1

 January 26, 2011

MEMORANDUM

SUBJECT: Solicitation of CASAC Advice on EPA’s Reconsideration of the 2008 Primary 

Ozone National Ambient Air Quality Standard

FROM: Lydia N. Wegman, Director /s/ 

Health and Environmental Impacts Division 

Office of Air Quality Planning and Standards 

TO: Holly Stallworth 

 Designated Federal Officer 

 Clean Air Scientific Advisory Committee 

 EPA Science Advisory Board Staff Office 

 The Environmental Protection Agency (EPA) is currently in the process of reconsidering 

the national ambient air quality standards (NAAQS) for ozone (O3) set in 2008. EPA issued a 

proposal to reconsider the 2008 Ozone NAAQS in January 2010, (75 FR 2938; January 19, 

2010), and this proposal took into account prior CASAC advice, received before, during and 

after the 2008 O3 NAAQS rulemaking.1 In addition, the Clean Air Scientific Advisory 

Committee’s (CASAC) Ozone Review Panel for the Reconsideration of the 2008 NAAQS 

(CASAC Ozone Reconsideration Panel; the Panel) also reviewed the 2010 O3 NAAQS 

reconsideration proposal and provided additional comment and advice on EPA’s proposed O3

NAAQS (Samet, February 19, 2010). EPA is requesting additional advice from the CASAC 

Ozone Reconsideration Panel about the strengths and limitations of the scientific evidence and 

technical information to aid in the reconsideration. 

The EPA is now in the process of reaching final decisions on the reconsideration of the 

2008 O3 NAAQS, which requires the deliberative evaluation of the extensive body of scientific 

and technical information available in the 2008 review and the many comments received on the 

proposed reconsideration. In the process of evaluating this information and determining how to 

exercise her judgment concerning the appropriate O3 NAAQS to set, the EPA Administrator has 

determined that additional advice from CASAC would be useful and important in evaluating the 

scientific and technical information from the 2008 review upon which the reconsideration of the 

primary (health-based) standard is based.2

 The EPA’s Office of Air Quality Planning and 

Standards (OAQPS) has prepared charge questions (Attachment 1) to solicit further advice from 

 

1

 Advice provided to the EPA Administrator in letters on the second draft Staff Paper (Henderson, 2006), the final 

2007 Staff Paper (Henderson, 2007), the 2008 final decision (Henderson, 2008), and the 2010 reconsideration 

proposal (Samet, 2010). 

2

 The EPA is also reconsidering the secondary (welfare-based) O3 NAAQS, but is not soliciting additional CASAC 

advice on that standard. 
2

the CASAC Ozone Reconsideration Panel, with the expectation that CASAC’s advice would 

help the Administrator in most appropriately weighing the strengths and limitations of the 

scientific evidence and other information before her, and thus aid her in the exercise of judgment 

as to the appropriate primary standard for O3. To provide background and context for 

considering these charge questions, relevant information from the 2010 O3 NAAQS 

reconsideration proposal is summarized below. 

In January 2010, based on consideration of the entire body of evidence and information 

available in the 2008 rulemaking, including exposure and risk estimates, as well as the 

recommendations of CASAC, the Administrator initiated a rulemaking to reconsider the O3

NAAQS set in 2008, at which time the primary O3 NAAQS was revised from a level of 0.08 

ppm to 0.075 ppm. In the proposal, the Administrator concluded that it was appropriate to set 

the level of the O3 primary standard to a level “well below 0.080 ppm, a level at which the 

evidence provides a high degree of certainty about the adverse effects of O3 exposure in healthy 

people” (75 FR 2996, Section II.C.5., “Administrator’s Proposed Conclusions”). The 

Administrator also agreed with CASAC’s conclusion that important public health protections can 

be achieved by a standard set below 0.075 ppm, and concluded that “a standard set as high as 

0.075 ppm would not be considered requisite to protect public health with an adequate margin of 

safety” (75 FR 2996). Having concluded that consideration of lower levels was warranted, the 

Administrator proposed to set the level of the primary 8-hour O3 standard to a level within the 

range of 0.060 to 0.070 ppm. In reaching this proposed decision, the Administrator noted the 

following: 

A standard level within this range would reduce the risk of a variety of health 

effects associated with exposure to O3, including the respiratory symptoms and 

lung function effects demonstrated in the controlled human exposure studies, and 

the respiratory-related emergency department visits, hospital admissions and 

mortality effects observed in the epidemiological studies. All of these effects are 

indicative of a much broader array of O3-related health endpoints, such as school 

absences and increased medication use, that are plausibly linked to these observed 

effects. Depending on the weight placed on the evidence and information 

available in the 2008 rulemaking, as well as the uncertainties and limitations in 

the evidence and information, a standard could be set within this range at a level 

that would be requisite to protect public health with an adequate margin of safety. 

(75 FR 2998) 

In the 2010 reconsideration proposal, two different approaches to interpreting the 

available evidence and exposure/risk-based information were presented as the basis for 

concluding that 0.070 ppm and 0.060 ppm were appropriate upper and lower ends, respectively, 

for a range of standard levels that was appropriate to propose (75 FR 2997). The proposal of 

0.070 ppm as the upper end of the range was based on an approach that would place “significant 

weight on uncertainties and limitations in the information to avoid potentially overestimating 

public health risks and protection...” The proposal of 0.060 ppm as the lower end of the range 

was based on an approach that would place “less weight on uncertainties and limitations in the 

information so as to avoid potentially underestimating public health improvements...” The 
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considerations that formed the basis for each of these approaches are discussed on page 2997 of 

the 2010 reconsideration proposal. 

The Administrator is now in the process of reaching a final decision as to the specific 

primary standard level that is requisite to protect public health, including the health of 

susceptible populations, with an adequate margin of safety, in light of the indicator, averaging 

time, and form of the standard. The standard that is chosen is to be sufficient but not more than 

necessary to achieve that result. As noted in the 2010 reconsideration proposal: 

The assessment of a standard level calls for consideration of both the degree of 

risk to public health at alternative levels of the standard as well as the certainty 

that such risk will occur at any specific level. Based on the information available 

in the 2008 rulemaking, there is no evidence-based bright line that indicates a 

single appropriate level. Instead there is a combination of scientific evidence and 

other information that needs to be considered as a whole in making this public 

health policy judgment, and selecting a standard level from a range of potentially 

reasonable values (75 FR 2996). 

In selecting a primary standard level within the proposed range, the Administrator stated 

in the proposal that it is appropriate to consider the following information: 

(1) The strong body of evidence from controlled human exposure studies 

evaluating healthy people at exposure levels of 0.080 ppm and above that 

demonstrated lung function decrements, respiratory symptoms, pulmonary 

inflammation, and other medically significant airway responses, as well as limited 

but important evidence of lung function decrements and respiratory symptoms in 

healthy people down to O3 exposure levels of 0.060 ppm; (2) the substantial body 

of evidence from controlled human exposure and epidemiological studies 

indicating that people with asthma are likely to experience larger and more 

serious effects than healthy people; (3) the body of epidemiological evidence 

indicating associations are observed for a wide range of serious health effects, 

including respiratory related emergency department visits and hospital admissions 

and premature mortality, across distributions of ambient O3 concentrations that 

extend below the 2008 standard level of 0.075 ppm, as well as questions of 

biological plausibility in attributing the observed effects to O3 alone at the lower 

end of the concentration ranges extending down to background levels; and (4) the 

estimates of exposures of concern and risks for a range of health effects that 

indicate that important improvements in public health are very likely associated 

with O3 levels just meeting alternative standards, especially for standards set at 

0.070 and 0.064 ppm (the lowest levels included in the assessment), relative to 

standards set at and above 0.080 ppm (75 FR 2996). 

The attached charge questions specifically solicit further advice on these four areas of 

information. We recognize that CASAC has previously provided advice on the scientific and 

technical information that informed the 2008 review of the primary O3 NAAQS and the 2010 

proposed reconsideration, including information in the 2006 Ozone Air Quality Criteria 
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Document, the exposure and health risk assessments, and the 2007 Ozone Staff Paper. To 

facilitate the Panel’s response to these charge questions, specific references to prior CASAC 

advice are contained within the charge questions. For your convenience, prior CASAC advisory 

letters are attached (Attachment 2). The charge questions also contain specific references to the 

2010 reconsideration proposal, which is also attached (Attachment 3). In addition, the 2010 

proposal contains specific references to the 2006 Ozone Air Quality Criteria Document and the 

2007 Staff Paper where more detailed information can be found.3

 In the charge questions, we 

cite the 2010 reconsideration proposal, recognizing that the discussion in the proposal further 

cites the 2006 Ozone Air Quality Criteria Document and the 2007 Staff Paper. 

In reaching a final decision on the level of an 8-hour O3 primary standard that is requisite 

to protect public health with an adequate margin of safety, the Administrator is mindful that this 

choice includes making “judgments based on an interpretation of the evidence and other 

information that neither overstates nor understates the strength and limitations of the evidence 

and information” (75 FR 2993). To ensure that this final decision on the reconsideration of the 

2008 O3 primary standard is based on the most appropriate interpretation of the scientific 

evidence and exposure/risk information that was available in the 2008 review, the Administrator 

is asking the CASAC Ozone Reconsideration Panel to provide further advice about the strengths 

and limitations of the scientific evidence and the results of the exposure and health risk 

assessments to aid in her interpretation of this information. In providing this advice, we ask the 

Panel members to focus on the attached charge questions, though we would appreciate any 

further advice that CASAC wishes to provide. We also ask the Panel members to be mindful 

that they should consider only the information that was available in the record of the 2008 O3

NAAQS review, as information that has become available since the 2008 review is not relevant 

to EPA’s reconsideration of the 2008 O3 NAAQS. Such “new” information is being considered 

as part of EPA’s next periodic review of the O3 NAAQS, but is not part of the basis for this 

reconsideration (75 FR 2944). 

The prior advice from CASAC throughout the ozone NAAQS review process has been 

very useful to the Administrator. She appreciates and looks forward to CASAC’s consensus 

advice on these additional questions while she considers which standard, within the full range of 

0.060 to 0.070 ppm, is in her judgment requisite to protect public health with an adequate margin 

of safety as required by the Clean Air Act. We look forward to the upcoming CASAC Ozone 

Reconsideration Panel review meeting and to receiving further CASAC advice on EPA’s 

ongoing reconsideration of the 2008 primary O3 NAAQS. Should you have any questions, 

please contact me (919-541-5505; email wegman.lydia@epa.gov) or Dr. Karen Martin (919-541-

5274; email martin.karen@epa.gov). 

cc: Vanessa Vu, SAB. OA 

 Gina McCarthy, OAR 

 Janet McCabe, OAR 

 Steve Page, OAR/OAQPS 

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 These documents are available on the Web; the 2006 Ozone Air Quality Criteria 

Document is at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923#Download and the 2007 

Staff Paper is at: http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007_07_ozone_staff_paper.pdf. 
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Karen Martin, OAR/OAQPS 

Susan Stone, OAR/OAQPS 

John Vandenberg, ORD/NCEA-RTP 

Debra Walsh, ORD/NCEA-RTP 

Mary Ross, ORD/NCEA-RTP 

James Brown, ORD/NCEA-RTP
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Attachment 1 

Charge Questions 

 We have prepared the following charge questions to facilitate further advice from the CASAC 

Panel to the Administrator about the strengths and limitations of the scientific evidence and the 

results of the exposure and health risk assessments to aid in her interpretation of this information. 

As noted in the cover memorandum, two different approaches to interpreting the available 

evidence and exposure/risk based information were presented as the basis for proposing 0.070 

ppm and 0.060 ppm as the appropriate upper and lower ends, respectively, of the proposed range 

(75 FR 2997). The approach that led to selecting 0.070 ppm as the upper end of the proposed 

range was based on placing significant weight on uncertainties and limitations in the information 

so as to avoid potentially overestimating public health risks from exposure to O3. The approach 

that led to selecting 0.060 ppm as the lower end of the proposed range was based on placing less 

weight on uncertainties and limitations in the information so as to avoid potentially 

underestimating public health improvements. 

Taking into account the considerations that formed the basis for these two approaches to 

interpreting the evidence and exposure/risk-based information available in the 2008 review, we 

ask you to address questions related to the specific aspects of the scientific and technical 

information as well as the first overarching charge question. In order to facilitate the Panel’s 

response, we have prepared specific charge questions in the following sections on the four lines 

of information that the Administrator focused on in the 2010 proposal, including evidence and 

information from: (1) controlled human exposure studies; (2) controlled human exposure and 

epidemiological studies about susceptible populations; (3) epidemiological evidence about a 

wide range of serious health effects; and, (4) quantitative estimates of exposures of concern, and 

risks for a range of health effects. After consideration of these specific points, we ask you to 

address the following overarching charge question. 

1. What is your advice on the overall strengths and limitations of the evidence from controlled 

human exposure and epidemiological studies and the results of the exposure and risk 

assessments, in the context of EPA's selection of a standard level within the proposed range that 

would be requisite to protect public health with an adequate margin of safety, including the need 

to protect susceptible populations, such as children and people with asthma? 

Controlled human exposure studies 

As noted in the 2010 proposal, the most certain evidence of adverse health effects from exposure 

to O3 comes from the controlled human exposure studies, and the large bulk of this evidence 

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

At those levels, there is consistent evidence of lung function decrements and 

respiratory symptoms in healthy young adults, as well as evidence of O3-induced 

pulmonary inflammation, airway responsiveness, impaired host defense 

capabilities, and other medically significant airway responses. Moreover, there is 

no evidence that the 0.080 ppm exposure level is a threshold for any of these 

types of respiratory effects. Rather, there is now controlled human exposure 
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evidence, including studies of lung function decrements and respiratory symptoms 

at the 0.060 ppm exposure level, that strengthens our previous understanding that 

this array of respiratory responses are likely to occur in some healthy adults at 

such lower levels (75 FR 2993). 

In particular, there were two studies by Adams (2002, 2006), newly available in the 2008 

rulemaking, that examined lung function (measured in terms of FEV1) and respiratory symptom 

effects associated with prolonged O3 exposures at levels below 0.080 ppm, down to an exposure 

level of 0.060 ppm. These studies analyzed hour-by-hour changes in responses. At the 0.060 

ppm exposure level the author reported no statistically significant differences in lung function, 

although some statistically significant increases in respiratory symptoms were observed, based 

on differences in hour-by-hour exposure patterns. EPA conducted an analysis (Brown, 2007) of 

the data from the Adams (2006) study that addressed the different and more fundamental 

question of whether there were statistically significant changes in lung function from a 6.6-hour 

exposure to 0.060 ppm O3 versus filtered air and used a standard statistical method appropriate 

for a simple paired comparison. This analysis found small group mean lung function decrements 

in healthy adults at the 0.060 ppm exposure level to be statistically significantly different from 

responses associated with filtered air exposure. 

In deciding the weight to place on the information from the Adams studies, relative to the entire 

body of evidence from controlled human exposure studies, EPA has recognized several 

important considerations. The controlled human exposure studies at 0.060 ppm O3 are limited, 

with only two published studies (Adams 2002 and 2006) available from one investigator. 

However, the Adams studies are well-designed and employed an exposure protocol that was 

consistent with earlier studies (Horstman et al., 1990; McDonnell et al., 1991). At the 0.080 

ppm level, the subjects did not appear to be more responsive to O3 than subjects in previous 

studies, as the observed response was similar to that of previous studies (Adams, 2003a,b; 

Horstman et al., 1990; McDonnell et al., 1991). Although of much smaller magnitude, the 

temporal pattern of the 0.060 ppm response was generally consistent with the temporal patterns 

of response to higher concentrations of O3 in this and other studies. These findings are not 

unexpected because the previously observed group mean FEV1 responses to 0.080 ppm were in 

the range of 6–9% suggesting that exposure to lower concentrations of O3 would result in 

smaller, but real group mean FEV1 decrements, i.e., the responses to 0.060 ppm O3 are consistent 

with the presence of a smooth exposure-response curve with responses that do not end abruptly 

below 0.080 ppm (75 FR 2950). The EPA’s analysis of the data from the Adams (2006) study at 

a 0.060 ppm exposure level found small, but statistically significant group mean differences in 

lung function decrements in healthy adults at the 0.060 ppm exposure level. 

Moreover, 7 to 20% of the subjects in the Adams studies experienced lung function decrements 

(≥ 10%) at the 0.060 ppm exposure level. While for active healthy people, moderate levels of 

functional responses (e.g., FEV1 decrements of ≥ 10% but < 20%) and/or moderate respiratory 

symptom responses would likely interfere with normal activity for relatively few responsive 

individuals, for people with lung disease, even moderate functional or symptomatic responses 

would likely interfere with normal activity for many individuals, and would likely result in more 

frequent use of medication (75 FR at 2986). The CASAC panel indicated that a focus on the 

lower end of the range of moderate levels of functional responses (e.g., FEV1 decrements ≥ 10%) 
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is most appropriate for estimating potentially adverse lung function decrements in people with 

lung disease (Henderson, 2006c). 

In the 2010 proposal it was concluded that the evidence from the Adams studies provide limited 

but important evidence which adds to the overall body of evidence that informs the 

Administrator’s proposed decision on the range of levels within which a standard could be set 

that would be requisite to protect public health with an adequate margin of safety, including the 

health of susceptible populations such as people with lung disease (75 FR at 2993). A number 

of questions were raised on the 2010 proposal about the weight that should be placed on the 

Adams studies and EPA’s focus on the proportion of subjects experiencing moderate lung 

function decrements. 

2. Recognizing that controlled human exposure studies at 0.080 ppm O3 and above have 

provided evidence of other health effects, including inflammation and increased airway 

responsiveness which may occur through different physiological mechanisms than the reduction 

in FEV1, how should the results of these studies inform our understanding the health effects to 

healthy adults at exposures levels from 0.060 to 0.070 ppm? 

 

3. How should the results of the controlled human exposure studies at 0.060 ppm O3, showing 

effects on FEV1 and respiratory symptoms, in the context of the larger body of evidence from 

controlled human exposure studies, mentioned above, inform our understanding of the health 

effects to healthy adults at exposure levels from 0.060 to 0.070 ppm? 

4. With respect to the information from controlled human exposure studies at 0.060 ppm O3, 

what is the scientific importance of the small, group mean FEV1 decrements relative to the 

findings that 7 to 20% of the subjects experienced FEV1 decrements ≥ 10%? Please consider this 

question from both a public health and a clinical perspective. 

Controlled human exposure and epidemiological studies about susceptible populations 

The 2010 proposal noted that in looking more broadly at evidence from animal toxicological, 

controlled human exposure, and epidemiological studies, there is substantial evidence, new in the 

2008 rulemaking, that people with asthma and other preexisting pulmonary diseases are among 

those at increased risk from O3 exposure. 

Altered physiological, morphological, and biochemical states typical of 

respiratory diseases like asthma, COPD, and chronic bronchitis may render people 

sensitive to additional oxidative burden induced by O3 exposure. Children and 

adults with asthma are the group that has been studied most extensively. Evidence 

from controlled human exposure studies indicates that asthmatics and people with 

allergic rhinitis may exhibit larger lung function decrements in response to O3

exposure than healthy subjects and that they can have larger inflammatory 

responses. The Administrator also notes that two large U.S. epidemiological 

studies, as well as several smaller U.S. and international studies, have reported 

fairly robust associations between ambient O3 concentrations and measures of 

lung function and daily symptoms (e.g., chest tightness, wheeze, shortness of 
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breath) in children with moderate to severe asthma and between O3 and increased 

asthma medication use. These more serious responses in asthmatics and others 

with lung disease provide biological plausibility for the respiratory morbidity 

effects observed in epidemiological studies, such as respiratory-related emergency 

department visits and hospital admissions (75 FR 2994). 

The 2010 proposal goes on to note that the body of evidence from controlled human exposure 

and epidemiological studies indicates that controlled human exposure studies of lung function 

decrements and respiratory symptoms that evaluate only healthy, non-asthmatic subjects likely 

underestimate the effects of O3 exposure on asthmatics and other susceptible populations. 

Therefore, relative to the healthy, non-asthmatic subjects used in most controlled human 

exposure studies, including the Adams (2002, 2006) studies, a greater proportion of people with 

asthma may be affected, and those who are affected may have as large or larger lung function 

and symptomatic responses at ambient exposures to 0.060 ppm O3 (75 FR 2987-2988). With 

respect to the results of the Adams studies, this means that potentially more than 7 to 20% of 

people with asthma may experience moderate or greater functional or symptomatic responses 

would likely interfere with normal activity for many individuals, and would likely result in more 

frequent use of medication (75 FR 2986). This also indicates that the lowest-observed-effects 

levels demonstrated in controlled human exposure studies that use only healthy subjects may not

reflect the lowest levels at which people with asthma or other lung diseases may respond (75 FR 

2987-88). 

The CASAC panel in its 2006 comments on the second draft Staff Paper generally supported this 

view: 

Furthermore, we have evidence from recently reported controlled clinical studies 

of healthy adult human volunteers exposed for 6.6 hours to 0.08, 0.06, or 0.04 

ppm ozone, or to filtered air alone during moderate exercise (Adams, 2006). 

Statistically-significant decrements in lung function were observed at the 0.08 

ppm exposure level. Importantly, adverse lung function effects were also 

observed in some individuals at 0.06 ppm (Adams, 2006). .... It should be noted 

these findings were observed in healthy volunteers; similar studies in sensitive 

groups such as asthmatics have yet to be conducted. However, people with 

asthma, and particularly children, have been found to be more sensitive and to 

experience larger decrements in lung function in response to ozone exposures than 

would healthy volunteers (Mortimer et al., 2002). (Henderson, 10/24/06, p. 3)

5. The evidence, including that summarized above, indicates that susceptible populations may 

have greater responses than healthy people. In light of this evidence, how can we appropriately 

use the results of controlled human exposure studies conducted on healthy adults, as well as the 

epidemiological studies of susceptible groups, to inform a judgment on the effects of ozone 

exposure on susceptible populations? 
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Epidemiological studies 

The 2010 proposal states that with regard to epidemiological studies, statistically significant 

associations between ambient O3 levels and a wide array of respiratory symptoms and other 

morbidity outcomes including school absences, emergency department visits, and hospital 

admissions have been reported in a large number of studies. More specifically, positive and 

robust associations were found between ambient O3 concentrations and respiratory hospital 

admissions and emergency department visits, when focusing particularly on the results of warm 

season analyses. Taken together, the overall body of evidence from controlled human exposure, 

toxicological, and epidemiological studies supports the inference of a causal relationship 

between acute ambient O3 exposures and increased respiratory morbidity outcomes resulting in 

increased emergency department visits and hospitalizations during the warm season. Further, 

recent epidemiological evidence is highly suggestive that O3 directly or indirectly contributes to 

non-accidental and cardiopulmonary-related mortality (75 FR 2994). 

In the 2010 proposal the Administrator stated that while some studies provide some indication 

of possible 8-hour average threshold levels from below about 0.025 to 0.035 ppm (within the 

range of background concentrations) up to approximately 0.050 ppm, other studies observe linear 

concentration-response functions suggesting that there may be no effects thresholds at the 

population level above background concentrations. In addition, other studies conducted subset 

analyses that included only days with ambient O3 concentrations below the level of the then 

current standard, or below even lower O3 concentrations, including a level as low as 0.061 ppm, 

and continue to report statistically significant associations. The Administrator noted that the 

relationships between ambient 

O3 concentrations and lung function decrements, respiratory symptoms, indicators of respiratory 

morbidity including increased respiratory-related emergency department visits and hospital 

admissions, and possibly mortality reported in a large number of studies likely extend down to 

ambient O3 concentrations well below the level of the standard set in 2008 (0.075 ppm), in that 

the highest level at which there is any indication of a threshold is approximately 0.050 ppm. The 

Administrator noted as well that toward 

the lower end of the range of O3 concentrations observed in such studies, ranging down to 

background levels (i.e., 0.035 to 0.015 ppm), 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. She also noted that there are 

limitations in epidemiological studies that make discerning population thresholds difficult, as 

discussed above, such that there is the possibility that thresholds for individuals may exist in 

reported associations at fairly low levels within the range of air quality observed in the studies 

but not be detectable as population thresholds in epidemiological analyses (75 FR 2993-2994). 

6. To what extent does your confidence that the effects observed in epidemiological studies are 

attributable specifically to O3 lessen or otherwise change, if at all, at the lower levels in the 

proposed range as compared to the higher levels? 
6

Exposure and risk assessments 

In addition to the evidence-based considerations discussed above, in the 2010 proposal the 

Administrator also considered quantitative estimates of exposures and health risks estimated to 

occur associated with air quality simulated to just meet various standard levels. The standard 

levels assessed included 0.084, 0.074, and 0.064 ppm, which were selected to represent standards 

of 0.08, 0.07 and 0.06 ppm, combined with the rounding convention in effect for the 0.08 ppm 

standard at that time. We also assessed a standard level of 0.070 ppm to represent a standard of 

0.07 ppm, but without such rounding convention. This information was considered to help 

inform judgments about a range of standard levels for consideration that could provide an 

appropriate degree of public health protection. In so doing, she was mindful of the important 

uncertainties and limitations that are associated with the exposure and risk assessments4

 (75 FR 

2994).

With respect to the results of the exposure assessment, the Administrator focused on the extent to 

which alternative standard levels, approximately at and below the 0.075 ppm O3 standard set in 

the 2008 final rule, are estimated to reduce exposures over the 0.060 and 0.070 ppm health 

effects benchmark levels, for all and asthmatic school age children in the 12 urban areas included 

in the assessment. The Administrator also took note that the lowest standard level included in 

the exposure and health risk assessments was 0.064 ppm and that additional reductions in 

exposures over the selected health benchmark levels would be anticipated for just meeting a 

0.060 ppm standard (75 FR 2994). 

In the 2010 proposal the term ‘‘exposures of concern” is defined as personal exposures while at 

moderate or greater exertion to 8-hour average ambient O3 levels at and above specific 

benchmark levels which represent exposure levels at which O3-related health effects are known 

or can reasonably be inferred to occur in some individuals (75 FR 2945, 2976-77). EPA 

emphasized that although the analysis of ‘‘exposures of concern’’ was conducted using three 

discrete benchmark levels (i.e., 0.080, 0.070, and 0.060 ppm), the concept is more appropriately 

viewed as a continuum with greater confidence and less uncertainty about the existence of health 

effects at the upper end and less confidence and greater uncertainty as one considers increasingly 

lower O3 exposure levels.5

 Within the context of this continuum, estimates of exposures of 

concern at discrete benchmark levels provide some perspective on the public health impacts of 

O3-related health effects that have been demonstrated in controlled human exposure and 

toxicological studies but cannot be evaluated in quantitative risk assessments, such as lung 

 

4

 Uncertainties are discussed in more detail in the 2007 Staff Paper, and in sections II.B (75 FR 2974-2985) and 

II.C.1.b (75 FR 2988-2991) of the 2010 proposal. Important limitations related to the exposure and risk analyses 

include: insufficient information to evaluate all relevant at-risk groups (e.g., outdoor workers); insufficient 

information to evaluate all O3-related health outcomes (e.g., increased medication use, school absences, emergency 

department visits); and, the geographic scope of the analyses was generally limited (i.e., estimating exposures and 

risks in 12 urban areas across the U.S., and to only five or just one area for some health effects). Thus, it is clear 

that national-scale public health impacts of ambient O3 exposures are much larger than the numbers of children 

likely to experience exposures of concern and the quantitative estimates of O3-related incidences of adverse health 

effects associated with meeting alternative standards. 5

 For the reasons discussed in section II.C.1.b in the 2010 proposal (75 FR 2988-2991) above, the Administrator 

concluded that it is appropriate to focused on both the 0.060 and 0.070 ppm health effect benchmarks for her 

decision on the primary standard (75 FR 2995).
7

inflammation, increased airway responsiveness, and changes in host defenses. They also help in 

understanding the extent to which such impacts have the potential to be reduced by meeting 

various standards. These O3-related physiological effects are plausibly linked to the increased 

morbidity seen in epidemiological studies (e.g., as indicated by increased medication use in 

asthmatics, school absences in all children, and emergency department visits and hospital 

admissions in people with lung disease) (75 FR 2946, 2994-95). EPA recognized that there is no 

sharp breakpoint within the continuum ranging from at and above 0.080 ppm down to 0.060 

ppm, and that in considering estimates of exposures of concern it is important to balance 

concerns about the potential for health effects and their severity with the increasing uncertainty 

associated with our understanding of the likelihood of such effects at lower O3 levels (75 FR 

2945-6, 2994-95). 

Estimates of the number of people likely to experience exposures of concern cannot be directly 

translated into quantitative estimates of the number of people likely to experience specific health 

effects, since sufficient information to draw such comparisons is not available—if such 

information were available, these health outcomes would have been included in the quantitative 

risk assessment. Due to individual variability in responsiveness, only a subset of individuals 

who have exposures at and above a specific benchmark level can be expected to experience such 

adverse health effects, and susceptible subpopulations such as those with asthma are expected to 

be affected more by such exposures than healthy individuals (75 FR 2995). The amount of 

weight to place on the estimates of exposures of concern at any of these benchmark levels 

depends in part on the weight of the scientific evidence concerning health effects associated with 

O3 exposures at and above that benchmark level. It also depends on judgments about the 

importance from a public health perspective of the health effects that are known or can 

reasonably be inferred to occur as a result of exposures at and above the benchmark level (75 FR 

at 2946). 

Based on the exposure and risk considerations discussed in detail in the 2007 Staff Paper and 

presented in sections II.B (75 FR 2974-2985) and II.C.1.b (75 FR 2988-2991) of the 2010 

proposal, the Administrator noted the following important observations from these assessments: 

(1) There is a similar pattern for all children and asthmatic school age children in terms of 

exposures of concern over selected benchmark levels when estimates are expressed in terms of 

percentage of the population; (2) the aggregate estimates of exposures of concern reflecting 

estimates for the 12 urban areas included in the assessment are considerably larger for the 

benchmark level of 0.060 ppm compared to the 0.070 ppm benchmark; (3) there is notable yearto-year variability in exposure and risk estimates with higher exposure and risk estimates 

occurring in simulations involving a year with generally poorer air quality in most areas (2002) 

compared to a year with generally better air quality (2004); and (4) there is significant city-tocity variability in exposure and risk estimates, with some cities receiving considerably less 

protection associated with air quality just meeting the same standard. The Administrator stated 

that it is appropriate to consider not just the aggregate estimates across all cities, but also to 

consider the public health impacts in cities that receive relatively less protection from alternative 

standards under consideration. Similarly, year-to-year variability should also be considered in 

making judgments about which standards will protect public health with an adequate margin of 

safety (75 FR 2995). 
8

Considering the exposure information, as shown in Table 3 in the proposal (75 FR 2990-2991), a 

standard set at 0.070 ppm would likely substantially limit exposures of concern relative to the 

0.070 ppm benchmark level, while affording far less protection against exposures of concern 

relative to the 0.060 ppm benchmark level. To the extent that more weight is placed on 

protection relative to the higher benchmark level, and more weight is placed on the uncertainties 

associated with the epidemiological evidence, a standard set at 0.070 ppm might be considered to 

be adequately protective (75 FR 2997). A standard set at 0.064 ppm (which was the lowest 

standard level evaluated in the exposure assessment as discussed above) would likely essentially 

eliminate exposures of concern relative to the 0.070 ppm benchmark level, while appreciably 

limiting exposures of concern relative to the 0.060 ppm benchmark level to approximately 6 

percent of asthmatic children in the aggregate across 12 cities and up to 16 percent in the city 

that would receive the least protection. While not addressed in the exposure assessment done as 

part of the 2008 rulemaking, a standard set at 0.060 ppm would be expected to provide somewhat 

greater protection from such exposures, which is important to the extent that more weight is 

placed on providing protection relative to the lower benchmark level (75 FR 2997). 

The CASAC panel in its 2006 comments on the second draft Staff Paper endorsed the concept of 

considering a range of health effects (e.g., school absenteeism) that cannot be quantified in a 

health risk assessment. 

Going beyond spirometric decrements, adverse health effects due to lowconcentration exposure to ambient ozone (that is, below the current primary 8-hour 

NAAQS) found in the broad range of epidemiologic and controlled exposure studies 

cited above include: an increase in school absenteeism; increases in respiratory 

hospital emergency department visits among asthmatics and patients with other 

respiratory diseases; an increase in hospitalizations for respiratory illnesses; an 

increase in symptoms associated with adverse health effects, including chest tightness 

and medication usage; and an increase in mortality (non-accidental, cardiorespiratory 

deaths) reported at exposure levels well below the current standard. The CASAC 

considers each of these findings to be an important indicator of adverse health 

effects. (Henderson, 10/24/06, p. 3). 

With respect to the results from the quantitative risk assessment, the Administrator notes that 

EPA’s risk assessment estimates comparable risk reductions in going from a 0.074 ppm standard 

to a 0.064 ppm standard as were estimated in going from the then current 0.084 ppm standard 

down to a 0.074 ppm standard for an array of health effects analyzed. These estimates include 

reductions in risk for lung function decrements in all and asthmatic school age children, 

respiratory symptoms in asthmatic children, respiratory-related hospital admissions, and nonaccidental mortality (75 FR 2996). The Administrator also recognizes that the risk estimates for 

health outcomes included in the risk assessment are limited and that the overall health effects 

evidence is indicative of a much broader array of O3-related health effects 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, doctor’s visits, and 

emergency department visits), some of which have a greater impact on at-risk groups (75 FR 

2995). 
9

The CASAC panel in its 2006 comments on the second draft Staff Paper is generally supportive 

of the use of the entire range of effects quantified in the health risk assessment. 

Beneficial effects in terms of reduction of adverse health effects were calculated 

to occur at the lowest concentration considered (i.e., 0.064 ppm). (Henderson, 

10/24/06, p.4) 

Also, while measures of FEV1 are quantitative and readily obtainable in humans, they 

are not the only measures — and perhaps not the most sensitive measures — of the 

adverse health effects induced by ozone exposure. As stated on page 6-32 of the Final 

Ozone AQCD, “Spirometric responses to ozone are independent from inflammatory 

responses and markers of epithelial injury (Balmes et al., 1996; Bloomberg et al., 

1999; Hazucha et al., 1996; Torres et al., 1997). Significant inflammatory responses 

to ozone exposures that did not elicit significant spirometric responses have been 

reported (Holz et al., 2005; McBride et al., 1994).” Agency staff’s analyses placed 

most emphasis on spirometric evidence and not enough emphasis on serious 

morbidity (e.g., hospital admissions) and mortality observed in epidemiology studies 

(see page 6-44). (Henderson, 10/24/06, p.4) 

7. EPA’s exposure assessment quantified the number of all children and asthmatic children 

likely to be exposed to specific benchmark levels of ozone, including in particular 0.060 and 

0.070 ppm. Considering the patterns of change in the estimates of exposures of concern at and 

above the 0.060 and 0.070 ppm benchmark levels, and the uncertainties and limitations in the 

estimates, what is the relative importance from a public health perspective of the estimated 

reductions in exposures of concern, as well as the exposures remaining, for alternative standards 

across the proposed range? 

