concentrations in the Moderate 

category of the AQI. 

2. Specific Comments Related to Monitoring and the Secondary Standard 
145

(1) Comment: Several commenters questioned whether the current monitoring system will be 

sufficient for monitoring a new standard, such as W126, particularly in rural areas. For 

example, the ACC noted that “there is also the very practical problem of the lack of a 

rural monitor network to support a W126 standard. Thus, even if evidence is directionally 

pointing to establishing a cumulative standard, it is premature to do so now.” With 

regard to how to address the lack of a rural monitoring network, Alan Leston noted that 

“EPA should more fully address the coverage and quality of non-urban ozone monitoring 

by regulation. As a starting point EPA might require that 10% of a State’s ozone 

monitoring sites (or at least 2 sites, whichever is greater) be located in non-urban areas.” 

The Iowa Department of Natural Resources urged EPA to include monitoring 

requirements regarding the secondary standard – in particular requiring monitoring in 

areas that contain ozone-sensitive crops or ecosystems. 

Response: In light of the Administrator’s decision to revise the 8-hour secondary standard 

by setting it identical in all respects to the 8-hour primary standard, EPA believes that it 

is appropriate to consider whether the existing urban-based monitoring requirements are 

adequate and appropriate to characterize the exposure in more rural areas where O3-

sensitive plant species and more sensitive ecosystems exist, and where resulting 

vegetation damage would adversely affect land usage. Such areas would likely include 

public lands that are protected areas of national interest (e.g., national parks, wilderness 

areas). In consideration of the spatial gaps that currently exist in the rural ozone 

monitoring network, and to the extent that the existence of such gaps has contributed to 

the overall uncertainty that exists in the understanding of ambient O3 levels that occur 

throughout rural areas, EPA believes that there is merit in considering whether additional 

monitoring requirements in certain rural areas would help support ongoing ecosystem 

research studies as well as future reviews of the O3 NAAQS by providing a more robust 

data set with which to assess the relationship of vegetation damage to O3 concentrations. 

Accordingly, as part of its separate monitoring rulemaking, EPA intends to consider 

specific requirements for a minimum number of rural monitors per State, with detailed 

rule language to ensure that States locate such monitors in appropriate areas. For 

example, these areas could include Federal, State, or Tribal lands characterized by areas 

of sensitive vegetation species subject to visible foliar injury, seedling and mature tree 

biomass loss, and other adverse impacts to a degree that could be considered adverse 

depending on the intended use of the plant and its significance to the public welfare. 

(2) Comment: NESCAUM recommended that EPA and the states explore together how the 

CASTNET (Clean Air Status and Trends Network) program might be augmented and 

made more efficient and cost-effective to enhance the monitoring network, especially in 

rural areas. Some commenters expressed concern about the quality assurance practices at 

CASTNET sites with regard to certain aspects of O3 monitoring. They recommended 

that EPA upgrade such practices to meet the 40 CFR Part 58 Appendix A quality 

assurance requirements already followed by the States so that the resulting data could be 

used in assessing compliance with the revised secondary standard. 

Response: EPA agrees that CASTNET sites represent a valuable resource to help 

provide rural monitoring coverage in support of the revised level of the secondary O3
146

NAAQS. EPA notes that O3 monitoring technology and procedural upgrades have been 

completed at some of the CASTNET sites, and that such upgrades will be completed at 

all CASTNET sites by 2009. The resulting O3 ambient data from the upgraded sites will 

meet Appendix A requirements as is presently the case for O3 data from State operated 

monitors and NPS monitors. These data will be deemed acceptable for NAAQScomparison objectives and available in the AQS database beginning in 2008. 

(3) Comment: The National Park Service noted that the level of monitoring in non-urban and 

natural areas, such as Class I areas in national parks and wilderness areas, is inadequate 

to identify all areas that might violate a secondary standard. NPS urged EPA to consider 

alternative monitoring approaches since typical monitoring may not be possible in some 

areas due to lack of electricity and other restrictions. 

Response: While EPA notes the value of non-traditional monitoring approaches to meet 

certain research oriented objectives, we believe that monitors intended for demonstrating 

compliance with the primary and secondary NAAQS must employ federally approved 

reference or equivalent methods to insure that data of known and acceptable quality are 

used in the designation of areas as attainment or non-attainment. EPA is aware of the 

potential logistical difficulty of locating monitors in remote areas and that the lack of 

monitoring data may complicate the assessment of areas with the regard to compliance 

with the revised level of the secondary NAAQS. Future guidance or rulemaking on O3

implementation issues may deal with this issue. 

III. RESPONSES TO LEGAL, ADMINISTRATIVE, AND PROCEDURAL ISSUES AND 

MISPLACED COMMENTS 

A number of comments were received that addressed a wide range of issues including 

legal, administrative, and procedural issues. Many legal issues are addressed generally 

throughout the preamble to the final rule. Specific legal issues are more fully addressed below in 

section III.A. In addition, a number of comments were submitted related to issues that are not 

germane to the review of the NAAQS, including implementation issues. Implementation issues 

are addressed generally in section I.C of the preamble to the final rule. Comments on 

implementation and other issues that have been categorized as “misplaced” comments are 

included in section III.B below. 

A. Legal, Administrative and Procedural Issues 

(1) Comment: By law, the Clean Air Scientific Advisory Committee (CASAC) is charged 

with performing both a scientific review and policy advice function (Clean Air Act, 

section 109(d)(2)). This means that EPA must be extraordinarily careful in how it listens 

to CASAC to ensure that it clearly distinguishes scientific insight from policy 

prescription (NAM, pp. 53-54). 
147

CASAC’s primary scientific responsibility is to perform a scientific peer review of EPA’s 

various risk assessment documents, including Criteria Documents and Staff Papers. 

CASAC is directed to “complete a review of the criteria published under section 108,” 

which requires that air pollution criteria “accurately reflect the latest scientific 

knowledge.” CASAC’s primary duty is to ensure that EPA’s risk assessment is accurate, 

clear and unbiased. CASAC is not charged with performing a de novo synthesis of the 

science, which is EPA’s job through preparation of the Criteria Document. Since the 

Criteria Document should be completely free of policy considerations, there is no reason 

why CASAC should ever stray into policy matters (NAM, p. 55). 

CASAC’s review of the EPA Staff Paper is necessarily different, for the Staff Paper is by 

design a complex mix of science and policy recommendations from Agency staff. In 

principle, the design of the Staff Paper should make it relatively easy for CASAC to 

maintain a clear distinction between its scientific review and policy advocacy roles. 

CASAC does not seem to have adhered to that principle. It is difficult to discern where it 

is commenting on science and opining about policy (NAM, p. 55). 

CASAC’s members also are invited to provide the Administrator with their opinions 

regarding how he ought to exercise his statutory discretion in revising or retaining 

NAAQS. Because their principal charge is scientific, the public might reasonably expect 

CASAC members to limit their advice to matters of a strictly scientific nature, as 

befitting their technical expertise. However, the law does not limit CASAC to advising 

on matters of science, nor does it constrain them from providing pure policy advice 

reflecting their personal values and preferences (NAM, p. 56). 

The law invites CASAC to provide policy advice several ways. First, it specifies that one 

member of the committee must represent State air pollution agencies. Like EPA, these 

agencies are regulatory rather than scientific in nature, function, or organization, and they 

are populated with personnel who quite reasonably share their agency’s (and EPA’s) air 

pollution control mission. Furthermore the act of representation is inherently a 

stakeholder role (NAM, p. 56). 

 CASAC members are asked to “recommend to the Administrator any new national 

ambient air quality standards and revisions of existing criteria and standards as may be 

appropriate” (section 109(d)(2)(B)). In short, they are invited to speculate as to how they 

think they would exercise the Administrator’s statutory discretion if they were standing in 

his shoes. Despite the fact that CASAC members all have scientific training and have 

distinguished themselves in one or more scientific fields, there is nothing scientific about 

this assignment (NAM, p. 57). 

Response: Under section 109(d)(2)(B) of the Clean Air Act, CASAC “shall complete a 

review of the [air quality criteria] and [the NAAQS] and shall recommend to the 

Administrator any new national ambient air quality standards and revisions of existing 

criteria and standards as may be appropriate under section 108 and subsection (b) of this 

section.” Thus CASAC has two primary responsibilities: to review the air quality 

criteria and advise EPA on appropriate revisions to the criteria, and to review the 
148

NAAQS and advise EPA on appropriate new or revised NAAQS. The Act does not 

distinguish between these obligations and does not establish different ranking or priority 

between them; instead they are of equal statutory status. 

 The Act does not specify how CASAC is to perform its statutory function. For example, 

it neither requires nor prohibits CASC from conducting a “de novo synthesis” of the 

science. For many years, as in this review, the method employed by CASAC in 

discharging its advisory role has been to provide comments, advice, and 

recommendations to EPA on draft and final versions of the air quality criteria document, 

Staff Paper, and related exposure and/or risk assessments. In certain cases, as it has here, 

CASAC has also provided advice and recommendations on a range of potential 

alternative standards. EPA has found this overall approach to be a very constructive and 

useful method for CASAC to provide its advice. Since passage of the CAA Amendments 

in 1977, EPA has carefully considered all such advice and recommendations provided by 

CASAC. 

EPA recognizes that CASAC serves in an advisory capacity and that the judgments 

required under section 109(b) are made by the Administrator and not CASAC. Advice of 

the CASAC is available to the Administrator to use as deemed appropriate in making 

decisions on the proposal and final rulemaking. The Administrator has followed that 

approach in this rulemaking. 

 In providing advice and recommendations to EPA on these various documents, CASAC 

has properly provided both their views on the science as well as their views on 

appropriate new or revised NAAQS. It is the latter advice, on new or revised NAAQS, 

that EPA understands NAM to mean by the term “policy advice.” Providing advice and 

recommendations on new or revised NAAQS calls for CASAC to apply its understanding 

of the science to the criteria in section 109(b) for setting the NAAQS. This by definition 

means providing advice and recommendations on the public health and welfare policy 

judgments inherent in judging, for example, what primary standard would be requisite to 

protect public health with an adequate margin of safety. This is fully appropriate based 

on the charge to CASAC in the CAA. In general, as in this case, CASAC has provided 

such advice by recommending a range of possible new or revised standards, as compared 

to recommending a single standard, recognizing that section 109 calls for the 

Administrator to exercise his own public health and welfare policy judgment. 

In considering CASAC’s advice and recommendations EPA fully agrees that it is very 

important to pay close attention to the content of the advice and weigh it carefully, 

whether it be advice on the science or advice on policy matters related to new or revised 

NAAQS. EPA in fact does this, as seen in the many and varied revisions made to the 

draft documents CASAC has reviewed and commented on, such as the air quality criteria 

document, the Staff Paper, and the related exposure and risk assessments. It can also be 

seen in the careful attention paid by the Administrator to CASAC’s advice in both the 

proposed rule and in this final rule. The Administrator has carefully explained where he 

has accepted CASAC’s advice and where he has not, and explained in detail his 

reasoning. 
149

In general, EPA has found CASAC’s science and policy advice to be very important and 

helpful. The result has been a robust and comprehensive peer review of the various 

documents noted above, all of which have informed EPA’s proposed and final rule in this 

review. EPA recognizes that the nature of the advice and recommendations from 

CASAC, whether on the science or on the policy judgments in applying the science to the 

criteria for the NAAQS, does vary depending whether the focus of the document at issue 

is on the science, as in the Criteria Document, or on applying the science to the standardsetting criteria of section 109(b), as in the Staff Paper or the proposal. EPA also agrees 

that advice and recommendations from CASAC are most useful when the science and/or 

policy basis of the advice are clearly expressed and identified. 

In this rulemaking, EPA is confident that it has been able to clearly differentiate 

CASAC’s science advice from the policy advice on the appropriateness of new or revised 

NAAQS. NAM has not identified examples where it believes EPA has failed to so 

differentiate, nor examples where CASAC has improperly mixed science and policy in 

providing its advice. For example NAM has not identified where CASAC’s science 

advice on the air quality criteria was improper because it was based on policy instead of 

science considerations. Nor has NAM identified any area where it believes CASAC is 

speculating about new or revised NAAQS, as compared to exercising their judgment. 

EPA fully agrees that it needs to pay close attention when evaluating the advice of 

CASAC to properly understand its scientific basis as well as its policy basis; however, 

NAM has provided no example where EPA has failed to do so or where EPA has 

confused or misunderstood the basis for CASAC's advice. In fact, this rule indicates that 

EPA is fully capable of disagreeing with CASAC on its advice and recommendations, 

and explaining why EPA either was not persuaded or did not agree with CASAC’s 

reasoning or conclusions. 

(2) Comment: Because it is an independent body outside of the Agency’s control, CASAC is 

exempt from federal information quality guidelines. However, EPA is not exempt when 

it disseminates or uses information provided by CASAC. EPA cannot simply cite 

CASAC as a scientific authority without regard for whether their content adheres to 

applicable information quality standards. Where EPA disseminates covered information 

obtained from CASAC in a manner that a reasonable person would construe as Agency 

agreement, EPA must ensure that the information satisfies applicable information quality 

standards as if the Agency itself had produced the information (NAM, p. 54). 

EPA’s Notice of Proposed Rulemaking contains numerous subsections in which the input 

it received from CASAC is summarized. In some places, this input is clearly described 

as scientific information, subject to applicable information quality guidelines. But in 

most instances, EPA does not carefully distinguish CASAC’s scientific review from its 

policy advice. This is entirely understandable insofar as CASAC itself did not make 

these distinctions clear. However, adherence to information quality guidelines is EPA’s 

responsibility and not that of CASAC. Moreover, in its charge to CASAC, EPA did not 

ask the committee to clearly distinguish between its scientific review and its policy 

recommendations. For example, EPA did not ask CASAC to apply the Agency’s 
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information quality guidelines, and CASAC didn’t do so. Nor did EPA disclose any predissemination review of the input it received from CASAC (or any other third party) to 

ensure that applicable information quality requirements were met (NAM, p. 57). 

 To minimize the number of error correction requests they receive, agencies are required 

by OMB’s government-wide information quality guidelines to establish effective 

procedures for dissemination review. In EPA’s own guidelines the Agency states that it 

has in place sufficient pre-dissemination review procedures to ensure that information 

quality error is rare. The problem, though, is that none of the documents subject to this 

RFC contain any text suggesting that pre-dissemination review actually occurred. 

Information quality and its associated concepts and definitions simply don’t appear 

(NAM, pp. 57-58). 

 

Response: CASAC is a separate entity from EPA and, as such, assesses scientific and 

other documents produced by EPA independently of Agency oversight. While EPA 

gives careful consideration to the advice provided by CASAC members, EPA cannot 

subject CASAC recommendations to information quality standards. In using CASAC 

panel advice, however, EPA agrees that it is subject to following information quality 

guidelines. 

EPA’s Guidelines for Ensuring and Maximizing the Quality, Objectivity, Utility, and 

Integrity of Information Disseminated does not require the Agency to discuss, separately, 

whether the pre-dissemination review actually occurred. The Guidelines, rather, provide a 

process for developing quality actions, of which the pre-dissemination review procedures 

are a part. This process is also a part of EPA’s Action Development Process (ADP). 

EPA’s ADP is a mechanism that assists the Agency in achieving the objectivity and 

transparency of information used in developing regulations. The stakeholder involvement 

and consultation that is a part of the ADP are a valuable component of pre-dissemination 

review. In fact, NAM’s comments are also a part of this process to ensure that the 

information EPA disseminates is of appropriate quality. 

 Throughout this O3 NAAQS review there has been public review and comment of drafts 

of the Criteria Document, the Staff Paper, the risk and exposure assessments, and 

comment on the proposal notice. In addition, the CASAC meetings were open to the 

public, and interested parties had the opportunity to submit comments and/or present oral 

testimony. In EPA’s view, this process has ensured a robust review of the science. EPA 

believes that this lengthy and transparent process is an effective procedure for 

dissemination review. 

 The discussions in both the proposed and final rule of the science, the risk and exposure 

assessment, and the public health and welfare judgments supporting the proposed and 

final standards make clear not only the basis for the Administrator’s decision but also 

what advice was received form CASAC, and how EPA differentiated between advice on 

the science and advice on the policy matters relevant to setting the NAAQS. It also 

shows where EPA disagreed with CASAC and the basis for any such disagreement. 
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NAM has not identified any example where EPA failed to properly differentiate between 

science and policy advice from CASAC. 

(3) Comment: NAM contends that EPA demonstrates presentational bias through selective 

citation of statements made by the CASAC for the purpose of conveying the impression 

that CASAC endorsed all or virtually all of the EPA staff analyses. In the first set of 

examples, NAM contends that EPA demonstrates this presentational bias by citing text 

from a paragraph that supports its analyses, but does not cite other text in the same 

paragraph that does not. In the second set of examples that allegedly demonstrate 

presentational bias, NAM finds important scientific comments from the CASAC O3 Panel 

that it contends do not support EPA’s interpretation of the data and also contends that 

these comments do not appear in the NPRM. (NAM, pp. 23-27) 

First set of examples: 

 1. NAM contends that EPA did not fully present the CASAC O3 Panel’s concerns about 

the utility of time-series mortality studies and whether use of such studies allows us to 

confidently attribute observed effects specifically to individual pollutants. 

2. NAM contends that EPA did not fully present the CASAC O3 Panel’s concerns about 

the limited information on the specific chemical composition, toxicity and, equally 

importantly, the population exposure of oxidant pollutants other than O3. 

3. NAM contends that EPA did not fully present the CASAC O3 Panel’s comments 

concerning inclusion of health endpoints in the risk assessment and the CASAC advice to 

qualitatively discuss other health endpoints. 

Second set of examples: 

4. NAM contends that EPA did not fully include in the proposal notice CASAC’s 

comments concerning exposure measurement error which were expressed in CASAC’s 

letter on the final Criteria Document (Henderson, 2006b, pp.3-4) and that in NAM’s view 

these CASAC comments support the view that 1) data from ambient monitors yield 

upwardly biased estimates of risk, 2) personal exposure cannot be correlated with 

ambient exposures and thus associations between data from ambient monitors and 

mortality are spurious, and 3) that short-term studies do not provide supportive evidence 

that positive associations in time series results are true. 

5. NAM contends that EPA did not present the CASAC O3 Panel’s comment that O3

measurement error would be expected to upwardly bias estimates of risk and have a 

substantial impact on the ability to detect a threshold of the concentration-response 

relationship below which no ozone effects are discernible. NAM also contends that this 

aspect of O3 measurement error would undermine EPA’s risk assessment. 

6. NAM contends that EPA did not present in the proposal notice CASAC’s comments 

recommending an alternative approach to calculate risks relative to the current standard 

which would avoid the problem of estimating PRB. 
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7. NAM contends that EPA did not present in the proposal notice CASAC’s comments 

on the final Criteria Document (Henderson, 2006b, p. 4) that NAM states support 

conclusions that “attributing the observed associations between ozone and mortality in 

time-series studies masks the underlying factor(s) actually responsible” (NAM, p.27) and 

“If ozone is not the relevant factor, and its control will not serendipitously reduce the 

relevant factor(s) then the risk reductions predicted by EPA will not be realized” (NAM, 

p. 27). 

Response: EPA strongly denies NAM’s contention that it demonstrated presentational 

bias. As an initial matter, EPA is not required to quote verbatim all of an important 

comment made by the CASAC O3 Panel. Doing so in the Staff Paper or NPRM could 

have the effect of obstructing clear communication of the concepts involved rather than 

facilitating communication. Most of the examples listed above were comments made by 

the CASAC O3 Panel to point out issues that were not fully addressed in the final Criteria 

Document that it wanted to have addressed in the final Staff Paper. The issues were fully 

addressed in the final Staff Paper and thoroughly discussed in the NPRM. If these issues 

had not been fully addressed, the CASAC O3 Panel would have noted that in its final 

review of the Staff Paper, but it did not. Instead it praised the final Staff Paper in its 

March 26, 2007 letter: 

Members of the CASAC Ozone Review Panel were pleased to review EPA’s 

Final Ozone Staff Paper. The members of CASAC and the Ozone Panel were 

unanimous in their praise of both the responsiveness of the Agency to our 

previous recommendations and of the clarity of this document. (Henderson, 

2007) (emphasis added) 

With respect to the specific examples cited by NAM, EPA’s responses are given below. 

First set of examples: 

1. Contrary to NAM’s contention, EPA fully presented the CASAC O3 Panel’s views on 

the utility of time-series studies, and addressed this issue in both the Staff Paper and the 

NPRM. In section 3.4 of the Staff Paper, EPA described important issues related to 

assessment of epidemiological studies and this included discussion of NAM’s examples 

1, 5 and 2 above, respectively: the general issue of the utility of time-series 

epidemiological studies in assessing the risks from exposure to O3 and other criteria 

pollutants, as well as related issues about exposure measurement error in O3 mortality 

time-series studies and O3 as a surrogate for the broader mix of photochemical oxidant 

pollution in time-series studies. EPA further goes on to note that the implications of 

these three issues for staff conclusions about the adequacy of the current O3 NAAQS and 

the identification of options for consideration are considered in Chapter 6. 

With regard to whether use of time-series studies allows us to confidently attribute 

observed effects specifically to individual pollutants, in section 6.3.4.1 of the Staff Paper, 

on the evidence-based considerations in selecting the level of the standard, staff generally 

concludes that: 
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Toward the lower end of the range of O3 concentrations observed in such studies, ranging 

down to background levels, however, we conclude that there is increasing uncertainty as 

to whether the observed associations remain plausibly related to exposures to ambient O3, 

rather than to the broader mix of air pollutants present in the ambient atmosphere. (EPA 

2007a, p.6-61) 

This conclusion is carried over to section II.D.4.a, the discussion of the evidence based 

considerations from the Staff Paper the level section in the NPRM (72 FR 37875). The 

uncertainty about whether observed associations remain plausibly related to exposures to 

ambient O3 at the lower end of the range was among the uncertainties that were included 

in the rationale for concluding that a standard level below 0.070 ppm would not be 

appropriate. In this rationale the Administrator judged that evidence of a causal 

relationship between adverse health outcomes and O3 exposures becomes increasingly 

uncertain at lower levels of exposure. (72 FR 37880) 

Moreover, EPA highlights this issue in section 6.4 of the Staff Paper as a key uncertainty 

that merits more research in the future. In this section staff notes: 

Most epidemiological studies of short-term exposure effects have been time-series studies 

in large populations. Time-series studies remain subject to uncertainty due to use of 

ambient fixed-site data serving as a surrogate for ambient exposures, to the difficulty of 

determining the impact of any single pollutant among the mix of pollutants in the ambient 

air, to limitations in existing statistical models, or to a combination of all of these factors. 

Independent variables for air pollution have generally been measurements made at 

stationary outdoor monitors, but the accuracy with which these measurements actually 

reflect subjects’ exposure is not yet fully understood. Also, additional research is needed 

to improve the characterization of the degree to which discrepancy between stationary 

monitor measurements and actual pollutant exposures introduces error into statistical 

estimates of pollutant effects in time-series studies. (EPA 2007a, p. 6-89) 

2. Contrary to NAM’s contention, EPA fully presented the CASAC O3 Panel’s views on 

the limited information on the specific chemical composition, toxicity and the population 

exposure of oxidant pollutants other than O3, and addressed this issue in both the Staff 

Paper and the NPRM. As noted above, EPA first described this issue in section 3.4 of the 

Staff Paper. In section 6.3.2 of the Staff Paper, in the discussion of the most appropriate 

surrogate for ambient photochemical oxidants, EPA again discusses this issue. In section 

6.3.6 of the Staff Paper, summary of staff conclusions and recommendations on the 

primary O3 NAAQS, staff concludes:

It is appropriate to continue to use O3 as the indicator for a standard that is 

intended to address effects associated with exposure to O3, alone or in 

combination with related photochemical oxidants. Based on the available 

information, and consistent with the views of CASAC and public commenters, we 

concluded that there is no basis for considering any alternative indicator at this 

time. Staff notes that while the new body of time-series epidemiological evidence 

cannot resolve questions about the relative contribution of other photochemical 
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oxidant species to the range of morbidity and mortality effects associated with O3

in these types of studies, control of ambient O3 levels is generally understood to 

provide the best means of controlling photochemical oxidants in general, and thus 

of protecting against effects that may be associated with individual species and/or 

the broader mix of photochemical oxidants, independent of effects specifically 

related to O3. (Staff Paper, p. 6-85) 

The CASAC O3 Panel obviously endorsed this assessment because in its letter on the 

final Staff Paper it notes that the panel, “agreed with the choice of indicator, statistical 

form and averaging time for the primary Ozone NAAQS suggested by Agency staff.” 