8. EPA’s quantitative risk assessment estimated the numbers of occurrences of various ozonerelated health effects associated with just meeting alternative standard levels down to a standard 

level of 0.064 ppm. Considering the patterns of change in the estimates of health effects in the 

risk assessment at the alternative standard levels, and the uncertainties and limitations in the 

estimates, what is the relative importance from a public health perspective of the estimated 

reductions in risk, as well as the risk remaining, for alternative standards across the proposed 

range? Please consider this question in light of the scientific evidence as a whole. 
10

References 

Adams, W. C. (2002) Comparison of chamber and face-mask 6.6-hour exposures to ozone on 

pulmonary function and symptoms responses. Inhalation Toxicol. 14: 745-764. 

Adams, W. C. (2003a) Comparison of chamber and face mask 6.6-hour exposure to 0.08 ppm 

ozone via square-wave and triangular profiles on pulmonary responses. Inhalation 

Toxicol. 15: 265-281. 

Adams, W. C. (2003b) Relation of pulmonary responses induced by 6.6 hour exposures to 0.08 

ppm ozone and 2-hour exposures to 0.30 ppm via chamber and face-mask inhalation. 

Inhalation Toxicol. 15: 745-759. 

Adams, W. C. (2006) Comparison of chamber 6.6 hour exposures to 0.04-0.08 ppm ozone via 

square-wave and triangular profiles on pulmonary responses. Inhalation Toxicol. 18: 

127-136. 

Balmes, J. R.; Chen, L. L.; Scannell, C.; Tager, I.; Christian, D.; Hearne, P. Q.; Kelly, T.; Aris, 

R. M. (1996) Ozone-induced decrements in FEV1 and FVC do not correlate with 

measures of inflammation. Am. J. Respir. Crit. Care Med. 153: 904-909. 

Bell, M. L.; McDermott, A.; Zeger, S. L.; Samet, J. M.; Dominici, F. (2004) Ozone and shortterm mortality in 95 US urban communities, 1987-2000. JAMA J. Am. Med. Assoc. 292: 

2372-2378. 

Bell, M. L.; Peng, R. D.; Dominici, F. (2006) The exposure-response curve for ozone and risk of 

mortality and the adequacy of current ozone regulations. Environ. Health Perspect.: 

doi:10.1289/ehp.8816. Available online at: http://dx.doi.org/ [23 January, 2006]. 

Blomberg, A.; Mudway, I. S.; Nordenhäll, C.; Hedenström, H.; Kelly, F. J.; Frew, A. J.; Holgate, 

S. T.; Sandström, T. (1999) Ozone-induced lung function decrements do not correlate 

with early airway inflammatory or antioxidant responses. Eur. Respir. J. 13: 1418-1428. 

Burnett, R. T.; Brook, J. R.; Yung, W. T.; Dales, R. E.; Krewski, D. (1997a) Association 

between ozone and hospitalization for respiratory diseases in 16 Canadian cities. Environ. 

Res. 72: 24-31. 

Burnett, R. T.; Cakmak, S.; Brook, J. R.; Krewski, D. (1997b) The role of particulate size and 

chemistry in the association between summertime ambient air pollution and 

hospitalization for cardiorespiratory diseases. Environ. Health Perspect. 105: 614-620. 

Environmental Protection Agency (2006) Air Quality Criteria for Ozone and Related 

Photochemical Oxidants. (Final) Washington, DC: National Center for Environmental 

Assessment; EPA report no. EPA/600/R-05/004aB-cB. Available online at: 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923. 
11

Environmental Protection Agency (2007) Review of the national ambient air quality standards 

for ozone: assessment of scientific and technical information. OAQPS staff paper. 

(Updated Final) July 2007. Research Triangle Park, NC: Office of Air Quality Planning 

and Standards; EPA report no. EPA-452/R-07-007. Available online at: 

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

Gryparis, A.; Forsberg, B.; Katsouyanni, K.; Analitis, A.; Touloumi, G.; Schwartz, J.; Samoli, 

E.; Medina, S.; Anderson, H. R.; Niciu, E. M.; Wichmann, H.-E.; Kriz, B.; Kosnik, M.; 

Skorkovsky, J.; Vonk, J. M.; Dörtbudak, Z. (2004) Acute effects of ozone on mortality 

from the "air pollution and health: a European approach" project. Am. J. Respir. Crit. 

Care Med. 170: 1080-1087. 

Hazucha, M. J.; Madden, M.; Pape, G.; Becker, S.; Devlin, R.; Koren, H. S.; Kehrl, H.; 

Bromberg, P. A. (1996) Effects of cyclo-oxygenase inhibition on ozone-induced 

respiratory inflammation and lung function changes. Eur. J. Appl. Physiol. Occup. Med. 

73: 17-27. 

Henderson, R. (2006) Letter from CASAC Chairman Rogene Henderson to EPA Administrator 

Stephen Johnson. October 24, 2006, EPA–CASAC–07–001. 

Henderson, R. (2007) Letter from CASAC Chairman Rogene Henderson to EPA Administrator 

Stephen Johnson. March 26, 2007, EPA-CASAC-07-002. 

Henderson, R. (2008) Letter from CASAC Chairman Rogene Henderson to EPA Administrator 

Stephen Johnson. April 7, 2008, EPA-CASAC-08-009. 

Holz, O.; Tal-Singer, R.; Kanniess, F.; Simpson, K. J.; Gibson, A.; Vessey, R. S. J.; Janicki, S.; 

Magnussen, H.; Jörres, R. A.; Richter, K. (2005) Validation of the human ozone 

challenge model as a tool for assessing anti-inflammatory drugs in early development. J. 

Clin. Pharmacol. 45: 498-503. 

Horstman, D. H.; Folinsbee, L. J.; Ives, P. J.; Abdul-Salaam, S.; McDonnell, W. F. (1990) Ozone 

concentration and pulmonary response relationships for 6.6-hr exposures with five hours 

of moderate exercise to 0.08, 0.10, and 0.12 ppm. Am. Rev. Respir. Dis. 142: 1158-1163. 

Kim, S.-Y.; Lee, J.-T.; Hong, Y.-C.; Ahn, K.-J.; Kim, H. (2004) Determining the threshold effect 

of ozone on daily mortality: an analysis of ozone and mortality in Seoul, Korea, 1995-

1999. Environ. Res. 94: 113-119. 

McBride, D. E.; Koenig, J. Q.; Luchtel, D. L.; Williams, P. V.; Henderson, W. R., Jr. (1994) 

Inflammatory effects of ozone in the upper airways of subjects with asthma. Am. J. Respir. 

Crit. Care Med. 149: 1192-1197. 

McDonnell, W. F.; Kehrl, H.R.; Abdul-Salaam, S.; Ives, P.J.; Folinsbee, L.J.; Devlin, R.B.; 

O’Neil, J.J.; Horstman, D. H. (1991) Respiratory response of humans exposed to low 

levels of ozone for 6.6 hours. Arch. Environ. Health 46: 145-150. 
12

Mortimer, K. M.; Neas, L. M.; Dockery, D. W.; Redline, S.; Tager, I. B. (2002) The effect of air 

pollution on inner-city children with asthma. Eur. Respir. J. 19: 699-705. 

Samet, J (2010) Letter from CASAC Chairman Jonathan Samet to EPA Administrator Lisa 

Jackson. February 19, 2010, EPA–CASAC–10–007. 

Torres, A.; Utell, M. J.; Morow, P. E.; Voter, K. Z.; Whitin, J. C.; Cox, C.; Looney, R. J.; Speers, 

D. M.; Tsai, Y.; Frampton, M. W. (1997) Airway inflammation in smokers and 

nonsmokers with varying responsiveness to ozone. Am. J. Respir. Crit. Care Med. 156: 

728-736. 

Vedal, S.; Brauer, M.; White, R.; Petkau, J. (2003) Air pollution and daily mortality in a city 

with low levels of pollution. Environ. Health Perspect. 111: 45-51. 
Attachment 2

CASAC Advisory Letters

Advice provided to the EPA Administrator in letters on the second draft Staff Paper (Henderson, 2006), the final

2007 Staff Paper (Henderson, 2007), the 2008 final decision (Henderson, 2008), and the 2010 reconsideration

proposal (Samet, 2010).
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

 WASHINGTON D.C. 20460 

OFFICE OF THE ADMINISTRATOR 

SCIENCE ADVISORY BOARD 

October 24, 2006 

EPA-CASAC-07-001 

Honorable Stephen L. Johnson 

Administrator 

U.S. Environmental Protection Agency 

1200 Pennsylvania Avenue, NW 

Washington, DC 20460 

Subject: Clean Air Scientific Advisory Committee’s (CASAC) Peer Review of the 

Agency’s 2nd Draft Ozone Staff Paper 

Dear Administrator Johnson: 

EPA is in the process of reviewing the national ambient air quality standards (NAAQS) 

for ozone (O3) and related photochemical oxidants, which the Agency most recently revised in 

July 1997. As part of its ongoing review of the ozone NAAQS, EPA’s Office of Air Quality 

Planning and Standards (OAQPS) developed a 2nd Draft Ozone Staff Paper, entitled, Review of 

the National Ambient Air Quality Standards for Ozone: Policy Assessment of Scientific and 

Technical Information (July 2006). At the request of the Agency, EPA’s Clean Air Scientific 

Advisory Committee (CASAC or Committee), supplemented by subject-matter-expert panelists 

— collectively referred to as the CASAC Ozone Review Panel (Ozone Panel) — met in a public 

meeting in Durham, NC, on August 24-25, 2006, to conduct a peer review of this draft Ozone 

Staff Paper and three related draft technical support documents. 

In its summary of EPA staff conclusions on the primary (health-related) ozone NAAQS 

found in Chapter 6 of the 2nd Draft Ozone Staff Paper, OAQPS set-forth two options with regard 

to revising the level and the form of the standard: (1) retain the current primary eight-hour (8-hr) 

NAAQS of 0.08 parts per million (ppm); or (2) consider a reduction in the level of the primary 

O3 NAAQS within the range of alternative 8-hr standards included in Staff’s exposure and risk 

assessments (which included a range from 0.064 to 0.084 ppm) with primary focus on an O3 

level of 0.07 ppm with a range of forms from third- through fifth-highest daily maximum. The 

Ozone Panel unanimously concludes that: 

1. There is no scientific justification for retaining the current primary 8-hr NAAQS of 0.08 

parts per million (ppm), and 

1 
2. The primary 8-hr NAAQS needs to be substantially reduced to protect human health, 

particularly in sensitive subpopulations. 

Therefore, the CASAC unanimously recommends a range of 0.060 to 0.070 ppm for the 

primary ozone NAAQS. With regard to the secondary (welfare-related) ozone NAAQS, the 

Ozone Panel is in strong agreement with the scientific and technical evidence presented in the 

summary of EPA staff conclusions on the secondary ozone NAAQS found in Chapter 8 of the 

draft Staff Paper in support of the alternative secondary standard of cumulative form that 

extends over an entire growing season. 

The Ozone Panel members agree that this letter adequately represents their views. The 

chartered Clean Air Scientific Advisory Committee fully endorses the Panel’s letter and hereby 

forwards it to you as the Committee’s consensus report on this subject. A discussion of each 

chapter in the 2nd Draft Ozone Staff Paper follows this letter, and the comments of individual 

Panel members on the 2nd Draft Ozone Staff Paper and three related draft technical support 

documents are attached as Appendix D. 

1. Background 

2

Section 109(d)(1) of the CAA requires that the Agency periodically review and revise, as 

appropriate, the air quality criteria and the NAAQS for the “criteria” air pollutants, including 

ambient ozone. Pursuant to sections 108 and 109 of the Act, EPA is in the process of reviewing 

the ozone NAAQS. OAQPS, within the Office of Air and Radiation (OAR), developed the 2nd 

Draft Ozone Staff Paper as part of this activity. In February 2006, the Agency’s National Center 

for Environmental Assessment, Research Triangle Park, NC (NCEA-RTP), within the Agency’s 

Office of Research and Development (ORD), released its final Air Quality Criteria for Ozone 

and Related Photochemical Oxidants, Volumes I, II, and III, (EPA/600/R-05/004aF-cF, Final 

Ozone Air Quality Criteria Document) for this current review cycle for the ozone NAAQS. The 

nd Draft Ozone Staff Paper evaluates the policy implications of the key scientific and technical 

information contained in the Final Ozone AQCD and identifies critical elements that the Agency 

believes should be considered in its review of the ozone NAAQS. The Ozone Staff Paper is 

intended to “bridge the gap” between the scientific review contained in the Ozone AQCD and 

the public health and welfare policy judgments required of the EPA Administrator in reviewing 

the ozone NAAQS. 

The Ozone Panel met in a public meeting on December 8, 2005 to conduct a consultation 

on EPA’s 1st Draft Ozone Staff Paper and two related technical support documents. However, 

given that the OAQPS’ first draft Staff Paper did not contain Agency staff conclusions about 

whether to retain or revise the existing primary and secondary Ozone standards, the CASAC’s 

activity only amounted to a technical assessment of that document. The Committee’s letter to 

you from that meeting (EPA-CASAC-CON-06-003), dated February 16, 2006, is posted at URL: 

http://www.epa.gov/sab/pdf/casac_con_06_003.pdf. 

2
2. CASAC Ozone Review Panel’s Peer Review of the 2nd Draft Ozone Staff Paper and 

Related Technical Support Documents 

The Ozone Panel reviewed the 2nd Draft Ozone Staff Paper and found it improved over 

the earlier version that had been reviewed as part of a consultation process. However, the Panel 

did not agree with the EPA staff conclusions that it was appropriate to consider retaining the 

current NAAQS as an option that would be protective of public health and welfare. The Ozone 

Panel’s recommendations for reducing the level of the primary ozone standard, and its rationale 

for these recommendations, are provided immediately below. Following a detailed discussion on 

the primary and secondary NAAQS are the Panel’s major, chapter-specific comments. Finally, 

the individual written comments of Ozone Panel members on the 2nd Draft Ozone Staff Paper 

and the three related draft technical support documents are attached in Appendix D. Panelists’ 

responses to the Agency’s charge questions are included in these individual review comments. 

Primary Ozone NAAQS 

New evidence supports and build-upon key, health-related conclusions drawn in the 1997 

Ozone NAAQS review. Indeed, in the 2nd Draft Ozone Staff Paper, EPA staff themselves arrived 

at this same conclusion: 

“Based on the above considerations and findings from the [Final Ozone AQCD], while being 

mindful of important remaining uncertainties, staff concludes that the newly available 

information generally reinforces our judgments about causal relationships between O3 exposure 

and respiratory effects observed in the last review and broadens the evidence of O3 -related 

associations to include additional respiratory-related endpoints, newly identified cardiovascularrelated health endpoints, and mortality. Newly available evidence also has identified increased 

susceptibility in people with asthma. While recognizing that important uncertainties and research 

questions remain, we also conclude that progress has been made since the last review in 

advancing our understanding of potential mechanisms by which ambient O3, alone and in 

combination with other pollutants, is causally linked to a range of respiratory- and cardiovascularrelated health endpoints.” (Pages 6-6 and 6-7) 

2

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. (See 

the numerous ozone epidemiological single-city studies shown in Figure 3-4 on page 3-53 of the 

nd Draft Staff Paper and, in addition, Appendix 3B of the staff paper, which contains the 

summary of effect estimates and air quality data for these studies and multi-city epidemiological 

studies.) These studies are backed-up by evidence from controlled human exposure studies that 

also suggest that the current primary ozone NAAQS is not adequate to protect human health 

(Adams, 2002; McDonnell, 1996). 

Furthermore, we have evidence from recently reported controlled clinical studies of 

healthy adult human volunteers exposed for 6.6 hours to 0.08, 0.06, or 0.04 ppm ozone, or to 

filtered air alone during moderate exercise (Adams, 2006). Statistically-significant decrements 

in lung function were observed at the 0.08 ppm exposure level. Importantly, adverse lung 

function effects were also observed in some individuals at 0.06 ppm (Adams, 2006). These 

3
results indicate that the current ozone standard of 0.08 ppm is not sufficiently health-protective 

with an adequate margin of safety. It should be noted these findings were observed in healthy 

volunteers; similar studies in sensitive groups such as asthmatics have yet to be conducted. 

However, people with asthma, and particularly children, have been found to be more sensitive 

and to experience larger decrements in lung function in response to ozone exposures than would 

healthy volunteers (Mortimer et al., 2002). 

Going beyond spirometric decrements, adverse health effects due to low-concentration 

exposure to ambient ozone (that is, below the current primary 8-hour NAAQS) found in the 

broad range of epidemiologic and controlled exposure studies cited above include: an increase in 

school absenteeism; increases in respiratory hospital emergency department visits among 

asthmatics and patients with other respiratory diseases; an increase in hospitalizations for 

respiratory illnesses; an increase in symptoms associated with adverse health effects, including 

chest tightness and medication usage; and an increase in mortality (non-accidental, 

cardiorespiratory deaths) reported at exposure levels well below the current standard. The 

CASAC considers each of these findings to be an important indicator of adverse health effects. 

As demonstrated in Chapter 5 of the 2nd Draft Ozone Staff Paper (specifically, Figures 5.5, 5.7, 

5.8, and 5.9), a significant decrease in adverse effects due to ozone exposures can be achieved by 

lowering the exposure concentrations below the current standard, which is effectively 0.084 

ppm. Beneficial effects in terms of reduction of adverse health effects were calculated to occur 

at the lowest concentration considered (i.e., 0.064 ppm). (See also Figure 3-4, “Effect estimates 

(with 95% confidence intervals) for associations between short-term ozone exposure and 

respiratory health outcomes,” on page 3-53.) 

The justification provided in the 2nd Draft Ozone Staff Paper for retaining the current 

level of the primary ozone standard as an option for the Administrator was based on results of 

controlled human exposure studies measuring modest declines in FEV1 after exposures to 0.08 

ppm ozone. However, as stated in the Staff Paper (page 3-6), while average decrements in the 

FEV1 were relatively small, 26% of the subjects had greater than 10% decrements, which can be 

clinically significant. Also, while measures of FEV1 are quantitative and readily obtainable in 

humans, they are not the only measures — and perhaps not the most sensitive measures — of the 

adverse health effects induced by ozone exposure. As stated on page 6-32 of the Final Ozone 

AQCD, “Spirometric responses to ozone are independent from inflammatory responses and 

markers of epithelial injury (Balmes et al., 1996; Bloomberg et al., 1999; Hazucha et al., 1996; 

Torres et al., 1997). Significant inflammatory responses to ozone exposures that did not elicit 

significant spirometric responses have been reported (Holz et al., 2005; McBride et al., 1994).” 

Agency staff’s analyses placed most emphasis on spirometric evidence and not enough emphasis 

on serious morbidity (e.g., hospital admissions) and mortality observed in epidemiology studies 

(see page 6-44). 

Therefore, on the basis of the large amount of recent data evaluating adverse health 

effects at levels at and below the current NAAQS for ozone, it is the unanimous opinion of the 

CASAC that the current primary ozone NAAQS is not adequate to protect human health. 

Furthermore, the Ozone Panel is in complete agreement both that: the EPA staff conclusion in 

Section 6.3.6 arguing that “consideration could be given to retaining the current 8-hr ozone 

standard” is not supported by the relevant scientific data; and that the current primary 8-hr 

4
standard of 0.08 ppm needs to be substantially reduced to be protective of human health, 

particularly in sensitive subpopulations. 

Additionally, we note that the understanding of the associated science has progressed to 

the point that there is no longer significant scientific uncertainty regarding the CASAC’s 

conclusion that the current 8-hr primary NAAQS must be lowered. A large body of data clearly 

demonstrates adverse human health effects at the current level of the 8-hr primary ozone 

standard. Retaining this standard would continue to put large numbers of individuals at risk for 

respiratory effects and/or significant impact on quality of life including asthma exacerbations, 

emergency room visits, hospital admissions and mortality. (Scientific uncertainty does exist with 

regard to the lower level of ozone exposure that would be fully-protective of human health. The 

Ozone Panel concludes that it is possible that there is no threshold for an ozone-induced impact 

on human health and that some adverse events may occur at policy-relevant background.) 

Moreover, EPA staff concluded that changes in the concentration-based form of the 

standard (i.e., whether to use the third-, fourth-, or fifth-highest daily maximum 8-hr average 

concentration) should also be considered. The analysis found in the 2nd Draft Ozone Staff Paper 

indicates that modest changes in the form of the standard can have substantial impacts on the 

frequency of adverse health effects. Therefore, the CASAC recommends that the Agency 

conduct a broader evaluation of alternative concentration-based forms of the primary 8-hr ozone 

standard and the implications of those alternative forms on public-health protection and stability 

(i.e., with respect to yearly variability to ensure a stable target for control programs). 

The CASAC further recommends that the ozone NAAQS should reflect the capability of 

current monitoring technology, which allows accurate measurement of ozone concentrations 

with a precision of parts per billion, or equivalently to the third decimal place on the parts-permillion scale. In addition, given that setting a level of the ozone standard to only two decimal 

places inherently reflects upward or downward “rounding,” e.g., 0.07 ppm includes actual 

measurements from 0.0651 ppm to 0.0749 ppm, the CASAC chooses to express its 

recommended level, immediately below, to the third decimal place. 

Accordingly, the CASAC unanimously recommends that the current primary ozone 

NAAQS be revised and that the level that should be considered for the revised standard be from 

0.060 to 0.070 ppm, with a range of concentration-based forms from the third- to the fifthhighest daily maximum 8-hr average concentration. While data exist that adverse health effects 

may occur at levels lower than 0.060 ppm, these data are less certain and achievable gains in 

protecting human health can be accomplished through lowering the ozone NAAQS to a level 

between 0.060 and 0.070 ppm. 

Secondary Ozone NAAQS 

An important difference between the effects of acute exposures to ozone on human health 

and the effects of ozone exposures on welfare is that vegetation effects are more dependent on 

the cumulative exposure to, and uptake of, ozone over the course of the entire growing season 

(defined to be a minimum of at least three months). Therefore, there is a clear need for a 

5
secondary standard which is distinctly different from the primary standard in averaging time, 

level and form. Developing a biologically-relevant ozone air quality index would be directly 

responsive to the 2004 National Research Council (NRC) recommendations on Air Quality 

Management in the United States (NAS, 1994) and will help support important new Agency 

initiatives to enhance ecosystem-related program tracking and accountability. 

In its 1996 review of the ozone NAAQS, EPA staff proposed several cumulative seasonal 

ozone exposure indices, including SUM06, the concentration-weighted metric (i.e., the seasonal 

sum of all hourly average concentrations > 0.06 ppm), and W126, the integrated exposure index 

with a sigmoidal weighting function, as candidates for a secondary standard. The Administrator 

considered a three-month, 12-hr SUM06 secondary standard at a level of 25 ppm-hr as an 

appropriate, biologically-relevant secondary standard, but ultimately rejected this option in favor 

of simply setting the secondary standard equal to the primary. It was rationalized that efforts to 

attain the new 8-hr primary standard would also eliminate most adverse effects on vegetation, 

and at that time there were uncertainties in how cumulative seasonal exposures would change 

with efforts to reduce peak 8-hour concentrations. Additionally, it was assumed that future 

ozone/vegetation effects research over the coming years would clarify the very uncertain 

quantitative relationships between ozone exposures and vegetation/ecological responses under 

ambient field conditions. 

Unfortunately, however, the Agency has supported very little new vegetation/ecological 

ozone effects research over the past decade. The net result is that the quantitative evidence 

linking specific ozone concentrations to specific vegetation/ecological effects must continue to 

be characterized as having high uncertainties due to the lack of data for verification of those 

relationships. It is not surprising that substantial research needs remain, as indicated both in 

Chapter 8 and in individual reviewer comments. The quantitative evidence linking specific 

ozone concentrations to specific vegetation effects — especially at the complex ecosystem level 

2

— must continue to be characterized as having high uncertainties due to the lack of data for 

verification of those relationships. To a large extent, this is an unavoidable consequence of the 

inherent complexities of ecosystem structure and function, interactions among biotic and abiotic 

stressors and stimuli, variability among species and genotype, detoxification and compensatory 

mechanisms, etc. Nevertheless, the compelling weight of evidence provided in Chapter 7 of the 

nd Draft Ozone Staff Paper results from the convergence of results from many various and 

disparate assessment methods including chamber and free air exposure, crop yield and tree 

seedling biomass experimental studies, foliar injury data from biomonitoring plots, and modeled 

mature tree growth. 

Despite limited recent research, it has become clear since the last review that adverse 

effects on a wide range of vegetation including visible foliar injury are to be expected and have 

been observed in areas that are below the level of the current 8-hour primary and secondary 

ozone standards. Such effects are observed in areas with seasonal 12-hr SUM06 levels below 25 

ppm-hr (the lower end of the range of a SUM06 secondary standard suggested in the 1996 

review and the upper end of the range suggested in Chapter 8 of the 2nd Draft Ozone Staff 

Paper). Seasonal SUM06 (or equivalent W126) ranges well below 25 ppm-hr were 

recommended for protecting various managed and unmanaged crops and tree seedlings in the 

1997 workshop on secondary ozone standards (Heck and Cowling, 1997). The absence of clear6
cut lower effects thresholds for sensitive vegetation combined with the lower recent estimates of 

policy-relevant background (typical range of 0.015 to 0.035 ppm) emphasizes the importance of 

efforts to reduce low- to mid-range environmental exposures below 0.060 ppm. 

Based on the Ozone Panel’s review of Chapters 7 and 8, the CASAC unanimously agrees 

that it is not appropriate to try to protect vegetation from the substantial, known or anticipated, 

direct and/or indirect, adverse effects of ambient ozone by continuing to promulgate identical 

primary and secondary standards for ozone. Moreover, the members of the Committee and a 

substantial majority of the Ozone Panel agrees with EPA staff conclusions and encourages the 

Administrator to establish an alternative cumulative secondary standard for ozone and related 

photochemical oxidants that is distinctly different in averaging time, form and level from the 

currently existing or potentially revised 8-hour primary standard. The suggested approach to the 

secondary standard is a cumulative seasonal growing standard such as the indices SUM06 or 

W126 aggregated over at least the three summer months exhibiting the highest cumulative ozone 

levels and includes the ozone exposures from at least 12 daylight hours. The CASAC suggests a 

range of 10 to 20 ppm-hours for the three-month growing season SUM06 index for agricultural 

crops rather than the 15-25 ppm-hours proposed in Chapter 8. 

However, the Ozone Panel views the three-month growing season W126 index as a 

potentially more biologically-relevant index than the 3-month growing season SUM06 index. 

This is because the W126 index has no absolute minimum ozone concentration threshold and 

only lightly weights the lower ozone concentrations. Therefore, a three-month seasonal W126 

that is the approximate equivalent of the SUM06 at 10 to 20 ppm-hr is preferred. As shown by 

the references cited at the end of Chapter 8, the consensus view among expert persons in the 

ecological communities of both this country and elsewhere around the world is that a secondary 

standard of cumulative form and extending over an entire growing season will be far more 

effective than a secondary standard that is not cumulative in form and does not include the whole 

growing season. 

In conclusion, the Clean Air Scientific Advisory Committee is pleased to provide its 

scientific advice and recommendations to the Agency on the primary and secondary ozone 

NAAQS. We recognize that our recommendation of lowering of the current primary ozone 

standard would likely result in a large portion of the U.S. being in non-attainment. Nevertheless, 

we take very seriously the statutory mandate in the Clean Air Act not only for the Administrator 

to establish, but also for the CASAC to recommend to the Administrator, a primary standard that 

provides for an “adequate margin of safety ... requisite to protect the public health.” 

Finally, as announced during the Ozone Panel’s August meeting, once the Agency 

releases the Final Ozone Staff Paper in early January 2007, the CASAC intends to hold a public 

teleconference in late January or early February 2007 for the members of the Ozone Panel to 

review — and, prospectively, to offer additional, unsolicited advice to the Agency concerning — 

Chapter 6 (Staff Conclusions on Primary O3 NAAQS) and Chapter 8 (Staff Conclusions on 

Secondary O3 NAAQS) in that final Agency document. The purpose of such advice would be to 

7
inform EPA’s efforts as it develops the forthcoming, proposed rule for ozone and related 

photochemical oxidants. As always, the CASAC wishes EPA well in this important endeavor. 

 Sincerely,

 /Signed/ 

Dr. Rogene Henderson, Chair 

 Clean Air Scientific Advisory Committee 

Appendix A – Clean Air Scientific Advisory Committee Roster (FY 2006) 

Appendix B – CASAC Ozone Review Panel Roster 

Appendix C – Charge to the CASAC Ozone Review Panel 

Appendix D – Review Comments from Individual CASAC Ozone Review Panel Members 

8
CASAC Chapter-Specific Discussion Comments on 

EPA’s 2nd Draft Ozone Staff Paper 

Sub-groups of the CASAC Ozone Review Panel who led the discussion on individual 

chapters of the Staff Paper summarized their comments in the following paragraphs: 

Chapter 2 (Air Quality Characterization): A better introduction to the central role of 

photochemical oxidation reactions as the key reactions governing the behavior of air pollutants 

in the atmosphere would improve this chapter. Ozone is the key indicator of the extent of 

oxidative chemistry and serves to integrate multiple pollutants. Oxidation in the atmosphere 

leads to the formation of particulate matter from SO2, NOX, and volatile organic compounds 

(VOCs) as well as gas phase irritants (formaldehyde, acrolein, etc). Thus, although ozone itself 

has direct effects on human health and ecosystems, it can also be considered as indicator of the 

mixture of photochemical oxidants and of the oxidizing potency of the atmosphere. Section 2.2.6 

only briefly covers the relationship of ozone to other photochemical oxidants. It would be 

beneficial to add a short paragraph outlining the role of ozone and other photochemical oxidants 

in the atmospheric transformation processes that may results in the formation of more toxic 

products (both in an outdoor and indoor environment), as provided in the individual comments 

appended to this letter. 

The section on policy-relevant background (2.7) continues to have problems. Although 

the section briefly cites the results of comparison of different models and measurements, it does 

not adequately address the uncertainties of the global GEOS-CHEM model, and how these 

uncertainties are reflected in the health risk analysis. Since ozone health effects are observed 

down to concentrations of the order of 0.04–0.05 ppm, it is important to know how the PRB is 

related to the considered primary ozone standard and what uncertainties there are in the risk 

attributed to controllable sources. 

Chapter 3 (Policy-Relevant Assessment of Health Effects Evidence): The latest draft 

of Chapter 3 is much improved over the previous draft. Efforts to respond to some of the earlier 

concerns expressed by the CASAC are appreciated. While in general this chapter is well written, 

and is a credible basis for the risk analyses that follow, there are inconsistencies and inaccuracies 

that still need to be addressed. Typically, there is appropriate use of cautionary phrases when the 

data are not as strong as they might be, but this use is inconsistent across the chapter, and there 

are instances where EPA staff appear to be stretching to infer that data support their statement. 

While the individual comments of Ozone Panel members attached to this letter provide specifics 

on these points, some of the Panel’s more significant concerns are discussed briefly below. 

Discussion of measurement error is convoluted, confusing, and contains some mistakes. 

The primary issue in the use of central ambient monitors for ozone in time-series 

epidemiological studies is whether they provide any information at all that reflects daily personal 

ozone exposure in susceptible populations. The discussion on p. 3-37 of the impact of various 

types of exposure measurement error is incorrect; the difference between true and measured 

ambient concentrations is an example of classical measurement error that results in bias of effect 

9
estimates to the null, not just an increase in standard error. Claiming that the difference between 

average personal exposure and ambient concentrations results in “attenuation of risk” is not 

appropriate. 

The Ozone Panel does not completely agree with staff’s conclusion that “the use of 

routinely monitored ambient ozone concentrations as a surrogate for personal exposures is not 

generally expected to change the principal conclusions from ozone epidemiological studies.” 

Indeed, Panel members have little insight as to what we would find if we had actual exposure 

measurements. Personal 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. 

Some statements about which individuals are at greatest risk of ozone-induced effects are 

not adequately supported by the information discussed in the chapter. Individuals with chronic 

obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) are likely to be at 

increased risk, but the hypothesis that such “hyper-responsiveness” can be used to identify 

individuals with COPD or CVD who are at greatest risk of O3-induced health effects has not 

been confirmed. A more appropriate conclusion would be that individuals with COPD and CVD 

are at increased risk of O3-induced health effects. 

The discussion of the ranges for changes in FEV1 that are considered to be small, 

moderate, or large for persons with impaired respiratory systems is not consistent. While EPA 

staff state that the table values for the ranges do not need to be changed, staff indirectly 

acknowledge that a 10% reduction in this variable in asthmatics could have serious 

consequences, an interpretation that is used in Chapters 4-6. 

The 30 subjects studied by Adams had a great influence on the analyses presented in 

Chapters 5 and 6. While the discussion of the low-level exposures used in the controlled human 

studies by Adams and colleagues is technically correct that no statistically significant changes 

were found in FEV1 for ozone at 40 to 60 ppb compared to filtered air, there were clearly a few 

individuals who experienced declines in lung function at these lower concentrations. These were 

healthy subjects, so the percentage of asthmatic subjects, if they had been studied, would most 

likely be considerably greater. 

The lack of statistical power is consistently offered in Chapter 3 for why there appears to 

be an inconsistent effect seen for COPD mortality. Coherence of respiratory effects for ozone 

suffers from neither no more nor no less power considerations that do those for particulate matter 

(PM). Yet the Agency did not argue a lack of power when assessing PM risks, so consistency is 

needed here relative to ozone effect estimates for COPD mortality. 

The relatively strong and relatively consistent effect of ozone on emergency department 

visits for respiratory disease, especially asthma, as evidenced in Figure 3-4 is misrepresented in 

several places in the Chapter (and in Chapters 5 and 6) as “inconclusive” or “inconsistent.” This 

should be corrected. 

10
Chapter 4 (Characterization of Human Exposure to Ozone): The second draft of 

Chapter 4 has responded to many of the comments made on the first draft, and is thus clearer 

than before. The panel was pleased to see the reanalysis for 2002 in addition to 2004. 

It would be helpful to have the estimated exposures for current (2002 and 2004) levels 

displayed in Tables 4-8 & 4-9 (p. 4-32) and Figures 4-4 to 4-21 (pp. 4-33 to 4-41), in addition to 

only those for just meeting the current standard and alternative more stringent standards. This 

would be analogous to the way estimated effects are displayed in Chapter 5 (Figures 5-5 to 5-9 

[pp.5-58 to 5-65]). 