(Henderson, 2007) 

However, the CASAC O3 Panel further noted that “There is an urgent need to fund more 

research on the effects on sensitive subpopulations of low levels of the photochemical 

oxidant mixture for which ozone is used as a surrogate. More information on the effects 

of low levels of oxidant mixtures on public health is essential to inform the future 

decision-making process.” (Henderson, 2007) This view about the need for additional 

research mirrored the view expressed by EPA Staff in Section 6.4 of the Staff Paper, 

summary of key uncertainties and research recommendations related to setting a primary 

O3 standard, which noted: 

The extent to which the broad mix of photochemical oxidants and more generally 

other copollutants in the ambient air (e.g., PM, NO2, SO2, etc.) may play a role in 

modifying or contributing to the observed associations between ambient O3 and 

various morbidity effects and mortality continues to be an important research 

question. Ozone has long been known as an indicator of health effects of the 

entire photochemical oxidant mix in the ambient air and has served as a surrogate 

for control purposes. A better understanding of sources of the broader pollutant 

mix, of human exposures, and of how other pollutants may modify or contribute 

to the health effects of O3 in the ambient air, and vice versa, is needed to better 

inform future NAAQS reviews. (Staff Paper, p. 6-88) 

In the NPRM, the issue of the limited information on the specific chemical composition, 

toxicity and the population exposure of oxidant pollutants other than O3 was discussed in 

section II.D.1 on the indicator for the primary standard. (72 FR 37872) 

3. EPA rejects NAM’s contention that EPA did not present the CASAC O3 Panel’s 

comments in the proposal notice regarding CASAC’s advice on health effects which it 

should discuss qualitatively. In the proposal notice EPA states, 

However as noted by CASAC (Henderson, 2007) and in the Staff Paper, there are a 

number of health endpoints (e.g., increased lung inflammation, ...and increased school 

absences) for which there currently is insufficient information to develop quantitative risk 

estimates, but which are important to consider in assessing the overall public health 

impacts associated with exposure to O3. (72 FR 37856) 
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With respect to the first part of the CASAC letter quote that EPA omitted, CASAC was 

simply agreeing that the health endpoints based on epidemiological evidence that EPA 

included in its risk assessment were appropriate. EPA stated in the proposal notice that 

“the CASAC O3 Panel concluded “... that the selection of health endpoints for inclusion 

in the quantitative risk assessment was appropriate” (72 FR 37856) 

Second set of examples: 

4. EPA rejects NAM’s contention that EPA did not fully discuss the issues raised by 

CASAC with respect to the role of exposure measurement error in O3 mortality timeseries studies. EPA does not agree with the set of conclusions that NAM draws from the 

CASAC comments with regard to whether this issue undermines the use of 

epidemiological studies in risk assessment. Rather, EPA concludes that until more data 

on personal O3 exposure becomes available, the use of routinely monitored ambient O3

concentrations as a surrogate for personal exposures is not generally expected to change 

the principal conclusions from O3 epidemiologic studies. Therefore, population health 

risk estimates derived using ambient O3 levels from currently available observational 

studies, with appropriate caveats about personal exposure considerations, remain useful. 

As noted in the general response to this comment, evidently the CASAC O3 Panel agreed 

with this assessment in the final Staff Paper. Far from downplaying this issue, EPA 

highlights it again in section 6.4 of the Staff Paper as a key uncertainty that merits more 

research in the future. (EPA 2007a, p. 6-88) The discussion of measurement error and 

the overall conclusion about the usefulness of epidemiological studies in estimating 

population risk can be found in section II.A.3.a, assessment of evidence from 

epidemiological studies, in the proposal notice (72 FR 37838). 

5 and 7. EPA rejects NAM’s contentions that EPA did not present the CASAC O3

Panel’s comments that O3 measurement error would be expected to have a substantial 

impact on the ability to detect a threshold of the concentration-response relationship 

below which no ozone effects are discernible and that attributing the observed 

associations between O3 and mortality in time-series studies masks the underlying 

factor(s) actually responsible. EPA also disagrees with NAM’s contention that this issue 

undermines EPA’s risk assessment. 

EPA has thoroughly discussed the issue of measurement error and the impact on the 

ability to detect a threshold in section 3.4 of the Staff Paper. In this section, EPA notes 

that: 

...the use of ambient O3 concentrations may obscure the presence of thresholds in 

epidemiologic studies (CD p. 7-9). Brauer et al. (2002) concluded that surrogate 

measures of exposure, such as those from centrally located ambient monitors, that 

were not highly correlated with personal exposures obscured the presence of 

thresholds in epidemiologic studies at the population level, even if a common 

threshold exists for individuals within the population. (Staff Paper, p. 3-41) 

With regard to whether the issue of exposure measurement error undermines the use of 

epidemiological studies in risk assessment, EPA reaches a different conclusion than 
156

NAM. EPA concludes that until more data on personal O3 exposure becomes available, 

the use of routinely monitored ambient O3 concentrations as a surrogate for personal 

exposures is not generally expected to change the principal conclusions from O3

epidemiologic studies. Therefore, population health risk estimates derived using ambient 

O3 levels from currently available observational studies, with appropriate caveats about 

personal exposure considerations, remain useful. As noted in the general response to this 

comment, evidently the CASAC O3 Panel agreed with this assessment in the final Staff 

Paper. Far from downplaying this issue, EPA highlights it again in section 6.4 of the 

Staff Paper as a key uncertainty that merits more research in the future. (EPA 2007a, p. 

6-88) The discussion of measurement error obscuring population thresholds and the 

overall conclusion about the usefulness of epidemiological studies in estimating 

population risk can be found in section II.A.3.a, assessment of evidence from 

epidemiological studies, in the proposal notice. (72 FR 37838) 

6. EPA has included CASAC’s comments related to PRB and its suggested alternative 

approach and EPA’s response to this comment above in section II.A.5 (see comment 

number (20)). 

 

(4) Comment: NAM claims that it is a violation of the information quality standard of 

objectivity to use terms such as "likely" in ways that conflict with their actual use in 

appropriate context or without clear definition. NAM contends that EPA must establish 

clear rules and procedures for how such terms will be used based on the following 

principals: (1) where possible assign quantitative values to statements about likelihood to 

reduce interpretative heterogeneity, (2) the values assigned by EPA to likelihood 

statements and probability descriptors must be consistent with both intuition and 

scientific research about such terms, (3) to adhere to applicable information quality 

standards EPA must at a minimum make transparent what it means when it uses 

likelihood statements and probability descriptors, and (4) EPA must have full and 

complete documentation of what it proposes and subject its work to pre-dissemination 

review (such as peer review by qualified psychologists). 

Response: EPA agrees that where available information provides a basis for assigning 

quantitative values to probabilistic statements that it is generally appropriate to do so. On 

the other hand, EPA does not agree that it is appropriate to interpret information in 

quantitative terms if available information does not provide a basis to do so, which would 

have the effect of communicating a higher degree of precision than is warranted, or that 

the Information Quality Guidelines either require such an interpretation or that EPA 

establish clear rules and procedures for how commonly used probabilistic terms will be 

used in a NAAQS review. The commenter specifically refers to EPA’s use of the term 

“likely” as an example of a probabilistic statement that should be assigned quantitative 

values. EPA disagrees. EPA has used this and other similar types of words throughout 

the relevant documents based on their common definitions when appropriate, in the 

absence of information that would support a more quantitative statement. In so doing, 

EPA has been consistent in using such words and has explained the scientific and logical 

basis for the statements in which such words appear. For example, the word “likely” is 

intended to convey its common meaning, i.e., having the qualities or characteristics that 
157

make something probable. This meaning reflects a judgment, for which EPA provides a 

reasoned basis in these documents. NAM has not identified any specific instance in 

which the Agency’s use of terms such as “likely” or “unlikely” is not consistent with the 

common meaning of these terms. EPA does not agree that the process that NAM 

suggests would add to the accuracy, clarity, completeness, or unbiased dissemination of 

information in NAAQS reviews or would be an appropriate use of Agency resources. 

(5) Comment: One commenter (NAM, pp. 47-49) contends that EPA used default values in 

its assessments and that this violates information quality principles. 

Response: EPA rejects NAM’s contention that it used default values in its assessments. 

More specifically, EPA used the best available scientific information and included 

distributions based on available scientific and technical data in its exposure and health 

risk assessments to characterize variability. Further, the commenter offered no specific 

examples of where EPA used default values. 

(6) Comment: One commenter (NAM, pp. 20-21, 56 fn. 31) states that EPA needs to draw a 

distinction between studies included in the last review (“old” studies) and subsequent 

studies (“new” studies). EPA should discuss old studies only to set the stage for the 

review of new studies, since the Administrator's charge under section 108 and 109 is to 

utilize the best available new scientific information. None of the old studies has utility in 

deciding in this review whether to change the standard, absent some finding of error or 

other reason to change the prior evaluation of the old study. CASAC’s advice includes 

reference to various studies published between 1988 and 1993, noting that the relevance 

of these studies is unclear given CASAC’s charge to focus on new research. 

Response: EPA disagrees with the construct suggested by the commenter, on both legal 

and scientific grounds. Section 108 calls for the air quality criteria to “accurately reflect 

the latest scientific knowledge useful in indicating the kinds and extent of all identifiable 

effects on public health or welfare.” EPA implements this charge by reviewing the 

newest scientific information, and conducting this review not in isolation but by 

synthesizing and integrating the newest information with the prior scientific knowledge. 

An integrated synthesis of the entire body of evidence allows all of the evidence to be 

evaluated in context, without artificially segregating new from old information. It allows 

EPA to draw the most appropriate implications and conclusions from the evidence when 

seen as a whole. The commenter’s approach would instead call for freezing our 

understanding of the information gained from the “old” studies, and would not allow 

EPA to fully evaluate what the old studies teach us in drawing proper implications from 

the entire body of evidence. The commenter’s approach is not grounded in scientific 

principles, and would interfere with developing the most useful analysis of the evidence. 

The commenter’s approach is neither required nor appropriate. 

(7) Comment: One commenter (NAM, pp. 45, 65) stated that the overall result of various 

errors in the risk assessment is that the Administrator has been misled to believe that the 

risk estimates are much more certain than they actually are. For these and various other 

errors, the risk assessment should only be used for purposes of a screening level 
158

assessment, and should not be used for making the important public health decision in 

this review. 

Response: In both the preamble and this Response to Comments document EPA has 

responded to a wide variety of comments on the risk assessment, as well as comments on 

the Staff Paper and Criteria Document. The exposure and risk assessment, the Staff 

paper and the Criteria Document have all carefully identified the many sources of 

uncertainty in the science or the analysis reported. Throughout the development of these 

documents EPA received comments on many of these same issues, and addressed them 

appropriately in many cases by recognizing and describing or otherwise characterizing 

the uncertainties. 

As in prior NAAQS reviews, the degree of uncertainty in the science and the analyses 

developed using the science is a critical component of decision making by the 

Administrator. In this review the Administrator has been fully aware of all of these 

sources of uncertainty. He has taken them into account in making provisional decisions 

in the proposal, as well as in making decisions in the final rule. For example, 

uncertainties associated with the exposure and risk assessment results was discussed 

extensively in the proposal (See e.g. 72 FR 37851, 37852, 37856, and 37862). The 

Administrator explained that he took these uncertainties into consideration when 

evaluating the adequacy of the current standard, and when evaluating what range of 

standards would be appropriate (72 FR 37871, 37880). As described in the preamble to 

the final rule, the Administrator has fully considered the uncertainties in the science and 

in the exposure and risk assessment. Based on this consideration, he has placed primary 

emphasis on the scientific evidence and implications drawn from it. He has also placed 

more emphasis on the exposure assessment than the risk assessment. This reflects a 

reasoned approach that considers and evaluates the uncertainties, and places more weight 

where there is more certainty and less weight where there is less certainty. The lengthy 

public process leading to this final rule has provided a full and comprehensive review of 

both the science and the various analyses based on the science, as well as the type and 

degree of uncertainties in each of these areas. 

(8) Comment: One commenter, NAM, submitted a Request for Correction (RFC) concerning 

certain information it claims was disseminated by EPA in its proposal notice. In its RFC, 

NAM describes numerous alleged information quality errors in the description, analysis, 

and presentation of scientific information and information quality errors in the 

assessment of human health risks. NAM also claims the existence of information quality 

errors in the consideration of reports from CASAC, in the rollback assumption, and in the 

description of PRB. 

Response: The RFC has been treated as a comment on our proposal notice. EPA has 

reviewed NAM’s RFC and finds that there is no merit to their objections. EPA disagrees 

with NAM’s allegations that EPA has not complied with the requirements of the 

Information Quality Act or the Agency's policies for ensuring information quality. EPA 

has responded to NAM’s significant comments in the preamble to the final rule or in this 

document. 
159

(9) Comment: Some commenters argued that EPA has not provided any rational justification 

for disagreeing with CASAC’s recommendations, in violation of the requirements of 

section 307 (d) (ALA et al.). 