On the whole, Chapter 4 provides a clear “road map” for what was done to characterize 

available knowledge about human exposure to ozone in the framework of generally accepted 

modeling approaches of appropriately selected populations in 12 urban areas of the U.S. Much 

of the text reads like a basic textbook on human exposure assessment using state-of-the-art 

modeling approaches, such as the Air Pollutants Exposure Model (APEX), including adjustments 

for lung ventilation of delivered ozone dose. This extension, beyond exposure characterization, 

is particularly important for ozone where the extent of measurable human responses is very 

sensitive to the amount of ozone inhaled and to where it deposits along the respiratory tract. 

Further extension of the methodology to estimate dose would have important implications and 

should be discussed. 

There is an explicit discussion of the limitations of the APEX model in terms of 

variability and the quality of the input data, which is appropriate and fine as far as it goes. There 

are good reasons presented for selection of urban areas and the time periods to be modeled. 

However, there was inadequate consideration of the populations selected for modeling. Those 

selected were appropriate, but the omission of the elderly, the population most at risk for ozoneassociated premature daily mortality, was notable and not even mentioned in terms of why it was 

not considered. 

The chapter was very good at exposition and clear presentation of modeling results, but 

was deficient it its discussion of seemingly counterintuitive results, and of a potentially large 

influence of measurement biases. As an example of the first of these issues, the children in LA 

& Houston are estimated to have far fewer exposures above 0.07 ppm (8-hr) than in most other 

cities with lower ozone concentrations and fewer children. This was likely due to the greater 

within-day and sampler-to-sampler variations in concentration within these two cities than in the 

others, the fact that the entire year was modeled while for other sites the winter was not included 

and/or the greater extent of air conditioning, especially in Houston. Whatever the reasons, there 

should have been some discussion of the causes. The quadratic rollback methodology should 

have been better described since this strategy has important consequences for the modeled 

results. 

The second issue that was presented, but left hanging without an adequate discussion is at 

the bottom of page 4-47, where it was simply stated that “in general, APEX systematically 

under-predicts the measured values by 0.001 to 0.02 ppm (zero to 50 percent).” If this is so, is it 

due to a really serious failure of the APEX model, or to unreliable measurements? The 

measurements at issue were six-day average concentrations based on the use of passive 

11
(diffusion) samplers, which are known to be subject to significant errors when the air velocity 

across the inlet is variable. The comparison of measured and modeled concentrations depicted in 

Figure 4-22 is certainly worthy of further analysis and discussion. 

Chapter 5 (Characterization of Health Risks): Generally the panel found Chapter 5 

and its accompanying risk assessment to be well done, balanced and reasonably communicated. 

Additional text is needed at the beginning and end of the chapter to put the limited risk 

assessment into the context of the much larger body of evidence of ozone health effects. The 

discussion of uncertainty in these risk estimates is expanded in section 5.3.2.5. Although a 

number of issues are raised, their impacts on the estimates have not been thoroughly explored. 

Additional sensitivity analyses seem warranted. In particular, it is essential that the sensitivity of 

the risk assessment to the shape of the dose-response curve for FEV1 be evaluated. Although the 

3 parameter logistic (3PL) model emulates the pattern seen in the five “data points,” these points 

are aggregates of the original data, and may give a misleadingly optimistic picture of the quality 

of the fit. More importantly, although the problem of model uncertainty is noted it has not been 

addressed even though methods exist for doing so. Even if only the linear and logistic models 

were included in the analysis, the error bands around the estimated response probabilities would 

likely increase to better reflect that uncertainty. In addition, a suggestion to deal with the 

uncertainties surrounding estimation of PRB, particularly as related to Table 5.5 (for lung 

function) and Table 5.11 (mortality), would be to change the form of the analyses to assess the 

impact of the concentration change in the expected number of health effects relative to the 

current standard. The key advantage of estimating the effect of concentration change is that it 

does not depend on the choice of the PRB. 

With regard to the controlled human exposure studies, Ozone Panel members believe that 

the selection of changes in pulmonary function expressed as percent change in FEV1 in children 

is a fair indicator of an adverse effect at 15% change in all active children; and, in asthmatic 

children, a 10% change is indicative of adverse effects. However, the presentation of the figures 

showing these effects needs to be revised to indicate the uncertainties in the results used, 

particularly at the lower levels of exposure. The potential mechanisms whereby these changes 

are a reflection of both pain on breathing, partial inflammation of smaller airways, other effects 

on airways, and potentially triggers for more significant respiratory morbidity, particularly in 

asthmatic children, are not adequately discussed. In addition, some added discussion is 

necessary to indicate that these measures are generally taken in areas with relatively high 

background levels of ozone exposure, and that the role that tolerance may play in minimizing the 

degree of adverse effect observed needs to be considered. 

From the perspective of the epidemiological data, the Ozone Panel judged the selection 

of: respiratory symptoms in moderate/severe asthmatic children (ages zero [birth] to 12); hospital 

admissions for respiratory illness among asthmatic children; and premature total non-accidental 

and cardiorespiratory mortality for inclusion in the quantitative risk assessment to be appropriate. 

However, the CASAC believes that several other endpoints should be discussed qualitatively to 

support the findings that these endpoints indicate that significant adverse effects are occurring at 

exposure concentrations well below the current standard. Other endpoints deemed worthy of 

additional discussion included respiratory emergency department visits among asthmatics and 

patients with other respiratory diseases, increased medication usage, and increased 

12
symptomatology reported at exposure levels well below the current standard. Taken together, 

members of the Ozone Panel felt strongly that these findings preclude including the current 

standard as a scientifically defensible option for the Administrator (see discussion about Chapter 

6 found in the main portion of the letter above). 

Another problem in the health effects calculations (see Table 5-5 and 5-11) is that they 

are based on computations of the form Rx – RPRB, where Rx is the risk at a given concentration x 

of O3 and RPRB is the corresponding risk at policy-relevant background (PRB) for O3. As 

discussed at the Ozone Panel’s August meeting, the PRB is highly-problematic to calculate and 

is, in some sense, “unknowable.” One can avoid this problem by calculating the ∆ = R0.8 – Rx 

for various concentrations x. This form 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 ∆ is that it does not depend on 

the choice of PRB, and thus is free of the uncertainties surrounding estimation of PRB. 

Chapter 6 (Staff Conclusions on Primary O3 NAAQS): See the discussion on Chapter 

6 found in the main portion of the letter above. It would also be helpful to have the estimated 

exposures for current (2002 and 2004) levels displayed in figures 6-1 to 6-6 (pp. 6-34 to 6-39), in 

addition to only those for just meeting the current standard and alternative more stringent 

standards. This would be analogous to the way estimated effects are displayed in Chapter 5 

(Figures 5-5 to 5-9 [pp.5-58 to 5-65]). 

Chapters 7 (Policy-Relevant Assessment of Welfare Effects Evidence) and 8 (Staff 

Conclusions on Secondary O3 NAAQS): Chapter 7 is a well-developed and persuasively 

presented assessment of the welfare effects of ozone on vegetation, which forms the technical 

basis for the range of secondary standards recommended in Chapter 8. That having been said, 

the potential for significant propagation of error/uncertainty in the underlying technical 

documentation draws into question the conclusions drawn by EPA Staff. As observed in the 

Agency’s 1989 and 1996 Ozone Staff Papers, ozone remains the most prevalent phytotoxic 

compound in the ambient air “impairing crop production and injuring native vegetation and 

ecosystems more than any other air pollutant” (USEPA 1989, 1996). Furthermore, as has been 

noted in the current assessment of human health effects, there also appears to be no safe 

threshold concentration below which ozone effects on sensitive vegetation are eliminated. See 

the additional discussion on Chapter 8 found in the main portion of the letter above. 

13
Appendix A – Clean Air Scientific Advisory Committee Roster (FY 2006) 

U.S. Environmental Protection Agency 

Science Advisory Board (SAB) Staff Office 

Clean Air Scientific Advisory Committee (CASAC) 

CHAIR 

Dr. Rogene Henderson, Scientist Emeritus, Lovelace Respiratory Research Institute, 

Albuquerque, NM 

MEMBERS 

Dr. Ellis Cowling, University Distinguished Professor-at-Large, North Carolina State 

University, Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina 

State University, Raleigh, NC 

Dr. James D. Crapo, Professor, Department of Medicine, National Jewish Medical and 

Research Center, Denver, CO 

Dr. Frederick J. Miller, Consultant, Cary, NC 

Mr. Richard L. Poirot, Environmental Analyst, Air Pollution Control Division, Department of 

Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT

Dr. Frank Speizer, Edward Kass Professor of Medicine, Channing Laboratory, Harvard 

Medical School, Boston, MA 

Dr. Barbara Zielinska, Research Professor, Division of Atmospheric Science, Desert Research 

Institute, Reno, NV 

SCIENCE ADVISORY BOARD STAFF 

Mr. Fred Butterfield, CASAC Designated Federal Officer, 1200 Pennsylvania Avenue, N.W., 

Washington, DC, 20460, Phone: 202-343-9994, Fax: 202-233-0643 (butterfield.fred@epa.gov) 

(Physical/Courier/FedEx Address: Fred A. Butterfield, III, EPA Science Advisory Board Staff 

Office (Mail Code 1400F), Woodies Building, 1025 F Street, N.W., Room 3604, Washington, 

DC 20004, Telephone: 202-343-9994)

A-1 
Appendix B – CASAC Ozone Review Panel Roster 

U.S. Environmental Protection Agency 

Science Advisory Board (SAB) Staff Office 

Clean Air Scientific Advisory Committee (CASAC) 

CASAC Ozone Review Panel 

CHAIR 

Dr. Rogene Henderson*, Scientist Emeritus, Lovelace Respiratory Research Institute, 

Albuquerque, NM 

MEMBERS 

Dr. John Balmes, Professor, Department of Medicine, University of California San Francisco, 

University of California – San Francisco, San Francisco, California 

Dr. Ellis Cowling*, University Distinguished Professor-at-Large, North Carolina State 

University, Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina 

State University, Raleigh, NC 

Dr. James D. Crapo*, Professor, Department of Medicine, National Jewish Medical and 

Research Center, Denver, CO 

Dr. William (Jim) Gauderman, Associate Professor, Preventive Medicine, Medicine, 

University of Southern California, Los Angeles, CA 

Dr. Henry Gong, Professor of Medicine and Preventive Medicine, Medicine and Preventive 

Medicine, Keck School of Medicine, University of Southern California, Downey, CA 

Dr. Paul J. Hanson, Senior Research and Development Scientist, Environmental Sciences 

Division, Oak Ridge National Laboratory (ORNL), Oak Ridge, TN 

Dr. Jack Harkema, Professor, Department of Pathobiology, College of Veterinary Medicine, 

Michigan State University, East Lansing, MI 

Dr. Philip Hopke, Bayard D. Clarkson Distinguished Professor, Department of Chemical 

Engineering, Clarkson University, Potsdam, NY 

Dr. Michael T. Kleinman, Professor, Department of Community & Environmental Medicine, 

University of California – Irvine, Irvine, CA 

Dr. Allan Legge, President, Biosphere Solutions, Calgary, Alberta, Canada 

B-1 
Dr. Morton Lippmann, Professor, Nelson Institute of Environmental Medicine, New York 

University School of Medicine, Tuxedo, NY 

Dr. Frederick J. Miller*, Consultant, Cary, NC 

Dr. Maria Morandi, Assistant Professor of Environmental Science & Occupational Health, 

Department of Environmental Sciences, School of Public Health, University of Texas – Houston 

Health Science Center, Houston, TX 

Dr. Charles Plopper, Professor, Department of Anatomy, Physiology and Cell Biology, School 

of Veterinary Medicine, University of California – Davis, Davis, California 

Mr. Richard L. Poirot*, Environmental Analyst, Air Pollution Control Division, Department of 

Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT

Dr. Armistead (Ted) Russell, Georgia Power Distinguished Professor of Environmental 

Engineering, Environmental Engineering Group, School of Civil and Environmental 

Engineering, Georgia Institute of Technology, Atlanta, GA 

Dr. Elizabeth A. (Lianne) Sheppard, Research Professor, Biostatistics and Environmental & 

Occupational Health Sciences, Public Health and Community Medicine, University of 

Washington, Seattle, WA 

Dr. Frank Speizer*, Edward Kass Professor of Medicine, Channing Laboratory, Harvard 

Medical School, Boston, MA 

Dr. James Ultman, Professor, Chemical Engineering, Bioengineering Program, Pennsylvania 

State University, University Park, PA

Dr. Sverre Vedal, Professor of Medicine, Department of Environmental and Occupational 

Health Sciences, School of Public Health and Community Medicine, University of Washington, 

Seattle, WA

Dr. James (Jim) Zidek, Professor, Statistics, Science, University of British Columbia, 

Vancouver, BC, Canada 

Dr. Barbara Zielinska*, Research Professor, Division of Atmospheric Science, Desert Research 

Institute, Reno, NV 

SCIENCE ADVISORY BOARD STAFF 

Mr. Fred Butterfield, CASAC Designated Federal Officer, 1200 Pennsylvania Avenue, N.W., 

Washington, DC, 20460, Phone: 202-343-9994, Fax: 202-233-0643 (butterfield.fred@epa.gov) 

* Members of the statutory Clean Air Scientific Advisory Committee (CASAC) appointed by the EPA 

Administrator (FY 2006) 

B-2 
Appendix C – Charge to the CASAC Ozone Review Panel 

O3 air quality information and analyses (Chapter 2): 

1. To what extent are the air quality characterizations and analyses clearly communicated, 

appropriately characterized, and relevant to the review of the primary and secondary O3 

NAAQS? 

2. Does the information in Chapter 2 provide a sufficient air quality-related basis for the 

exposure, human health and environmental effects, health risk assessment, and 

environmental assessment presented in later chapters? 

O3-related health effects (Chapter 3): 

1. To what extent is the presentation of evidence from the health studies assessed in the AQCD 

and the integration of information from across the various health-related research areas 

drawn from the O3 AQCD technically sound, appropriately balanced, and clearly 

communicated? 

2. What are the views of the Panel on the appropriateness of staff’s discussion and conclusions 

in Chapter 3 on key issues related to quantitative interpretation of animal toxicology and 

controlled-exposure human experimental studies and epidemiologic study results, including, 

for example, exposure error, the influence of alternative model specification, potential 

confounding or effect modification by co-pollutants, and lag structure? 

3. What are the Panel’s view on the adequacy and clarity of staff discussion on the issue of 

potential thresholds in concentration-response relationships discussed in Chapter 3? 

Exposure Analysis (Second Draft Chapter 4 of the O3 Staff Paper, draft Exposure Analysis 

technical support document, and OAQPS Staff Memorandum on Uncertainty Analysis): 

1. To what extent are the assessment, interpretation, and presentation of the results of the 

exposure analysis as presented in Chapter 4 (and in the second draft Exposure Analysis 

technical support document) technically sound, appropriately balanced, and clearly 

communicated? 

2. Are the methods used to conduct the exposure analysis technically sound? Does the Panel 

have any comments on the methods used? 

3. To what extent are the uncertainties associated with the exposure analysis clearly and 

appropriately characterized in Chapter 4, the Exposure Analysis technical support document, 

and the uncertainty memorandum? 

C-1
4. To what extent is the plan for the remaining uncertainty assessment technically sound? Are 

there other important uncertainties which are not covered? What are the views of the Panel 

on sensitivity analyses conducted to evaluate the influence of uncertainties in the exposure 

analysis? 

Heath Risk Assessment (Second Draft Chapter 5 of the O3 Staff Paper and draft Health Risk 

Assessment technical support document): 

1. To what extent are the assessment, interpretation, and presentation of the results of the 

revised exposure analysis as presented in Chapter 5 (and in the second draft Risk Assessment 

technical support document) technically sound, appropriately balanced, and clearly 

communicated? 

2. In general, is the set of health endpoints and concentration-response and exposure-response 

functions used in this risk assessment appropriate for this review? 

3. Are the methods used to conduct the health risk assessment technically sound? Does the 

Panel have any comments on the methods used? 

4. To what extent are the uncertainties associated with the health risk assessment clearly and 

appropriately characterized in both the second draft Chapter 5 and the second draft Health 

Risk Assessment technical support documents? 

Staff Conclusions and Standard Options for the Primary O3 NAAQS (Chapter 6): 

1. What are the views of the Panel on the approach taken by staff (as discussed in Chapter 6) of 

using both evidence-based and quantitative exposure- and risk-based considerations in 

drawing conclusions and identifying options as to a range of standards to protect against 

health effects associated with exposure to O3, alone and in combination with the ambient mix 

of photochemical oxidants, for consideration in this review of the primary O3 NAAQS? 

2. Does the Panel generally agree that the range of alternative primary O3 standards identified in 

Chapter 6 is generally consistent with the available scientific information and is appropriate 

for consideration by the Administrator? 

3. What are the views of the Panel on the key uncertainties and O3 research recommendations 

discussed in Chapter 6? 

O3-related welfare effects and secondary standard options (Chapters 7): 

1. To what extent is the presentation of evidence drawn from the vegetation effects studies 

assessed in the O3 AQCD technically sound, appropriately balanced, and clearly 

communicated? 

C-2
2. What are the views of the Panel on the appropriateness of staff’s weight-of-evidence 

approach which assesses information from across the various vegetation-related research 

areas described in the O3 AQCD, including chamber and free air exposure crop yield and tree 

seedling biomass experimental studies, foliar injury data from biomonitoring plots, and 

modeled mature tree growth? 

3. To what extent are the methods used to conduct the exposure assessment and the 

interpretation and presentation of the results of the exposure assessment in the second draft 

Chapter 7 and the draft Environmental Assessment technical support document technically 

sound, appropriately balanced, and clearly communicated? 

4. To what extent are the uncertainties associated with the exposure analysis clearly and 

appropriately characterized in the second draft Chapter 7 and the draft Environmental 

Assessment technical support document? 

5. To what extent are the uncertainties associated with the vegetation risk assessment clearly 

and appropriately characterized in both the second draft Chapter 7 and the draft 

Environmental Assessment technical support document? 

6. Staff recognizes that gradients can exist between O3 levels measured at monitor probe heights 

and those measured over low vegetation canopies. What are the Panel’s views on the 

appropriateness of applying a single adjustment factor to hourly monitoring data to account 

for the range of potential gradients that can exist across sites and crop and tree seedling 

canopy structures? Are there alternative approaches or adjustment values the Panel would 

suggest? Are staff’s planned sensitivity analyses appropriate and sufficient? 

7. To what extent do the figures aid in clarifying the text? Should more or less information of 

this type be included in the final Chapter 7 or its Appendices? 

8. Given the lack of quantitative information on O3-related ecosystem effects, what are the 

Panel’s views on the appropriateness of how this topic is addressed in the second draft 

Chapter 7? 

Staff Conclusions and Standard Options for the Secondary O3 NAAQS (Chapter 8): 

1. Does the Panel generally agree that the secondary standard options identified by staff 

(including indicator, averaging time, form, and level) are generally consistent with the 

available scientific and technical information and are appropriate for consideration by the 

Administrator? 

C-3
NOTICE 

This report has been written as part of the activities of the U.S. Environmental 

Protection Agency’s (EPA) Clean Air Scientific Advisory Committee (CASAC), a 

Federal advisory committee administratively located under the EPA Science Advisory 

Board (SAB) Staff Office that is chartered to provide extramural scientific information 

and advice to the Administrator and other officials of the EPA. The CASAC is 

structured to provide balanced, expert assessment of scientific matters related to issue 

and problems facing the Agency. This report has not been reviewed for approval by the 

Agency and, hence, the contents of this report do not necessarily represent the views and 

policies of the EPA, nor of other agencies in the Executive Branch of the Federal 

government, nor does mention of trade names or commercial products constitute a 

recommendation for use. CASAC reports are posted on the SAB Web site at: 

http://www.epa.gov/sab. 
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

 WASHINGTON D.C. 20460 

OFFICE OF THE ADMINISTRATOR 

SCIENCE ADVISORY BOARD 

March 26, 2007 

EPA-CASAC-07-002 

Honorable Stephen L. Johnson 

Administrator 

U.S. Environmental Protection Agency 

1200 Pennsylvania Avenue, NW 

Washington, DC 20460 

Subject: Clean Air Scientific Advisory Committee’s (CASAC) Review of the Agency’s 

Final Ozone Staff Paper 

Dear Administrator Johnson: 

The Clean Air Scientific Advisory Committee (CASAC or Committee), augmented by 

subject-matter-expert Panelists — collectively referred to as the CASAC Ozone Review Panel 

(Ozone Panel) — completed its review of the Agency’s 2nd Draft Ozone Staff Paper in October 

2006 (EPA-CASAC-07-001). In that letter, dated October 24, 2006, the CASAC indicated it 

would review the Agency’s Final Ozone Staff Paper and offer additional, unsolicited advice to 

the Agency on the chapters concerned with setting the primary and secondary National Ambient 

Air Quality Standards (NAAQS) for ozone. 

On March 5, 2007, the Ozone Panel met via a public teleconference to review EPA’s 

Final Review of the National Ambient Air Quality Standards for Ozone: Policy Assessment of 

Scientific and Technical Information (Final Ozone Staff Paper, January 2007). The Panel 

focused on Chapter 6 (The Primary O3 NAAQS) and Chapter 8 (The Secondary O3 NAAQS). 

The CASAC roster is attached as found in Appendix A, the Ozone Panel roster is provided as 

Appendix B, and Ozone Panel members’ individual review comments are found in Appendix C. 

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. While the CASAC recognizes that the Ozone Staff Paper is a final 

document, the Committee offers the following advice to aid the Administrator and Agency staff 

in developing EPA’s proposed rule for ozone and related photochemical oxidants, to be 

published in June 2007. 

1 
Primary Standard 

• The CASAC Ozone Review Panel agreed with the choice of indicator, statistical form 

and averaging time for the primary Ozone NAAQS suggested by Agency staff. 

• The Final Ozone Staff Paper recommended that “consideration be given to a standard 

level within the range of somewhat below 0.080 ppm to 0.060 ppm,” adding that 

“[s]tandard levels within this range that were considered in staff analyses of air quality, 

exposure, and risk include 0.074, 0.070, and 0.064 ppm, representative of levels within 

the upper, middle, and lower parts of this range, respectively.” Reiterating what was 

stated in the CASAC’s previous letter to you on this review (EPA-CASAC-07-001), 

Ozone Panel members were unanimous in recommending that the level of the current 

primary ozone standard should be lowered from 0.08 ppm to no greater than 0.070 ppm. 

The above-referenced CASAC letter (from October 24, 2006), in addition to EPA’s own 

findings in the Final Ozone Air Quality Criteria Document (AQCD) and the Final Ozone 

Staff Paper, provide overwhelming scientific evidence for this recommendation. 

Furthermore, the Ozone Panel recommends that the NAAQS should be specified to the 

third decimal place of the ppm scale to avoid any rounding issues — as indicated by the 

standard levels that the Agency itself considered in the Final Ozone Staff Paper. 

• Pursuant to the Clean Air Act, the primary NAAQS for criteria air pollutants must be set 

to protect the public health with an adequate margin of safety. Significantly, the Final 

Ozone Staff Paper does not address the issue of a margin of safety. (On page 6-86, the 

authors conclude that the proposed standard would “...provide an appropriate degree of 

public health protection...;” however, there is no explicit mention of a margin of safety, 

per se.) Such a discussion should be added to the document and taken into consideration 

in setting the primary ozone standard. 

• There is an underestimation of the affected population when one considers only twelve 

urban “Metropolitan Statistical Areas” (MSAs). The CASAC acknowledges that EPA 

may have intended to illustrate a range of impacts rather than be comprehensive in their 

analyses. However, it must be recognized that ozone is a regional pollutant that will 

affect people living outside these 12 MSAs, as well as inside and outside other urban 

areas. 

• 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. In addition to the three field studies pointing to higher responses to the oxidant 

mixtures than to pure ozone that the Agency has already referenced in the Final Ozone 

AQCD (1–3), three other such studies are referenced below (4–6). More information on 

the effects of low levels of oxidant mixtures on public health is essential to inform the 

future decision-making process. 

• Finally, with respect to policy-relevant background (PRB), the Ozone Panel wishes to 

point out that the Final Ozone Staff Paper does not provide a sufficient base of evidence 

from the peer-reviewed literature to suggest that the current approach to determining a 

PRB is the best method to make this estimation. One reason is that part of the PRB is not 

2
controllable by EPA. It would require international cooperation beyond the bounds of 

North America. A better scientific understanding of the PRB and its relationship to 

intercontinental transport of air pollutants could serve as the basis for a more concerted 

effort to control its growth and preserve the gains in air quality achieved by control 

efforts within the U.S. In any case, there is no apparent need to define PRP in the context 

of establishing a health-based (primary) ozone NAAQS. The effects of inhaled ozone on 

decreases in respiratory function have been seen in healthy children exposed to ozone 

within ambient air mixtures in summer camps (1–6). Furthermore, the concentrationresponse functions above 40 ppb are either linear, or indistinguishable from linear. Thus, 

PRB is irrelevant to the discussion of where along the concentration-response function a 

NAAQS with an 8-hour averaging time that provides enhanced public health protection 

should be. 

Secondary Standard 

• The CASAC Ozone Review Panel members were unanimous in supporting the 

recommendation in the Final Ozone Staff Paper that protection of managed agricultural 

crops and natural terrestrial ecosystems requires a secondary Ozone NAAQS that is 

substantially different from the primary ozone standard in averaging time, level and 

form. 

• The recommended metric for the secondary ozone standard is the (sigmoidally-weighted) 

W126 index, accumulated over at least the 12 “daylight” hours and over at least the three 

maximum ozone months of the summer “growing season.” 

• The Ozone Panel agrees with EPA Staff recommendations that the lowest bound of the 

range within which a seasonal W126 welfare-based (secondary) ozone standard should be 

considered is 7.5 ppm-hrs; however, it does not agree with Staff’s recommendations that 

the upper bound of the range should be as high as 21 ppm-hours. Rather, the Panel 

recommends that the upper bound of the range considered should be no higher than 15 

ppm-hour, which the Panel estimates is approximately equivalent to a seasonal 12-hour 

SUM06 level of 20 ppm-hours. 

• Multi-year averaging to promote a “stable” secondary Ozone NAAQS is less appropriate 

for a cumulative, seasonal secondary standard than for a primary standard based on 

maximum eight-hour concentrations. If multi-year averaging is employed to increase the 

stability of the secondary standard, the level of the standard should be revised downward 

to assure that the desired threshold is not exceeded in individual years. 

• There was an effective, Federally-funded program of ozone environmental effects 

research during the 1970s and 1980s, but such research support has been neglected in 

recent years. It is reasonable to conclude that changes in the distribution and genetic 

makeup of crop cultivars and naturally occurring plant species has and will take place 

over time along with modification of levels and distribution of ambient ozone exposures. 

Therefore, future refinements of the secondary Ozone NAAQS will require both: (1) a 

significant future investment in effects research to ensure that data for plant response to 

ozone are representative of the species and genetic composition of current crop and forest 

3
species utilized by society; and (2) a clear understanding of the sources and propagation 

of uncertainty in the results of that research. 

Additional details on the general recommendations listed above are provided in the 

comments of the individual members of the Ozone Panel that are included in Appendix C. 

The CASAC appreciate this opportunity to work with the Agency is using science to help 

inform the setting of primary and secondary NAAQS to protect public health. While this is the 

last of a long series of Agency NAAQS-related staff papers, the Committee will continue to 

provide you with scientific advice related to setting criteria air pollutant standards protective of 

the public health and public welfare under EPA’s revised NAAQS review process. As always, 

the CASAC wishes the Agency well in this important endeavor. 

 Sincerely, 

/Signed/ 

Dr. Rogene Henderson, Chair 

 Clean Air Scientific Advisory Committee 

Appendix A – Roster of the Clean Air Scientific Advisory Committee 

Appendix B – Roster of the CASAC Ozone Review Panel 

Appendix C – Review Comments from Individual CASAC Ozone Review Panel Members 

References 

1. Spector, D.M., Lippmann, M., Lioy, P.J., Thurston, G.D., Citak, K., James, D.J., Bock, N., 

Speizer, F.E., and Hayes, C. Effects of ambient ozone on respiratory function in active 

normal children. Am. Rev. Respir. Dis. 137:313-320 (1988). 

2. Spektor, D.M., Lippmann, M., Thurston, G.D., Lioy, P.J., Stecko, J., O'Connor, G., 

Garshick, E., Speizer, F.E., and Hayes, C. Effects of ambient ozone on respiratory function 

in healthy adults exercising outdoors. Am. Rev. Respir. Dis. 138:821-828 (1988). 

3. Thurston, G.D., Lippmann, M., Scott, M.B., and Fine, J.M. Summertime haze air pollution 

and children with asthma. Am. J. Respir. Crit. Care Med. 155:654-660 (1997). 

4. Lippmann, M. Health effects of ozone: A critical review. JAPCA 39:672-695 (1989). 

5. Spektor, D.M., Thurston, G.D., Mao, J., He, D., Hayes, C., and Lippmann, M. Effects of 

single and multi-day ozone exposures on respiratory function in active normal children. 

Environ. Res. 55:107-122 (1991). 

6. Lippmann, M. Health effects of tropospheric ozone: Implications of recent research 

findings to ambient air quality standards. J. Exposure Anal. Environ. Epidemiol. 3:103-129 

(1993). 

4
Appendix A – Roster of the Clean Air Scientific Advisory Committee 

U.S. Environmental Protection Agency 

Science Advisory Board (SAB) Staff Office 

Clean Air Scientific Advisory Committee (CASAC) 

CHAIR 

Dr. Rogene Henderson, Scientist Emeritus, Lovelace Respiratory Research Institute, 

Albuquerque, NM 

MEMBERS 

Dr. Ellis Cowling, University Distinguished Professor At-Large, North Carolina State 

University, Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina 

State University, Raleigh, NC 

Dr. James D. Crapo, Professor, Department of Medicine, National Jewish Medical and 

Research Center, Denver, CO 

Dr. Douglas Crawford-Brown, Director, Carolina Environmental Program; Professor, 

Environmental Sciences and Engineering; and Professor, Public Policy, Department of 

Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel 

Hill, NC 

Mr. Richard L. Poirot, Environmental Analyst, Air Pollution Control Division, Department of 

Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT

Dr. Armistead (Ted) Russell, Georgia Power Distinguished Professor of Environmental 

Engineering, Environmental Engineering Group, School of Civil and Environmental 

Engineering, Georgia Institute of Technology, Atlanta, GA 

Dr. Frank Speizer, Edward Kass Professor of Medicine, Channing Laboratory, Harvard 

Medical School, Boston, MA 

SCIENCE ADVISORY BOARD STAFF 

Mr. Fred Butterfield, CASAC Designated Federal Officer, 1200 Pennsylvania Avenue, N.W., 

Washington, DC, 20460, Phone: 202-343-9994, Fax: 202-233-0643 (butterfield.fred@epa.gov) 

(Physical/Courier/FedEx Address: Fred A. Butterfield, III, EPA Science Advisory Board Staff 

Office (Mail Code 1400F), Woodies Building, 1025 F Street, N.W., Room 3604, Washington, 

DC 20004, Telephone: 202-343-9994) 

A-1 
Appendix B – Roster of the CASAC Ozone Review Panel 

U.S. Environmental Protection Agency 

Science Advisory Board (SAB) Staff Office 

Clean Air Scientific Advisory Committee (CASAC) 

CASAC Ozone Review Panel 

CHAIR 

Dr. Rogene Henderson*, Scientist Emeritus, Lovelace Respiratory Research Institute, Albuquerque, NM 

MEMBERS 

Dr. John Balmes, Professor, Department of Medicine, University of California San Francisco, University 

of California – San Francisco, San Francisco, California 

Dr. Ellis Cowling*, University Distinguished Professor At-Large, North Carolina State University, 

Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina State University, 

Raleigh, NC 

Dr. James D. Crapo*, Professor, Department of Medicine, National Jewish Medical and Research 

Center, Denver, CO 

Dr. Douglas Crawford-Brown*, Director, Carolina Environmental Program; Professor, Environmental 

Sciences and Engineering; and Professor, Public Policy, Department of Environmental Sciences and 

Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC 

Dr. William (Jim) Gauderman, Associate Professor, Preventive Medicine, Medicine, University of 

Southern California, Los Angeles, CA 

Dr. Henry Gong, Professor of Medicine and Preventive Medicine, Medicine and Preventive Medicine, 

Keck School of Medicine, University of Southern California, Downey, CA 

Dr. Paul J. Hanson, Senior Research and Development Scientist, Environmental Sciences Division, Oak 

Ridge National Laboratory (ORNL), Oak Ridge, TN 

Dr. Jack Harkema, Professor, Department of Pathobiology, College of Veterinary Medicine, Michigan 

State University, East Lansing, MI 

Dr. Philip Hopke, Bayard D. Clarkson Distinguished Professor, Department of Chemical Engineering, 

Clarkson University, Potsdam, NY 

Dr. Michael T. Kleinman, Professor, Department of Community & Environmental Medicine, University 

of California – Irvine, Irvine, CA 

Dr. Allan Legge, President, Biosphere Solutions, Calgary, Alberta, Canada 

B-1 
Dr. Morton Lippmann, Professor, Nelson Institute of Environmental Medicine, New York University 

School of Medicine, Tuxedo, NY 

Dr. Frederick J. Miller, Consultant, Cary, NC 

Dr. Maria Morandi, Assistant Professor of Environmental Science & Occupational Health, Department 

of Environmental Sciences, School of Public Health, University of Texas – Houston Health Science 

Center, Houston, TX 

Dr. Charles Plopper, Professor, Department of Anatomy, Physiology and Cell Biology, School of 

Veterinary Medicine, University of California – Davis, Davis, California 

Mr. Richard L. Poirot*, Environmental Analyst, Air Pollution Control Division, Department of 

Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT 

Dr. Armistead (Ted) Russell*, Georgia Power Distinguished Professor of Environmental Engineering, 

Environmental Engineering Group, School of Civil and Environmental Engineering, Georgia Institute of 

Technology, Atlanta, GA 

Dr. Elizabeth A. (Lianne) Sheppard, Research Professor, Biostatistics and Environmental & 

Occupational Health Sciences, Public Health and Community Medicine, University of Washington, 

Seattle, WA 

Dr. Frank Speizer*, Edward Kass Professor of Medicine, Channing Laboratory, Harvard Medical 

School, Boston, MA 

Dr. James Ultman, Professor, Chemical Engineering, Bioengineering Program, Pennsylvania State 

University, University Park, PA 

Dr. Sverre Vedal, Professor of Medicine, Department of Environmental and Occupational Health 

Sciences, School of Public Health and Community Medicine, University of Washington, Seattle, WA 

Dr. James (Jim) Zidek, Professor, Statistics, Science, University of British Columbia, Vancouver, BC, 

Canada 

Dr. Barbara Zielinska, Research Professor, Division of Atmospheric Science, Desert Research Institute, 

Reno, NV 

SCIENCE ADVISORY BOARD STAFF 

Mr. Fred Butterfield, CASAC Designated Federal Officer, 1200 Pennsylvania Avenue, N.W., 

Washington, DC, 20460, Phone: 202-343-9994, Fax: 202-233-0643 (butterfield.fred@epa.gov) 

* Members of the statutory Clean Air Scientific Advisory Committee (CASAC) appointed by the EPA 

Administrator 

B-2 
NOTICE 

This report has been written as part of the activities of the U.S. Environmental 

Protection Agency’s (EPA) Clean Air Scientific Advisory Committee (CASAC), a 

Federal advisory committee administratively located under the EPA Science Advisory 

Board (SAB) Staff Office that is chartered to provide extramural scientific information 

and advice to the Administrator and other officials of the EPA. The CASAC is 

structured to provide balanced, expert assessment of scientific matters related to issue 

and problems facing the Agency. This report has not been reviewed for approval by the 

Agency and, hence, the contents of this report do not necessarily represent the views and 

policies of the EPA, nor of other agencies in the Executive Branch of the Federal 

government, nor does mention of trade names or commercial products constitute a 

recommendation for use. CASAC reports are posted on the SAB Web site at: 

http://www.epa.gov/sab. 
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

 WASHINGTON D.C. 20460 

OFFICE OF THE ADMINISTRATOR 

SCIENCE ADVISORY BOARD 

April 7, 2008 

EPA-CASAC-08-009

Honorable Stephen L. Johnson 

Administrator 

U.S. Environmental Protection Agency 

1200 Pennsylvania Avenue, NW

Washington, DC 20460 

Subject: Clean Air Scientific Advisory Committee Recommendations Concerning the 

Final Rule for the National Ambient Air Quality Standards for Ozone 

Dear Administrator Johnson: 

 

The Clean Air Scientific Advisory Committee (CASAC or Committee), augmented by 

subject-matter-expert Panelists — collectively referred to as the CASAC Ozone Review Panel — 

met via a public advisory teleconference on March 28, 2008. The purpose of this conference call 

was to hold follow-on discussions concerning the Final Rule for the National Ambient Air Quality Standards (NAAQS) for ozone, which the Agency published on March 12, 2008. The Ozone 

Panel roster is attached as Appendix A. 