Response: The EPA disagrees with this characterization of its explanation at proposal, 

and refers also to its detailed response in sections II.A regarding decisions not to accept 

CASAC’s recommendations regarding the level of the 8-hour standard for O3. 

(10) Comment: The standards must protect these vulnerable populations – including persons 

with heart disease, hypertension, diabetes, and chronic bronchitis or asthma -- with an 

adequate margin of safety, the same standards that apply to the general population (ALA 

et al.). 

Response: The EPA agrees with this comment, and has carefully considered effects on 

vulnerable subpopulations in considering whether and how to revise the O3 NAAQS (See 

e.g. section II.A.2). 

(11) Comment: Some commenters (e.g., ALA et al.) argued that EPA must adopt a 

precautionary approach to the standard setting process, and set standards in a manner that 

deals with uncertainty not by ignoring uncertain effects but rather by protecting against 

adverse health effects even where those effects may be uncertain. In support of its

argument, the ALA et al. specifically cited ATA III, 283 F. 3d at 369 (EPA must 

promulgate protective NAAQS even where risks cannot be qualified or precisely 

identified) and Lead Industries, 647 F. 2d at 1155 (requiring EPA to wait until it can 

conclusively demonstrate that a particular effect is adverse to human health is 

inconsistent with the statute’s preventative and precautionary orientation). 

Response: The EPA agrees generally with this comment, but notes further that a general 

invocation of precautionary principles does not determine where in the range of 

reasonable values EPA could establish the level of a standard --in this case, the 8-hour 

average O3 standard. Section II.C.4 to the preamble to the final rule explains in detail 

why it is appropriate to set the level of the 8-hour standard at 0.075 ppm. The EPA notes 

further that this choice is consistent with case law in the D.C. Circuit (not cited by the 

commenter) that the Administrator is to carefully examine all of the relevant studies in 

the record, but need not base the level of the standard on either the highest or lowest 

value in these studies. Rather, an informed judgment is called for. API, 665 F. 2d at 

1187; NRDC v. EPA, 902 F. 2d 962, 970. Section II.C.4 to the preamble to the final rule 

states the basis for the Administrator’s exercise of informed judgment here, in particular, 

setting the level of the 8-hour standard below the level at which health effects related to 

O3 have been clearly demonstrated to occur (i.e. at and above 0.080 ppm) in controlled 

human exposure studies. 

Far from “ignoring uncertain effects,” the Administrator has focused closely on the issue 

of “uncertain effects” in determining where the 8-hour level should be set, recognizing 

the significant uncertainty over whether adverse effects occur from exposure at various 
160

ambient levels of O3. As discussed above, Lead Industries is not on point as the issue in 

that case concerned when an effect should be considered adverse, and the authority to 

determine that an effect was adverse before there was clear evidence that the effect was 

harmful. Here there is no issue that mortality and serious morbidity are adverse. 

(12) Comment: Environmental Defense commented that EPA’s proposed alternative to set 

the secondary standards at the same level as the primary standard flouts the 

recommendations of both CASAC and Staff, and is scientifically unsupportable. The 

commenter stated that EPA provides no reasoned basis for rejecting CASAC’s 

recommendation on this score, and that EPA concedes that the cumulative seasonal 

W126 standard is the most biologically relevant way to protect against adverse welfare 

effects on vegetation. Environmental Defense claims that EPA cites no scientific or other 

rational relationship between the proposed primary standards and protection of vegetation 

against adverse welfare effects. Because there is no rational connection between the 

proposed primary standard and the level of protection needed to protect vegetation 

against adverse O3-induced welfare effects, any EPA finding that the primary standards 

would be sufficient for secondary standards purposes would be arbitrary. The most that 

EPA asserts is that there could be significant overlap in the areas protected by the 8-hour 

and W126 forms, and that the proposed primary standards. 

Response: EPA agrees that the W126 form is currently the most biologically relevant 

form available for reflecting vegetation response to O3 exposures. However, EPA does 

not agree that a biologically relevant form is a mandatory requirement in setting a 

secondary standard, under all circumstances. Indeed, EPA has a long history of judging 

that a secondary standard set identical to the primary standard form and level will be 

requisite to protect public welfare, based on the entire body of information available at 

that time. This judgment has often been made, in large part, as a result of the often 

significant uncertainties that remain regarding what combination of form and level are 

most appropriate for a secondary standard, as was the case at the conclusion of the last O3

NAAQS review in 1997. EPA’s reasons for adopting an 8-hour average standard are 

discussed in the preamble. 

(13) Comment: Environmental Defense commented that EPA’s proposal to set a W126 

secondary standard in the range of 7-21 ppm-hrs unlawfully and arbitrarily departs from 

CASAC’s recommendation and the supporting science. The commenter stated that the 

Act and settled principles of administrative law require EPA to provide a reasoned 

justification for departing from CASAC’s recommendation with respect to the upper 

bound of the proposed W126 standard and EPA has failed to provide such a justification 

here. The Agency merely asserts that “[g]iven the uncertainty in determining the risk 

attributable to various levels of exposure to O3, the Administrator believes as a public 

welfare policy judgment that this is a reasonable range to propose” 72 Fed. Reg. 37,903. 

The commenter claimed that this bare assertion is grossly deficient as a basis for 

departing from CASAC’s recommendation, as described in paragraphs (a) through (c) 

below. 
161

(a) The commenter asserted that EPA fails to identify its basis for claiming uncertainty 

in determining the risk attributable to various O3 levels or explain why the degree of 

alleged uncertainty is so great as to render the findings of adverse effects at those levels 

improbable. The agency cites no facts supporting the claim of uncertainty and does not 

explain any rational connection between the degree of alleged uncertainty and specified 

levels of the standard. The agency does not show, nor does the record support a finding 

that uncertainty of the evidence of adverse effects at 15 ppm-hours is materially greater 

than at 21 ppm-hours, or that any alleged uncertainty of adverse effects at 15 ppm-hours 

is so great as to render adverse effects at that level improbable. To the contrary, the 

record shows that conclusions of a consensus workshop of independent scientists that 

limits below 15 ppm-hours are requisite to protect against adverse effects to vegetation. 

72 Fed. Reg. 37902/2. Evidence in the Criteria Document and analysis in the Staff paper 

provides further support for these consensus recommendations, and indeed the Staff 

found nothing in more recent information to call these recommendations into question. 

(b) EPA does not meet its burden of rationally justifying its choice of standards and its 

rejection of CASAC’s recommendation merely by asserting that its decision is a “policy 

judgment.” The Criteria Document and other evidence in the record support a finding of 

adverse welfare effects on vegetation at W126 levels at and below 15 ppm-hours. To 

justify setting the secondary standard at a higher level than that, EPA must provide a 

reasoned justification for disregarding or giving limited weight to the studies and 

scientific findings of adverse effects at and below 15, and for rejecting CASAC’s 

recommendation. 

(c) Based on the evidence of adverse welfare effects on vegetation from O3 levels as low 

as 7 ppm-hours, EPA must set the secondary standard at the lowest end of the range. 

Section 109 (b) (2) of the Act requires EPA to set the secondary standard at a level 

“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.” Because the record 

documents known or anticipated adverse O3 welfare effects on vegetation at levels of 7 

ppm-hours (and even below), EPA must set the standard at or below that level. 

Response: Congress explicitly recognized that in making judgments about how to use 

uncertain evidence to set standards, the Administrator may not always agree with his 

scientific advisors, see CAA 307(d)(3), but EPA agrees that where the NAAQS differs in 

any important respect from the advice of CASAC, it must provide an explanation of the 

reasons for such differences. EPA fully considered CASAC’s advice with regard to the 

range of W126 levels proposed, as is clear from the expansion of the original range 

identified in the second draft Staff Paper (range 13 to 21 ppm-hours) to include the lower 

end of the CASAC recommended range (7 ppm-hours), and explained that the level 

selected within the range of 7 to 21 ppm-hrs is largely a policy judgment as to the 

requisite level of protection needed. Specifically, the Staff Paper states “In the absence 

of any information regarding a threshold of O3 exposures for vegetation, staff recognizes 

that the level selected is largely a policy judgment as to the requisite level of protection 

needed. In determining the requisite level of protection for crops and trees, the 

Administrator will need to weigh the importance of the predicted risks of these effects in 
162

the overall context of public welfare protection, along with a determination as to the 

appropriate weight to place on the associated uncertainties and limitations of this 

information.” (EPA, 2007a) 

(a) With regard to the Commenter’s assertion that EPA fails to identify its basis for 

claiming uncertainty in determining the risks attributable to various O3 levels, EPA refers 

the Commenter to the Staff Paper discussions regarding the nature and scope of 

uncertainties associated with the exposure (Staff Paper, pp.7-34 to 7-37), risks (Staff 

Paper pp. 7-43 to 7-47 for crops; 7-69 to 7-70 for trees,) and benefits (Staff Paper, pp. 7-

52 to 7-53) assessments as well as similar discussions in parallel sections of the proposal 

notice (e.g., 72 FR 37897). The uncertainties associated with each of these assessments 

translate into uncertain levels of risks to vegetation for each of the different air quality 

scenarios evaluated. EPA, in being careful to discharge its mandate to provide the 

requisite level of public welfare protection, i.e. sufficient but not more than necessary, 

took into account to the best of its ability, all the information it had available to help 

inform its judgments on requisite protection. EPA’s intention to do so is clearly 

articulated throughout the proposal notice (e.g., 72 FR 37904/5). EPA notes that the 

uncertainties associated with the exposure and risk assessments affect the predictions of 

risk to vegetation at different levels equally, so they do not, by themselves, make the risks 

at one level of exposure any more or less probable than another. What they do show, 

however, is that at lower and lower levels of O3 air quality, remaining risks to vegetation 

appear to decline so that the relative risks among the different air quality scenarios can be 

compared to each other. 

However, in addition to comparing the relative risks of effects occurring at any given 

level, EPA must make a further determination as to the significance of those remaining 

risks to the public welfare and at what level those risks could reasonably be considered 

adverse to the public welfare. Thus, it is not only the uncertainty associated with 

reductions in the presence of effects but the uncertainties associated with the degree of 

public welfare impact of those reduced levels of effect that must be weighed. 

(b) Based on the statutory language in the section 109(b) (2) of the CAA, EPA notes that 

Congress clearly envisioned a role for “the judgment of the Administrator” in identifying 

the “requisite level of protection” for the public welfare. As stated in the proposal notice, 

“the level selected is largely a policy judgment as to the requisite level of protection 

needed. In determining the requisite level of protection for crops and trees, the Staff 

Paper recognizes that it is appropriate to weigh the importance of the predicted risks of 

these effects in the overall context of public welfare protection, along with a 

determination as to the appropriate weight to place on the associated uncertainties and 

limitations of this information.” (72 FR 37903). Comments received following proposal 

further helped inform EPA’s judgments both as to the likelihood of predicted risks 

occurring and potential adversity in the context of public welfare. In particular, 

comments regarding the significance of the uncertainties and limitations associated with 

the exposure and risk assessments, as well as the field based data, helped inform EPA’s 

judgments regarding how much weight to place on these uncertainties, in reaching a 

decision regarding what standard is requisite to protect the public welfare. 
163

EPA disagrees that it has not provided a reasoned justification for departing from the 

CASAC recommended form and range. This justification is described in the proposal 

notice and further refined in the preamble to the final rule to take into account comments 

received on the proposal notice. The Administrator notes that he is in general agreement 

with the CASAC Panel’s views concerning the interpretation of the scientific evidence. 

The Administrator also notes that there is no bright line clearly directing the choice of 

standard for any of the effects of concern, and the choice of what standard is appropriate 

is clearly a public welfare policy judgment entrusted to the Administrator. This judgment 

must include consideration of the strengths and limitations of the evidence and the 

appropriate inferences to be drawn from the evidence and the exposure and risk 

assessments. In reviewing the basis for the CASAC Panel’s recommendations for the 

form and range of the secondary O3 standard, the Administrator observes that the 

CASAC Panel apparently placed appreciable weight on the combined science and policy 

views contained in a report from a 1996 consensus building workshop held by a group of 

independent scientists to inform its policy judgments on standard levels that would be 

protective against various types of O3-related effects. While the Administrator finds the 

views expressed in that report to be relevant and of interest, he does not see in that report 

clear linkages between the underlying scientific information and the recommended 

standard levels. Lacking such linkages, the Administrator can find no appropriate 

scientific basis for deferring to the policy judgments reflected in that report. Similarly, in 

presenting their recommendations, the CASAC Panel did not provide clear linkages 

between their interpretation of the scientific evidence, the substantial uncertainties 

associated with that evidence, and their recommended range of levels. The Administrator 

more heavily weighs the implications of the uncertainties associated with the scientific 

evidence and with the Agency’s vegetation exposure and risk assessments than the 

CASAC Panel apparently does, and disagrees with CASAC that the evidence and 

assessment results appropriately serve as a basis for concluding that a seasonal standard 

with a level no higher than 15 ppm-hours is required for an annual standard, or that an 

even lower level is required for a standard averaged over three years. 