In our most-recent letters to you on this subject — EPA-CASAC-07-001, dated October 

24, 2006, and EPA-CASAC-07-002, dated March 26, 2007 — the CASAC unanimously recommended selection of an 8-hour average Ozone NAAQS within the range of 0.060 to 0.070 parts 

per million for the primary (human health-based) Ozone NAAQS. Moreover, with regard to the 

secondary (welfare-related) ozone standard, the Committee recommended an alternative secondary standard of cumulative form that is substantially different from the primary Ozone NAAQS 

in averaging time, level and form — specifically, the W126 index within the range of 7 to 15 

ppm-hours, accumulated over at least the 12 “daylight” hours and the three maximum ozone 

months of the summer growing season. 

The CASAC now wishes to convey, by means of this letter, its additional, unsolicited advice with regard to the primary and secondary Ozone NAAQS. In doing so, the participating 

members of the CASAC Ozone Review Panel are unanimous in strongly urging you or your successor as EPA Administrator to ensure that these recommendations be considered during the 

next review cycle for the Ozone NAAQS that will begin next year. 
March 12, 2008 was the first time since 1997 that the primary standard for ozone was updated, and the CASAC commends you for taking a step in the right direction by lowering the primary eight-hour ozone standard from 0.08 parts per million to 0.075 ppm. The Committee is 

also pleased that the Agency has abandoned the artificial use of only two decimal places for the 

standard, as reported in ppm. As noted in the CASAC’s previous letters to you on this subject, 

this practice has allowed the rounding-down of ozone concentrations as high as 0.084 ppm to 

meet the previous standard of 0.08 ppm.

Nevertheless, the members of the CASAC Ozone Review Panel do not endorse the new 

primary ozone standard as being sufficiently protective of public health. The CASAC — as the 

Agency’s statutorily-established science advisory committee for advising you on the national 

ambient air quality standards — unanimously recommended decreasing the primary standard to 

within the range of 0.060–0.070 ppm. It is the Committee’s consensus scientific opinion that 

your decision to set the primary ozone standard above this range fails to satisfy the explicit stipulations of the Clean Air Act that you ensure an adequate margin of safety for all individuals, including sensitive populations. 

As you are well aware, numerous medical organizations and public health groups have 

also expressed their support of these CASAC recommendations. We sincerely hope that, in light 

of these scientific judgments and the supporting scientific evidence, you or your successor will 

select a more health-protective primary ozone standard during the upcoming review cycle. 

The CASAC was also greatly disappointed that you failed to change the form of the secondary standard to make it different from the primary standard. As stated in the preamble to the 

Final Rule, even in the previous 1996 ozone review, “there was general agreement between the 

EPA staff, CASAC, and the Administrator, ... that a cumulative, seasonal form was more biologically relevant than the previous 1-hour and new 8-hour average forms (61 FR 65716)” for the 

secondary standard. Therefore, in both the previous review and in this review, the Agency staff 

and its advisors agreed that a change in the form of the secondary standard was scientifically 

well-justified. 

The CASAC was pleased to see that the EPA Deputy Administrator clearly articulated a 

robust scientific defense of this position when he responded to Ms. Susan Dudley of the Office 

of Management and Budget (OMB) in a memorandum dated March 7, 2008 that, “In light of the 

available information, EPA believes that ozone-related effects on vegetation are clearly linked to 

cumulative, seasonal exposures and are not appropriately characterized by the use of a short-term

(8-hour) daily measure of ozone exposure.” However, the Committee was disappointed and surprised that written correspondence from OMB to the Agency apparently thwarted the opportunity 

to take a major step forward in setting a separate secondary ozone standard that is different in 

form from the primary standard. The CASAC is particularly dismayed at the suggestion that setting a secondary NAAQS that is different from the primary NAAQS is somehow against the law 

— which is not only at odds with a plain-language reading of the Clean Air Act but is also contrary to the Agency’s previous actions in setting a separate secondary standard for the initial 

NAAQS for both particulate matter and sulfur oxides, the latter of which (i.e., for SO2) remains 

in effect.

2
Unfortunately, this scientifically-sound approach of using a cumulative exposure index 

for welfare effects was not adopted, and the default position of using the primary standard for the 

secondary standard was once again instituted. Keeping the same form for the secondary Ozone 

NAAQS as for the primary standard is not supported by current scientific knowledge indicating 

that different indicator variables are needed to protect vegetation compared to public health. The 

CASAC was further disappointed that a secondary standard of the W126 form was not considered from within the Committee’s previously-recommended range of 7 to 15 ppm-hours. The 

CASAC sincerely hopes that, in the next round of Ozone NAAQS review, the Agency will be able 

to support and establish a reasonable and scientifically-defensible cumulative form for the secondary standard. 

We recognize that it will be difficult to bring the country into compliance with lower 

primary and secondary ozone standards. However, the fact that it is difficult does not mean that 

it is not achievable. The substantial progress made to date in lowering ambient ozone levels testifies to this. The CASAC believes that, in the future, we as a nation can devise effective and 

efficient ways to decrease ambient ozone concentrations to a sufficiently health- and welfareprotective level. However, in order to support this vital objective, EPA’s recent record of not 

adequately funding ozone research must end. The CASAC strongly supports the provision of 

additional funds to address the research needs that Agency staff have identified as being necessary for informing the process of setting both the primary and secondary ozone standards. 

As always, the members of the CASAC wish the Agency well in our crucial — and mutual — efforts to protect both human health and the environment. 

 

 Sincerely,

 /Signed/ 

Dr. Rogene F. Henderson, Chair 

 Clean Air Scientific Advisory Committee 

Attachment: Appendix A

3
NOTICE 

This report has been written as part of the activities of the U.S. Environmental 

Protection Agency’s (EPA) Clean Air Scientific Advisory Committee (CASAC), a Federal advisory committee administratively-located under the EPA Science Advisory Board 

(SAB) Staff Office that is chartered to provide extramural scientific information and advice to the Administrator and other officials of the EPA. The CASAC is structured to 

provide balanced, expert assessment of scientific matters related to issue and problems 

facing the Agency. This report has not been reviewed for approval by the Agency and, 

hence, the contents of this report do not necessarily represent the views and policies of

the EPA, nor of other agencies in the Executive Branch of the Federal government, nor 

does mention of trade names or commercial products constitute a recommendation for 

use. CASAC reports are posted on the SAB Web site at: http://www.epa.gov/casac. 

4
Appendix A – Roster of the CASAC Ozone Review Panel 

U.S. Environmental Protection Agency 

Science Advisory Board (SAB) Staff Office 

Clean Air Scientific Advisory Committee (CASAC) 

CASAC Ozone Review Panel

CASAC MEMBERS 

Dr. Rogene Henderson (Chair), Scientist Emeritus, Lovelace Respiratory Research Institute, Albuquerque, NM 

Dr. Ellis Cowling, University Distinguished Professor At-Large, Emeritus, Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina State University, Raleigh, NC 

Dr. James D. Crapo [M.D.], Professor, Department of Medicine, National Jewish Medical and Research 

Center, Denver, CO 

Dr. Douglas Crawford-Brown,

§

 Director, Carolina Environmental Program; Professor, Environmental 

Sciences and Engineering; and Professor, Public Policy, Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC 

Dr. Donna Kenski,

†

 Director of Data Analysis, Lake Michigan Air Directors Consortium (LADCO), 

Rosemont, IL 

Dr. Armistead (Ted) Russell,

§

 Georgia Power Distinguished Professor of Environmental Engineering, 

Environmental Engineering Group, School of Civil and Environmental Engineering, Georgia Institute of 

Technology, Atlanta, GA 

Dr. Jonathan Samet [M.D.],

†

 Professor and Chairman, Department of Epidemiology, Bloomberg School 

of Public Health, Johns Hopkins University, Baltimore, MD 

PANEL MEMBERS 

Dr. John Balmes, Professor, Department of Medicine, University of California San Francisco, University

of California – San Francisco, San Francisco, California 

Dr. William (Jim) Gauderman, Professor, Department of Preventive Medicine, School of Medicine, 

University of Southern California, Los Angeles, CA 

Dr. Paul J. Hanson, Senior Research and Development Scientist, Environmental Sciences Division, Oak 

Ridge National Laboratory (ORNL), Oak Ridge, TN 

Dr. Jack Harkema,* Professor, Department of Pathobiology, College of Veterinary Medicine, Michigan 

State University, East Lansing, MI 

Dr. Philip Hopke, Bayard D. Clarkson Distinguished Professor, Department of Chemical Engineering, 

Clarkson University, Potsdam, NY 

A-1
Dr. Michael T. Kleinman, Professor, Department of Community & Environmental Medicine, University 

of California – Irvine, Irvine, CA 

Dr. Allan Legge, President, Biosphere Solutions, Calgary, Alberta, Canada 

Dr. Morton Lippmann, Professor, Nelson Institute of Environmental Medicine, New York University 

School of Medicine, Tuxedo, NY 

Dr. Frederick J. Miller, Consultant, Cary, NC 

Dr. Maria Morandi, Assistant Professor of Environmental Science & Occupational Health, Department 

of Environmental Sciences, School of Public Health, University of Texas – Houston Health Science Center, Houston, TX 

Dr. Charles Plopper, Professor, Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California – Davis, Davis, California 

Mr. Richard L. Poirot, Environmental Analyst, Air Pollution Control Division, Department of Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT 

Dr. Elizabeth A. (Lianne) Sheppard, Research Professor, Biostatistics and Environmental & Occupational Health Sciences, Public Health and Community Medicine, University of Washington, Seattle, WA 

Dr. Frank Speizer, Edward Kass Professor of Medicine, Channing Laboratory, Harvard Medical School, 

Boston, MA 

Dr. James Ultman, Professor, Chemical Engineering, Bioengineering Program, Pennsylvania State University, University Park, PA

Dr. Sverre Vedal, Professor of Medicine, Department of Environmental and Occupational Health Sciences, School of Public Health and Community Medicine, University of Washington, Seattle, WA 

Dr. James (Jim) Zidek, Professor, Statistics, Science, University of British Columbia, Vancouver, BC, 

Canada 

Dr. Barbara Zielinska, Research Professor, Division of Atmospheric Science, Desert Research Institute, 

Reno, NV 

SCIENCE ADVISORY BOARD STAFF 

Mr. Fred Butterfield, CASAC Designated Federal Officer, 1200 Pennsylvania Avenue, N.W., Washington, DC, 20460, Phone: 202-343-9994, Fax: 202-233-0643 (butterfield.fred@epa.gov) 

§

Dr. Crawford-Brown was appointed to the Clean Air Scientific Advisory Committee in October 2006; Dr. Russell 

was a member of the CASAC Ozone Review Panel and was appointed to the Clean Air Scientific Advisory Committee in October 2006. 

†

Dr. Kenski and Dr. Samet were appointed to the Clean Air Scientific Advisory Committee in October 2007. 

*Dr. Harkema did not participate in this current CASAC Ozone Review Panel activity.

A-2
 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON D.C. 20460 

 

OFFICE OF THE ADMINISTRATOR 

 SCIENCE ADVISORY BOARD 

February 19, 2010 

EPA-CASAC-10-007 

The Honorable Lisa P. Jackson 

Administrator 

U.S. Environmental Protection Agency 

1200 Pennsylvania Avenue, N.W. 

Washington, D.C. 20460 

Subject: Review of EPA’s proposed Ozone National Ambient Air Quality Standard 

(Federal Register, Vol. 75, Nov. 11, January 19, 2010) 

Dear Administrator Jackson: 

At the request of EPA’s Office of Air Quality Planning and Standards (OAQPS), the 

Clean Air Scientific Advisory Committee (CASAC) Ozone Review Panel for the 

Reconsideration of the 2008 National Ambient Air Quality Standard (NAAQS) met via 

teleconference on January 25, 2010 to review EPA’s proposed NAAQS for ozone announced in 

the Federal Register on January 19, 2010 (see Enclosure for roster.) OAQPS asked CASAC for 

any “additional comment” on EPA’s proposed ozone (O3) standards. 

CASAC fully supports EPA’s proposed range of 0.060 – 0.070 parts per million (ppm) 

for the 8-hour primary ozone standard. CASAC considers this range to be justified by the 

scientific evidence as presented in the Air Quality Criteria for Ozone and Related Photochemical 

Oxidants (March 2006) and Review of the National Ambient Air Quality Standards for Ozone: 

Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper (July 2007). As 

stated in our letters of October 24, 2006, March 26, 2007 and April 7, 2008 to former 

Administrator Stephen L. Johnson, CASAC unanimously recommended selection of an 8-hour 

average ozone NAAQS within the range proposed by EPA (0.060 to 0.070 ppm).* In proposing 

this range, EPA has recognized the large body of data and risk analyses demonstrating that 

retention of the current standard would leave large numbers of individuals at risk for respiratory 

effects and/or other significant health impacts including asthma exacerbations, emergency room 

visits, hospital admissions and mortality. 

CASAC also supports EPA’s secondary ozone standard as proposed: a new cumulative, 

 

*

 See Letters from CASAC Chair Rogene Henderson, EPA-CASAC-07-001 (October 24, 2006), EPA-CASAC-07-

002 (March 26, 2007) and EPA-CASAC-08-000 (April 7, 2008) respectively. 
 2

seasonal standard expressed as an annual index of the sum of weighted hourly concentrations 

(i.e., the W126 form), cumulated over 12 hours per day (8am to 8pm) during the consecutive 3-

month period within the ozone season with the maximum index value, set as a level within the 

range of 7 to 5 ppm-hours. This W126 metric can be supported as an appropriate option for 

relating ozone exposure to vegetation responses, such as visible foliar injury and reductions in 

plant growth. We found the Agency’s reasoning, as stated in the Federal Register notice of 

January 19, 2010, to be supported by the extensive scientific evidence considered in the last 

review cycle. In choosing the W126 form for the secondary standard, the Agency acknowledges 

the distinction between the effects of acute exposures to ozone on human health and the effects 

of chronic ozone exposures on welfare, namely that vegetation effects are more dependent on the 

cumulative exposure to, and uptake of, ozone over the course of the entire growing season 

(defined to be a minimum of at least three months). In this proposal, the Agency is responding 

to the clear need for a secondary standard that is different from the primary standard in averaging 

time, level and form. 

As required by the law, CASAC’s recommendations are made without consideration of 

the cost or feasibility of implementation, considerations that are a part of the regulatory impact 

analysis. Although health and welfare effects of ozone will occur regardless of the origin of the 

ozone (i.e., natural, U.S. anthropogenic emissions or internationally transported emissions), we 

note that as levels for ozone standards move closer to “background” levels, new issues may arise 

with implementation. As the Agency moves forward with the next ozone review cycle, it would 

be well advised to carefully consider any new monitoring and implementation issues that may 

arise, particularly as background levels vary throughout the country. In addition, with 

implementation of the new W126 form for the secondary standard, we suggest that EPA collect 

information and seek additional research that could be used to inform continued refinement of 

the standard as well as its implementation. 

As always, we thank the Agency for the opportunity to provide advice on the proposed 

ozone NAAQS. 

Sincerely, 

 /Signed/ 

Dr. Jonathan M. Samet, Chair 

Clean Air Scientific Advisory Committee 

Enclosure 
 3

 

Enclosure 

U.S. Environmental Protection Agency 

Clean Air Scientific Advisory Committee (CASAC) 

Ozone Review Panel for the Reconsideration of the 2008 NAAQS 

CHAIR 

Dr. Jonathan M. Samet, Professor and Flora L. Thornton Chair, Department of Preventive 

Medicine, University of Southern California, Los Angeles, CA 

 

MEMBERS 

Dr. Joseph D. Brain, Cecil K. and Philip Drinker Professor of Environmental Physiology, 

Department of Environmental Health, Harvard School of Public Health, Boston, MA 

Dr. H. Christopher Frey, Professor, Department of Civil, Construction and Environmental 

Engineering, College of Engineering, North Carolina State University, Raleigh, NC 

Dr. Donna Kenski, Data Analysis Director, Lake Michigan Air Directors Consortium, 

Rosemont, IL 

Dr. Armistead (Ted) Russell, Professor, Department of Civil and Environmental Engineering, 

Georgia Institute of Technology, Atlanta, GA 

Dr. Helen Suh, Associate Professor, Department of Environmental Health, School of Public 

Health, Harvard University, Boston, MA 

Dr. Kathleen Weathers,*

 Senior Scientist, Cary Institute of Ecosystem Studies, Millbrook, NY 

CONSULTANTS 

Dr. John R. Balmes, Professor, Department of Medicine, Division of Occupational and 

Environmental Medicine, University of California, San Francisco, CA 

Dr. Ellis B. Cowling, University Distinguished Professor At-Large Emeritus, Colleges of 

Natural Resources and Agriculture and Life Sciences, North Carolina State University, Raleigh, 

NC 

*

 Did not participate in this review. 
 4

Dr. James Crapo, Professor of Medicine, Department of Medicine , National Jewish Medical 

and Research Center, Denver, CO 

Dr. William (Jim) Gauderman, Professor, Department of Preventive Medicine, University of 

Southern California, Los Angeles, CA 

Dr. Paul J. Hanson, Distinguished R&D Staff Member, Environmental Sciences Division, Oak 

Ridge National Laboratory, Oak Ridge, TN 

Dr. Jack Harkema, Professor, Department of Pathobiology, College of Veterinary Medicine, 

Michigan State University, East Lansing, MI 

Dr. Rogene Henderson, Senior Scientist Emeritus, Lovelace Respiratory Research Institute, 

Albuquerque, NM 

Dr. Philip Hopke, Bayard D. Clarkson Distinguished Professor, Department of Chemical and 

Biomolecular Engineering, Clarkson University, Potsdam, NY 

Dr. Michael T. Kleinman, Professor, Department of Medicine, Division of Occupational and 

Environmental Medicine, University of California, Irvine, Irvine, CA 

Dr. Allan Legge, President, Biosphere Solutions, Calgary, Alberta, Canada 

Dr. Morton Lippmann, Professor, Nelson Institute of Environmental Medicine, New York 

University School of Medicine, Tuxedo, NY 

Dr. Frederick J. Miller, Independent Consultant, Cary, NC 

Dr. Maria Morandi, Assistant Professor, Division of Environmental and Occupational Health, 

School of Public Health, University of Texas, Houston, TX 

Mr. Richard L. Poirot, Environmental Analyst, Air Pollution Control Division, Department of 

Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT 

Dr. Charles Plopper, Professor, Department of Anatomy, Physiology and Cell Biology, School 

of Veterinary Medicine, University of California, Davis, California 

Dr. Elizabeth A. (Lianne) Sheppard, Professor, Biostatistics and Environmental & 

Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA 

Dr. Frank Speizer, Edward Kass Professor of Medicine, Channing Laboratory, Harvard 

Medical School, Boston, MA 

Dr. James Ultman, Professor, Chemical Engineering, Bioengineering Program, Pennsylvania 

State University, University Park, PA 
 5

Dr. Sverre Vedal, Professor, Department of Environmental and Occupational Health Sciences, 

School of Public Health, University of Washington, Seattle, WA 

Dr. Barbara Zielinska, Research Professor, Division of Atmospheric Sciences, Desert Research 

Institute, Reno, NV 

SCIENCE ADVISORY BOARD STAFF 

Dr. Holly Stallworth, Designated Federal Officer, Science Advisory Board Staff Office, 

Washington, D.C. 
Attachment 3

2010 Reconsideration Proposal
2938 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Parts 50 and 58 

[EPA–HQ–OAR–2005–0172; FRL–9102–1] 

RIN 2060–AP98 

National Ambient Air Quality 

Standards for Ozone 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Proposed rule. 

SUMMARY: Based on its reconsideration 

of the primary and secondary national 

ambient air quality standards (NAAQS) 

for ozone (O3) set in March 2008, EPA 

proposes to set different primary and 

secondary standards than those set in 

2008 to provide requisite protection of 

public health and welfare, respectively. 

With regard to the primary standard for 

O3, EPA proposes that the level of the 

8-hour primary standard, which was set 

at 0.075 ppm in the 2008 final rule, 

should instead be set at a lower level 

within the range of 0.060 to 0.070 parts 

per million (ppm), to provide increased 

protection for children and other ‘‘at 

risk’’ populations against an array of O3- 

related adverse health effects that range 

from decreased lung function and 

increased respiratory symptoms to 

serious indicators of respiratory 

morbidity including emergency 

department visits and hospital 

admissions for respiratory causes, and 

possibly cardiovascular-related 

morbidity as well as total nonaccidental and cardiopulmonary 

mortality. With regard to the secondary 

standard for O3, EPA proposes that the 

secondary O3 standard, which was set 

identical to the revised primary 

standard in the 2008 final rule, should 

instead be a new cumulative, seasonal 

standard expressed as an annual index 

of the sum of weighted hourly 

concentrations, cumulated over 12 

hours per day (8 am to 8 pm) during the 

consecutive 3-month period within the 

O3 season with the maximum index 

value, set at a level within the range of 

7 to 15 ppm-hours, to provide increased 

protection against O3-related adverse 

impacts on vegetation and forested 

ecosystems. 

DATES: Written comments on this 

proposed rule must be received by 

March 22, 2010. 

Public Hearings: Three public 

hearings are scheduled for this proposed 

rule. Two of the public hearings will be 

held on February 2, 2010 in Arlington, 

Virginia, and Houston, Texas. The third 

public hearing will be held on February 

4, 2010 in Sacramento, California. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

OAR–2005–0172, by one of the 

following methods: 

• http://www.regulations.gov: Follow 

the on-line instructions for submitting 

comments. 

• E-mail: a-and-r-Docket@epa.gov. 

• Fax: 202–566–9744. 

• Mail: Docket No. EPA–HQ–OAR– 

2005–0172, Environmental Protection 

Agency, Mail code 6102T, 1200 

Pennsylvania Ave., NW., Washington, 

DC 20460. Please include a total of two 

copies. 

• Hand Delivery: Docket No. EPA– 

HQ–OAR–2005–0172, Environmental 

Protection Agency, EPA West, Room 

3334, 1301 Constitution Ave., NW., 

Washington, DC. Such deliveries are 

only accepted during the Docket’s 

normal hours of operation, and special 

arrangements should be made for 

deliveries of boxed information. 

Public Hearings: Three public 

hearings are scheduled for this proposed 

rule. Two of the public hearings will be 

held on February 2, 2010 in Arlington, 

Virginia and Houston, Texas. The third 

public hearing will be held on February 

4, 2010 in Sacramento, California. The 

hearings will be held at the following 

locations: 

Arlington, Virginia—February 2, 2010 

Hyatt Regency Crystal City @ Reagan 

National Airport, Washington Room 

(located on the Ballroom Level), 2799 

Jefferson Davis Highway, Arlington, 

Virginia 22202, Telephone: 703–418– 

1234. 

Houston, Texas—February 2, 2010 

Hilton Houston Hobby Airport, Moody 

Ballroom (located on the ground 

floor), 8181 Airport Boulevard, 

Houston, Texas 77061, Telephone: 

713–645–3000. 

Sacramento, California—February 4, 

2010 

Four Points by Sheraton Sacramento 

International Airport, Natomas 

Ballroom, 4900 Duckhorn Drive, 

Sacramento, California 95834, 

Telephone: 916–263–9000. 

See the SUPPLEMENTARY INFORMATION

under ‘‘Public Hearings’’ for further 

information. 

Instructions: Direct your comments to 

Docket ID No. EPA–HQ–OAR–2005– 

0172. The EPA’s policy is that all 

comments received will be included in 

the public docket without change and 

may be made available online at 

www.regulations.gov, including any 

personal information provided, unless 

the comment includes information 

claimed to be Confidential Business 

Information (CBI) or other information 

whose disclosure is restricted by statute. 

Do not submit information that you 

consider to be CBI or otherwise 

protected through www.regulations.gov 

or e-mail. The www.regulations.gov Web 

site is an ‘‘anonymous access’’ system, 

which means EPA will not know your 

identity or contact information unless 

you provide it in the body of your 

comment. If you send an e-mail 

comment directly to EPA without going 

through www.regulations.gov, your email address will be automatically 

captured and included as part of the 

comment that is placed in the public 

docket and made available on the 

Internet. If you submit an electronic 

comment, EPA recommends that you 

include your name and other contact 

information in the body of your 

comment and with any disk or CD–ROM 

you submit. If EPA cannot read your 

comment due to technical difficulties 

and cannot contact you for clarification, 

EPA may not be able to consider your 

comment. Electronic files should avoid 

the use of special characters, any form 

of encryption, and be free of any defects 

or viruses. 

Docket: All documents in the docket 

are listed in the www.regulations.gov 

index. Although listed in the index, 

some information is not publicly 

available, e.g., CBI or other information 

whose disclosure is restricted by statute. 

Certain other material, such as 

copyrighted material, will be publicly 

available only in hard copy. Publicly 

available docket materials are available 

either electronically in 

www.regulations.gov or in hard copy at 

the Air and Radiation Docket and 

Information Center, EPA/DC, EPA West, 

Room 3334, 1301 Constitution Ave., 

NW., Washington, DC. The Public 

Reading Room is open from 8:30 a.m. to 

4:30 p.m., Monday through Friday, 

excluding legal holidays. The telephone 

number for the Public Reading Room is 

(202) 566–1744 and the telephone 

number for the Air and Radiation 

Docket and Information Center is (202) 

566–1742. 

FOR FURTHER INFORMATION CONTACT: Ms. 

Susan Lyon Stone, Health and 

Environmental Impacts Division, Office 

of Air Quality Planning and Standards, 

U.S. Environmental Protection Agency, 

Mail Code C504–06, Research Triangle 

Park, NC 27711; telephone: 919–541– 

1146; fax: 919–541–0237; e-mail: 

stone.susan@epa.gov. 

SUPPLEMENTARY INFORMATION: 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 2939 

General Information 

What Should I Consider as I Prepare My 

Comments for EPA? 

1. Submitting CBI. Do not submit this 

information to EPA through http:// 

www.regulations.gov or e-mail. Clearly 

mark the part or all of the information 

that you claim to be CBI. For CBI 

information in a disk or CD–ROM that 

you mail to EPA, mark the outside of the 

disk or CD–ROM as CBI and then 

identify electronically within the disk or 

CD–ROM the specific information that 

is claimed as CBI. In addition to one 

complete version of the comment that 

includes information claimed as CBI, a 

copy of the comment that does not 

contain the information claimed as CBI 

must be submitted for inclusion in the 

public docket. Information so marked 

will not be disclosed except in 

accordance with procedures set forth in 

40 CFR part 2. 

2. Tips for Preparing Your Comments. 

When submitting comments, remember 

to: 

• Identify the rulemaking by docket 

number and other identifying 

information (subject heading, Federal 

Register date and page number). 

• Follow directions—The Agency 

may ask you to respond to specific 

questions or organize comments by 

referencing a Code of Federal 

Regulations (CFR) part or section 

number. 

• Explain why you agree or disagree, 

suggest alternatives, and substitute 

language for your requested changes. 

• Describe any assumptions and 

provide any technical information and/ 

or data that you used. 

• Provide specific examples to 

illustrate your concerns, and suggest 

alternatives. 

• Explain your views as clearly as 

possible, avoiding the use of profanity 

or personal threats. 

• Make sure to submit your 

comments by the comment period 

deadline identified. 

Availability of Related Information 

A number of documents relevant to 

this rulemaking are available on EPA 

web sites. The Air Quality Criteria for 

Ozone and Related Photochemical 

Oxidants (2006 Criteria Document) (two 

volumes, EPA/and EPA/, date) is 

available on EPA’s National Center for 

Environmental Assessment Web site. To 

obtain this document, go to http:// 

www.epa.gov/ncea, and click on Ozone 

in the Quick Finder section. This will 

open a page with a link to the March 

2006 Air Quality Criteria Document. 

The 2007 Staff Paper, human exposure 

and health risk assessments, vegetation 

exposure and impact assessment, and 

other related technical documents are 

available on EPA’s Office of Air Quality 

Planning and Standards (OAQPS) 

Technology Transfer Network (TTN) 

web site. The updated final 2007 Staff 

Paper is available at: http://epa.gov/ttn/ 

naaqs/standards/ozone/s_o3_cr_sp.html 

and the exposure and risk assessments 

and other related technical documents 

are available at http://www.epa.gov/ttn/ 

naaqs/standards/ozone/ 

s_o3_cr_td.html. The Response to 

Significant Comments Document is 

available at: http://www.epa.gov/ttn/ 

naaqs/standards/ozone/ 

s_o3_cr_rc.html. These and other related 

documents are also available for 

inspection and copying in the EPA 

docket identified above. 

Public Hearings 

The public hearings on February 2, 

2010 and February 4, 2010 will provide 

interested parties the opportunity to 

present data, views, or arguments 

concerning the proposed rule. The EPA 

may ask clarifying questions during the 

oral presentations, but will not respond 

to the presentations at that time. Written 

statements and supporting information 

submitted during the comment period 

will be considered with the same weight 

as any oral comments and supporting 

information presented at the public 

hearing. Written comments must be 

received by the last day of the comment 

period, as specified in this proposed 

rulemaking. 

The public hearings will begin at 9:30 

a.m. and continue until 7:30 p.m. (local 

time) or later, if necessary, depending 

on the number of speakers wishing to 

participate. The EPA will make every 

effort to accommodate all speakers that 

arrive and register before 7:30 p.m. A 

lunch break is scheduled from 12:30 

p.m. until 2 p.m. 

If you would like to present oral 

testimony at the hearings, please notify 

Ms. Tricia Crabtree (C504–02), U.S. 

EPA, Research Triangle Park, NC 27711. 

The preferred method for registering is 

by e-mail (crabtree.tricia@epa.gov). Ms. 

Crabtree may be reached by telephone at 

(919) 541–5688. She will arrange a 

general time slot for you to speak. The 

EPA will make every effort to follow the 

schedule as closely as possible on the 

day of the hearing. 

Oral testimony will be limited to five 

(5) minutes for each commenter to 

address the proposal. We will not be 

providing equipment for commenters to 

show overhead slides or make 

computerized slide presentations unless 

we receive special requests in advance. 

Commenters should notify Ms. Crabtree 

if they will need specific audiovisual 

(AV) equipment. Commenters should 

also notify Ms. Crabtree if they need 

specific translation services for nonEnglish speaking commenters. The EPA 

encourages commenters to provide 

written versions of their oral testimonies 

either electronically on computer disk, 

CD–ROM, or in paper copy. 

The hearing schedules, including lists 

of speakers, will be posted on EPA’s 

Web site for the proposal at http:// 

www.epa.gov/ttn/naaqs/standards/ 

ozone/s_o3_cr_fr.html prior to the 

hearing. Verbatim transcripts of the 

hearings and written statements will be 

included in the rulemaking docket. 

Children’s Environmental Health 

Consideration of children’s 

environmental health plays a central 

role in the reconsideration of the 2008 

final decision on the O3 NAAQS and 

EPA’s decision to propose to set the 

8-hour primary O3 standard at a level 

within the range of 0.060 to 0.070 ppm. 

Technical information that pertains to 

children, including the evaluation of 

scientific evidence, policy 

considerations, and exposure and risk 

assessments, is discussed in all of the 

documents listed above in the section 

on the availability of related 

information. These documents include: 

the Air Quality Criteria for Ozone and 

Other Related Photochemical Oxidants; 

the 2007 Staff Paper; exposure and risk 

assessments and other related 

documents; and the Response to 

Significant Comments. All of these 

documents are available on the Web, as 

described above, and are in the public 

docket for this rulemaking. The public 

is invited to submit comments or 

identify peer-reviewed studies and data 

that assess effects of early life exposure 

to O3. 

Table of Contents 

The following topics are discussed in 

this preamble: 

I. Background 

A. Legislative Requirements 

B. Related Control Requirements 

C. Review of Air Quality Criteria and 

Standards for O3

D. Reconsideration of the 2008 O3 NAAQS 

Final Rule 

1. Decision to Initiate a Rulemaking to 

Reconsider 

2. Ongoing Litigation 

II. Rationale for Proposed Decision on the 

Level of the Primary Standard 

A. Health Effects Information 

1. Overview of Mechanisms 

2. Nature of Effects 

3. Interpretation and Integration of Health 

Evidence 

4. O3-Related Impacts on Public Health 

B. Human Exposure and Health Risk 

Assessments 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
2940 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

1The legislative history of section 109 indicates 

that a primary standard is to be set at ‘‘the 

maximum permissible ambient air level * * * 

which will protect the health of any [sensitive] 

group of the population,’’ and that for this purpose 

‘‘reference should be made to a representative 

sample of persons comprising the sensitive group 

rather than to a single person in such a group’’ [S. 

Rep. No. 91–1196, 91st Cong., 2d Sess. 10 (1970)]. 

2Welfare effects as defined in section 302(h) (42 

U.S.C. 7602(h)) include, but are not limited to, 

‘‘effects on soils, water, crops, vegetation, man-made 

materials, animals, wildlife, weather, visibility, and 

climate, damage to and deterioration of property, 

and hazards to transportation, as well as effects on 

economic values and on personal comfort and wellbeing.’’ 

1. Exposure Analyses 

2. Quantitative Health Risk Assessment 

C. Reconsideration of the Level of the 

Primary Standard 

1. Evidence and Exposure/Risk-Based 

Considerations 

2. CASAC Views Prior to 2008 Decision 

3. Basis for 2008 Decision on the Primary 

Standard 

4. CASAC Advice Following 2008 Decision 

5. Administrator’s Proposed Conclusions 

D. Proposed Decision on the Level of the 

Primary Standard 

III. Communication of Public Health 

Information 

IV. Rationale for Proposed Decision on the 

Secondary Standard 

A. Vegetation Effects Information 

1. Mechanisms 

2. Nature of Effects 

3. Adversity of Effects 

B. Biologically Relevant Exposure Indices 

C. Vegetation Exposure and Impact 

Assessment 

1. Exposure Characterization 

2. Assessment of Risks to Vegetation 

D. Reconsideration of Secondary Standard 

1. Considerations Regarding 2007 Proposed 

Cumulative Seasonal Standard 

2. Considerations Regarding 2007 Proposed 

8-Hour Standard 

3. Basis for 2008 Decision on the 

Secondary Standard 

4. CASAC Views Following 2008 Decision 

5. Administrator’s Proposed Conclusions 

E. Proposed Decision on the Secondary O3

Standard 

V. Revision of Appendix P—Interpretation of 

the NAAQS for O3 and Proposed 

Revisions to the Exceptional Events Rule 

A. Background 

B. Interpretation of the Secondary O3

Standard 

C. Clarifications Related to the Primary 

Standard 

D. Revisions to Exceptions From Standard 

Data Completeness Requirements for the 

Primary Standard 

E. Elimination of the Requirement for 90 

Percent Completeness of Daily Data 

Across Three Years 

F. Administrator Discretion To Use 

Incomplete Data 

G. Truncation Versus Rounding 

H. Data Selection 

I. Exceptional Events Information 

Submission Schedule 

VI. Ambient Monitoring Related to Proposed 

O3 Standards 

A. Background 

B. Urban Monitoring Requirements 

C. Non-Urban Monitoring Requirements 

D. Revisions to the Length of the Required 

O3 Monitoring Season 

VII. Implementation of Proposed O3

Standards 

A. Designations 

B. State Implementation Plans 

C. Trans-boundary Emissions 

VIII. Statutory and Executive Order Reviews 

A. Executive Order 12866: Regulatory 

Planning and Review 

B. Paperwork Reduction Act 

C. Regulatory Flexibility Act 

D. Unfunded Mandates Reform Act 

E. Executive Order 13132: Federalism 

F. Executive Order 13175: Consultation 

and Coordination With Indian Tribal 

Governments 

G. Executive Order 13045: Protection of 

Children From Environmental Health 

and Safety Risks 

H. Executive Order 13211: Actions That 

Significantly Affect Energy Supply, 

Distribution or Use 

I. National Technology Transfer and 

Advancement Act 

J. Executive Order 12898: Federal Actions 

To Address Environmental Justice in 

Minority Populations and Low-Income 

Populations 

References 

I. Background 

The proposed decisions presented in 

this notice are based on a 

reconsideration of the 2008 O3 NAAQS 

final rule (73 FR 16436, March 27, 

2008), which revised the level of the 8- 

hour primary O3 standard to 0.075 ppm 

and revised the secondary O3 standard 

by making it identical to the revised 

primary standard. This reconsideration 

is based on the scientific and technical 

information and analyses on which the 

March 2008 O3 NAAQS rulemaking was 

based. Therefore, much of the 

information included in this notice is 

drawn directly from information 

included in the 2007 proposed rule (72 

FR 37818, July 11, 2007) and the 2008 

final rule (73 FR 16436). 

A. Legislative Requirements 

Two sections of the Clean Air Act 

(CAA) govern the establishment and 

revision of the NAAQS. Section 108 (42 

U.S.C. 7408) directs the Administrator 

to identify and list ‘‘air pollutants’’ that 

in her ‘‘judgment, cause or contribute to 

air pollution which may reasonably be 

anticipated to endanger public health or 

welfare’’ and satisfy two other criteria, 

including ‘‘whose presence * * * in the 

ambient air results from numerous or 

diverse mobile or stationary sources’’ 

and to issue air quality criteria for those 

that are listed. Air quality criteria are 

intended to ‘‘accurately reflect the latest 

scientific knowledge useful in 

indicating the kind and extent of all 

identifiable effects on public health or 

welfare which may be expected from the 

presence of [a] pollutant in the ambient 

air. * * *’’ 

Section 109 (42 U.S.C. 7409) directs 

the Administrator to propose and 

promulgate ‘‘primary’’ and ‘‘secondary’’ 

NAAQS for pollutants for which air 

quality criteria are issued. Section 

109(b)(1) defines a primary standard as 

one ‘‘the attainment and maintenance of 

which in the judgment of the 

Administrator, based on such criteria 

and allowing an adequate margin of 

safety, are requisite to protect the public 

health.’’ 1 A secondary standard, as 

defined in section 109(b)(2), must 

‘‘specify a level of air quality the 

attainment and maintenance of which, 

in the judgment of the Administrator, 

based on such criteria, is requisite to 

protect the public welfare from any 

known or anticipated adverse effects 

associated with the presence of such air 

pollutant in the ambient air.’’ 2

The requirement that primary 

standards include an adequate margin of 

safety was intended to address 

uncertainties associated with 

inconclusive scientific and technical 

information available at the time of 

standard setting. It was also intended to 

provide a reasonable degree of 

protection against hazards that research 

has not yet identified. Lead Industries 

Association v. EPA, 647 F.2d 1130, 1154 

(DC Cir 1980), cert. denied, 449 U.S. 

1042 (1980); American Petroleum 

Institute v. Costle, 665 F.2d 1176, 1186 

(DC Cir. 1981), cert. denied, 455 U.S. 

1034 (1982). Both kinds of uncertainties 

are components of the risk associated 

with pollution at levels below those at 

which human health effects can be said 

to occur with reasonable scientific 

certainty. Thus, in selecting primary 

standards that include an adequate 

margin of safety, the Administrator is 

seeking not only to prevent pollution 

levels that have been demonstrated to be 

harmful but also to prevent lower 

pollutant levels that may pose an 

unacceptable risk of harm, even if the 

risk is not precisely identified as to 

nature or degree. The CAA does not 

require the Administrator to establish a 

primary NAAQS at a zero-risk level or 

at background concentration levels, see 

Lead Industries Association v. EPA, 647 

F.2d at 1156 n. 51, but rather at a level 

that reduces risk sufficiently so as to 

protect public health with an adequate 

margin of safety. 

In addressing the requirement for an 

adequate margin of safety, EPA 

considers such factors as the nature and 

severity of the health effects involved, 

the size of the population(s) at risk, and 

the kind and degree of the uncertainties 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 2941 

3See EPA report, Evaluating Ozone Control 

Programs in the Eastern United States: Focus on the 

NOX Budget Trading Program, 2004. 

that must be addressed. The selection of 

any particular approach to providing an 

adequate margin of safety is a policy 

choice left specifically to the 

Administrator’s judgment. Lead 

Industries Association v. EPA, 647 F.2d 

at 1161–62; Whitman v. American 

Trucking Associations, 531 U.S. 457, 

495 (2001). 

In setting standards that are 

‘‘requisite’’ to protect public health and 

welfare, as provided in section 109(b), 

EPA’s task is to establish standards that 

are neither more nor less stringent than 

necessary for these purposes. Whitman 

v. America Trucking Associations, 531 

U.S. 457, 473. In establishing ‘‘requisite’’ 

primary and secondary standards, EPA 

may not consider the costs of 

implementing the standards. Id. at 471. 

Section 109(d)(1) of the CAA requires 

that ‘‘not later than December 31, 1980, 

and at 5-year intervals thereafter, the 

Administrator shall complete a 

thorough review of the criteria 

published under section 108 and the 

national ambient air quality standards 

* * * and shall make such revisions in 

such criteria and standards and 

promulgate such new standards as may 

be appropriate. * * *’’ Section 109(d)(2) 

requires that an independent scientific 

review committee ‘‘shall complete a 

review of the criteria * * * and the 

national primary and secondary ambient 

air quality standards * * * and shall 

recommend to the Administrator any 

new * * * standards and revisions of 

existing criteria and standards as may be 

appropriate. * * *’’ This independent 

review function is performed by the 

Clean Air Scientific Advisory 

Committee (CASAC) of EPA’s Science 

Advisory Board. 

B. Related Control Requirements 

States have primary responsibility for 

ensuring attainment and maintenance of 

ambient air quality standards once EPA 

has established them. Under section 110 

of the Act (42 U.S.C. 7410) and related 

provisions, States are to submit, for EPA 

approval, State implementation plans 

(SIPs) that provide for the attainment 

and maintenance of such standards 

through control programs directed to 

emission sources. 

The majority of man-made nitrogen 

oxides (NOX) and volatile organic 

compounds (VOC) emissions that 

contribute to O3 formation in the United 

States come from three types of sources: 

Mobile sources, industrial processes 

(which include consumer and 

commercial products), and the electric 

power industry.3 Mobile sources and 

the electric power industry were 

responsible for 78 percent of annual 

NOX emissions in 2004. That same year, 

99 percent of man-made VOC emissions 

came from industrial processes 

(including solvents) and mobile sources. 

Emissions from natural sources, such as 

trees, may also comprise a significant 

portion of total VOC emissions in 

certain regions of the country, especially 

during the O3 season, which are 

considered natural background 

emissions. 

The EPA has developed new 

emissions standards for many types of 

stationary sources and for nearly every 

class of mobile sources in the last 

decade to reduce O3 by decreasing 

emissions of NOX and VOC. These 

programs complement State and local 

efforts to improve O3 air quality and 

meet the 0.084 ppm 8-hour national 

standards. Under title II of the CAA, 42 

U.S.C. 7521–7574), EPA has established 

new emissions standards for nearly 

every type of automobile, truck, bus, 

motorcycle, earth mover, and aircraft 

engine, and for the fuels used to power 

these engines. EPA also established new 

standards for the smaller engines used 

in small watercraft, lawn and garden 

equipment. In March 2008, EPA 

promulgated new standards for 

locomotive and marine diesel engines 

and in August 2009, proposed to control 

emissions from ocean-going vessels. 

Benefits from engine standards 

increase modestly each year as older, 

more-polluting vehicles and engines are 

replaced with newer, cleaner models. In 

time, these programs will yield 

substantial emission reductions. 

Benefits from fuel programs generally 

begin as soon as a new fuel is available. 

The reduction of VOC emissions from 

industrial processes has been achieved 

either directly or indirectly through 

implementation of control technology 

standards, including maximum 

achievable control technology, 

reasonably available control technology, 

and best available control technology 

standards; or are anticipated due to 

proposed or upcoming proposals based 

on generally available control 

technology or best available controls 

under provisions related to consumer 

and commercial products. These 

standards have resulted in VOC 

emission reductions of almost a million 

tons per year accumulated starting in 

1997 from a variety of sources including 

combustion sources, coating categories, 

and chemical manufacturing. EPA has 

also finalized emission standards and 

fuel requirements for new stationary 

engines. In the area of consumer and 

commercial products, EPA has finalized 

new national VOC emission standards 

for aerosol coatings and is working 

toward amending existing rules to 

establish new nationwide VOC content 

limits for household and institutional 

consumer products and architectural 

and industrial maintenance coatings. 

The aerosol coatings rule took effect in 

July 2009; the compliance date for both 

the amended consumer product rule 

and architectural coatings rule is 

anticipated to be January 2011. These 

actions are expected to yield significant 

new VOC reductions—about 200,000 

tons per year. Additionally, in ozone 

nonattainment areas, we anticipate 

reductions of an additional 25,000 tons 

per year as States adopt rules this year 

implementing control techniques 

recommendations issued in 2008 for 4 

additional categories of consumer and 

commercial products, typically surface 

coatings and adhesives used in 

industrial manufacturing operations. 

These emission reductions primarily 

result from solvent controls and 

typically occur where and when the 

solvent is used, such as during 

manufacturing processes. 

The power industry is one of the 

largest emitters of NOX in the United 

States. Power industry emission sources 

include large electric generating units 

(EGU) and some large industrial boilers 

and turbines. The EPA’s landmark Clean 

Air Interstate Rule (CAIR), issued on 

March 10, 2005, was designed to 

permanently cap power industry 

emissions of NOX in the eastern United 

States. The first phase of the cap was to 

begin in 2009, and a lower second phase 

cap was to begin in 2015. The EPA had 

projected that by 2015, the CAIR and 

other programs would reduce NOX

emissions during the O3 season by about 

50 percent and annual NOX emissions 

by about 60 percent from 2003 levels in 

the Eastern U.S. However, on July 11, 

2008 and December 23, 2008, the U.S. 

Court of Appeals for the DC Circuit 

issued decisions on petitions for review 

of the CAIR. In its July 11 opinion, the 

court found CAIR unlawful and decided 

to vacate CAIR and its associated 

Federal implementation plans (FIPs) in 

their entirety. On December 23, the 

court granted EPA’s petition for 

rehearing to the extent that it remanded 

without vacatur for EPA to conduct 

further proceedings consistent with the 

Court’s prior opinion. Under this 

decision, CAIR will remain in place 

only until replaced by EPA with a rule 

that is consistent with the Court’s July 


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11 opinion. The EPA recognizes the 

need in our CAIR replacement effort to 

address the reconsidered ozone 

standard, and we are currently assessing 

our options for the best way to 

accomplish this. It should also be noted 

that new electric generating units 

(EGUs) are also subject to NOX limits 

under New Source Performance 

Standards (NSPS) under CAA section 

111, as well as either nonattainment 

new source review or prevention of 

significant deterioration requirements. 

With respect to agricultural sources, 

the U.S. Department of Agriculture 

(USDA) has approved conservation 

systems and activities that reduce 

agricultural emissions of NOX and VOC. 

Current practices that may reduce 

emissions of NOX and VOC include 

engine replacement programs, diesel 

retrofit programs, manipulation of 

pesticide applications including timing 

of applications, and animal feeding 

operations waste management 

techniques. The EPA recognizes that 

USDA has been working with the 

agricultural community to develop 

conservation systems and activities to 

control emissions of O3 precursors. 

These conservation activities are 

voluntarily adopted through the use of 

incentives provided to the agricultural 

producer. In cases where the States need 

these measures to attain the standard, 

the measures could be adopted. The 

EPA will continue to work with USDA 

on these activities with efforts to 

identify and/or improve the control 

efficiencies, prioritize the adoption of 

these conservation systems and 

activities, and ensure that appropriate 

criteria are used for identifying the most 

effective application of conservation 

systems and activities. 

The EPA will work together with 

USDA and with States to identify 

appropriate measures to meet the 

primary and secondary standards, 

including site-specific conservation 

systems and activities. Based on prior 

experience identifying conservation 

measures and practices to meet the PM 

NAAQS requirements, the EPA will use 

a similar process to identify measures 

that could meet the O3 requirements. 

The EPA anticipates that certain USDAapproved conservation systems and 

activities that reduce agricultural 

emissions of NOX and VOC may be able 

to satisfy the requirements for 

applicable sources to implement 

reasonably available control measures 

for purposes of attaining the primary 

and secondary O3 NAAQS. 

C. Review of Air Quality Criteria and 

Standards for O3

In 1971, EPA first established primary 

and secondary NAAQS for 

photochemical oxidants (36 FR 8186). 

Both primary and secondary standards 

were set at a level of 0.08 parts per 

million (ppm), 1-hr average, total 

photochemical oxidants, not to be 

exceeded more than one hr per year. In 

1977, EPA announced the first periodic 

review of the air quality criteria in 

accordance with section 109(d)(1) of the 

Act. The EPA published a final decision 

in 1979 (44 FR 8202). Both primary and 

secondary standard levels were revised 

from 0.08 to 0.12 ppm. The indicator 

was revised from photochemical 

oxidants to O3, and the form of the 

standards was revised from a 

deterministic to a statistical form, which 

defined attainment of the standards as 

occurring when the expected number of 

days per calendar year with maximum 

hourly average concentration greater 

than 0.12 ppm is equal to or less than 

one. In 1983, EPA announced that the 

second periodic review of the primary 

and secondary standards for O3 had 

been initiated. Following review and 

publication of air quality criteria and a 

supplement, EPA published a proposed 

decision (57 FR 35542) in August 1992 

that announced EPA’s intention to 

proceed as rapidly as possible with the 

next review of the air quality criteria 

and standards for O3 in light of 

emerging evidence of health effects 

related to 6- to 8-hr O3 exposures. In 

March 1993, EPA concluded the review 

by deciding that revisions to the 

standards were not warranted at that 

time (58 FR 13008). 

In August 1992 (57 FR 35542), EPA 

announced plans to initiate the third 

periodic review of the air quality criteria 

and O3 NAAQS. On the basis of the 

scientific evidence contained in the 

1996 CD (U.S. EPA 1996a) and the 1996 

Staff Paper (U.S. EPA, 1996b), and 

related technical support documents, 

linking exposures to ambient O3 to 

adverse health and welfare effects at 

levels allowed by the then existing 

standards, EPA proposed to revise the 

primary and secondary O3 standards in 

December 1996 (61 FR 65716). The EPA 

proposed to replace the then existing 

1-hour primary and secondary standards 

with 8-hour average O3 standards set at 

a level of 0.08 ppm (equivalent to 0.084 

ppm using standard rounding 

conventions). The EPA also proposed, 

in the alternative, to establish a new 

distinct secondary standard using a 

biologically based cumulative seasonal 

form. The EPA completed the review in 

July 1997 (62 FR 38856) by setting the 

primary standard at a level of 0.08 ppm, 

based on the annual fourth-highest daily 

maximum 8-hr average concentration, 

averaged over three years, and setting 

the secondary standard identical to the 

revised primary standard. 

The EPA initiated the most recent 

periodic review of the air quality criteria 

and standards for O3 in September 2000 

with a call for information (65 FR 

57810; September 26, 2000) for the 

development of a revised Air Quality 

Criteria Document for O3 and Other 

Photochemical Oxidants (henceforth the 

‘‘2006 Criteria Document’’). A project 

work plan (EPA, 2002) for the 

preparation of the Criteria Document 

was released in November 2002 for 

CASAC and public review. The EPA 

held a series of workshops in mid-2003 

on several draft chapters of the Criteria 

Document to obtain broad input from 

the relevant scientific communities. 

These workshops helped to inform the 

preparation of the first draft Criteria 

Document (EPA, 2005a), which was 

released for CASAC and public review 

on January 31, 2005; a CASAC meeting 

was held on May 4–5, 2005 to review 

the first draft Criteria Document. A 

second draft Criteria Document (EPA, 

2005b) was released for CASAC and 

public review on August 31, 2005, and 

was discussed along with a first draft 

Staff Paper (EPA, 2005c) at a CASAC 

meeting held on December 6–8, 2005. In 

a February 16, 2006 letter to the 

Administrator, CASAC provided 

comments on the second draft Criteria 

Document (Henderson, 2006a), and the 

final 2006 Criteria Document (EPA, 

2006a) was released on March 21, 2006. 

In a June 8, 2006 letter to the 

Administrator (Henderson, 2006b), 

CASAC provided additional advice to 

the Agency concerning chapter 8 of the 

final 2006 Criteria Document 

(Integrative Synthesis) to help inform 

the second draft Staff Paper. 

A second draft Staff Paper (EPA, 

2006b) was released on July 17, 2006 

and reviewed by CASAC on August 24– 

25, 2006. In an October 24, 2006 letter 

to the Administrator, CASAC provided 

advice and recommendations to the 

Agency concerning the second draft 

Staff Paper (Henderson, 2006c). A final 

2007 Staff Paper (EPA, 2007a) was 

released on January 31, 2007. In a March 

26, 2007 letter (Henderson, 2007), 

CASAC offered additional advice to the 

Administrator with regard to 

recommendations and revisions to the 

primary and secondary O3 NAAQS. 

The schedule for completion of the 

2008 rulemaking was governed by a 

consent decree resolving a lawsuit filed 

in March 2003 by a group of plaintiffs 

representing national environmental 


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4American Lung Association v. Whitman (No. 

1:03CV00778, D.DC 2003). 

5The level of the 8-hour primary ozone standard 

was set at 0.075 ppm, while CASAC unanimously 

recommended a range between 0.060 and 0.070 

ppm. 

6The Administrator also noted the exchange that 

had occurred between EPA and the Office of 

Management and Budget (OMB) with regard to the 

final decision on the secondary standard, as 

discussed in the 2008 final rule (73 FR 16497). 

and public health organizations, 

alleging that EPA had failed to complete 

the review within the period provided 

by statute.4 The modified consent 

decree that governed the 2008 

rulemaking, entered by the court on 

December 16, 2004, provided that EPA 

sign for publication notices of proposed 

and final rulemaking concerning its 

review of the O3 NAAQS no later than 

March 28, 2007 and December 19, 2007, 

respectively. That consent decree was 

further modified in October 2006 to 

change these proposed and final 

rulemaking dates to no later than May 

30, 2007 and February 20, 2008, 

respectively. These dates for signing the 

publication notices of proposed and 

final rulemaking were further extended 

to no later than June 20, 2007 and 

March 12, 2008, respectively. The 

proposed decision was signed on June 

20, 2007 and published in the Federal 

Register on July 11, 2007 (72 FR 37818). 

Public hearings on the proposed 

decision were held on Thursday, August 

30, 2007 in Philadelphia, PA and Los 

Angeles, CA. On Wednesday, September 

5, 2007, hearings were held in Atlanta, 

GA, Chicago, IL, and Houston, TX. A 

large number of comments were 

received from various commenters on 

the 2007 proposed revisions to the O3

NAAQS. A comprehensive summary of 

all significant comments, along with 

EPA’s responses (henceforth ‘‘Response 

to Comments’’), can be found in the 

docket for the 2008 rulemaking, which 

is also the docket for this 

reconsideration rulemaking. 

The EPA’s final decision on the O3

NAAAQS was published in the Federal 

Register on March 27, 2008 (73 FR 

16436). In the 2008 rulemaking, EPA 

revised the level of the 8-hour primary 

standard for O3 to 0.075 parts per 

million (ppm), expressed to three 

decimal places. With regard to the 

secondary standard for O3, EPA revised 

the 8-hour standard by making it 

identical to the revised primary 

standard. The EPA also made 

conforming changes to the Air Quality 

Index (AQI) for O3, setting an AQI value 

of 100 equal to 0.075 ppm, 8-hour 

average, and making proportional 

changes to the AQI values of 50, 150 

and 200. 

D. Reconsideration of the 2008 O3

NAAQS Final Rule 

Consistent with a directive of the new 

Administration regarding the review of 

new and pending regulations (Emanuel 

memorandum, 74 FR 4435; January 26, 

2009), the Administrator reviewed a 

number of actions that were taken in the 

last year by the previous 

Administration. The 2008 final rule was 

included in this review in recognition of 

the central role that the NAAQS play in 

enabling EPA to fulfill its mission to 

protect the nation’s public health and 

welfare. In her review, the 

Administrator was mindful of the need 

for judgments concerning the NAAQS to 

be based on a strong scientific 

foundation which is developed through 

a transparent and credible NAAQS 

review process, consistent with the core 

values highlighted in President Obama’s 

memorandum on scientific integrity 

(March 9, 2009). 

1. Decision To Initiate a Rulemaking To 

Reconsider 

In her review of the 2008 final rule, 

several aspects of the final rule related 

to the primary and secondary standards 

stood out to the Administrator. As an 

initial matter, the Administrator noted 

that the 2008 final rule concluded that 

the 1997 primary and secondary O3

standards were not adequate to protect 

public health and public welfare, and 

that revisions were necessary to provide 

increased protection. With respect to 

revision of the primary standard, the 

Administrator noted that the revised 

level established in the 2008 final rule 

was above the range that had been 

unanimously recommended by 

CASAC.5 She also noted that EPA 

received comments from a large number 

of commenters from the medical and 

public health communities, including 

EPA’s Children’s Health Protection 

Advisory Committee, all of which 

endorsed levels within CASAC’s 

recommended range. 

With respect to revision of the 

secondary O3 standard, the 

Administrator noted that the 2008 final 

rule differed substantially from 

CASAC’s recommendations that EPA 

adopt a new secondary O3 standard 

based on a cumulative, seasonal 

measure of exposure. The 2008 final 

rule revised the secondary standard to 

be identical to the revised primary 

standard, which is based on an 8-hour 

daily maximum measure of exposure. 

She also noted that EPA received 

comments from a number of 

commenters representing environmental 

interests, all of which endorsed 

CASAC;s recommendation for a new 

cumulative, seasonal secondary 

standard.6

Subsequent to issuance of the 2008 

final rule, in April 2008, CASAC took 

the unusual step of sending EPA a letter 

expressing strong, unanimous 

disagreement with EPA’s decisions on 

both the primary and secondary 

standards (Henderson, 2008). The 

CASAC explained that it did not 

endorse the revised primary O3 standard 

as being sufficiently protective of public 

health because it failed to satisfy the 

explicit stipulation of the Act to provide 

an adequate margin of safety. The 

CASAC also expressed the view that 

failing to revise the secondary standard 

to a cumulative, seasonal form was not 

supported by the available science. In 

addition to CASAC’s letter, the 

Administrator noted a recent adverse 

ruling issued by the U.S. Court of 

Appeals for the District of Columbia 

Circuit on another NAAQS decision. In 

February 2009, the DC Circuit remanded 

the Agency’s decisions on the primary 

annual and secondary standards for fine 

particles (PM2.5). In so doing, the Court 

found that EPA had not adequately 

explained the basis for its decisions, 

including why CASAC’s 

recommendations for a more healthprotective primary annual standard and 

for secondary standards different from 

the primary standards were not 

accepted. American Farm Bureau v. 

EPA, 559 F.3d. 512 (DC Cir. 2009). 

Based on her review of the 

information described above, the 

Administrator is initiating a rulemaking 

to reconsider parts of the 2008 final 

rule. Specifically, the Administrator is 

reconsidering the level of the primary 

standard to ensure that it is sufficiently 

protective of public health, as discussed 

in section II below, and is reconsidering 

all aspects of the secondary standard to 

ensure that it appropriately reflects the 

available science and is sufficiently 

protective of public welfare, as 

discussed in section IV below. Based on 

her review, the Administrator has 

serious cause for concern regarding 

whether the revisions to the primary 

and secondary O3 standards adopted in 

the 2008 final rule satisfy the 

requirements of the CAA, in light of the 

body of scientific evidence before the 

Agency. In addition, the importance of 

the O3 NAAQS to public health and 

welfare weigh heavily in favor of 

reconsidering parts of the 2008 final 

rule as soon as possible, based on the 

scientific and technical information 

upon which the 2008 final rule was 

based. 


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7The EPA also separately announced that it will 

move quickly to implement any new standards that 

might result from this reconsideration. To reduce 

the workload for states during the interim period of 

reconsideration, the Agency intends to propose to 

defer compliance with the CAA requirement to 

designate areas as attainment or nonattainment. 

EPA will work with states, local governments and 

tribes to ensure that air quality is protected during 

that time. 

8The use of O3 as the indicator for photochemical 

oxidants was adopted in the 1979 final rule and 

retained in subsequent rulemaking. An 8-hour 

averaging time and a form based on the annual 

fourth-highest daily maximum 8-hour 

concentration, averaged over 3 years, were adopted 

in the 1997 final rule and retained in the 2008 

rulemaking. 

Also, EPA conducted a provisional 

assessment of ‘‘new’’ scientific papers 

(EPA, 2009) of scientific literature 

evaluating health and ecological effects 

of O3 exposure published since the close 

of the 2006 Criteria Document upon 

which the 2008 O3 NAAQS were based. 

The Administrator notes that the 

provisional assessment of ‘‘new’’ science 

found that such studies did not 

materially change the conclusions in the 

2006 Criteria Document. This 

provisional assessment is supportive of 

the Administrator’s decision to 

reconsider parts of the 2008 final rule at 

this time, based on the scientific and 

technical information available for the 

2008 final rule, as compared to 

foregoing such reconsideration and 

taking appropriate action in the future 

as part of the next periodic review of the 

air quality criteria and NAAQS, which 

will include such scientific and 

technical information. 

The reconsideration of parts of the 

2008 final rule discussed in this notice 

is based on the scientific and technical 

record from the 2008 rulemaking, 

including public comments and CASAC 

advice and recommendations. The 

information that was assessed during 

the 2008 rulemaking includes 

information in the 2006 Criteria 

Document (EPA, 2006a), the 2007 Policy 

Assessment of Scientific and Technical 

Information, referred to as the 2007 Staff 

Paper (EPA, 2007b), and related 

technical support documents including 

the 2007 REAs (U.S. EPA, 2007c; Abt 

Associates, 2007a,b). Scientific and 

technical information developed since 

the 2006 Criteria Document will be 

considered in the next periodic review, 

instead of this reconsideration 

rulemaking, allowing the new 

information to receive careful and 

comprehensive review by CASAC and 

the public before it is used as a basis in 

a rulemaking that determines whether to 

revise the NAAQS. 

2. Ongoing Litigation 

In May 2008, following publication of 

the 2008 final rule, numerous groups, 

including state, public health, 

environmental, and industry petitioners, 

challenged EPA’s decisions in federal 

court. The challenges were consolidated 

as State of Mississippi, et al. v. EPA (No. 

08–1200, DC Cir. 2008). On March 10, 

2009, EPA filed an unopposed motion 

requesting that the Court vacate the 

briefing schedule and hold the 

consolidated cases in abeyance. The 

Agency stated its desire to allow time 

for appropriate officials from the new 

Administration to review the O3

standards to determine whether they 

should be maintained, modified or 

otherwise reconsidered. The EPA 

further requested that it be directed to 

notify the Court and all the parties of 

any actions it has taken or intends to 

take, if any, within 180 days of the 

Court vacating the briefing schedule. On 

March 19, 2009, the Court granted EPA’s 

motion. Pursuant to the Court’s order, 

on September 16, 2009 EPA notified the 

Court and the parties of its decision to 

initiate a rulemaking to reconsider the 

primary and secondary O3 standards set 

in March 2008 to ensure they satisfy the 

requirements of the CAA.7 In its notice 

to the Court, EPA stated that this notice 

of proposed rulemaking would be 

signed by December 21, 2009, and that 

the final rule will be signed by August 

31, 2010. 

II. Rationale for Proposed Decision on 

the Level of the Primary Standard 

As an initial matter, the Administrator 

notes that the 2008 final rule concluded 

that the 1997 primary O3 standard was 

‘‘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’’ (73 FR 16472). The 

Administrator is not reconsidering this 

aspect of the 2008 decision, which is 

based on the reasons discussed in 

section II.B of the 2008 final rule (73 FR 

16443–16472). The Administrator also 

notes that the 2008 final rule concluded 

that it was appropriate to retain the O3

indicator, the 8-hour averaging time, 

and form of the primary O3 standard 

(specified as the annual fourth-highest 

daily maximum 8-hour concentration, 

averaged over 3 years), while 

concluding that revision of the standard 

level was appropriate.8 The 

Administrator is not reconsidering these 

aspects of the 2008 decision, which are 

based on the reasons discussed in 

sections II.C.1–3 of the 2008 final rule, 

which address the indicator, averaging 

time, and form, respectively, of the 

primary O3 standard (73 FR 16472– 

16475). For these reasons, the 

Administrator is not reopening the 2008 

decision with regard to the need to 

revise the 1997 primary O3 standard nor 

with regard to the indicator, averaging 

time, and form of the 2008 primary O3

standard. Thus, the information that 

follows in this section specifically 

focuses on a reconsideration of level of 

the primary O3 standard. 

This section presents the rationale for 

the Administrator’s proposed decision 

that the O3 primary standard, which was 

set at a level of 0.075 ppm in the 2008 

final rule, should instead be set at a 

lower level within the range from 0.060 

to 0.070 ppm. As discussed more fully 

below, the rationale for the proposed 

range of standard levels is based on a 

thorough review of the latest scientific 

information on human health effects 

associated with the presence of O3 in 

the ambient air presented in the 2006 

Criteria Document. This rationale also 

takes into account: (1) Staff assessments 

of the most policy-relevant information 

in the 2006 Criteria Document and staff 

analyses of air quality, human exposure, 

and health risks, presented in the 2007 

Staff Paper, upon which staff 

recommendations for revisions to the 

primary O3 standard in the 2008 

rulemaking were based; (2) CASAC 

advice and recommendations, as 

reflected in discussions of drafts of the 

2006 Criteria Document and 2007 Staff 

Paper at public meetings, in separate 

written comments, and in CASAC’s 

letters to the Administrator both before 

and after the 2008 rulemaking; and (3) 

public comments received during the 

development of these documents, either 

in connection with CASAC meetings or 

separately, and on the 2007 proposed 

rule. 

In developing this rationale, the 

Administrator recognizes that the CAA 

requires her to reach a public health 

policy judgment as to what standard 

would be requisite to protect public 

health with an adequate margin of 

safety, based on scientific evidence and 

technical assessments that have 

inherent uncertainties and limitations. 

This judgment requires making 

reasoned decisions as to what weight to 

place on various types of evidence and 

assessments, and on the related 

uncertainties and limitations. Thus, in 

selecting standard levels to propose, and 

subsequently in selecting a final level, 

the Administrator is seeking not only to 

prevent O3 levels that have been 

demonstrated to be harmful but also to 

prevent lower O3 levels that may pose 

an unacceptable risk of harm, even if the 

risk is not precisely identified as to 

nature or degree. 

In this proposed rule, EPA has drawn 

upon an integrative synthesis of the 

entire body of evidence, published 


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9 In its assessment of the epidemiological 

evidence judged to be most relevant to making 

decisions on the level of the O3 primary standard, 

EPA has placed greater weight on U.S. and 

Canadian epidemiologic studies, since studies 

conducted in other countries may well reflect 

different demographic and air pollution 

characteristics. 