After carefully taking the above comments and considerations into account, and fully 

considering the scientific and policy views of the CASAC, the Administrator has decided 

to set the secondary standard equal to the primary standard, as discussed in the preamble. 

(c) EPA disagrees that it must set the standard at the lowest level for which there are 

known adverse effects. As stated above in (b), the CAA does not require that secondary 

standards be set at a zero-risk level, but rather at a level that reduces risk sufficiently but 

not more than what is necessary to protect public welfare from known or anticipated 

adverse effects. EPA further notes that the same effect may have different degrees of 

adversity to the public welfare, depending on the intended use of the plant and where it is 

growing. In addition, in concluding that the appropriate range for EPA to consider was 

between 7-15 ppm-hours, the CASAC Panel, as stated in (b) above, apparently placed 

appreciable weight on the combined science and policy views contained in a report from 

a 1996 consensus building workshop held by a group of independent scientists to inform 

its policy judgments on standard levels that would be protective against various types of 
164

O3-related effects. However, though EPA found the views expressed in that report to be 

relevant and of interest, as stated in section II.B.2.c above, it concludes that these views 

fall far short of providing a scientific basis for determining at what level these effects 

become adverse to the public welfare. 

(14) Comment: EPA also asks for comment on setting differing levels of protection for 

different types of vegetation. Because EPA has not proposed the specific levels for such 

a proposal, or methods for implementing it, the agency cannot pursue it further without 

additional notice and comment. 

Response: EPA agrees that should such an alternative approach have been chosen, EPA 

may have needed to issue a supplemental proposal providing more detail on a proposed 

approach. EPA notes that since the Agency did not choose this alternative path, such a 

supplemental proposal is not necessary. 

(15) Comment: UARG states in a footnote that “EPA has previously noted that ‘striking 

anomalies arise in attempting to set welfare-based air quality standards according to some 

welfare effects but not others.’ 49 Fed. Reg. 10,408, 10,417 (March 20, 1984). The 

Agency did not then resolve how such anomalies should be addressed. Nor has the 

Agency ever considered whether and how the beneficient [sic] effects of a pollutant (e.g., 

protection provided by tropospheric O3 against UV-B radiation-related health effects such 

as cataracts and melanoma) should be considered in selecting a secondary NAAQS that 

differs from the primary one. Should the Administrator decide in this rulemaking to set a 

secondary standard different from the primary one, these are issues that he would be 

compelled to address. 

Response: In the 1984 notice of proposed rulemaking cited by UARG, the question as to 

whether EPA could consider the costs of implementation in setting the secondary 

standard had not been resolved by a court. Although EPA explained that the better view 

of the CAA was that EPA could not consider costs in setting the standard, it noted that it 

was uncertain whether a court would reach the same conclusion. The “striking 

anomalies” noted by EPA arose from the possibility that EPA could consider the costs of 

implementation in setting a secondary NAAQS. As the Supreme Court has now 

resolved the issue of whether EPA may consider the costs of implementation in setting a 

secondary standard, the Agency need not resolve how such “anomalies” described in the 

1984 NPRM should be addressed. 

B. Misplaced Comments 

Some comments received on the proposed O3 NAAQS addressed issues that are not 

relevant for consideration in the review of the NAAQS. These include several comments that 

address implementation issues. In addition to comments related to implementation of the O3

NAAQS that are generally addressed in section I.C of the preamble to the final rule, these 

comments and other “misplaced” comments are discussed more fully below. 
165

(1) Comment: Many commenters noted that the current standard has not yet been fully 

implemented and felt that EPA should allow time for existing regulations to work before 

revising the ozone standard. State agencies and industry have spent years planning and 

implementing strategies for how best to implement reductions mandated by current 

regulatory programs, and a revised standard could undo much of that planning. 

Numerous commenters expressed concern over the substantial burden placed on states to 

adopt a new set of implementation plans. Further, state plans to achieve a revised 

standard would probably be due in 2013, which is in the middle of the current attainment 

effort and before the results of current activities will be known. Several commenters 

believed that more significant public health gains can be achieved by focusing all 

resources on meeting the current 8-hour standard versus starting the SIP process over 

again. One commenter felt that EPA should not propose to lower the current 8-hour 

ozone standard until such time as NOx reductions from federal programs are realized. 

One commenter stated that a tighter ozone standard could discourage the use and 

development of greenhouse-gas-friendly energy and biofuels. The commenter believes 

that reducing reliance on imported fossil fuels and developing technologies to reduce 

greenhouse gas emissions is more important than a “marginal change in ozone levels.” 

(2) Comment: Numerous commenters from state environmental organizations, industry, and 

private citizens stated that they did not believe that the proposed standard was attainable. 

Several commenters expressed concern over the impact of additional nonattainment areas 

on regulatory agencies charged with planning for attainment of the new standards. 

Several commenters expressed concern that neither state agencies nor industry will be 

able to devise a successful compliance strategy for the proposed standard because the 

control technology does not exist. Others commented that as nonattainment counties 

become more rural, the choice of sources that can be controlled becomes very limited and 

offsets would not be as available, which would hinder the economy. 

(3) Comment: Several commenters representing industry and economic development 

associations felt that if the lower standard is not achievable, that it calls into question the 

validity of the asserted health benefits of such a standard. The Gulf Coast Lignite 

Coalition stated that the proposed standard was overly conservative and would not benefit 

the health of residents in many newly designated nonattainment areas that are relatively 

rural, large in size, and have a low population density. The Coalition did not believe that 

monitoring data was appropriate for estimating exposure. 

(4) Comment: Several organizations believed that international and interstate impacts on 

ambient ozone levels will likely result in more stringent requirements placed on facilities 

that are not significant contributors to local air quality. Other commenters stressed that 

improving air quality in areas affected by transport of ozone and ozone precursors 

depends largely on reducing ozone levels in areas currently in nonattainment. In some 

cases, reducing local production of ozone would not attain a lower standard. For 

example, the Associated Industries of Massachusetts indicated that Massachusetts will be 

in nonattainment for the foreseeable future if the standard was lowered to 0.070 ppm. 

The issue is a result of upwind pollution transported into Massachusetts and there are no 
166

further reductions that can be made. Similarly, the Gila River Indian Community asked 

that EPA acknowledge and address in the final rule the problem of identifying the 

Community as a nonattainment area when the largest source of ozone precursors is one 

over which the Community does not have jurisdiction.

(5) Comment: Several commenters questioned EPA’s focus on mean background rather than 

the extremes of the background, believing that it resulted in EPA’s failure to propose an 

attainable standard. Further, others mentioned that when EPA established the current 

primary standard for ozone, the EPA Administrator specifically rejected a standard of 

0.070 ppm as being too close to background levels. The AAM stated that reliance on one 

particular global model is not a scientifically sound way to estimate the contribution of 

uncontrollable ozone to an extreme value standard. Some industry groups believed that 

the proposed welfare standard should be dropped until the issue of background ozone 

levels and achievable ozone limits is better understood and assessed.

Response to Comments 1-5: Questions of implementation or attainability consequences 

of a NAAQS are legally irrelevant in determining which standards are requisite to protect 

public health with an adequate margin of safety. API v. Costle, 665 F. 2d at 1185-86. In 

addition, section 109(d) requires EPA to reevaluate the NAAQS no later than five years 

after completion of the last review, and determine whether new or revised NAAQS are 

appropriate in light of current science, as reflected in the updated air quality criteria. 

Issues of implementation or attainability are not a basis to delay conducting and finishing 

the review and making the decisions required under section 109(d). The EPA therefore 

did not consider these comments in its decision-making process. 

(6) Comment: Several organizations, including the American Association of State Highway 

and Transportation Officials and the Association of Metropolitan Planning Organizations, 

recommend that EPA initiate research to identify innovative new strategies and 

technologies including new federal emission control programs that will assist regional or 

multi-state nonattainment areas in meeting the existing standard or any new standard that 

is adopted. They also suggest that EPA address regional pollutant transport issues, 

including research, guidance on offsets, and attainment dates. The Fertilizer Institute 

recommended that chemical interactions that lead to ground-level ozone formation 

clearly need to be further studied prior to mandating further source reductions in 

precursor compounds.

(7) Comment: The Texas Department of Transportation commented that EPA should 

evaluate the effects and address the applicability of W126 on transportation and general 

conformity. If conformity does not apply, the commenter recommended that EPA 

provide a mechanism to exempt transportation programs from the conformity provision 

in areas where on-road mobile sources are not a significant contributor to the 

nonattainment problems, and also in areas where nonattainment is largely caused by 

ozone transport. The Washington Department of Ecology also commented about the 

implementation of the secondary standard, and stated that EPA needs to consult with and 

assist states that are inexperienced with dealing with a secondary standard. The National 

Association of Regional Councils also noted that creating two standards of evaluation 
167

would make planning infrastructure complicated; the same primary and secondary 

standard would be a simpler approach.

(8) Comment: Several organizations expressed concerns about how the implementation of a 

revised standard would be coordinated with other policies and programs. The U.S. 

Chamber of Commerce and several other organizations commented that the proposed 

NAAQS standard would be in force at the “Twenty in Ten” target date set for a 35-

billion-gallon renewable fuel standard and will last eight years past that date. The 

commenter believes that ozone precursors will rise significantly with the renewable fuels 

standard, which will impact compliance with the ozone NAAQS. 

(9) Comment: Several commenters, including the Indian Nations Council of Governments 

and others, recommended that EPA provide for better synchronization of various 

programs and policies at the federal level, including the Regional Haze Program, HeavyDuty Highway Rule, and Regional Transport from Ground-Level Ozone Program. 

Several commenters were concerned about the impacts that a revised standard would 

have on current NOx emission control activities under EPA’s NOx SIP call, CAIR, and 

Regional Haze Program (e.g., Best Available Retrofit Technology and reasonable 

progress). One commenter requested that EPA provide funding commensurate with that 

provided to these other air quality programs.

(10) Comment: Several commenters stated that designation of additional nonattainment areas 

would significantly impact the Congestion Mitigation and Air Quality Program. One 

commenter predicted that the revision could possibly create unfunded mandates for many 

regions. Local governments do not have the resources or controls to address the 

changing requirements. Another commenter suggested that program funding be 

increased and protected from budget cuts.

(11) Comment: With respect to implementing a revised standard, many commenters 

expressed that EPA needs to issue timely implementation guidance, identifying 

reasonable practical measures that can aid stakeholders, and work with state and local 

governments to develop national strategies to address ozone. They also noted that EPA 

should provide the maximum time allowed under the CAA to set the standards and 

implement and attain such standards. The South Carolina Department of Health and 

Environmental Control felt that the implementation process should reward and provide 

flexibility to programs that attain the standards on an accelerated basis.

(12) Comment: Numerous commenters asked that EPA consider simultaneous strengthening 

of other national policies/measures that affect ozone nationwide. Several felt that more 

stringent controls on mobile sources would be appropriate to help achieve the standard 

and avoid undue burden on stationary sources. One commenter stated that because 

mobile source emission controls rest solely with the federal government, the reductions 

needed to meet attainment under the current standard are greater than the amount of 

emissions that the State of Texas currently regulates. One commenter suggested that 

EPA further tighten standards for on-road heavy-duty and off-road new diesel engines to 

further reduce ozone levels. 
168

(13) Comment: One commenter recommended that if EPA revises the current standard that it 

should adopt SIP criteria to allow states to factor out background ozone and transported 

ozone from emission rollback requirements in their nonattainment SIPs. The commenter 

further suggested that EPA adopt an optional form of identifying reasonable progress 

toward attainment based on making reductions in the population and magnitude-weighted 

exposure to ozone levels remaining above the standard. 

(14) Comment: One commenter recommended that if EPA revises the current standard that it 

should adopt SIP criteria to allow states to factor out background ozone and transported 

ozone from emission rollback requirements in their nonattainment SIPs. The commenter 

further suggested that EPA adopt an optional form of identifying reasonable progress 

toward attainment based on making reductions in the population and magnitude-weighted 

exposure to ozone levels remaining above the standard. 

(15) Comment: Several commenters, including public citizens and industry organizations, 

suggested technologies and practices to help reduce ozone: hybrid cars, low emission 

engines, solar energy, low-carbon fuel, and a carbon tax. Other commenters called on 

EPA to make educational, modeling or policy changes to promote the integration of landuse and transportation planning and implementation. Another commenter was concerned 

about the potential consequences of expanded use of reformulated gasoline on refiners 

and consumers.

Response to Comments 6-15: As noted above, comments concerning implementation of 

a NAAQS are legally irrelevant in determining which standards are requisite to protect 

public health with an adequate margin of safety. API v. Costle, 665 F. 2d at 1185-86. 

The EPA therefore did not consider this comment in its decision making process. For the 

purpose of informing the public, a variety of information on control strategies is 

discussed in the RIA. 

(16) Comment: Numerous comments were received regarding significant issues associated 

with the Regulatory Impact Analysis (RIA), including the scope, assumptions and 

methodology, and additional analyses suggested. 

Response: Because the costs of implementation cannot be considered in setting or 

revising the NAAQS (see section I.B of the preamble to the final rule), the results of the 

RIA were not considered in EPA’s decisions on the O3 standards. For the same reason, 

comments on the RIA were not considered in the decisions. Comments on the Interim 

RIA were considered, as appropriate, in developing the RIA for the final rule. 
169

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Midwest Ozone Group (2007) Letter and Comments Sent to Docket No. OAR-2005-0172 re: 

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Docket No. OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality Standards 

for Ozone. Docket No. OAR-2005-0172-4274. October 9, 2007. 

National Association of Regional Councils (2007) Letter and Comments Sent to Docket No. 

OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. 

Docket No. OAR-2005-0172-4504. October 9, 2007. 

National Association of Manufacturers (NAM) (2007) Letter and Comments Sent to Molly A. 

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Information Officer) re: Proposed Rule – National Ambient Air Quality Standards for 

Ozone. Docket No. OAR-2005-0172-4275. October 9, 2007. 
181

National Cattlemen’s Beef Association (2007) Letter and Comments Sent to Docket No. OAR2005-0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. 

Docket No. OAR-2005-0172-4132. October 9, 2007. 

National Park Service (NPS) Letter and Comments Sent to Docket No. OAR-2005-0172 re: 

Proposed Rule – National Ambient Air Quality Standards for Ozone. Docket No. OAR2005-0172-4934. September 27, 2007 

National Tribal Air Association (NTAA) (2007) Letter and Comments Sent to Docket No. OAR2005-0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. 

Docket No. OAR-2005-0172-4169. October 9, 2007. 

Nevada Department of Conservation & Natural Resources(2007) Letter and Comments Sent to 

Docket No. OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality Standards 

for Ozone. Docket No. OAR-2005-0172-4173. October 9, 2007. 

New Jersey Clean Air Council (2007) Letter and Comments Sent to Docket No. OAR-2005-0172 

re: Proposed Rule – National Ambient Air Quality Standards for Ozone. Docket No. OAR2005-0172-4119. October 9, 2007. 

New York State Department of Environmental Conservation (2007) Letter and Comments Sent 

to Docket No. OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality 

Standards for Ozone. Docket No. OAR-2005-0172-4099. October 9, 2007. 

New York State Department of Transportation (2007) Letter and Comments Sent to Docket No. 

OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. 

Docket No. OAR-2005-0172-4865. October 9, 2007. 

New Mexico Environment Department Air Quality Bureau (2007) Letter and Comments Sent to 

Docket No. OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality Standards 

for Ozone. Docket No. OAR-2005-0172-4195. October 5, 2007. 

North Carolina Department of Environment and Natural Resources (NCDENR) (2007) Letter 

Sent to Stephen L. Johnson re: Proposed Rule – National Ambient Air Quality Standards 

for Ozone. Docket No. OAR-2005-0172-4497. October 9, 2007. 

Northeast States for Coordinated Air Use Management (NESCAUM) (2007) Letter and 

Comments Sent to Stephen Johnson, Administrator re: Proposed Rule – National Ambient 

Air Quality Standards for Ozone. Docket No. OAR-2005-0172-4165. October 4, 2007 

Occidental Chemical Corporation (2007) Letter and Comments Sent to Docket No. OAR-2005-

0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. Docket No. 

OAR-2005-0172-4866. October 9 2007. 
182

Oklahoma Department of Transportation (2007) Letter and Comments Sent to Docket No. OAR2005-0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. 

Docket No. OAR-2005-0172-4365. October 5, 2007. 

Ontario Minister of the Environment (2007) Comments Sent to Docket No. OAR-2005-0172 re: 

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Oregon Department of Environmental Quality (2007) Letter and Comments Sent to Docket No. 

OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. 

Docket No. OAR-2005-0172-4014. September 20, 2007. 

Ozone Transport Commission (OTC) (2007) Letter and Comments Sent to Docket No. OAR2005-0172 re: Proposed Rule – National Ambient Air Quality Standards for Ozone. 

Docket No. OAR-2005-0172-4135. October 5, 2007. 

Ozone (8-hour) SIP Coalition (2007) Letter and Comments Sent to Docket No. OAR-2005-0172 

re: Proposed Rule – National Ambient Air Quality Standards for Ozone. Docket No. OAR2005-0172-4168. October 9 2007. 

Pennsylvania Department of Environmental Protection (2007) Letter and Comments Sent to 

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e/epec02009a.pdf 
Appendix 

Provisional Consideration of Recent Studies 

EPA has provisionally considered the recent literature related to the health and ecological effects 

of ozone (O3) to identify pertinent “new” studies that were not included in the O3 Criteria 

Document. The O3 Criteria Document included a rigorous and thorough review of the pertinent 

literature that included studies accepted for publication through December 2004. More recent 

studies accepted for publication in 2005 and 2006 were also included in the 2006 Criteria 

Document. These papers were identified by EPA staff, or by public comments and the Clean Air 

Scientific Advisory Committee (CASAC) as adding significantly to the existing body of data on 

critically important topics. Typically, these studies examined effects at lower O3 levels than 

previously reported or discussed epidemiologic methodological issues. The Criteria Document 

forms the scientific basis for this review of the national ambient air quality standards (NAAQS) 

for O3. 

A number of commenters submitted more recently published studies along with their public 

comments on the proposed revisions to the NAAQS. In addition, EPA has screened and 

surveyed the recent literature and provisionally considered those “new” studies of potentially 

greatest relevance to place them in the context of the findings of the 2006 O3 Criteria Document. 

The intent of this effort is to determine if the new studies published since the Criteria Document 

materially change the conclusions of that document. Overall, EPA’s provisional consideration of 

“new” studies, as discussed below, concludes that, taken in context, the “new” information and 

findings do not materially change any of the broad scientific conclusions regarding the health 

and ecological effects of ozone exposure made in the O3 Criteria Document. 

 

This effort cannot be considered a complete literature review. While the papers have been 

individually peer-reviewed, this provisional consideration has not been subjected to peer review 

or the public comment process, and it has not been reviewed by the CASAC, as is done in the 

development of the Criteria Document and Staff Paper. 

The following sections highlight findings of recent studies from three scientific disciplines that 

were the major focus for the relevant recent studies submitted by public commenters: (1) 

epidemiology, (2) human exposure, and (3) ecology. 

1. Epidemiologic Studies of Ozone-Related Health Effects 

EPA has screened and surveyed the recent epidemiologic literature and identified a number of 

“new” studies on the health effects associated with O3 exposure. This process has identified 

approximately 90 epidemiologic studies that encompass the majority of health outcomes 

addressed in the O3 Criteria Document. The following sections summarize the results of EPA’s 

provisional consideration of these epidemiologic studies for a range of health outcomes; the 
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overall conclusions from the O3 Criteria Document are presented at the beginning of each 

section. 

1.1. Human Health Effects Associated with Short-Term Exposures to Ozone 

1.1.1 Mortality 

The analysis of several large multi-city studies, single-city studies, and additional meta-analyses 

of these studies in the O3 Criteria Document found a “positive association between increasing 

ambient O3 concentrations and excess risk for non-accidental and cardio-pulmonary-related daily 

mortality (EPA, 2006).” The O3 Criteria Document, therefore, concluded that the literature is 

“highly suggestive that O3 directly or indirectly contributes to non-accidental and 

cardiopulmonary-related mortality,” but the underlying mechanisms by which such effects occur 

are not entirely clear (EPA, 2006). 

This provisional consideration identified a number of “new” short-term O3 exposure mortality 

studies; however, not all of them focused solely on O3-related health effects.9 These are 

summarized below. 

One of the studies examined potential confounding in the O3-mortality relationship using the 

multicity data from the National Morbidity, Mortality, and Air Pollution Study (NMMAPS). In 

Bell et al. (2007), confounding was investigated by analyzing the effect of PM on the association 

between short-term exposure to O3 and mortality using data from 98 U.S. communities. By 

estimating the correlation between daily PM and O3 concentrations, along with including PM as 

a covariate in various models, Bell et al. (2007) concluded that neither PM10 nor PM2.5 is a likely 

confounder of the observed O3 and mortality relationship. 

The additional short-term exposure mortality studies identified consisted of studies that were 

conducted in: Italy (Forastiere et al. (2005), Parodi et al. (2005)), China (Qian et al. (2007)), 

South America (Cakmak et al. (2007), Australia (Simpson et al. (2005)), and one that was 

conducted in the U.S. (Zanobetti and Schwartz (2007)). Forastiere et al. (2005) and Qian et al. 

(2007) did not find an association between short-term O3 exposure and out-of hospital coronary 

deaths in Rome, and non-accidental mortality in Wuhan, China, respectively. The lack of an 

association in these two studies may be attributed to the fact neither study focused specifically on 

the “O3 season.” Several studies reported associations between O3 and mortality: 

• Zanobetti and Schwartz (2007) examined mortality displacement, which postulates that 

deaths associated with exposure to air pollutants are occurring in frail individuals, by 

studying an unconstrained and smooth distributed lag of O3 with 21 lags. The authors 

found that the effect size estimate was greatest when observing 21 days of ozone instead 

of a single day, which indicates that the effect observed is not due to mortality 

 

9

 Two of studies identified did not focus on O3-related mortality: Kan et al. (2007) studied the effect of short-term 

exposures to PM on mortality; whereas, Medina-Ramon et al. (2007) focused solely on the temperature-mortality 

relationship. 
A-3

displacement. As a result, the authors concluded that single day lags may underestimate 

the true effect of short-term O3 exposure on mortality. 

• Parodi et al. (2005) and Cakmak et al. (2007) both investigated the association between 

O3 and mortality in populations consisting primarily of elderly inhabitants. In Genoa, 

Italy, Parodi et al. found an association between both total and cardiovascular mortality 

throughout the whole year, but the effects were more pronounced during the warm season 

(May-October). Similarly, Cakmak et al. in their study in Chile concluded that the very 

elderly, >85, had the largest percent increase in mortality due to O3 exposure compared to 

rest of the population. 

• Simpson et al. (2005) assessed the effect of air pollution on mortality in four Australian 

cities (Brisbane, Melbourne, Perth, and Sydney). The authors found an association 

between short-term exposure to O3 and respiratory-related mortality. 

The remaining short-term exposure mortality studies identified (Ren et al. (2007a), Ren et al. 

(2007b), Rainham et al. (2005), Gonçalves et al. (2007)), analyzed the potential modification of 

the effect of O3 on mortality due to various weather variables, including temperature.10 In two 

separate studies, Ren et al. (2007a, 2007b) analyzed whether temperature modified the O3-

mortality effect and whether O3 modified the temperature-mortality effect, respectively. Ren et 

al. (2007a) found in a study of 60 large eastern U.S. communities that temperature 

synergistically modifies the O3-mortality effect, but the modification varies depending on the 

geographic location. On the other hand, Ren et al. (2007b) found in a study of 95 large U.S. 

communities, using the NMMAPS data, that O3 modified the temperature effect on 

cardiovascular mortality across all regions of the U.S. Unlike the two Ren et al. studies, 

Rainham et al. (2005) and Gonçalves et al. (2007) analyzed the overall effect of weather on the 

air pollution-mortality association. Rainham et al. (2005), in a study in Toronto, Canada, did not 

find a systematic pattern of modification, but a modification effect seems dependent on the type 

of synoptic climatology category11 analyzed. Similarly, Gonçalves et al. (2007), in a study of 

cardiovascular mortality in Sao Paulo, Brazil, did not find an association between weather 

variables and O3 concentrations on cardiovascular mortality. 

1.1.2 Respiratory Morbidity 

Results from controlled human exposure studies and animal toxicological studies analyzed 

during the completion of the O3 Criteria Document “provide clear evidence of causality for the 

associations observed between acute (≤ 24 h) O3 exposure and relatively small, but statistically 

 

10 In addition to the studies that focused on the potential modification of the O3 effect, the 

literature search identified three studies that investigated the effect of ambient O3 concentrations 

and temperature on mortality in response to the European heat wave that occurred in the summer 

of 2003 (Dear et al. (2003), Filleul et al. (2006), Keatinge et al. (2006)). 