10The exposure assessment done as part of the 

2008 final rulemaking considered several air quality 

scenarios, including just meeting what was then the 

current standard set at a level of 0.084 ppm, as well 

as just meeting alternative standards at levels of 

0.080, 0.074, 0.070, and 0.064 ppm. 

11Exposures of concern were also considered in 

the 1997 review of the O3 NAAQS, and were judged 

by EPA to be an important indicator of the public 

health impacts of those O3-related effects for which 

information was too limited to develop quantitative 

estimates of risk but which had been observed in 

humans at and above the benchmark level of 0.08 

ppm for 6- to 8-hour exposures * * * including 

increased nonspecific bronchial responsiveness (for 

example, aggravation of asthma), decreased 

pulmonary defense mechanisms (suggestive of 

increased susceptibility to respiratory infection), 

and indicators of pulmonary inflammation (related 

Continued 

through early 2006, on human health 

effects associated with the presence of 

O3 in the ambient air. As discussed 

below in section II.A, this body of 

evidence addresses a broad range of 

health endpoints associated with 

exposure to ambient levels of O3 (EPA, 

2006a, chapter 8), and includes over one 

hundred epidemiologic studies 

conducted in the U.S., Canada, and 

many countries around the world.9 In 

reconsidering this evidence, EPA 

focuses on those health endpoints that 

have been demonstrated to be caused by 

exposure to O3, or for which the 2006 

Criteria Document judges associations 

with O3 to be causal, likely causal, or for 

which the evidence is highly suggestive 

that O3 contributes to the reported 

effects. This rationale also draws upon 

the results of quantitative exposure and 

risk assessments, discussed below in 

section II.B. Section II.C focuses on the 

considerations upon which the 

Administrator’s proposed conclusions 

on the level of the primary standard are 

based. Policy-relevant evidence-based 

and exposure/risk-based considerations 

are discussed, and the rationale for the 

2008 final rulemaking on the primary 

standard and CASAC advice, given both 

prior to the development of the 2007 

proposed rule and following the 2008 

final rule, are summarized. Finally, the 

Administrator’s proposed conclusions 

on the level of the primary standard are 

presented. Section II.D summarizes the 

proposed decision on the level of the 

primary O3 standard and the solicitation 

of public comments. 

Judgments made in the 2006 Criteria 

Document and 2007 Staff Paper about 

the extent to which relationships 

between various health endpoints and 

short-term exposures to ambient O3 are 

likely causal have been informed by 

several factors. As discussed below in 

section II.A, these factors include the 

nature of the evidence (i.e., controlled 

human exposure, epidemiological, and/ 

or toxicological studies) and the weight 

of evidence, which takes into account 

such considerations as biological 

plausibility, coherence of evidence, 

strength of association, and consistency 

of evidence. 

In assessing the health effects data 

base for O3, it is clear that human 

studies provide the most directly 

applicable information for determining 

causality because they are not limited 

by the uncertainties of dosimetry 

differences and species sensitivity 

differences, which would need to be 

addressed in extrapolating animal 

toxicology data to human health effects. 

Controlled human exposure studies 

provide data with the highest level of 

confidence since they provide human 

health effects data under closely 

monitored conditions and can provide 

exposure-response relationships. 

Epidemiological data provide evidence 

of associations between ambient O3

levels and more serious acute and 

chronic health effects (e.g., hospital 

admissions and mortality) that cannot 

be assessed in controlled human 

exposure studies. For these studies the 

degree of uncertainty introduced by 

potentially confounding variables (e.g., 

other pollutants, temperature) and other 

factors affects the level of confidence 

that the health effects being investigated 

are attributable to O3 exposures, alone 

and in combination with other 

copollutants. 

In using a weight of evidence 

approach to inform judgments about the 

degree of confidence that various health 

effects are likely to be caused by 

exposure to O3, confidence increases as 

the number of studies consistently 

reporting a particular health endpoint 

grows and as other factors, such as 

biological plausibility and strength, 

consistency, and coherence of evidence, 

increase. Conclusions regarding 

biological plausibility, consistency, and 

coherence of evidence of O3-related 

health effects are drawn from the 

integration of epidemiological studies 

with mechanistic information from 

controlled human exposure studies and 

animal toxicological studies. As 

discussed below, this type of 

mechanistic linkage has been firmly 

established for several respiratory 

endpoints (e.g., lung function 

decrements, lung inflammation) but 

remains far more equivocal for 

cardiovascular endpoints (e.g., 

cardiovascular-related hospital 

admissions). For epidemiological 

studies, strength of association refers to 

the magnitude of the association and its 

statistical strength, which includes 

assessment of both effects estimate size 

and precision. In general, when 

associations yield large relative risk 

estimates, it is less likely that the 

association could be completely 

accounted for by a potential confounder 

or some other bias. Consistency refers to 

the persistent finding of an association 

between exposure and outcome in 

multiple studies of adequate power in 

different persons, places, circumstances 

and times. For example, the magnitude 

of effect estimates is relatively 

consistent across recent studies showing 

association between short-term, but not 

long-term, O3 exposure and mortality. 

Based on the information discussed 

below in sections II.A.1–II.A.3, 

judgments concerning the extent to 

which relationships between various 

health endpoints and ambient O3

exposures are likely causal are 

summarized below in section II.A.3.c. 

These judgments reflect the nature of 

the evidence and the overall weight of 

the evidence, and are taken into 

consideration in the quantitative 

exposure and risk assessments, 

discussed below in section II.B. 

To put judgments about health effects 

that have been demonstrated to be 

caused by exposure to O3, or for which 

the 2006 Criteria Document judges 

associations with O3 to be causal, likely 

causal, or for which the evidence is 

highly suggestive that O3 contributes to 

the reported effects into a broader 

public health context, EPA has drawn 

upon the results of the quantitative 

exposure and risk assessments. These 

assessments provide estimates of the 

likelihood that individuals in particular 

population groups that are at risk for 

various O3-related physiological health 

effects would experience ‘‘exposures of 

concern’’ and specific health endpoints 

under varying air quality scenarios (i.e., 

just meeting various standards 10), as 

well as characterizations of the kind and 

degree of uncertainties inherent in such 

estimates. 

In the 2008 final rulemaking and in 

this reconsideration, the term 

‘‘exposures of concern’’ is defined as 

personal exposures while at moderate or 

greater exertion to 8-hour average 

ambient O3 levels at and above specific 

benchmark levels which represent 

exposure levels at which O3-related 

health effects are known or can 

reasonably be inferred to occur in some 

individuals, as discussed below in 

section II.B.1.11 The EPA emphasizes 


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to potential aggravation of chronic bronchitis or 

long-term damage to the lungs). (62 FR 38868) 

that although the analysis of ‘‘exposures 

of concern’’ was conducted using three 

discrete benchmark levels (i.e., 0.080, 

0.070, and 0.060 ppm), the concept is 

more appropriately viewed as a 

continuum with greater confidence and 

less uncertainty about the existence of 

health effects at the upper end and less 

confidence and greater uncertainty as 

one considers increasingly lower O3

exposure levels. The EPA recognizes 

that there is no sharp breakpoint within 

the continuum ranging from at and 

above 0.080 ppm down to 0.060 ppm. In 

considering the concept of exposures of 

concern, it is important to balance 

concerns about the potential for health 

effects and their severity with the 

increasing uncertainty associated with 

our understanding of the likelihood of 

such effects at lower O3 levels. 

Within the context of this continuum, 

estimates of exposures of concern at 

discrete benchmark levels provide some 

perspective on the public health 

impacts of O3-related health effects that 

have been demonstrated in controlled 

human exposure and toxicological 

studies but cannot be evaluated in 

quantitative risk assessments, such as 

lung inflammation, increased airway 

responsiveness, and changes in host 

defenses. They also help in 

understanding the extent to which such 

impacts have the potential to be reduced 

by meeting various standards. These O3- 

related physiological effects are 

plausibly linked to the increased 

morbidity seen in epidemiological 

studies (e.g., as indicated by increased 

medication use in asthmatics, school 

absences in all children, and emergency 

department visits and hospital 

admissions in people with lung 

disease). Estimates of the number of 

people likely to experience exposures of 

concern cannot be directly translated 

into quantitative estimates of the 

number of people likely to experience 

specific health effects, since sufficient 

information to draw such comparisons 

is not available—if such information 

were available, these health outcomes 

would have been included in the 

quantitative risk assessment. Due to 

individual variability in responsiveness, 

only a subset of individuals who have 

exposures at and above a specific 

benchmark level can be expected to 

experience such adverse health effects, 

and susceptible subpopulations such as 

those with asthma are expected to be 

affected more by such exposures than 

healthy individuals. The amount of 

weight to place on the estimates of 

exposures of concern at any of these 

benchmark levels depends in part on 

the weight of the scientific evidence 

concerning health effects associated 

with O3 exposures at and above that 

benchmark level. It also depends on 

judgments about the importance from a 

public health perspective of the health 

effects that are known or can reasonably 

be inferred to occur as a result of 

exposures at and above the benchmark 

level. Such public health policy 

judgments are embodied in the NAAQS 

standard setting criteria (i.e., standards 

that, in the judgment of the 

Administrator, are requisite to protect 

public health with an adequate margin 

of safety). 

As discussed below in section II.B.2, 

the quantitative health risk assessment 

conducted as part of the 2008 final 

rulemaking includes estimates of risks 

of lung function decrements in 

asthmatic and all school age children, 

respiratory symptoms in asthmatic 

children, respiratory-related hospital 

admissions, and non-accidental and 

cardiorespiratory-related mortality 

associated with recent ambient O3

levels, as well as risk reductions and 

remaining risks associated with just 

meeting the then current 0.084 ppm 

standard and various alternative O3

standards in a number of example urban 

areas. There are two parts to this risk 

assessment: one part is based on 

combining information from controlled 

human exposure studies with modeled 

population exposure, and the other part 

is based on combining information from 

community epidemiological studies 

with either monitored or adjusted 

ambient concentrations levels. This 

assessment provides estimates of the 

potential magnitude of O3-related health 

effects, as well as a characterization of 

the uncertainties and variability 

inherent in such estimates. This 

assessment also provides insights into 

the distribution of risks and patterns of 

risk reductions associated with meeting 

alternative O3 standards. 

As discussed below, a substantial 

amount of new research conducted 

since the 1997 review of the O3 NAAQS 

was available to inform the 2008 final 

rulemaking, with important new 

information coming from epidemiologic 

studies as well as from controlled 

human exposure, toxicological, and 

dosimetric studies. The research studies 

newly available in the 2008 final 

rulemaking that were evaluated in the 

2006 Criteria Document and the 

exposure and risk assessments 

presented in the 2007 Staff Paper have 

undergone intensive scrutiny through 

multiple layers of peer review and many 

opportunities for public review and 

comment. While important 

uncertainties remain in the qualitative 

and quantitative characterizations of 

health effects attributable to exposure to 

ambient O3, and while different 

interpretations of these uncertainties 

can result in different public health 

policy judgments, the review of this 

information has been extensive and 

deliberate. In the judgment of the 

Administrator, this intensive evaluation 

of the scientific evidence provides an 

adequate basis for this reconsideration 

of the 2008 final rulemaking. 

A. Health Effects Information 

This section outlines key information 

contained in the 2006 Criteria 

Document (chapters 4–8) and in the 

2007 Staff Paper (chapter 3) on known 

or potential effects on public health 

which may be expected from the 

presence of O3 in ambient air. The 

information highlighted here 

summarizes: (1) New information 

available on potential mechanisms for 

health effects associated with exposure 

to O3; (2) the nature of effects that have 

been associated directly with exposure 

to O3 and indirectly with the presence 

of O3 in ambient air; (3) an integrative 

interpretation of the evidence, focusing 

on the biological plausibility and 

coherence of the evidence; and (4) 

considerations in characterizing the 

public health impact of O3, including 

the identification of ‘‘at risk’’ 

populations. 

The decision in the 1997 review 

focused primarily on evidence from 

short-term (e.g., 1 to 3 hours) and 

prolonged (6 to 8 hours) controlledexposure studies reporting lung 

function decrements, respiratory 

symptoms, and respiratory 

inflammation in humans, as well as 

epidemiology studies reporting excess 

hospital admissions and emergency 

department (ED) visits for respiratory 

causes. The 2006 Criteria Document 

prepared for the 2008 rulemaking 

emphasized the large number of 

epidemiological studies published since 

the last review with these and 

additional health endpoints, including 

the effects of acute (short-term and 

prolonged) and chronic exposures to O3

on lung function decrements and 

enhanced respiratory symptoms in 

asthmatic individuals, school absences, 

and premature mortality. It also 

emphasized important new information 

from toxicology, dosimetry, and 

controlled human exposure studies. 

Highlights of the evidence include: 

(1) Two new controlled humanexposure studies are now available that 

examine respiratory effects associated 

with prolonged O3 exposures at levels 

below 0.080 ppm, which was the lowest 


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12While most of the available evidence addresses 

mechanisms for O3, O3 clearly serves as an indicator 

for the total photochemical oxidant mixture found 

in the ambient air. Some effects may be caused by 

one or more components in the overall pollutant 

mix, either separately or in combination with O3. 

However, O3 clearly dominates these other oxidants 

with their concentrations only being a few percent 

of the O3 concentration. 

13 In previous Staff Papers and Federal Register 

notices announcing proposed and final decisions on 

the O3 and other NAAQS, EPA has used the phrase 

Continued 

exposure level that had been examined 

in the 1997 review. 

(2) Numerous controlled humanexposure studies have examined 

indicators of O3-induced inflammatory 

response in both the upper respiratory 

tract (URT) and lower respiratory tract 

(LRT), and increased airway 

responsiveness to allergens in subjects 

with allergic asthma and allergic rhinitis 

exposed to O3, while other studies have 

examined changes in host defense 

capability following O3 exposure of 

healthy young adults. 

(3) Animal toxicology studies provide 

new information regarding mechanisms 

of action, increased susceptibility to 

respiratory infection, and the biological 

plausibility of acute effects and chronic, 

irreversible respiratory damage. 

(4) Numerous acute exposure 

epidemiological studies published 

during the past decade offer added 

evidence of ambient O3-related lung 

function decrements and respiratory 

symptoms in physically active healthy 

subjects and greater responses in 

asthmatic subjects, as well as evidence 

on new health endpoints, such as the 

relationships between ambient O3

concentrations and asthma medication 

use and school absenteeism, and 

between ambient O3 and cardiac-related 

physiological endpoints. 

(5) Several additional studies have 

been published over the last decade 

examining the temporal associations 

between O3 exposures and emergency 

department visits for asthma and other 

respiratory diseases and respiratoryrelated hospital admissions. 

(6) A large number of newly available 

epidemiological studies have examined 

the effects of acute exposure to PM and 

O3 on mortality, notably including large 

multicity studies that provide much 

more robust and credible information 

than was available in the 1997 review, 

as well as recent meta-analyses that 

have evaluated potential sources of 

heterogeneity in O3-mortality 

associations. 

1. Overview of Mechanisms 

Evidence on possible mechanisms by 

which exposure to O3 may result in 

acute and chronic health effects is 

discussed in chapters 5 and 6 of the 

2006 Criteria Document.12 Evidence 

from dosimetry, toxicological, and 

human exposure studies has contributed 

to an understanding of the mechanisms 

that help to explain the biological 

plausibility and coherence of evidence 

for O3-induced respiratory health effects 

reported in epidemiological studies. 

More detailed information about the 

physiological mechanisms related to the 

respiratory effects of short- and longterm exposure to O3 can be found in 

section II.A.3.b.i and II.A.3.b.iii, 

respectively. In the past, however, little 

information was available to help 

explain potential biological mechanisms 

which linked O3 exposure to premature 

mortality or cardiovascular effects. As 

discussed more fully in section 

II.A.3.b.ii below, since the 1997 review 

an emerging body of animal toxicology 

and controlled human exposure 

evidence is beginning to suggest 

mechanisms that may mediate acute O3

cardiovascular effects. While much is 

known about mechanisms that play a 

role in O3-related respiratory effects, 

additional research is needed to more 

clearly understand the role that O3 may 

have in contributing to cardiovascular 

effects. 

With regard to the mechanisms 

related to short-term respiratory effects, 

scientific evidence discussed in the 

2006 Criteria Document (section 5.2) 

indicates that reactions of O3 with lipids 

and antioxidants in the epithelial lining 

fluid and the epithelial cell membranes 

of the lung can be the initial step in 

mediating deleterious health effects of 

O3. This initial step activates a cascade 

of events that lead to oxidative stress, 

injury, inflammation, airway epithelial 

damage and increased alveolar 

permeability to vascular fluids. 

Inflammation can be accompanied by 

increased airway responsiveness, which 

is an increased bronchoconstrictive 

response to airway irritants and 

allergens. Continued respiratory 

inflammation also can alter the ability of 

the body to respond to infectious agents, 

allergens and toxins. Acute 

inflammatory responses to O3 in some 

healthy people are well documented, 

and precursors to lung injury are 

observed within 3 hours after exposure 

in humans. Repeated respiratory 

inflammation can lead to a chronic 

inflammatory state with altered lung 

structure and lung function and may 

lead to chronic respiratory diseases such 

as fibrosis and emphysema (EPA, 2006a, 

section 8.6.2). The severity of symptoms 

and magnitude of response to acute 

exposures depend on inhaled dose, as 

well as on individual susceptibility to 

O3, as discussed below. At the same O3

dose, individuals who are more 

susceptible to O3 will have a larger 

response than those who are less 

susceptible; among individuals with 

similar susceptibility, those who receive 

a larger dose will have a larger response 

to O3. 

The inhaled dose is the product of O3

concentration (C), minute ventilation or 

ventilation rate, and duration of 

exposure (T), or (C × ventilation rate × 

T). A large body of data regarding the 

interdependent effect of these 

components of inhaled dose on 

pulmonary responses was assessed in 

the 1986 and 1996 O3 Criteria 

Documents. In an attempt to describe O3

dose-response characteristics, acute 

responses were modeled as a function of 

total inhaled O3 dose, which was 

generally found to be a better predictor 

of response than O3 concentration, 

ventilation rate, or duration of exposure, 

alone, or as a combination of any two 

of these factors (EPA 2006a, section 6.2). 

Predicted O3-induced decrements in 

lung function have been shown to be a 

function of exposure concentration, 

duration and exercise level for healthy, 

young adults (McDonnell et al., 1997). A 

meta-analysis of 21 studies (Mudway 

and Kelly, 2004) showed that markers of 

inflammation and increased cellular 

permeability in healthy subjects are 

associated with total O3 dose. 

The 2006 Criteria Document 

summarizes information on potentially 

susceptible and vulnerable groups in 

section 8.7. As described there, the term 

susceptibility refers to innate (e.g., 

genetic or developmental) or acquired 

(e.g., personal risk factors, age) factors 

that make individuals more likely to 

experience effects with exposure to 

pollutants. A number of population 

groups and lifestages have been 

identified as potentially susceptible to 

health effects as a result of O3 exposure, 

including people with existing lung 

diseases, including asthma, children 

and older adults, and people who have 

larger than normal lung function 

responses that may be due to genetic 

susceptibility. In addition, some 

population groups and lifestages have 

been identified as having increased 

vulnerability to O3-related effects due to 

increased likelihood of exposure while 

at elevated ventilation rates, including 

healthy children and adults who are 

active outdoors, for example, outdoor 

workers, and joggers. Taken together, 

the susceptible and vulnerable groups 

are more commonly referred to as ‘‘atrisk’’ groups,13 as discussed more fully 

below in section II.A.4.b. 


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‘‘sensitive population groups’’ to include both 

population groups that are at increased risk because 

they are more intrinsically susceptible and 

population groups that are more vulnerable due to 

an increased potential for exposure. In this notice, 

we use the phrase, ‘‘at risk’’ populations to include 

both types of population groups. 

Based on a substantial body of new 

evidence from animal, controlled 

human exposure and epidemiological 

studies, the 2006 Criteria Document 

concludes that people with asthma and 

other preexisting pulmonary diseases 

are likely to be among those at increased 

risk from O3 exposure. Altered 

physiological, morphological and 

biochemical states typical of respiratory 

diseases like asthma, COPD and chronic 

bronchitis may render people sensitive 

to additional oxidative burden induced 

by O3 exposure (EPA 2006a, section 

8.7). Children and adults with asthma 

are the group that has been studied most 

extensively. Evidence from controlled 

human exposure studies indicates that 

asthmatics may exhibit larger lung 

function decrements in response to O3

exposure than healthy controls. As 

discussed more fully in section 

II.A.4.b.ii below, asthmatics present a 

differential response profile for cellular, 

molecular, and biochemical parameters 

(EPA, 2006a, section 8.7.1) that are 

altered in response to acute O3

exposure. They can have larger 

inflammatory responses, as manifested 

by larger increases in markers of 

inflammation such as white bloods cells 

(e.g., PMNs) or inflammatory cytokines. 

Asthmatics, and people with allergic 

rhinitis, are more likely to mount an 

allergic-type response upon exposure to 

O3, as manifested by increases in white 

blood cells associated with allergy (i.e., 

eosinophils) and related molecules, 

which increase inflammation in the 

airways. The increased inflammatory 

and allergic responses also may be 

associated with the larger late-phase 

responses that asthmatics can 

experience, which can include 

increased bronchoconstrictor responses 

to irritant substances or allergens and 

additional inflammation. In addition to 

the experimental evidence of lung 

function decrements, respiratory 

symptoms, and other respiratory effects 

in asthmatic populations, two large U.S. 

epidemiological studies as well as 

several smaller U.S. and international 

studies, have reported fairly robust 

associations between ambient O3

concentrations and measures of lung 

function and daily symptoms (e.g., chest 

tightness, wheeze, shortness of breath) 

in children with moderate to severe 

asthma and between O3 and increased 

asthma medication use (EPA, 2007a, 

chapter 6). These responses in 

asthmatics and others with lung disease 

provide biological plausibility for the 

more serious respiratory morbidity 

effects observed in epidemiological 

studies, such as emergency department 

visits and hospital admissions. 

Children with and without asthma 

were found to be particularly 

susceptible to O3 effects on lung 

function and generally have greater lung 

function responses than older people. 

The American Academy of Pediatrics 

(2004) notes that children and infants 

are among the population groups most 

susceptible to many air pollutants, 

including O3. This is in part because 

their lungs are still developing. For 

example, eighty percent of alveoli are 

formed after birth, and changes in lung 

development continue through 

adolescence (Dietert et al., 2000). 

Moreover, children have high minute 

ventilation rates and relatively high 

levels of physical activity which also 

increases their O3 dose (Plunkett et al., 

1992). Thus, children are at-risk due to 

both their susceptibility and 

vulnerability. 

Looking more broadly at age-related 

differences in susceptibility, several 

mortality studies have investigated agerelated differences in O3 effects (EPA, 

2006a, section 7.6.7.2), primarily in the 

older adult population. Among the 

studies that observed positive 

associations between O3 and mortality, 

a comparison of all age or younger age 

(65 years of age) O3-mortality effect 

estimates to that of the elderly 

population (>65 years) indicates that, in 

general, the elderly population is more 

susceptible to O3 mortality effects. 

There is supporting evidence of agerelated differences in susceptibility to 

O3 lung function effects. The 2006 

Criteria Document (section 7.6.7.2) 

concludes that the elderly population 

(>65 years of age) appear to be at greater 

risk of O3-related mortality and 

hospitalizations compared to all ages or 

younger populations, and children (<18 

years of age) experience other 

potentially adverse respiratory health 

outcomes with increased O3 exposure. 

Controlled human exposure studies 

have also indicated a high degree of 

interindividual variability in some of 

the pulmonary physiological 

parameters, such as lung function 

decrements. The variable effects in 

individuals have been found to be 

reproducible, in other words, a person 

who has a large lung function response 

after exposure to O3 will likely have 

about the same response if exposed 

again to the same dose of O3 (EPA 

2006a, section 6.1). In controlled human 

exposure studies, group mean responses 

are not representative of this segment of 

the population that has much larger 

than average responses to O3. Recent 

studies, discussed in section II.A.4.b.iv 

below, reported a role for genetic 

polymorphism (i.e., the occurrence 

together in the same population of more 

than one allele or genetic marker at the 

same locus with the least frequent allele 

or marker occurring more frequently 

than can be accounted for by mutation 

alone) in observed differences in 

antioxidant enzymes and genes 

involved in inflammation to modulate 

pulmonary function and inflammatory 

responses to O3 exposure. These 

observations suggest a potential role for 

these markers in the innate 

susceptibility to O3, however, the 

validity of these markers and their 

relevance in the context of prediction to 

population studies needs additional 

experimentation. 

Controlled human exposure studies 

that provide information about 

mechanisms of the initial response to O3

(e.g., lung function decrements, 

inflammation, and injury to the lung) 

also inform the selection of appropriate 

lag times to analyze in epidemiological 

studies through elucidation of the time 

course of these responses (EPA 2006a, 

section 8.4.3). Based on the results of 

these studies, it would be reasonable to 

expect that lung function decrements 

could be detected epidemiologically 

within lags of 0 (same day) or 1 to 2 

days following O3 exposure, given the 

rapid onset of lung function changes 

and their persistence for 24 to 48 hours 

among more responsive human subjects 

in controlled human exposure studies. 

Other responses take longer to develop 

and can persist for longer periods of 

time. For example, although asthmatic 

individuals may begin to experience 

symptoms soon after O3 exposure, it 

may take anywhere from 1 to 3 days 

after exposure for these subjects to seek 

medical attention as a result of 

increased airway responsiveness or 

inflammation that may persist for 2 to 

3 days. This may be reflected by 

epidemiologic observations of 

significantly increased risk for asthmarelated emergency department visits or 

hospital admissions with 1- to 3-day 

lags, or, perhaps, enhanced distributed 

lag risks (combined across 3 days) for 

such morbidity indicators. Analogously, 

one might project increased mortality 

within 0- to 3-day lags as a possible 

consequence of O3-induced increases in 

clotting agents arising from the cascade 

of events, starting with cell injury 

described above, occurring within 12 to 

24 hours of O3 exposure. The time 

course for many of these initial 

responses to O3 is highly variable. 


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14Health effects discussions are also drawn from 

the more detailed information and tables presented 

in the Criteria Document’s annexes. 

Moreover these observations pertain 

only to the initial response to O3. 

Consequent responses can follow. For 

example, Jo ̈rres et al., (1996) found that 

in subjects with asthma and allergic 

rhinitis, a maximum percent fall in 

FEV1 of 27.9% and 7.8%, respectively, 

occurred 3 days after O3 exposure when 

they were challenged with of the highest 

common dose of allergen. 

2. Nature of Effects 

The 2006 Criteria Document provides 

new evidence that notably enhances our 

understanding of short-term and 

prolonged exposure effects, including 

effects on lung function, symptoms, and 

inflammatory effects reported in 

controlled exposure studies. These 

studies support and extend the findings 

of the previous Criteria Document. 

There is also a significant body of new 

epidemiological evidence of 

associations between short-term and 

prolonged exposure to O3 and effects 

such as premature mortality, hospital 

admissions and emergency department 

visits for respiratory (e.g., asthma) 

causes. Key epidemiological and 

controlled human exposure studies are 

summarized below and discussed in 

chapter 3 of the 2007 Staff Paper, which 

is based on scientific evidence critically 

reviewed in chapters 5, 6, and 7 of the 

2006 Criteria Document, as well as the 

Criteria Document’s integration of 

scientific evidence contained in chapter 

8.14 Conclusions drawn about O3-related 

health effects are based upon the full 

body of evidence from controlled 

human exposure, epidemiological and 

toxicological data contained in the 2006 

Criteria Document. 

a. Morbidity 

This section summarizes scientific 

information on the effects of inhalation 

of O3, including public health effects of 

short-term, prolonged, and long-term 

exposures on respiratory morbidity and 

cardiovascular system effects, as 

discussed in chapters 6, 7 and 8 of the 

2006 Criteria Document and chapter 3 of 

the 2007 Staff Paper. This section also 

summarizes the uncertainty about the 

potential indirect effects on public 

health associated with changes due to 

increases in UV–B radiation exposure, 

such as UV–B radiation-related skin 

cancers, that may be associated with 

reductions in ambient levels of groundlevel O3, as discussed in chapter 10 of 

the 2006 Criteria Document and chapter 

3 of the 2007 Staff Paper. 

i. Effects on the Respiratory System 

From Short-term and Prolonged O3

Exposures 

Controlled human exposure studies 

have shown that O3 induces a variety of 

health effects, including: Lung function 

decrements, respiratory symptoms, 

increased airway responsiveness, 

respiratory inflammation and 

permeability, increased susceptibility to 

respiratory infection, and acute 

morphological effects. Epidemiology 

studies have reported associations 

between O3 exposures (i.e., 1-hour, 8- 

hour and 24-hour) and a wide range of 

respiratory-related health effects 

including: pulmonary function 

decrements; respiratory symptoms; 

increased asthma medication use; 

increased school absences; increased 

emergency department visits and 

hospital admissions. 

(a) Pulmonary Function Decrements, 

Respiratory Symptoms, and Asthma 

Medication Use 

(i) Results From Controlled Human 

Exposure Studies 

A large number of studies published 

prior to 1996 that investigated shortterm O3 exposure health effects on the 

respiratory system from short-term O3

exposures were reviewed in the 1986 

and 1996 Criteria Documents (EPA, 

1986, 1996a). In the 1997 review, 0.50 

ppm was the lowest O3 concentration at 

which statistically significant 

reductions in forced vital capacity (FVC) 

and forced expiratory volume in 1 

second (FEV1) were reported in 

sedentary subjects. During exercise, 

spirometric (lung function) and 

symptomatic responses were observed 

at much lower O3 exposures. When 

minute ventilation was considerably 

increased by continuous exercise (CE) 

during O3 exposures lasting 2 hour or 

less at ≥ 0.12 ppm, healthy subjects 

generally experienced decreases in 

FEV1, FVC, and other measures of lung 

function; increases in specific airway 

resistance (sRaw), breathing frequency, 

and airway responsiveness; and 

symptoms such as cough, pain on deep 

inspiration, shortness of breath, throat 

irritation, and wheezing. When 

exposures were increased to 4- to 8- 

hours in duration, statistically 

significant lung function and symptom 

responses were reported at O3

concentrations as low as 0.08 ppm and 

at lower minute ventilation (i.e., 

moderate rather than high level 

exercise) than the shorter duration 

studies. 

The most important observations 

drawn from studies reviewed in the 

1996 Criteria Document were that: (1) 

Young healthy adults exposed to O3

concentrations ≥ 0.080 ppm develop 

significant, reversible, transient 

decrements in pulmonary function if 

minute ventilation or duration of 

exposure is increased sufficiently; (2) 

children experience similar lung 

function responses but report lesser 

symptoms from O3 exposure relative to 

young adults; (3) O3-induced lung 

function responses are decreased in the 

elderly relative to young adults; (4) 

there is a large degree of intersubject 

variability in physiological and 

symptomatic responses to O3 but 

responses tend to be reproducible 

within a given individual over a period 

of several months; (5) subjects exposed 

repeatedly to O3 for several days show 

an attenuation of response upon 

successive exposures, but this 

attenuation is lost after about a week 

without exposure; and (6) acute O3

exposure initiates an inflammatory 

response which may persist for at least 

18 to 24 hours post exposure. 

The development of these respiratory 

effects is time-dependent during both 

exposure and recovery periods, with 

great overlap for development and 

disappearance of the effects. In healthy 

human subjects exposed to typical 

ambient O3 levels near 0.120 ppm, lung 

function responses largely resolve 

within 4 to 6 hours postexposure, but 

cellular effects persist for about 24 

hours. In these healthy subjects, small 

residual lung function effects are almost 

completely gone within 24 hours, while 

in hyperresponsive subjects, recovery 

can take as much as 48 hour to return 

to baseline. The majority of these 

responses are attenuated after repeated 

consecutive exposures, but such 

attenuation to O3 is lost one week 

postexposure. 

Since 1996, there have been a number 

of studies published investigating lung 

function and symptomatic responses 

that generally support the observations 

previously drawn. Recent studies for 

acute exposures of 1 to 2 hours and 6 

to 8 hours in duration are compiled in 

the 2007 Staff Paper (Appendix 3C). As 

summarized in more detail in the 2007 

Staff Paper (section 3.3.1.1), among the 

more important of the recent studies 

that examined changes in FEV1 in large 

numbers of subjects over a range of 

1–2 hours at exposure levels of 0.080 to 

0.40 ppm were studies by McDonnell et 

al. (1997) and Ultman et al. (2004). 

These studies observed considerable 

intersubject variability in FEV1

decrements, which was consistent with 

findings in the 1996 Criteria Document. 

For prolonged exposures (4 to 8 

hours) in the range of 0.080 to 0.160 

ppm O3 using moderate intermittent 


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15This study and other studies (Folinsbee et al., 

1988; Horstman et al., 1990; and McDonnell et al., 

1991), conducted in EPA’s human studies research 

facility in Chapel Hill, NC, measured ozone 

concentrations to within +/¥ 5 percent or +/¥ 

0.004 ppm at the 0.080 ppm exposure level. 16These studies, conducted at a facility at the 

University of California, in Davis, CA, reported O3

concentrations to be accurate within +/¥ 0.003 

ppm over the range of concentrations included in 

these studies. 

17These distributional results presented in the 

Criteria Document and Staff Paper for the Adams 

(2006) study are based on data for squate-wave 

exposures to 0.080 ppm that were not included in 

the publication but were obtained from the author. 

18 Dr. Adams submitted comments on EPA’s 

reanalysis in which he concluded that the FEV1

response in healthy young adults at the 0.060 ppm 

exposure level in his study (Adams, 2006a) does not 

demonstrate a significant mean effect by ordinarily 

acceptable statistical analysis, but is rather in 

somewhat of a gray area, both in terms of a 

biologically meaningful response and a statistically 

significant response (Adams, 2007). The EPA 

responded to these comments in the 2008 final rule 

(73 FR 16455) and in the Response to Comments 

(EPA, 2008, pp. 26–28). 

exercise and typically using squarewave exposure patterns (i.e., a constant 

exposure level during time of exposure), 

several pre- and post-1996 studies 

(Folinsbee et al., 1988,1994; Horstman 

et al., 1990; Adams, 2002, 2003a, 2006) 

have reported statistically significant 

lung function responses and increased 

symptoms in healthy adults with 

increasing duration of exposure, O3

concentration, and minute ventilation. 

Studies that employed triangular 

exposure patterns (i.e., integrated 

exposures that begin at a low level, rise 

to a peak, and return to a low level 

during the exposure) (Hazucha et al., 

1992; Adams 2003a, 2006) suggest that 

the triangular exposure pattern can 

potentially lead to greater FEV1

decrements and respiratory symptoms 

than square-wave exposures (when the 

overall O3 doses are equal). These 

results suggest that peak exposures, 

reflective of the pattern of ambient O3

concentrations in some locations, are 

important in terms of O3 health effects. 

McDonnell (1996) used data from a 

series of studies to investigate the 

frequency distributions of FEV1

decrements following 6.6 hour 

exposures and found statistically 

significant, but relatively small, group 

mean decreases in average FEV1

responses (between 5 and 10 percent) at 

0.080 ppm O3.15 Notably, about 26 

percent of the 60 exposed subjects had 

lung function decrements > 10 percent, 

including about 8 percent of the subjects 

that experienced large decrements (> 20 

percent) (EPA, 2007b, Figure 3–1A). 

These results (which were not corrected 

for exercise in filtered air responses) 

demonstrate that while average 

responses may be relatively small at the 

0.080 ppm exposure level, some 

individuals experience more severe 

effects that may be clinically significant. 

Similar results at the 0.080 ppm 

exposure level (for 6.6 hours during 

intermittent exercise) were seen in more 

recent studies of 30 healthy young 

adults by Adams (2002, 2006).16 In 

Adams (2006), relatively small but 

statistically significant lung function 

decrements and respiratory symptom 

responses were found (for both squarewave and triangular exposure patterns), 

with 17 percent of the subjects (5 of 30) 

experiencing ≥ 10 percent FEV1

decrements (comparing pre- and postexposures) when the results were not 

corrected for the effects of exercise 

alone in filtered air (EPA, 2007b, Figure 

3–1B) and with 23 percent of subjects (7 

of 30) experiencing such effects when 

the results were corrected (EPA, 2007b, 

p. 3–6).17

These studies by Adams (2002, 2006) 

were notable in that they were the only 

controlled exposure human studies 

available at the time of the 2008 

rulemaking that examined respiratory 

effects associated with prolonged O3

exposures at levels below 0.080 ppm, 

which was the lowest exposure level 

that had been examined in the 1997 

review. The Adams (2006) study 

investigated a range of exposure levels 

(0.000, 0.040, 0.060, and 0.080 ppm O3) 

using square-wave and triangular 

exposure patterns. The study was 

designed to examine hour-by-hour 

changes in pulmonary function (FEV1) 

and respiratory symptom responses 

(total subjective symptoms (TSS) and 

pain on deep inspiration (PDI)) between 

these various exposure protocols at six 

different time points within the 

exposure periods to investigate the 

effects of different patterns of exposure. 

At the 0.060 ppm exposure level, the 

author reported no statistically 

significant differences for FEV1

decrements nor for most respiratory 

symptoms responses. Statistically 

significant responses were reported only 

for TSS for the triangular exposure 

pattern toward the end of the exposure 

period, with the PDI responses being 

noted as following a closely similar 

pattern (Adams, 2006, p. 131–132). 

EPA’s reanalysis of the data from the 

Adams (2006) study addressed the more 

fundamental question of whether there 

were statistically significant differences 

in responses before and after the 6.6 

hour exposure period (Brown, 2007), 

and used a standard statistical method 

appropriate for a simple before-and-after 

comparison. The statistical method used 

by EPA had been used previously by 

other researchers to address this same 

question. EPA’s reanalysis of the data 

from the Adams (2006) study, 

comparing FEV1 responses pre- and 

post-exposure at the 0.060 ppm 

exposure level, found small group mean 

differences from responses to filtered air 

that were statistically significant 

(Brown, 2007).18

Further examination of the postexposure FEV1 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 doseresponse relationship 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. At the 0.08 ppm level, the 

subjects in this study did not appear to 

be more responsive to O3 than subjects 

in previous studies, as the observed 

response was similar to that of previous 

studies (Adams, 2003a,b; Horstman et 

al., 1990; McDonnell et al., 1991). 

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 O3 in this and 

other studies. These findings are not 

unexpected because the previously 

observed group mean FEV1 responses to 

0.08 ppm were in the range of 6–9% 

suggesting that exposure to lower 

concentrations of O3 would result in 

smaller, but real group mean FEV1

decrements, i.e., the responses to 0.060 

ppm O3 are consistent with the presence 

of a smooth exposure-response curve 

with responses that do not end abruptly 

below 0.080 ppm. 

Moreover, the Adams studies (2002, 

2006) also report a small percentage of 

subjects experiencing moderate lung 

function decrements (≥ 10 percent) at 

the 0.060 ppm exposure level. Based on 

study data (Adams, 2006) provided by 

the author, 7 percent of the subjects (2 

of 30 subjects) experienced notable 

FEV1 decrements (≥ 10 percent) with the 

square wave exposure pattern at the 

0.060 ppm exposure level (comparing 

pre- and post-exposures) when the 

results were corrected for the effects of 

exercise alone in filtered air (EPA, 

2007b, p. 3–6). Furthermore, in a prior 

publication (Adams, 2002), the author 

stated that, ‘‘some sensitive subjects 

experience notable effects at 0.06 ppm,’’ 

based on the observation that 20% of 

subjects exposed to 0.06 ppm O3 (in a 

face mask exposure study) had greater 

than a 10% decrement in FEV1 even 

though the group mean response was 

not statistically different from the 

filtered air response. The effects 

described by Adams (2002), along with 


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the reanalysis of the Adams (2006) data 

as described above, demonstrate 

considerable inter-individual variability 

in responses of healthy adults at the 

0.060 ppm level with some individuals 

experiencing greater than 10% 

decrements in FEV1. The observation of 

statistically significant small group 

mean lung function decrements in 

healthy adults at 0.060 ppm O3 lowers 

the lowest-observed-effects level found 

in controlled human exposure studies 

for lung function decrements and 

respiratory symptoms. 

Of potentially greater concern is the 

magnitude of the lung function 

decrements in the small group of 

healthy subjects who had the largest 

responses (i.e., FEV1 decrements ≥ 

10%). This is a concern because for 

active healthy people, moderate levels 

of functional responses (e.g., FEV1

decrements of ≥ 10% but < 20%) and/ 

or moderate symptomatic responses 

would likely interfere with normal 

activity for relatively few responsive 

individuals. However, for people with 

lung disease, even moderate functional 

or symptomatic responses would likely 

interfere with normal activity for many 

individuals, and would likely result in 

more frequent use of medication (see 

section II.A.4 below). 

(ii) Results of Epidemiological and Field 

Studies 

A relatively large number of field 

studies investigating the effects of 

ambient O3 concentrations, in 

combination with other air pollutants, 

on lung function decrements and 

respiratory symptoms has been 

published over the last decade that 

support the major findings of the 1996 

Criteria Document that lung function 

changes, as measured by decrements in 

FEV1 or peak expiratory flow (PEF), and 

respiratory symptoms in healthy adults 

and asthmatic children are closely 

correlated to ambient O3 concentrations. 

Pre-1996 field studies focused primarily 

on children attending summer camps 

and found O3-related impacts on 

measures of lung function, but not 

respiratory symptoms, in healthy 

children. The newer studies have 

expanded to evaluate O3-related effects 

on outdoor workers, athletes, the 

elderly, hikers, school children, and 

asthmatics. Collectively, these studies 

confirm and extend clinical 

observations that prolonged (i.e., 6–8 

hour) exposure periods, combined with 

elevated levels of exertion or exercise, 

increase the dose of O3 to the lungs at 

a given ambient exposure level and 

result in larger lung function effects. 

The results of one large study of hikers 

(Korrick et al., 1998), which reported 

outcome measures stratified by several 

factors (e.g., gender, age, smoking status, 

presence of asthma) within a population 

capable of more than normal exertion, 

provide useful insight. In this study, 

lung function was measured before and 

after hiking, and individual O3

exposures were estimated by averaging 

hourly O3 concentrations from ambient 

monitors located at the base and 

summit. The mean 8-hour average O3

concentration was 0.040 ppm (8-hour 

average concentration range of 0.021 

ppm to 0.074 ppm O3). Decreased lung 

function was associated with O3

exposure, with the greatest effect 

estimates reported for the subgroup that 

reported having asthma or wheezing, 

and for those who hiked for longer 

periods of time. 

Asthma panel studies conducted both 

in the U.S. and in other countries have 

reported that decrements in PEF are 

associated with routine O3 exposures 

among asthmatic and healthy people. 

One large U.S. multicity study, the 

National Cooperative Inner City Asthma 

Study or NCICAS, (Mortimer et al., 

2002) examined O3-related changes in 

PEF in 846 asthmatic children from 8 

urban areas and reported that the 

incidence of ≥ 10 percent decrements in 

morning PEF are associated with 

increases in 8-hour average O3 for a 5- 

day cumulative lag, suggesting that O3

exposure may be associated with 

clinically significant changes in PEF in 

asthmatic children; however, no 

associations were reported with evening 

PEF. The mean 8-hour average O3 was 

0.048 ppm across the 8 cities. Excluding 

days when 8-hour average O3 was 

greater than 0.080 ppm (less than 5 

percent of days), the associations with 

morning PEF remained statistically 

significant. Mortimer et al. (2002) 

discussed potential biological 

mechanisms for delayed effects on 

pulmonary function in asthma, which 

included increased nonspecific airway 

responsiveness secondary to airway 

inflammation due to O3 exposure. Two 

other panel studies (Romieu et al., 1996, 

1997) carried out simultaneously in 

northern and southwestern Mexico City 

with mildly asthmatic school children 

reported statistically significant O3- 

related reductions in PEF, with 

variations in effect depending on lag 

time and time of day. Mean 1-hour 

maximum O3 concentrations in these 

locations ranged from 0.190 ppm in 

northern Mexico City to 0.196 ppm in 

southwestern Mexico City. While 

several studies report statistically 

significant associations between O3

exposure and reduced PEF in 

asthmatics, other studies did not, 

possibly due to low levels of O3

exposure. EPA concludes that these 

studies collectively indicate that O3 may 

be associated with short-term declines 

in lung function in asthmatic 

individuals and that the Mortimer et al. 

(2002) study showed statistically 

significant effects at concentrations in 

the range below 0.080 ppm O3.

Most of the panel studies which have 

investigated associations between O3

exposure and respiratory symptoms or 

increased use of asthma medication are 

focused on asthmatic children. Two 

large U.S. studies (Mortimer et al., 2002; 

Gent et al., 2003) have reported 

associations between ambient O3

concentrations and daily symptoms/ 

asthma medication use, even after 

adjustment for copollutants. Results 

were more mixed, meaning that a 

greater proportion of studies were not 

both positive and statistically 

significant, across smaller U.S. and 

international studies that focused on 

these health endpoints. 

The NCICAS reported morning 

symptoms in 846 asthmatic children 

from 8 U.S. urban areas to be most 

strongly associated with a cumulative 

1- to 4-day lag of O3 concentrations 

(Mortimer et al., 2002). The NCICAS 

used standard protocols that included 

instructing caretakers of the subjects to 

record symptoms (including cough, 

chest tightness, and wheeze) in the daily 

diary by observing or asking the child. 

While these associations were not 

statistically significant in several cities, 

when the individual data are pooled 

from all eight cities, statistically 

significant effects were observed for the 

incidence of symptoms. The authors 

also reported that the odds ratios 

remained essentially the same and 

statistically significant for the incidence 

of morning symptoms when days with 

8-hour O3 concentrations above 0.080 

ppm were excluded. These days 

represented less than 5 percent of days 

in the study. 

Gent and colleagues (2003) followed 

271 asthmatic children under age 12 

and living in southern New England for 

6 months (April through September) 

using a daily symptom diary. They 

found that mean 1-hour max O3 and 8- 

hour max O3 concentrations were 

0.0586 ppm and 0.0513 ppm, 

respectively. The data were analyzed for 

two separate groups of subjects, those 

who used maintenance asthma 

medications during the follow-up 

period and those who did not. The need 

for regular medication was considered 

to be a proxy for more severe asthma. 

Not taking any medication on a regular 

basis and not needing to use a 

bronchodilator would suggest the 


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presence of very mild asthma. 

Statistically significant effects of 1-day 

lag O3 were observed on a variety of 

respiratory symptoms only in the 

medication user group. Both daily 

1-hour max and 8-hour max O3

concentrations were similarly related to 

symptoms such as chest tightness and 

shortness of breath. Effects of O3, but 

not PM2.5, remained significant and 

even increased in magnitude in twopollutant models. Some of the 

associations were noted at 1-hour max 

O3 levels below 0.060 ppm. In contrast, 

no effects were observed among 

asthmatics not using maintenance 

medication. In terms of person-days of 

follow-up, this is one of the larger 

studies currently available that address 

symptom outcomes in relation to O3 and 

provides supportive evidence for effects 

of O3 independent of PM2.5. Study 

limitations include the post-hoc nature 

of the population stratification by 

medication use. Also, the study did not 

account for all of the important 

meteorological factors that might 

influence these results, such as relative 

humidity or dew point. 

The multicity study by Mortimer et al. 

(2002), which examined an asthmatic 

population representative of the United 

States, and several single-city studies 

indicate a robust association of O3

concentrations with respiratory 

symptoms and increased medication use 

in asthmatics. While there are a number 

of well-conducted, albeit relatively 

smaller, U.S. studies which showed 

only limited or a lack of evidence for 

symptom increases associated with O3

exposure, these studies had less 

statistical power and/or were conducted 

in areas with relatively low 1-hour 

maximum average O3 levels, in the 

range of 0.03 to 0.09 ppm. The 2006 

Criteria Document concludes that the 

asthma panel studies, as a group, and 

the NCICAS in particular, indicate a 

positive association between ambient 

concentrations and respiratory 

symptoms and increased medication use 

in asthmatics. The evidence has 

continued to expand since 1996 and 

now is considered to be much stronger 

than in the 1997 review of the O3

primary standard. 

School absenteeism is another 

potential surrogate for the health 

implications of O3 exposure in children. 

The association between school 

absenteeism and ambient O3

concentrations was assessed in two 

relatively large field studies. The first 

study, Chen et al. (2000), examined total 

daily school absenteeism in about 

28,000 elementary school students in 

Nevada over a 2-year period (after 

adjusting for PM10 and CO 

concentrations) and found that ambient 

O3 concentrations with a distributed lag 

of 14 days were statistically 

significantly associated with an 

increased rate of school absences. The 

second study, Gilliland et al. (2001), 

studied O3-related absences among 

about 2,000 4th grade students in 12 

southern California communities and 

found statistically significant 

associations between 8-hour average O3

concentrations (with a distributed lag 

out to 30 days) and all absence 

categories, and particularly for 

respiratory causes. Neither PM10 nor 

NO2 were associated with any 

respiratory or nonrespiratory illnessrelated absences in single pollutant 

models. The 2006 Criteria Document 

concludes that these studies of school 

absences suggest that ambient O3

concentrations, accumulated over two to 

four weeks, may be associated with 

school absenteeism, and particularly 

illness-related absences, but further 

replication is needed before firm 

conclusions can be reached regarding 

the effect of O3 on school absences. In 

addition, more research is needed to 

help shed light on the implications of 

variation in the duration of the lag 

structures (i.e., 1 day, 5 days, 14 days, 

and 30 days) found both across studies 

and within data sets by health endpoint 

and exposure metric. 

(b) Increased Airway Responsiveness 

As discussed in more detail in the 

2006 Criteria Document (section 6.8) 

and the 2007 Staff Paper (section 

3.3.1.1.2), increased airway 

responsiveness, also known as airway 

hyperresponsiveness (AHR) or bronchial 

hyperreactivity, refers to a condition in 

which the propensity for the airways to 

bronchoconstrict due to a variety of 

stimuli (e.g., exposure to cold air, 

allergens, or exercise) becomes 

augmented. This condition is typically 

quantified by measuring the decrement 

in pulmonary function after inhalation 

exposure to specific (e.g., antigen, 

allergen) or nonspecific (e.g., 

methacholine, histamine) 

bronchoconstrictor stimuli. Exposure to 

O3 causes an increase in airway 

responsiveness as indicated by a 

reduction in the concentration of 

stimuli required to produce a given 

reduction in FEV1 or increase in airway 

obstruction. Increased airway 

responsiveness is an important 

consequence of exposure to O3 because 

its presence means that the airways are 

predisposed to narrowing on exposure 

to various stimuli, such as specific 

allergens, cold air or SO2. Statistically 

significant and clinically relevant 

decreases in pulmonary function have 

been observed in early phase allergen 

response in subjects with allergic 

rhinitis after consecutive (4-day) 3-hour 

exposures to 0.125 ppm O3 (Holz et al., 

2002). Similar increased airway 

responsiveness in asthmatics to house 

dust mite antigen 16 to 18 hours after 

exposure to a single dose of O3 (0.160 

ppm for 7.6 hours) was observed. These 

observations, based on O3 exposures to 

levels much higher than the 0.084 ppm 

standard level suggest that O3 exposure 

may be a clinically important factor that 

can exacerbate the response to ambient 

bronchoconstrictor substances in 

individuals with preexisting allergic 

asthma or rhinitis. Further, O3 may have 

an immediate impact on the lung 

function of asthmatics as well as 

contribute to effects that persist for 

longer periods. 

Kreit et al. (1989) found that O3 can 

induce increased airway responsiveness 

in asthmatic subjects to O3, who 

typically have increased airway 

responsiveness at baseline. A 

subsequent study (Jo ̈rres et al., 1996) 

suggested an increase in specific (i.e., 

allergen-induced) airway reactivity in 

subjects with allergic asthma, and to a 

lesser extent in subjects with allergic 

rhinitis after short-term exposure to 

higher O3 levels; other studies reported 

similar results. According to one study 

(Folinsbee and Hazucha, 2000), changes 

in airway responsiveness after O3

exposure resolve more slowly than 

changes in FEV1 or respiratory 

symptoms. Other studies of repeated 

exposure to O3 suggest that changes in 

airway responsiveness tend to be 

somewhat less affected by attenuation 

with consecutive exposures than 

changes in FEV1 (EPA, 2006a, section 

6.8). 

The 2006 Criteria Document (section 

6.8) concludes that O3 exposure is 

linked with increased airway 

responsiveness. Both human and animal 

studies indicate that increased airway 

responsiveness is not mechanistically 

associated with inflammation, and does 

not appear to be strongly associated 

with initial decrements in lung function 

or increases in symptoms. As a result of 

increased airway responsiveness 

induced by O3 exposure, human airways 

may be more susceptible to a variety of 

stimuli, including antigens, chemicals, 

and particles. Because asthmatic 

subjects typically have increased airway 

responsiveness at baseline, enhanced 

bronchial response to antigens in 

asthmatics raises potential public health 

concerns as they could lead to increased 

morbidity (e.g., medication usage, 

school absences, emergency room visits, 

hospital admissions) or to more 

persistent alterations in airway 


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19 Graham and Koren (1990) compared 

inflammatory mediators present in NL and BAL 

fluids of humans exposed to 0.4 ppm O3 for 2 hours 

and found similar increases in PMNs in both fluids, 

suggesting a qualitative correlation between 

inflammatory changes in the lower airways (BAL) 

and upper respiratory tract (NL). 

responsiveness (EPA 2006a, p. 8–21). As 

such, increased airway responsiveness 

after O3 exposure represents a plausible 

link between O3 exposure and increased 

hospital admissions. 

(c) Respiratory Inflammation and 

Increased Permeability 

Based on evidence from the 1997 

review, acute inflammatory responses in 

the lung have been observed subsequent 

to 6.6 hour O3 exposures to the lowest 

tested level—0.080 ppm—in healthy 

adults engaged in moderately high 

exercise (section 6.9 of the 2006 Criteria 

Document and section 3.3.1.3 of the 

2007 Staff Paper). Some of these prior 

studies suggest that inflammatory 

responses may be detected in some 

individuals following O3 exposures in 

the absence of O3-induced pulmonary 

decrements in those subjects. These 

studies also demonstrate that short-term 

exposures to O3 also can cause 

increased permeability in the lungs of 

humans and experimental animals. 

Inflammatory responses and epithelial 

permeability have been seen to be 

independent of spirometric responses. 

Not only are the newer lung 

inflammation and increased cellular 

permeability findings discussed in the 

2006 Criteria Document (section 8.4.2) 

consistent with the 1997 review, but 

they provide better characterization of 

the physiological mechanisms by which 

O3 causes these effects. 

Lung inflammation and increased 

permeability, which are distinct events 

controlled by different mechanisms, are 

two commonly observed effects of O3

exposure observed in all of the species 

studied. Increased cellular permeability 

is a disruption of the lung barrier that 

leads to leakage of serum proteins, 

influx of polymorphonuclear leukocytes 

(neutrophils or PMNs), release of 

bioactive mediators, and movement of 

compounds from the airspaces into the 

blood. 

A number of controlled human 

exposure studies have analyzed 

bronchoalveolar lavage (BAL) and nasal 

lavage (NL) 19 fluids and cells for 

markers of inflammation and lung 

damage (EPA, 2006a, Annex AX6). 

Increased lung inflammation is 

demonstrated by the presence of 

neutrophils found in BAL fluid in the 

lungs, which has long been accepted as 

a hallmark of inflammation. It is 

apparent, however, that inflammation 

within airway tissues may persist 

beyond the point that inflammatory 

cells are found in the BAL fluid. Soluble 

mediators of inflammation, such as 

cytokines and arachidonic acid 

metabolites have been measured in the 

BAL fluid of humans exposed to O3. In 

addition to their role in inflammation, 

many of these compounds have 

bronchoconstrictive properties and may 

be involved in increased airway 

responsiveness following O3 exposure. 

An in vitro study of epithelial cells from 

nonatopic and atopic asthmatics 

exposed to 0.010 to 0.100 ppm O3

showed significantly increased 

permeability compared to cells from 

normal persons. This indicates a 

potentially inherent susceptibility of 

cells from asthmatic individuals for O3- 

induced permeability. 

In the 1996 Criteria Document, 

assessment of controlled human 

exposure studies indicated that a single, 

acute (1 to 4 hours) O3 exposure (≥ 0.080 

to 0.100 ppm) of subjects engaged in 

moderate to heavy exercise could 

induce a number of cellular and 

biochemical changes suggestive of 

pulmonary inflammation and lung 

permeability (EPA, 2006a, p. 8–22). 

These changes persisted for at least 18 

hours. Markers from BAL fluid 

following both 2-hour and 4-hour O3

exposures repeated up to 5 days 

indicate that there is ongoing cellular 

damage irrespective of attenuation of 

some cellular inflammatory responses of 

the airways, pulmonary function, and 

symptom scores (EPA, 2006a, p. 8–22). 

Acute airway inflammation was shown 

in Devlin et al. (1990) to occur among 

adults exposed to 0.080 ppm O3 for 6.6 

hours with exercise. McBride et al. 

(1994) reported that asthmatic subjects 

were more sensitive than nonasthmatics to upper airway 

inflammation for O3 exposures that did 

not affect pulmonary function (EPA, 

2006a, p. 6–33). However, the public 

health significance of these changes is 

not entirely clear. 

The studies reporting inflammatory 

responses and markers of lung injury 

have clearly demonstrated that there is 

significant variation in response of 

subjects exposed, especially to 6.6 hours 

O3 exposures at 0.080 and 0.100 ppm. 

To provide some perspective on the 

public health impact for these effects, 

the 2007 Staff Paper (section 3.3.1.1.3) 

notes that one study (Devlin et al., 1991) 

showed that roughly 10 to 50 percent of 

the 18 young healthy adult subjects 

experienced notable increases (i.e., ≥ 2 

fold increase) in most of the 

inflammatory and cellular injury 

indicators analyzed, associated with 6.6- 

hour exposures at 0.080 ppm. Similar, 

although in some cases higher, fractions 

of the population of 10 healthy adults 

tested saw > 2 fold increases associated 

with 6.6-hour exposures to 0.100 ppm. 

The authors of this study expressed the 

view that ‘‘susceptible subpopulations 

such as the very young, elderly, and 

people with pulmonary impairment or 

disease may be even more affected’’ 

(Devlin et al., 1991). 

Since 1996, a substantial number of 

human exposure studies have been 

published which have provided 

important new information on lung 

inflammation and epithelial 

permeability. Mudway and Kelly (2004) 

examined O3-induced inflammatory 

responses and epithelial permeability 

with a meta-analysis of 21 controlled 

human exposure studies and showed 

that an influx in neutrophils and protein 

in healthy subjects is associated with 

total O3 dose (product of O3

concentration, exposure duration, and 

minute ventilation) (EPA, 2006a, p. 6– 

34). Results of the analysis suggest that 

the time course for inflammatory 

responses (including recruitment of 

neutrophils and other soluble 

mediators) is not clearly established, but 

there is evidence that attenuation 

profiles for many of these parameters 

are different (EPA, 2006a, p. 8–22). 

The 2006 Criteria Document (chapter 

8) concludes that interaction of O3 with 

lipid constituents of epithelial lining 

fluid (ELF) and cell membranes and the 

induction of oxidative stress is 

implicated in injury and inflammation. 

Alterations in the expression of 

cytokines, chemokines, and adhesion 

molecules, indicative of an ongoing 

oxidative stress response, as well as 

injury repair and regeneration 

processes, have been reported in animal 

toxicology and human in vitro studies 

evaluating biochemical mediators 

implicated in injury and inflammation. 

While antioxidants in ELF confer some 

protection, O3 reactivity is not 

eliminated at environmentally relevant 

exposures (2006 Criteria Document, p. 

8–24). Further, antioxidant reactivity 

with O3 is both species-specific and 

dose-dependent. 

(d) Increased Susceptibility to 

Respiratory Infection 

As discussed in more detail in the 

2006 Criteria Document (sections 5.2.2, 

6.9.6, and 8.4.2), short-term exposures 

to O3 have been shown to impair 

physiological defense capabilities in 

experimental animals by depressing 

alveolar macrophage (AM) functions 

and by altering the mucociliary 

clearance of inhaled particles and 

microbes resulting in increased 

susceptibility to respiratory infection. 


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20 Discussion of the reasons for focusing on warm 

season studies is found in the section 2.A.3.a below. 

Short-term O3 exposures also interfere 

with the clearance process by 

accelerating clearance for low doses and 

slowing clearance for high doses. 

Animal toxicological studies have 

reported that acute O3 exposures 

suppress alveolar phagocytosis and 

immune system functions. Impairment 

of host defenses and subsequent 

increased susceptibility to bacterial lung 

infection in laboratory animals has been 

induced by short-term exposures to O3

levels as low as 0.080 ppm. 

A single controlled human exposure 

study reviewed in the 1996 Criteria 

Document (p. 8–26) reported that 

exposure to 0.080 to 0.100 ppm O3 for 

6.6 hours (with moderate exercise) 

induced decrements in the ability of 

AMs to phagocytose microorganisms. 

Integrating the recent animal study 

results with human exposure evidence 

available in the 1996 Criteria Document, 

the 2006 Criteria Document concludes 

that available evidence indicates that 

short-term O3 exposures have the 

potential to impair host defenses in 

humans, primarily by interfering with 

AM function. Any impairment in AM 

function may lead to decreased 

clearance of microorganisms or 

nonviable particles. Compromised AM 

functions in asthmatics may increase 

their susceptibility to other O3 effects, 

the effects of particles, and respiratory 

infections (EPA, 2006a, p. 8–26). 

(e) Morphological Effects 

The 1996 Criteria Document found 

that short-term O3 exposures cause 

similar alterations in lung morphology 

in all laboratory animal species studied, 

including primates. As discussed in the 

2007 Staff Paper (section 3.3.1.1.5), cells 

in the centriacinar region (CAR) of the 

lung (the segment between the last 

conducting airway and the gas exchange 

region) have been recognized as a 

primary target of O3-induced damage 

(epithelial cell necrosis and remodeling 

of respiratory bronchioles), possibly 

because epithelium in this region 

receives the greatest dose of O3

delivered to the lower respiratory tract. 

Following chronic O3 exposure, 

structural changes have been observed 

in the CAR, the region typically affected 

in most chronic airway diseases of the 

human lung (EPA, 2006a, p. 8–24). 

Ciliated cells in the nasal cavity and 

airways, as well as Type I cells in the 

gas-exchange region, are also identified 

as targets. While short-term O3

exposures can cause epithelial cell 

profileration and fibrolitic changes in 

the CAR, these changes appear to be 

transient with recovery occurring after 

exposure, depending on species and O3

dose. The potential impacts of repeated 

short-term and chronic morphological 

effects of O3 exposure are discussed 

below in the section on effects from 

long-term exposures. Long-term or 

prolonged exposure has been found to 

cause chronic lesions similar to early 

lesions found in individuals with 

respiratory bronchiolitis, which have 

the potential to progress to fibrotic lung 

disease (2006 Criteria Document, p. 

8–25). 

Recent studies continue to show that 

short-term and sub-chronic exposures to 

O3 cause similar alterations in lung 

structure in a variety of experimental 

animal species. For example, a series of 

new studies that used infant rhesus 

monkeys and simulated seasonal 

ambient exposure (0.5 ppm 8 hours/day 

for 5 days, every 14 days for 11 

episodes) reported remodeling in the 

distal airways; abnormalities in tracheal 

basement membrane; eosinophil 

accumulation in conducting airways; 

and decrements in airway innervation 

(2006 Criteria Document, p. 8–25). 

Based on evidence from animal 

toxicological studies, short-term and 

sub-chronic exposures to O3 can cause 

morphological changes in the 

respiratory systems, particularly in the 

CAR, of a number of laboratory animal 

species (EPA, 2006a, section 5.2.4). 

(f) Emergency Department Visits/ 

Hospital Admissions for Respiratory 

Causes 

Increased summertime emergency 

department visits and hospital 

admissions for respiratory causes have 

been associated with ambient exposures 

to O3. As discussed in section 3.3.1.1.6 

of the 2007 Staff Paper, numerous 

studies conducted in various locations 

in the U.S. and Canada consistently 

have shown a relationship between 

ambient O3 levels and increased 

incidence of emergency department 

visits and hospital admissions for 

respiratory causes, even after controlling 

for modifying factors, such as weather 

and copollutants. Such associations 

between elevated ambient O3 during 

summer months and increased hospital 

admissions have a plausible biological 

basis in the human and animal evidence 

of functional, symptomatic, and 

physiologic effects discussed above and 

in the increased susceptibility to 

respiratory infections observed in 

laboratory animals. 

In the 1997 review of the O3 NAAQS, 

the Criteria Document evaluated 

emergency department visits and 

hospital admissions as possible 

outcomes following exposure to O3

(EPA, 2006a, section 7.3). The evidence 

was limited for emergency department 

visits, but results of several studies 

generally indicated that short-term 

exposures to O3 were associated with 

respiratory emergency department 

visits. The strongest and most consistent 

evidence, at both lower levels (i.e., 

below 0.120 ppm 1-hour max O3) and at 

higher levels (above 0.120 ppm 1-hour 

max O3), was found in the group of 

studies which investigated 

summertime 20 daily hospital 

admissions for respiratory causes in 

different eastern North American cities. 

These studies consistently demonstrated 

that ambient O3 levels were associated 

with increased hospital admissions and 

accounted for about one to three excess 

respiratory hospital admissions per 

million persons with each 0.100 ppm 

increase in 1-hour max O3, after 

adjustment for possible confounding 

effects of temperature and copollutants. 

Overall, the 1996 Criteria Document 

concluded that there was strong 

evidence that ambient O3 exposures can 

cause significant exacerbations of 

preexisting respiratory disease in the 

general public. Excess respiratoryrelated hospital admissions associated 

with O3 exposures for the New York 

City area (based on Thurston et al., 

1992) were included in the quantitative 

risk assessment in the 1997 review and 

are included in the current assessment 

along with estimates for respiratoryrelated hospital admissions in 

Cleveland, Detroit, and Los Angeles 

based on more recent studies (2007 Staff 

Paper, chapter 5). Significant 

uncertainties and the difficulty of 

obtaining reliable baseline incidence 

numbers resulted in emergency 

department visits not being used in the 

quantitative risk assessment in either 

the 1997 or the 2008 O3 NAAQS review. 

In the past decade, a number of 

studies have examined the temporal 

pattern associations between O3

exposures and emergency department 

visits for respiratory causes (EPA, 

2006a, section 7.3.2). These studies are 

summarized in the 2006 Criteria 

Document (chapter 7 Annex) and some 

are shown in Figure 1 (in section II.A.3). 

Respiratory causes for emergency 

department visits include asthma, 

bronchitis, emphysema, pneumonia, 

and other upper and lower respiratory 

infections, such as influenza, but 

asthma visits typically dominate the 

daily incidence counts. Most studies 

report positive associations with O3. 

Among studies with adequate controls 

for seasonal patterns, many reported at 

least one significant positive association 

involving O3. 


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In reviewing evidence for associations 

between emergency department visits 

for asthma and short-term O3 exposures, 

the 2006 Criteria Document (Figure 7– 

8, p. 7–68) notes that in general, O3

effect estimates from summer only 

analyses tended to be positive and larger 

compared to results from cool season or 

all year analyses. Several of the studies 

reported significant associations 

between O3 concentrations and 

emergency department visits for 

respiratory causes, in particular asthma. 

However, inconsistencies were observed 

which were at least partially attributable 

to differences in model specifications 

and analysis approach among various 

studies. For example, ambient O3

concentrations, length of the study 

period, and statistical methods used to 

control confounding by seasonal 

patterns and copollutants appear to 

affect the observed O3 effect on 

emergency department visits. 

Hospital admissions studies focus 

specifically on unscheduled admissions 

because unscheduled hospital 

admissions occur in response to 

unanticipated disease exacerbations and 

are more likely than scheduled 

admissions to be affected by variations 

in environmental factors, such as daily 

O3 levels. Results of a fairly large 

number of these studies published 

during the past decade are summarized 

in 2006 Criteria Document (chapter 7 

Annex), and results of U.S. and 

Canadian studies are shown in Figure 1 

below (in section II.A.3). As a group, 

these hospital admissions studies tend 

to be larger geographically and 

temporally than the emergency 

department visit studies and provide 

results that are generally more 

consistent. The strongest associations of 

respiratory hospital admissions with O3

concentrations were observed using 

short lag periods, in particular for a 0- 

day lag (same day exposure) and a 1-day 

lag (previous day exposure). Most 

studies in the United States and Canada 

indicated positive, statistically 

significant associations between 

ambient O3 concentrations and 

respiratory hospital admissions in the 

warm season. However, not all studies 

found a statistically significant 

relationship with O3, possibly because 

of very low ambient O3 levels. Analyses 

for confounding using multipollutant 

regression models suggest that 

copollutants generally do not confound 

the association between O3 and 

respiratory hospitalizations. Ozone 

effect estimates were robust to PM 

adjustment in all-year and warm-season 

only data. 

Overall, the 2006 Criteria Document 

concludes that positive and robust 

associations were found between 

ambient O3 concentrations and various 

respiratory disease hospitalization 

outcomes, when focusing particularly 

on results of warm-season analyses. 

Recent studies also generally indicate a 

positive association between O3

concentrations and emergency 

department visits for asthma during the 

warm season (EPA, 2006a, p. 7–175). 