11 Synoptic categories, which are also referred to as air mass categories were devised through a 

complex statistical approach that classifies various meteorological components (i.e., temperature, 

dew point, components of wind, cloud cover, and sea level pressure) into six categories. 
A-4

significant declines in lung function observed in numerous recent epidemiologic studies. 

Declines in lung function were particularly noted in children, asthmatics, and adults who work or 

exercise outdoors (EPA, 2006).” 

 

Respiratory morbidity studies analyzed in the O3 Criteria Document provide evidence of 

associations between acute exposure to ambient O3 and an increase in respiratory symptoms in 

asthmatic children. This consideration identified four studies that analyzed the effect of ambient 

O3 concentrations on asthma symptoms (Feo Brito et al. (2007), Ho et al. (2007), Kim et al. 

(2007), Schildcrout et al. (2006)). The first three report an association, which is consistent with 

the 2006 Criteria Document; however, one - Schildcrout et al. (2006) - did not observe an 

association between O3 and respiratory symptoms. 

The following observations were made from those studies that reported an association: 

• Ho et al. (2007) investigated the relationship between air pollution, including O3, and 

weather on asthma prevalence and asthma attack rate in a study of junior high school 

students in Taiwan. The authors found in models examining only the effect of air 

pollution on each outcome, that air pollution, including O3, is associated with asthma 

attack rate. 

• Kim et al. (2007) examined the effect of ambient O3 on pulmonary function and 

asthmatic symptoms in 17 moderate to severe asthmatics in Korea. The authors observed 

an association between O3 and asthma symptoms even at O3 concentrations below 80 

ppb. 

• Feo Brito et al. (2007), in a cohort of asthmatic patients in two Spanish towns, found an 

association between O3 concentrations and asthma symptoms. However, the study 

focused on the development of asthma symptoms during the pollen season, which also 

influences the presentation of asthma symptoms. 

Schildcrout et al. (2006) investigated the relation between ambient criteria pollutant 

concentrations and asthma exacerbations in a cohort of children in 8 U.S. cities. Schildcrout et 

al. included a population of children in which the severity of their asthma was not clearly 

identified. Other studies described in the 2006 Criteria Document, specifically Gent et al. (2003) 

and Mortimer et al. (2002), observed associations in children clearly defined as having severe 

asthma. Although the study population in Schildcrout et al. encompasses children that do not 

have severe asthma, the study results are generally consistent with the pattern of results observed 

in the larger body of evidence on the relation between O3 exposure and respiratory symptoms as 

reviewed in the O3 Criteria Document. The following issues were brought to the forefront by the 

primary author of the study, which further indicate that the lack of an association found in 

Schildcrout et al. is not inconsistent with the conclusions of the Criteria Document12: 

 

12 Jonathan Schildcrout provided an email to EPA discussing the results of the 2007 study in 

which he was the lead author on January 4, 2008. 
A-5

• Shildcrout et al. included a study population of 990 children with, on average, 12 

children being examined every day. The O3 analysis included the months May through 

September, which resulted in the study population being less than the 990 children 

observed during the course of the full study. As a result, the total number of children 

observed by Schildcrout et al. is not comparable to other large multi-city studies that 

examined the effect of O3 concentrations on asthma exacerbation, such as Mortimer et 

al. (2002). 

• Although Schildcrout et al. did not find an association between O3 concentrations and 

asthma exacerbation, Shildcrout does not imply the results are inconsistent with those 

previously found because a thorough evaluation of study populations, uncertainty in 

parameter estimates, precise scientific questions, and additional comparisons between 

studies that examined the effect of O3 exposure on asthma exacerbations has not been 

conducted. 

A few “new” studies were identified during the provisional consideration that addressed the 

effect of short-term O3 exposure on lung function. In two U.S. studies, Lagorio et al. (2006) a 

small panel study of individuals with co-morbid conditions (Chronic Obstructive Pulmonary 

Disease (COPD), asthma, or Ischemic Heart Disease (IHD)), and Girardot et al. (2006) an 

observational study of healthy hikers, no association was found between exposure to ambient O3

concentrations and a decrease in lung function (i.e., FEV1 or FVC). However, in the Girardot et 

al. study all measured O3 concentrations were below the current O3 NAAQS, which is below the 

concentration in which lung decrements have been consistently observed in exercising 

individuals. The final lung function study identified, Lewis et al. (2005), did find an association 

between increasing ambient O3 concentrations and reduced lung function (i.e., FEV1) in a study 

of 86 school age children in Detroit, but greater than 75% of the children included in the study 

were classified as having persistent asthma. 

1.1.2 Cardiovascular Morbidity 

The “generally limited body of evidence is highly suggestive that O3 directly and/or indirectly 

contributes to cardiovascular-related morbidity,” including physiologic effects (i.e., release of 

platelet activating factor (PAF)), heart rate variability (HRV), arrhythmias, and myocardial 

infarctions (EPA, 2006). However, the available body of evidence reviewed during the O3

Criteria Document does not “fully substantiate links between ambient O3 exposure and adverse 

cardiovascular outcomes (EPA, 2006).” 

Four “new” studies were identified (Sarnat et al. (2006), Rich et al. (2006a), Rich et al. (2006b), 

Metzger et al. (2007)) that investigated the effect of O3 on arrhythmias. Each study used 

different cardiac episodes to identify an arrhythmia event: Sarnat et al. (2006) used 

supraventricular and ventricular ectopy, Rich et al. (2006a) used paroxysmal atrial fibrillation 

episodes (PAF), Rich et al. (2006b) used ventricular arrhythmias, and Metzger et al. (2007) used 

tachyarrhythmic events. Of these studies, Sarnat et al. (2006) and Rich et al. (2006a) found an 

association between O3 concentrations and the onset of arrhythmias in a study of 32 nonsmoking older adults, and in a study of 203 patients with implantable cardiac devices (ICDs) in 

Boston, respectively. However, Rich et al. (2006b) in a study of 56 patients with ICD in St. 
A-6

Louis observed a weak association between O3 concentrations and arrhythmias, while Metzger et 

al. (2007) did not find any association in a study 518 patients with tachyarrhythmia that had 

ICDs in Atlanta. 

In addition, two studies were identified that examined physiologic effects, the release of PAF - a 

potential stroke precursor, and B-type natriuretic peptide (BNP) - a marker of congestive heart 

failure (HF) severity, in response to O3 exposure (Chuang et al. (2007), Wellenius et al. (2007)). 

Chuang at al. (2007) found an increase in PAF along with other cellular proteins (i.e., highsensitivity C-reactive protein (hs-CRP), 8-hydroxy-2'-deoxyguanosine (8-OHdG)) and HRV, in 

response to an increase in O3 concentrations. Two additional studies, one assessing the effect of 

O3 concentrations on HRV in a cohort of men in Boston (Park et al. (2007))13, and another 

observing the impact of O3 on stroke in France (Henrotin et al. (2007)) along with Chuang et al. 

(2007) contribute to the body of evidence suggesting a potential effect of O3 on HRV and stroke. 

In the Wellenius et al. (2007) study the authors did not observe any fluctuations in BNP, but this 

could be due to within-person variability in BNP levels. 

1.1.3 Respiratory/Cardiovascular Hospital Admissions and Emergency Department Visits 

Numerous population time-series studies have “observed that ambient O3 concentrations are 

positively and robustly associated with respiratory-related hospitalization and asthma emergency 

department (ED) visits during the warm season. These observations are strongly supported by 

the human clinical, animal toxicologic, and epidemiologic evidence for lung function 

decrements, increased respiratory symptoms, airway inflammation, and airway hyperreactivity. 

Taken together, the overall evidence supports a causal relationship between acute ambient O3

exposures and increased respiratory morbidity resulting in increased ED visits and 

hospitalizations during the warm season (EPA, 2006).” 

This provisional consideration identified numerous studies that focus on respiratory 

hospitalization and emergency department visits, of which one (Chen et al. (2007)) did not assess 

the effect of ozone, and, as a result, was excluded from this consideration. The remaining studies 

were conducted in the U.S. (Medina-Ramón et al. (2006), Babin et al. (2007)), Canada (Cakmak 

et al. (2006)), Australia (Erbas et al. (2005), Barnett et al. (2005)), Hong Kong (Ko et al. (2007), 

Lee et al. (2006)), Korea (Kim et al. (2007)), and Taiwan (Bell et al. (2007), Yang et al. (2007), 

Tsai et al. (2006)). All of these studies, except Barnett et al. (2005) found an association 

between ambient O3 concentrations and respiratory hospital admissions. A brief description of 

each of the multi-city analyses is outlined below: 

• Medina-Ramón et al. (2006) evaluated the effect of ambient O3 on respiratory hospital 

admissions in 36 U.S. cities. The authors found an association between O3 exposure 

and chronic obstructive pulmonary disease (COPD) and pneumonia hospital admissions 

during the warm season. 

 

13 Park et al. (2007) examined the effect of O3 on HRV, and the originating location of the 

ambient air. An association was only found when the air originated in the west. 
A-7

• Cakmak et al. (2006) examined whether community income and education modified the 

effect of gaseous pollutants, including O3, on respiratory hospitalizations in 10 large 

Canadian cities. Although the analysis focused on income and education variables, the 

study did find an association between O3 exposure and respiratory hospital admissions 

in a single pollutant model, which excluded both variables. 

“Highly suggestive evidence for O3-induced cardiovascular effects [has been] provided by a few 

population studies of cardiovascular hospital admissions, which reported positive O3 associations 

during the warm season between ambient O3 concentrations and cardiovascular hospitalizations 

[and ED visits] (EPA, 2006).” The O3 Criteria Document, therefore, concluded, that the 

“generally limited body of evidence is highly suggestive that O3 directly and/or indirectly 

contributes to cardiovascular morbidity, but more research is needed to further substantiate the 

links between ambient O3 exposure and adverse cardiovascular outcomes (EPA, 2006).” 

Five “new” cardiovascular hospital admission and ED visit studies were identified (Peel et al. 

(2007), Ballester et al. (2006), Chan et al. (2006), von Klot et al. (2005), Barnett et al. (2006)), 

all of which found an association between ambient O3 concentrations and either hospital 

admissions or ER visits except Barnett et al. (2006). Individual observations for two of these 

studies are presented below: 

• Peel et al. (2007) examined the effect of ambient O3 concentrations on cardiovascular 

ED visits from 31 hospitals in Atlanta for individuals inflicted with co-morbid 

conditions (e.g., hypertension, diabetes, COPD, etc.). The authors observed an increase 

in cardiovascular ED visits due to effect modification in individuals co-morbid with 

COPD in response to ambient O3 levels. These results add to the evidence that 

individuals co-morbid with various conditions, including COPD, have an increased 

susceptibility to ambient air pollution. 

• Ballester et al. (2006) evaluated the effect of ambient O3 concentrations on 

cardiovascular ED visits in 14 Spanish cities. Focusing specifically on the warm 

season when analyzing O3, the authors found an association between O3 concentrations 

and ED visits for both cardiovascular disease (CVD) and heart disease (HD). 

In addition to the respiratory and cardiovascular specific hospital admission and ED visit studies 

already presented, four studies examined the effect of ambient O3 concentrations on both 

respiratory and cardiovascular hospital admissions and ED visits (Zanobetti and Schwartz 

(2006), Hinwood et al. (2006), Chan et al. (2006), Simpson et al. (2005)). Hinwood et al. (2006) 

and Zanobetti and Schwartz (2006) both found that O3 was not associated with an increase in 

cardiovascular and respiratory, or myocardial and pneumonia hospital admissions, respectively. 

In contrast, Simpson et al. (2005) in a study conducted in four Australian cities found an 

association between O3 concentrations and hospital admissions for both asthma and COPD in the 

elderly for three of the four cities; whereas, Chan et al. (2006) found an association between O3

concentrations and cerebrovascular disease in Taiwan. 
A-8

1.2 Health Effects Associated with Long-Term Exposures to Ozone14

1.2.1 Mortality 

Few epidemiologic studies have assessed the relationship between long-term exposure to O3 and 

mortality. As a result, the O3 Criteria Document concluded that an insufficient amount of 

evidence exists “to suggest a causal relationship between chronic O3 exposure and increased risk 

for mortality in humans (EPA, 2006).” 

This provisional consideration identified a few studies that examined the association between 

long-term exposure to O3 and mortality. Two of these studies focused specifically on traffic 

density (Lipfert et al. (2006a), Lipfert et al. (2006b)), and therefore, were not addressed in this 

analysis. The remaining studies (Krewski et al. (2005), Jerret et al. (2005)) did analyze the effect 

of long-term exposure to O3 on mortality, but consistent with the conclusions of previous longterm O3 exposure studies, did not find a clear association with mortality. 

1.2.2 Lung Function 

 “The epidemiologic data, collectively, indicates that the current evidence is suggestive, but 

inconclusive for respiratory health effects from long-term O3 exposure (EPA, 2006).” This 

provisional review identified two15 well conducted cohort studies that assessed the effect of longterm exposure to O3 on lung function development (Islam et al. (2007), Rojas-Martinez et al. 

(2007)). A description of each of the aforementioned studies and their findings are presented 

below: 

 

• Islam et al. (2007) investigated the relationship between air pollution, lung 

function, and the subsequent development of asthma in a cohort of 9 and 10 year 

old children without asthma or wheeze from the Children’s Health Study. The 

authors found that long-term O3 exposure did not have any observable effect on 

forced expiratory flow (FEF), and, therefore, was not associated with lung 

damage or asthma development. 

• Rojas-Martinez et al. (2007) evaluated the association between long-term 

exposure to O3 and lung function development in Mexico City schoolchildren. In 

this study, the authors found that deficits in FVC and FEV1 were associated with 

O3 exposure. 

 

14 In addition to the studies presented in this section, three long-term O3 exposure studies were 

identified that did not warrant analysis because they either focused specifically on proximity to 

traffic (Meng et al. (2007), McConnell et al. (2006a)), or the impact of cat and/or dog ownership 

along with air pollution levels on asthmatic occurrences (McConnell et al. (2006b)). 

15 Morgan et al. (2005) also studied lung function and the development of wheeze; however, the 

study does not take into consideration the role of air pollution on both. As a result, it was 

excluded from this analysis. 
A-9

1.2.3 Lung Cancer 

“The weight of evidence from recent animal toxicological studies and a very limited number of 

epidemiologic studies do not support ambient O3 as a pulmonary carcinogen (EPA, 2006).” This 

provisional consideration identified two studies (Chen et al. (2006), Huen et al. (2006)), which 

both observed cytogenic damage (i.e., micronuclei formation and degenerated cells) in response 

to an increase in O3 exposure. Although cytogenic damage could potentially lead to cancer 

development, neither study concluded that O3 is a pulmonary carcinogen. 

1.2.4 Prenatal and Neonatal Outcomes 

A limited number of studies have examined the relationship between O3 exposure and birthrelated outcomes, including mortality, premature births, low birth weights, and birth defects. 

The O3 Criteria Document concluded that “O3 [is] not an important predictor of several birthrelated outcomes including intrauterine and infant mortality, premature births, and low birth 

weight (EPA, 2006).” 

This provisional consideration identified “new” studies that analyzed the effect of O3 exposure 

on various birth outcomes, including pre-term birth (Hansen et al. (2007)); low birth weight 

(LBW) (Salam et al. (2005), Dugandzic et al. (2006), Hansen et al. (2007)); respiratory 

effects/hospitalizations (Triche et al. (2006), Dales et al. (2006)); and mortality (Tsai et al. 

(2006a), Tsai et al. (2006b), Hajat et al. (2007)). A synopsis of the findings for each birth 

outcome is presented below: 

• Pre-Term Birth: Hansen et al. (2007) analyzed the association between O3

exposure during pregnancy and pre-term birth in 28,000 singleton births in 

Brisbane, Australia. The authors found that an increase in O3 exposure during the 

1st trimester was associated with pre-term birth. 

• Low Birth Weight (LBW): Salam et al. (2005) assessed the effect of increasing 

O3 concentrations on LBW in a population of infants born in California from 

1975 – 1987. The authors concluded that a positive association exists between an 

increase in O3 concentrations and LBW over the entire pregnancy with the 

association being the strongest in the 2nd and 3rd trimesters. Dugandzic et al 

(2006) and Hansen et al. (2007)16 also analyzed the effect of O3 on LBW in 

Canada and Australia, respectively. In both instances, neither study observed an 

association between O3 exposure and LBW during any trimester. 

• Respiratory: Triche et al. (2006) examined respiratory effects of O3 in infants of 

asthmatic mothers. The authors found that infants of asthmatic mothers had a 

greater likelihood of wheeze and difficulty breathing compared to infants whose 

mother did not have asthma for every interquartile-range increase in 24-hr 

 

16 Hansen et al. (2007) also observed the effect of O3 on Head Circumference and Crown-Heel 

Length. The authors also found no association between O3 exposure and these health effects. 
A-10

average ozone.17 In addition, Dales et al. (2006) tested the association between 

daily neonatal respiratory hospitalizations and ambient O3 concentrations in 11 

large Canadian cities. The authors concluded that current O3 levels are 

responsible for a significant proportion of hospitalizations in neonates. 

• Mortality: Tsai et al. (2006a), Tsai et al. (2006b), and Hajat et al. (2007) in 

studies conducted in Taiwan, Taiwan, and the United Kingdom, respectively, all 

found a weak association between O3 exposure and infant mortality. 

1.3 Vulnerability/Susceptibility 

1.3.1 Heightened Vulnerability 

Epidemiologic studies reviewed in the O3 Criteria Document suggest that “exercising (moderate 

to high physical exertion) children and adolescents appear to demonstrate increased 

responsiveness to ambient concentrations of O3 and may be more likely to experience O3-

induced health effects (EPA, 2006).” During this provisional consideration, a study was 

identified that examined the effect of exercise on O3-related health effects (Wong et al. (2007)), 

however, the study focused on mortality in individuals > 30, instead of more benign health 

effects in children and adolescents. In this study, Wong et al. (2007) examined the relationship 

between habitual exercise and air pollution associated mortality in Hong Kong. The authors 

found an association between O3 exposure and mortality in people ≥ 65 who never exercised. As 

a result, the authors concluded that habitual exercise may reduce the risk of premature death 

attributed to air pollution. 

1.3.2. Genetic Susceptibility 

Human clinical and epidemiologic studies analyzed in the O3 Criteria Document demonstrated 

that “genetic polymorphisms for antioxidant enzymes and inflammatory genes (GSTM1, NQO1, 

and Tnf-α) may modulate the effect of O3 exposure on pulmonary function and airway 

inflammation (EPA, 2006).” This provisional consideration identified three studies (Islam et al. 

(2007), Chen et al. (2007), Romieu et al. (2006)) along with two review papers (London (2007), 

McCunney (2005)), which found that genetic polymorphisms in antioxidant genes can lead to a 

decrease in lung function upon exposure to O3. 

 

17 An association was not observed for wheeze for an interquartile-range increase in 8-hr 

maximum or 1-hr maximum. 
A-11

1.4 Provisional Consideration of Epidemiologic Studies Summary 

EPA emphasizes that this is a provisional consideration of the recent literature, and it is not 

intended to serve as a supplement to the Criteria Document. This summary of “new” studies has 

not undergone the detailed and extensive review process entailed in the development of a Criteria 

Document, and it has not been discussed by CASAC. Overall, the “new” study results support 

and expand upon findings in the 2006 O3 Criteria Document. The essential conclusions of this 

provisional consideration are that the science supporting evaluation of the potential health 

impacts of O3 on human health continues to expand and hence provides a larger knowledge base 

for better characterizing the relationships between O3 and health effects. The “new” studies 

provide additional insights on the health effects of O3 exposure, but the results do not materially 

change any of the broad scientific conclusions regarding the health effects of O3 exposure made 

in the 2006 O3 Criteria Document. 

 

2. Human Exposure Studies 

Three “new” studies were identified that addressed the relationship of personal exposures to 

ambient O3 concentrations: Koutrakis et al. (2005), Sarnat et al. (2006), and McConnell et al. 

(2006c). The Koutrakis et al. (2005) study is a research report summarizing results presented in 

peer-reviewed publications that were reviewed in the O3 Criteria Document (Sarnat et al., 2000, 

2001, 2005). As described in these publications, the report found that ambient O3 concentrations 

were significantly associated with personal O3 exposures in a study in Boston during the 

summer, although a similar study conducted in Baltimore found that ambient O3 concentrations 

showed stronger associations with personal exposures to PM2.5 than to O3. The poor correlations 

observed during the winter between ambient concentrations and personal exposure 

measurements may be due to the inability of personal monitors to detect low O3 concentrations 

(below 5 ppb), along with differences in activity patterns and building ventilation compared to 

the summer. The study conducted in Steubenville, OH by Sarnat et al. (2006) observed 

significant associations between ambient O3 concentrations and personal O3 exposures in both 

summer and fall seasons, with higher associations observed for subjects spending time under 

high building ventilation conditions. A modeling study to quantitatively estimate the effect of 

NOx emissions on O3 concentrations near roadways (McConnell et al. (2006c)) predicted 

decreased O3 concentrations near roadways, contributing to increased spatial variability and poor 

associations between residential outdoor concentrations and measured at ambient monitors; 

however, mean O3 concentrations measured outside homes were within 3 ppb of fixed-site 

monitor values (33 ppb vs. 36 ppb). 

The results of these studies are generally consistent with, and do not materially change, the broad 

scientific conclusions reached in the 2006 O3 Criteria Document regarding the spatial variability 

of ambient O3 concentrations and relationships between personal exposures and ambient 

concentrations of O3. In one case (Koutrakis et al. (2005)), data from the study had been 

presented in peer-reviewed publications that were considered during preparation of the Criteria 

Document. 
A-12

3. Ecological Studies 

EPA has screened and surveyed the recent vegetation and ecological literature and identified a 

number of “new” studies on effects associated with O3 exposure. The following discussion 

summarizes the results of EPA’s provisional consideration of these studies for a range of issues 

related to the effects of O3 on vegetation and ecosystems. 

Two recently published companion papers (McLaughlin et al 2007a, McLaughlin et al 2007b) 

investigated the effects of ambient O3 on tree growth and hydrology at forest sites in the southern 

Appalachian Mountains. The authors reported that the cumulative effects of ambient levels of 

O3 decreased seasonal stem growth by 30-50% for most trees species in a high ozone year in 

comparison to a low O3 year (McLaughlin et al 2007a). The authors also report that high 

ambient O3 concentrations can disrupt whole tree water use and in turn, reduce late-season 

stream-flow (McLaughlin et al 2007b). 

Several new studies were published since the O3 Criteria Document from the Aspen FACE “free 

air” O3 and carbon dioxide exposure experiment in a forest in Wisconsin (Kubiske et al. 2006a, 

Kubiske et al. 2006b, Liu et al. 2007, Percy et al. 2007, Darbah et al. 2007). Kubiske et al. 

(2006b) reported that elevated O3 may change the intra- and inter-species competition. For 

example, O3 treatments increased the rate of conversion from a mixed aspen-birch community to 

a birch dominated community. In another study at this site, Percy et al. (2007) showed that 

negative growth effects were seen below the current 8-hour O3 standard level (0.084 ppm). The 

authors also attempted to compare different O3 metrics to predict effects on tree growth by using 

trees repeatedly measured over 5 years. The authors suggested that 4th highest maximum metric 

performed the best, but they did not include the 3-month 12-hr W126 in their analysis. 

Several new studies have been published on the incidence of foliar injury in the field due to 

ambient O3 concentrations (Kohut 2007, Chappelka et al. 2007, Davis 2007a, Davis 2007b, 

Davis & Orendovici 2006). Kohut (2007) presented a foliar injury assessment for 244 National 

parks over 5 years. The author reported that risk of foliar injury was high in 65 parks, moderate 

in 46 parks, and low in 131 parks. Chappelka et al. (2007) reported that the average incidence of 

O3-induced foliar injury of was 73% on milkweed in the Great Smokey Mountain National Park 

in the years 1992-1996. Three papers (Davis 2007a, Davis 2007b, Davis & Orendovici 2006) 

reported O3-induced foliar injury in several plants species in National Wildlife Refuges in Maine, 

Michigan and New Jersey. 

In a large-scale modeling analysis, Sitch et al. (2007) suggested that increasing ambient O3

concentrations across the globe suppresses the land carbon sink because O3 decreases plant 

productivity. As a consequence, more CO2 is accumulating in the atmosphere. The authors 

suggest that the radiative forcing of this extra CO2 is greater than the direct radiative forcing of 

O3 as a greenhouse gas alone. 
A-13

Overall, EPA’s provisional consideration of these “new” studies concludes that, taken in context, 

the new information and findings do not materially change any of the broad scientific 

conclusions regarding the effects of O3 exposure on vegetation and ecosystems made in the O3

Criteria Document. 
A-14

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