These positive and robust associations 

are supported by the controlled human 

exposure, animal toxicological, and 

epidemiological evidence for lung 

function decrements, increased 

respiratory symptoms, airway 

inflammation, and increased airway 

responsiveness. Taken together, the 

overall evidence supports a causal 

relationship between acute ambient O3

exposures and increased respiratory 

morbidity outcomes resulting in 

increased emergency department visits 

and hospitalizations during the warm 

season (EPA, 2006a, p. 8–77). 

ii. Effects on the Respiratory System of 

Long-Term O3 Exposures 

The 1996 Criteria Document 

concluded that there was insufficient 

evidence from the limited number of 

studies to determine whether long-term 

O3 exposures resulted in chronic health 

effects at ambient levels observed in the 

U.S. However, the aggregate evidence 

suggested that O3 exposure, along with 

other environmental factors, could be 

responsible for health effects in exposed 

populations. Animal toxicological 

studies carried out in the 1980’s and 

1990’s demonstrated that long-term 

exposures can result in a variety of 

morphological effects, including 

permanent changes in the small airways 

of the lungs, including remodeling of 

the distal airways and CAR and 

deposition of collagen, possibly 

representing fibrotic changes. These 

changes result from the damage and 

repair processes that occur with 

repeated exposure. Fibrotic changes 

were also found to persist after months 

of exposure providing a potential 

pathophysiologic basis for changes in 

airway function observed in children in 

some recent epidemiological studies. It 

appears that variable seasonal ambient 

patterns of exposure may be of greater 

concern than continuous daily 

exposures. 

Several studies published since 1996 

have investigated lung function changes 

over seasonal time periods (EPA, 2006a, 

section 7.5.3). The 2006 Criteria 

Document (p. 7–114) summarizes these 

studies which collectively indicate that 

seasonal O3 exposure is associated with 

smaller growth-related increases in lung 

function in children than they would 

have experienced living in areas with 

lower O3 levels. There is some limited 

evidence that seasonal O3 also may 

affect lung function growth in young 

adults, although the uncertainty about 

the role of copollutants makes it 

difficult to attribute the effects to O3

alone. 

Lung capacity grows during 

childhood and adolescence as body size 

increases, reaches a maximum during 

the twenties, and then begins to decline 

steadily and progressively with age. 

Long-term exposure to air pollution has 

long been thought to contribute to 

slower growth in lung capacity, 

diminished maximally attained 

capacity, and/or more rapid decline in 

lung capacity with age (EPA, 2006a, 

section 7.5.4). Toxicological findings 

evaluated in the 1996 Criteria Document 

demonstrated that repeated daily 

exposure of rats to an episodic profile of 

O3 caused small, but significant, 

decrements in growth-related lung 

function that were consistent with early 

indicators of focal fibrogenesis in the 

proximal alveolar region, without overt 

fibrosis. Because O3 at sufficient 

concentrations is a strong respiratory 

irritant and has been shown to cause 

inflammation and restructuring of the 

respiratory airways, it is plausible that 

long-term O3 exposures might have a 

negative impact on baseline lung 

function, particularly during childhood 

when these exposures might be 

associated with long-term risks. 

Several epidemiological studies 

published since 1996 have examined 

the relationship between lung function 

development and long-term O3

exposure. The most extensive and 

robust study of respiratory effects in 

relation to long-term air pollution 

exposures among children in the U.S. is 

the Children’s Health Study carried out 

in 12 communities of southern 

California starting in 1993. One analysis 

(Peters et al., 1999a) examined the 

relationship between long-term O3

exposures and self-reports of respiratory 

symptoms and asthma in a cross 

sectional analysis and found a limited 

relationship between outcomes of 

current asthma, bronchitis, cough and 

wheeze and a 0.040 ppm increase in 1- 

hour max O3 (EPA, 2006a, p. 7–115). 

Another analysis (Peters et al., 1999b) 

examined the relationship between lung 

function at baseline and levels of air 

pollution in the community. They 

reported evidence that annual mean O3

levels were associated with decreases in 

FVC, FEV1, PEF and forced expiratory 

flow (FEF25¥75) (the latter two being 

statistically significant) among females 

but not males. In a separate analysis 

(Gauderman et al., 2000) of 4th, 7th, and 


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10th grade students, a longitudinal 

analysis of lung function development 

over four years found no association 

with O3 exposure. The Children’s 

Health Study enrolled a second cohort 

of more than 1500 fourth graders in 

1996 (Gauderman et al., 2002). While 

the strongest associations with negative 

lung function growth were observed 

with acid vapors in this cohort, children 

from communities with higher 4-year 

average O3 levels also experienced 

smaller increases in various lung 

function parameters. The strongest 

relationship with O3 was with PEF. 

Specifically, children from the leastpolluted community had a small but 

statistically significant increase in PEF 

as compared to those from the mostpolluted communities. In two-pollutant 

models, only 8-hour average O3 and NO2

were significant joint predictors of FEV1

and maximal midexpiratory flow 

(MMEF). Although results from the 

second cohort of children are supportive 

of a weak association, the definitive 8- 

year follow-up analysis of the first 

cohort (Gauderman et al., 2004a) 

provides little evidence that long-term 

exposure to ambient O3 at current levels 

is associated with significant deficits in 

the growth rate of lung function in 

children. Avol et al. (2001) examined 

children who had moved away from 

participating communities in southern 

California to other states with improved 

air quality. They found that a negative, 

but not statistically significant, 

association was observed between O3

and lung function parameters. 

Collectively, the results of these reports 

from the children’s health cohorts 

provide little evidence to support an 

impact of long-term O3 exposures on 

lung function development. 

Evidence for a significant relationship 

between long-term O3 exposures and 

decrements in maximally attained lung 

function was reported in a nationwide 

study of first year Yale students (Kinney 

et al., 1998; Galizia and Kinney, 1999) 

(EPA, 2006a, p. 7–120). Males had much 

larger effect estimates than females, 

which might reflect higher outdoor 

activity levels and correspondingly 

higher O3 exposures during childhood. 

A similar study of college freshmen at 

University of California at Berkeley also 

reported significant effects of long-term 

O3 exposures on lung function (Ku ̈nzli 

et al., 1997; Tager et al., 1998). In a 

comparison of students whose city of 

origin was either Los Angeles or San 

Francisco, long-term O3 exposures were 

associated with significant changes in 

mid- and end-expiratory flow measures, 

which could be considered early 

indicators for pathologic changes that 

might progress to COPD. 

There have been a few studies that 

investigated associations between longterm O3 exposures and the onset of new 

cases of asthma (EPA, 2006a, section 

7.5.6). The Adventist Health and Smog 

(AHSMOG) study cohort of about 4,000 

was drawn from nonsmoking, nonHispanic white adult Seventh Day 

Adventists living in California (Greer et 

al., 1993; McDonnell et al., 1999). 

During the ten-year follow-up in 1987, 

a statistically significant increased 

relative risk of asthma development was 

observed in males, compared to a 

nonsignificant relative risk in females 

(Greer et al., 1993). In the 15-year 

follow-up in 1992, it was reported that 

for males, there was a statistically 

significant increased relative risk of 

developing asthma associated with 8- 

hour average O3 exposures, but there 

was no evidence of an association in 

females. Consistency of results in the 

two studies with different follow-up 

times provides supportive evidence of 

the potential for an association between 

long-term O3 exposure and asthma 

incidence in adult males; however, 

representativeness of this cohort to the 

general U.S. population may be limited 

(EPA, 2006a, p. 7–125). 

In a similar study (McConnell et al., 

2002) of incident asthma among 

children (ages 9 to 16 at enrollment), 

annual surveys of 3,535 children 

initially without asthma were used to 

identify new-onset asthma cases as part 

of the Children’s Health Study. Six 

high-O3 and six low-O3 communities 

were identified where the children 

resided. There were 265 children who 

reported new-onset asthma during the 

follow-up period. Although asthma risk 

was no higher for all residents of the six 

high-O3 communities versus the six 

low-O3 communities, asthma risk was 

3.3 times greater for children who 

played three or more sports as compared 

with children who played no sports 

within the high-O3 communities. This 

association was absent in the 

communities with lower O3

concentrations. No other pollutants 

were found to be associated with newonset asthma (EPA, 2006a, p. 7–125). 

Playing sports may result in extended 

outdoor activity and exposure occurring 

during periods when O3 levels are 

higher. It should be noted, however, that 

the results of the Children’s Health 

Study were based on a small number of 

new-onset asthma cases among children 

who played three or more sports. Future 

replication of these findings in other 

cohorts would help determine whether 

a causal interpretation is appropriate. 

In animal toxicology studies, the 

progression of morphological effects 

reported during and after a chronic 

exposure in the range of 0.50 to 1.00 

ppm O3 (well above current ambient 

levels) is complex, with inflammation 

peaking over the first few days of 

exposure, then dropping, then 

plateauing, and finally, largely 

disappearing (EPA, 2006a, section 

5.2.4.4). By contrast, fibrotic changes in 

the tissue increase very slowly over 

months of exposure, and, after exposure 

ceases, the changes sometimes persist or 

increase. Epithelial hyperplasia peaks 

soon after the inflammatory response 

but is usually maintained in both the 

nose and lungs with continuous 

exposure; it also does not return to preexposure levels after the end of 

exposure. Patterns of exposure in this 

same concentration range determine 

effects, with 18 months of daily 

exposure, causing less morphologic 

damage than exposures on alternating 

months. This is important as 

environmental O3 exposure is typically 

seasonal. Long-term studies by Plopper 

and colleagues (Evans et al., 2003; 

Schelegle et al., 2003; Chen et al., 2003; 

Plopper and Fanucchi, 2000) 

investigated infant rhesus monkeys 

exposed to simulated, seasonal O3 and 

demonstrated: (1) Remodeling in the 

distal airways, (2) abnormalities in 

tracheal basement membrane; (3) 

eosinophil accumulation in conducting 

airways; and (4) decrements in airway 

innervation (EPA, 2006a, p. 5–45). 

These findings provide additional 

information regarding possible injuryrepair processes occurring with longterm O3 exposures suggesting that these 

processes are only partially reversible 

and may progress following cessation of 

O3 exposure. Further, these processes 

may lead to nonreversible structural 

damage to lung tissue; however, there is 

still too much uncertainty to 

characterize the significance of these 

findings to human exposure profiles and 

effect levels (EPA, 2006a, p. 8–25). 

In summary, in the past decade, 

important new longitudinal studies 

have examined the effect of chronic O3

exposure on respiratory health 

outcomes. Limited evidence from recent 

long-term morbidity studies have 

suggested in some cases that chronic 

exposure to O3 may be associated with 

seasonal declines in lung function or 

reduced lung function development, 

increases in inflammation, and 

development of asthma in children and 

adults. Seasonal decrements or smaller 

increases in lung function measures 

have been reported in several studies; 

however, the extent to which these 


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changes are transient remains uncertain. 

While there is supportive evidence from 

animal studies involving effects from 

chronic exposures, large uncertainties 

still remain as to whether current 

ambient levels and exposure patterns 

might cause these same effects in 

human populations. The 2006 Criteria 

Document concludes that 

epidemiological studies of new asthma 

development and longer-term lung 

function declines remain inconclusive 

at present (EPA, 2006a, p. 7–134). 

iii. Effects on the Cardiovascular System 

of O3 Exposure 

At the time of the 1997 review, the 

possibility of O3-induced cardiovascular 

effects was largely unrecognized. Since 

then, a very limited body of evidence 

from animal, controlled human 

exposure, and epidemiologic studies has 

emerged that provides evidence for 

some potential plausible mechanisms 

for how O3 exposures might exert 

cardiovascular system effects, however 

further research is needed to 

substantiate these potential 

mechanisms. Possible mechanisms may 

involve O3-induced secretions of 

vasoconstrictive substances and/or 

effects on neuronal reflexes that may 

result in increased arterial blood 

pressure and/or altered 

electrophysiologic control of heart rate 

or rhythm. Some animal toxicology 

studies have shown O3-induced 

decreases in heart rate, mean arterial 

pressure, and core temperature. One 

controlled human exposure study that 

evaluated effects of O3 exposure on 

cardiovascular health outcomes found 

no significant O3-induced differences in 

ECG or blood pressure in healthy or 

hypertensive subjects but did observe a 

significant O3-induced increase the 

alveolar-to-arterial PO2 gradient and 

heart rate in both groups resulting in an 

overall increase in myocardial work and 

impairment in pulmonary gas exchange 

(Gong et al., 1998). In another controlled 

human exposure study, inhalation of a 

mixture of PM2.5 and O3 by healthy 

subjects increased brachial artery 

vasoconstriction and reactivity (Brook et 

al., 2002). 

The evidence from a few animal 

studies also includes potential direct 

effects such as O3-induced release from 

lung epithelial cells of platelet 

activating factor (PAF) that may 

contribute to blood clot formation that 

would have the potential to increase the 

risk of serious cardiovascular outcomes 

(e.g., heart attack, stroke, mortality). 

Also, interactions of O3 with surfactant 

components in epithelial lining fluid of 

the lung may result in production of 

oxysterols and reactive oxygen species 

that may exhibit PAF-like activity 

contributing to clotting and also may 

exert cytotoxic effects on lung and heart 

muscle cells. 

Epidemiological panel and field 

studies that examined associations 

between O3 and various cardiac 

physiologic endpoints have yielded 

limited evidence suggestive of a 

potential association between acute O3

exposure and altered heart rate 

variability (HRV), ventricular 

arrhythmias, and incidence of heart 

attacks (myocardial infarction or MI). A 

number of epidemiological studies have 

also reported associations between 

short-term exposures and 

hospitalization for cardiovascular 

diseases. As shown in Figure 7–13 of 

the 2006 Criteria Document, many of the 

studies reported negative or inconsistent 

associations. Some other studies, 

especially those that examined the 

relationship when O3 exposures were 

higher, have found robust positive 

associations between O3 and 

cardiovascular hospital admissions 

(EPA, 2006a, p. 7–82). For example, one 

study reported a positive association 

between O3 and cardiovascular hospital 

admissions in Toronto, Canada in a 

summer-only analysis (Burnett et al., 

1997b). The results were robust to 

adjustment for various PM indices, 

whereas the PM effects diminished 

when adjusted for gaseous pollutants. 

Other studies stratified their analysis by 

temperature (i.e., by warms days versus 

cool days). Several analyses using warm 

season days consistently produced 

positive associations. 

The epidemiologic evidence for 

cardiovascular morbidity is much 

weaker than for respiratory morbidity, 

with only one of several U.S. and 

Canadian studies showing statistically 

significant positive associations of 

cardiovascular hospitalizations with 

warm-season O3 concentrations. Most of 

the available European and Australian 

studies, all of which conducted all-year 

O3 analyses, did not find an association 

between short-term O3 concentrations 

and cardiovascular hospitalizations. 

Overall, the currently available evidence 

is inconclusive regarding an association 

between cardiovascular hospital 

admissions and ambient O3 exposure 

(EPA, 2006a, p. 7–83). 

In summary, based on the evidence 

from animal toxicology, controlled 

human exposure, and epidemiological 

studies, from the 2006 Criteria 

Document (p. 8–77) concludes that this 

generally limited body of evidence is 

suggestive that O3 can directly and/or 

indirectly contribute to cardiovascularrelated morbidity, but that much needs 

to be done to more fully integrate links 

between ambient O3 exposures and 

adverse cardiovascular outcomes. 

b. Mortality 

i. Mortality and Short-term O3 Exposure 

The 1996 Criteria Document 

concluded that an association between 

daily mortality and O3 concentration for 

areas with high O3 levels (e.g., Los 

Angeles) was suggested. However, due 

to a very limited number of studies 

available at that time, there was 

insufficient evidence to conclude that 

the observed association was likely 

causal. 

The 2006 Criteria Document included 

results from numerous epidemiological 

analyses of the relationship between O3

and mortality. Additional single city 

analyses have also been conducted since 

1996, however, the most pivotal studies 

in EPA’s (and CASAC’s) finding of 

increased support for the relationship 

between premature mortality and O3 is 

in part related to differences in study 

design—limiting analyses to warm 

seasons, better control for copollutants, 

particularly PM, and use of multicity 

designs (both time series and metaanalytic designs). Key findings are 

available from multicity time-series 

studies that report associations between 

O3 and mortality. These studies include 

analyses using data from 90 U.S. cities 

in the National Mortality, Morbidity and 

Air Pollution (NMMAPS) study 

(Dominici et al., 2003) and from 95 U.S. 

communities in an extension to the 

NMMAPS analyses (Bell et al., 2004). 

The original 90-city NMMAPS 

analysis, with data from 1987 to 1994, 

was primarily focused on investigating 

effects of PM10 on mortality. A 

significant association was reported 

between mortality and 24-hour average 

O3 concentrations in analyses using all 

available data as well as in the warm 

season only analyses (Dominici et al., 

2003). The estimate using all available 

data was about half that for the summeronly data at a lag of 1-day. The extended 

NMMAPS analysis included data from 

95 U.S. cities and included an 

additional 6 years of data, from 1987– 

2000 (Bell et al., 2004). Significant 

associations were reported between O3

and mortality in analyses using all 

available data. The effect estimate for 

increased mortality was approximately 

0.5 percent per 0.020 ppm change in 24- 

hour average O3 measured on the same 

day, and approximately 1.04 percent per 

0.020 ppm change in 24-hour average O3

in a 7-day distributed lag model (EPA, 

2006a, p. 7–88). In analyses using only 

data from the warm season, the results 

were not significantly different from the 

full-year results. The authors also report 


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21 In commenting on the Criteria Document, the 

CASAC Ozone Panel raised questions about the 

implications of these time-series results in a policy 

context, emphasizing that ‘‘* * * while the timeseries study design is a powerful tool to detect very 

small effects that could not be detected using other 

designs, it is also a blunt tool’’ (Henderson, 2006b). 

They note that ‘‘* * * not only is the interpretation 

of these associations complicated by the fact that 

the day-to-day variation in concentrations of these 

pollutants is, to a varying degree, determined by 

meteorology, the pollutants are often part of a large 

and highly correlated mix of pollutants, only a very 

few of which are measured’’ (Henderson, 2006b). 

Even with these uncertainties, the CASAC Ozone 

Panel, in its review of the Staff Paper, found ‘‘* * * 

premature total non-accidental and 

cardiorespiratory mortality for inclusion in the 

quantitative risk assessment to be appropriate.’’ 

(Henderson, 2006b) 

that O3-mortality associations were 

robust to adjustment for PM (EPA, 

2006a, p. 7–100). Using a subset of the 

NMMAPS data set, Huang et al. (2005) 

focused on associations between 

cardiopulmonary mortality and O3

exposure (24-hour average) during the 

summer season only. The authors report 

an approximate 1.47 percent increase 

per 0.020 ppm change in O3

concentration measured on the same 

day and an approximate 2.52 percent 

increase per 0.020 ppm change in O3

concentration using a 7-day distributed 

lag model. These findings suggest that 

the effect of O3 on mortality is 

immediate but also persists for several 

days. 

As discussed below in section 

II.A.3.a, confounding by weather, 

especially temperature, is complicated 

by the fact that higher temperatures are 

associated with the increased 

photochemical activities that are 

important for O3 formation. Using a 

case-crossover study design, Schwartz 

(2005) assessed associations between 

daily maximum concentrations and 

mortality, matching case and control 

periods by temperature, and using data 

only from the warm season. The 

reported effect estimate of 

approximately 0.92 percent change in 

mortality per 0.040 ppm O3 (1-hour 

maximum) was similar to time-series 

analysis results with adjustment for 

temperature (approximately 0.76 

percent per 0.040 ppm O3), suggesting 

that associations between O3 and 

mortality were robust to the different 

adjustment methods for temperature. 

An initial publication from APHEA, a 

European multicity study, reported 

statistically significant associations 

between daily maximum O3

concentrations and mortality in four 

cities in a full year analysis (Toulomi et 

al., 1997). An extended analysis was 

done using data from 23 cities 

throughout Europe (Gryparis et al., 

2004). In this report, a positive but not 

statistically significant association was 

found between mortality and 1-hour 

daily maximum O3 in a full year 

analysis. Gryparis et al. (2004) noted 

that there was a considerable seasonal 

difference in the O3 effect on mortality; 

thus, the small effect for the all-year 

data might be attributable to inadequate 

adjustment for confounding by 

seasonality. Focusing on analyses using 

summer measurements, the authors 

report statistically significant 

associations with total mortality, 

cardiovascular mortality and respiratory 

mortality (EPA, 2006a, p. 7–93, 7–99). 

Numerous single-city analyses have 

also reported associations between 

mortality and short-term O3 exposure, 

especially for those analyses using 

warm season data. As shown in Figure 

7–21 of the 2006 Criteria Document, the 

results of recent publications show a 

pattern of positive, often statistically 

significant associations between shortterm O3 exposure and mortality during 

the warm season. In considering results 

from year-round analyses, there remains 

a pattern of positive results but the 

findings are less consistent. In most 

single-city analyses, effect estimates 

were not substantially changed with 

adjustment for PM (EPA, 2006a, Figure 

7–22). 

In addition, several meta-analyses 

have been conducted on the 

relationship between O3 and mortality. 

As described in section 7.4.4 of the 2006 

Criteria Document, these analyses 

reported fairly consistent and positive 

combined effect estimates ranging from 

approximately 1.5 to 2.5 percent 

increase in mortality for a standardized 

change in O3 (EPA, 2006a, Figure 7–20). 

Three recent meta-analyses evaluated 

potential sources of heterogeneity in O3- 

mortality associations (Bell et al., 2005; 

Ito et al., 2005; Levy et al., 2005). The 

2006 Criteria Document (p. 7–96) 

observes common findings across all 

three analyses, in that all reported that 

effect estimates were larger in warm 

season analyses, reanalysis of results 

using default convergence criteria in 

generalized additive models (GAM) did 

not change the effect estimates, and 

there was no strong evidence of 

confounding by PM. Bell et al. (2005) 

and Ito et al. (2005) both provided 

suggestive evidence of publication bias, 

but O3-mortality associations remained 

after accounting for that potential bias. 

The 2006 Criteria Document concludes 

that the ‘‘positive O3 effects estimates, 

along with the sensitivity analyses in 

these three meta-analyses, provide 

evidence of a robust association 

between ambient O3 and mortality’’ 

(EPA, 2006a, p. 7–97). 

Most of the single-pollutant model 

estimates from single-city studies range 

from 0.5 to 5 percent excess deaths per 

standardized increments. Corresponding 

summary estimates in large U.S. 

multicity studies ranged between 0.5 to 

1 percent with some studies noting 

heterogeneity across cities and studies 

(EPA, 2006a, p. 7–110). 

Finally, from those studies that 

included assessment of associations 

with specific causes of death, it appears 

that effect estimates for associations 

with cardiovascular mortality are larger 

than those for total mortality. The metaanalysis by Bell et al. (2005) observed a 

slightly larger effect estimate for 

cardiovascular mortality compared to 

mortality from all causes. The effect 

estimate for respiratory mortality was 

approximately one-half that of 

cardiovascular mortality in the metaanalysis. However, other studies have 

observed larger effect estimates for 

respiratory mortality compared to 

cardiovascular mortality. The apparent 

inconsistency regarding the effect size of 

O3-related respiratory mortality may be 

due to reduced statistical power in this 

subcategory of mortality (EPA, 2006a, p. 

7–108). 

In summary, many single- and multicity studies observed positive 

associations of ambient O3

concentrations with total nonaccidental 

and cardiopulmonary mortality. The 

2006 Criteria Document finds that the 

results from U.S. multicity time-series 

studies provide the strongest evidence 

to date for O3 effects on acute mortality. 

Recent meta-analyses also indicate 

positive risk estimates that are unlikely 

to be confounded by PM; however, 

future work is needed to better 

understand the influence of model 

specifications on the risk coefficient 

(EPA, 2006a, p. 7–175). A meta-analysis 

that examined specific causes of 

mortality found that the cardiovascular 

mortality risk estimates were higher 

than those for total mortality. For 

cardiovascular mortality, the 2006 

Criteria Document (Figure 7–25, p. 7– 

106) suggests that effect estimates are 

consistently positive and more likely to 

be larger and statistically significant in 

warm season analyses. The findings 

regarding the effect size for respiratory 

mortality have been less consistent, 

possibly because of lower statistical 

power in this subcategory of mortality. 

The 2006 Criteria Document (p. 8–78) 

concludes that these findings are highly 

suggestive that short-term O3 exposure 

directly or indirectly contribute to nonaccidental and cardiopulmonary-related 

mortality, but additional research is 

needed to more fully establish 

underlying mechanisms by which such 

effects occur.21


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22This reanalysis report and the original 

prospective cohort study findings are discussed in 

more detail in section 8.2.3 of the Air Quality 

Criteria for Particulate Matter (EPA, 2004). 

ii. Mortality and Long-Term O3

Exposure 

Little evidence was available in the 

1997 review on the potential for 

associations between mortality and 

long-term exposure to O3. In the 

Harvard Six City prospective cohort 

analysis, the authors report that 

mortality was not associated with longterm exposure to O3 (Dockery et al., 

1993). The authors note that the range 

of O3 concentrations across the six cities 

was small, which may have limited the 

power of the study to detect associations 

between mortality and O3 levels (EPA, 

2006a, p. 7–127). 

As discussed in section 7.5.8 of the 

2006 Criteria Document, in this review 

there are results available from three 

prospective cohort studies: the 

American Cancer Society (ACS) study 

(Pope et al., 2002), the Adventist Health 

and Smog (AHSMOG) study (Beeson et 

al., 1998; Abbey et al., 1999), and the 

U.S. Veterans Cohort study (Lipfert et 

al., 2000, 2003). In addition, a major 

reanalysis report includes evaluation of 

data from the Harvard Six City cohort 

study (Krewski et al., 2000).22 This 

reanalysis also includes additional 

evaluation of data from the initial ACS 

cohort study report that had only 

reported results of associations between 

mortality and long-term exposure to fine 

particles and sulfates (Pope et al., 1995). 

This reanalysis was discussed in the 

2007 Staff Paper (section 3.3.2.2) but not 

in the 2006 Criteria Document. 

In this reanalysis of data from the 

previous Harvard Six City prospective 

cohort study, the investigators 

replicated and validated the findings of 

the original studies, and the report 

included additional quantitative results 

beyond those available in the original 

report (Krewski et al., 2000). In the 

reanalysis of data from the Harvard Six 

Cities study, the effect estimate for the 

association between long-term O3

concentrations and mortality was 

negative and nearly statistically 

significant (relative risk = 0.87, 95 

percent CI: 0.76, 1.00). 

The ACS study is based on health 

data from a large prospective cohort of 

approximately 500,000 adults and air 

quality data from about 150 U.S. cities. 

The initial report (Pope et al., 1995) 

focused on associations with fine 

particles and sulfates, for which 

significant associations had been 

reported in the earlier Harvard Six 

Cities study (Dockery et al., 1993). As 

part of the major reanalysis of these 

data, results for associations with other 

air pollutants were also reported, and 

the authors report that no significant 

associations were found between O3 and 

all-cause mortality. However, a 

significant association was reported for 

cardiopulmonary mortality in the warm 

season (Krewski et al., 2000). The ACS 

II study (Pope et al., 2002) reported 

results of associations with an extended 

data base; the mortality records for the 

cohort had been updated to include 16 

years of follow-up (compared with 8 

years in the first report) and more recent 

air quality data were included in the 

analyses. Similar to the earlier 

reanalysis, a marginally significant 

association was observed between longterm exposure to O3 and 

cardiopulmonary mortality in the warm 

season. No other associations with 

mortality were observed in both the fullyear and warm season analyses. 

The Adventist Health and Smog 

(AHSMOG) cohort includes about 6,000 

adults living in California. In two 

studies from this cohort, a significant 

association has been reported between 

long-term O3 exposure and increased 

risk of lung cancer mortality among 

males only (Beeson et al., 1998; Abbey 

et al., 1999). No significant associations 

were reported between long-term O3

exposure and mortality from all causes 

or cardiopulmonary causes. Due to the 

small numbers of lung cancer deaths (12 

for males, 18 for females) and the 

precision of the effect estimate (i.e., the 

wide confidence intervals), the 2006 

Criteria Document (p. 7–130) discussed 

concerns about the plausibility of the 

reported association with lung cancer. 

The U.S. Veterans Cohort study 

(Lipfert et al., 2000, 2003) of 

approximately 50,000 middle-aged 

males diagnosed with hypertension, 

reported some positive associations 

between mortality and peak O3

exposures (95th percentile level for 

several years of data). The study 

included numerous analyses using 

subsets of exposure and mortality 

follow-up periods which spanned the 

years 1960 to 1996. In the results of 

analyses using deaths and O3 exposure 

estimates concurrently across the study 

period, there were positive, statistically 

significant associations between peak O3

and mortality (EPA, 2006a, p. 7–129). 

Overall, the 2006 Criteria Document 

(p. 7–130) concludes that consistent 

associations have not been reported 

between long-term O3 exposure and allcause, cardiopulmonary or lung cancer 

mortality. 

c. Role of Ground-Level O3 in Solar 

Radiation-Related Human Health Effects 

Beyond the direct health effects 

attributable to inhalation exposure to O3

in the ambient air discussed above, the 

2006 Criteria Document also assesses 

potential indirect effects related to the 

presence of O3 in the ambient air by 

considering the role of ground-level O3

in mediating human health effects that 

may be directly attributable to exposure 

to solar ultraviolet radiation (UV–B). 

The 2006 Criteria Document (chapter 

10) focuses this assessment on three key 

factors, including those factors that 

govern (1) UV–B radiation flux at the 

earth’s surface, (2) human exposure to 

UV–B radiation, and (3) human health 

effects due to UV–B radiation. In so 

doing, the 2006 Criteria Document 

provides a thorough analysis of the 

current understanding of the 

relationship between reducing groundlevel O3 concentrations and the 

potential impact these reductions might 

have on increasing UV–B surface fluxes 

and indirectly contributing to UV–B 

related health effects. 

There are many factors that influence 

UV–B radiation penetration to the 

earth’s surface, including latitude, 

altitude, cloud cover, surface albedo, 

PM concentration and composition, and 

gas phase pollution. Of these, only 

latitude and altitude can be defined 

with small uncertainty in any effort to 

assess the changes in UV–B flux that 

may be attributable to any changes in 

tropospheric O3 as a result of any 

revision to the O3 NAAQS. Such an 

assessment of UV–B related health 

effects would also need to take into 

account human habits, such as outdoor 

activities (including age- and 

occupation-related exposure patterns), 

dress and skin care to adequately 

estimate UV–B exposure levels. 

However, little is known about the 

impact of these factors on individual 

exposure to UV–B. 

Moreover, detailed information does 

not exist regarding other factors that are 

relevant to assessing changes in disease 

incidence, including: Type (e.g., peak or 

cumulative) and time period (e.g., 

childhood, lifetime, current) of 

exposures related to various adverse 

health outcomes (e.g., damage to the 

skin, including skin cancer; damage to 

the eye, such as cataracts; and immune 

system suppression); wavelength 

dependency of biological responses; and 

interindividual variability in UV–B 

resistance to such health outcomes. 

Beyond these well recognized adverse 

health effects associated with various 

wavelengths of UV radiation, the 2006 

Criteria Document (section 10.2.3.6) also 


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discusses protective effects of UV–B 

radiation. Recent reports indicate the 

necessity of UV–B in producing vitamin 

D. 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 2006 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–B-induced health 

outcomes cannot yet be critically 

assessed within reasonable uncertainty 

(2006 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 1997 

review, EPA determined that the 

information linking (a) changes in 

patterns of ground-level O3

concentrations likely to occur as a result 

of programs implemented to attain the 

1997 O3 NAAQS to (b) changes in 

relevant exposures to UV–B radiation of 

concern to public health was too 

uncertain at that time to warrant any 

relaxation in the level of public health 

protection previously determined to be 

requisite to protect against the 

demonstrated direct adverse respiratory 

effects of exposure to O3 in the ambient 

air (68 FR 614). At that time, the more 

recent information on protective effects 

of UV–B radiation was not available, 

such that only adverse UV–B-related 

effects could be considered. Taking into 

consideration the more recent 

information available for the 2008 

review, the 2006 Criteria Document and 

2007 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–B-induced health outcomes, 

including whether these changes would 

ultimately result in increased or 

decreased incidence of UV–B-related 

diseases, cannot yet be critically 

assessed. 

3. Interpretation and Integration of 

Health Evidence 

As discussed below, in assessing the 

health evidence, the 2006 Criteria 

Document integrates findings from 

experimental (e.g., toxicological, 

dosimetric and controlled human 

exposure) and epidemiological studies, 

to make judgments about the extent to 

which causal inferences can be made 

about observed associations between 

health endpoints and exposure to O3. In 

evaluating the evidence from 

epidemiological studies, the EPA 

focuses on well-recognized criteria, 

including: The strength of reported 

associations, including the magnitude 

and precision of reported effect 

estimates and their statistical 

significance; the robustness of reported 

associations, or stability in the effect 

estimates after considering factors such 

as alternative models and model 

specification, potential confounding by 

co-pollutants, and issues related to the 

consequences of exposure measurement 

error; potential aggregation bias in 

pooling data; and the consistency of the 

effects associations as observed by 

looking across results of multiple- and 

single-city studies conducted by 

different investigators in different places 

and times. Consideration is also given to 

evaluating concentration-response 

relationships observed in 

epidemiological studies to inform 

judgments about the potential for 

threshold levels for O3-related effects. 

Integrating more broadly across 

epidemiological and experimental 

evidence, the 2006 Criteria Document 

also focuses on the coherence and 

plausibility of observed O3-related 

health effects to reach judgments about 

the extent to which causal inferences 

can be made about observed 

associations between health endpoints 

and exposure to O3 in the ambient air. 

a. Assessment of Evidence From 

Epidemiological Studies 

Key elements of the evaluation of 

epidemiological studies are briefly 

summarized below. 

(1) The strength of associations most 

directly refers to the magnitude of the 

reported relative risk estimates. Taking 

a broader view, the 2006 Criteria 

Document draws upon the criteria 

summarized in a recent report from the 

U.S. Surgeon General, which define 

strength of an association as ‘‘the 

magnitude of the association and its 

statistical strength’’ which includes 

assessment of both effect estimate size 

and precision, which is related to the 

statistical power of the study (CDC, 

2004). In general, when associations are 

strong in terms of yielding large relative 

risk estimates, it is less likely that the 

association could be completely 

accounted for by a potential confounder 

or some other source of bias, whereas 

with associations that yield small 

relative risk estimates it is especially 

important to consider potential 

confounding and other factors in 

assessing causality. Effect estimates 

between O3 and some of the health 

outcomes are generally small in size and 

could thus be characterized as weak. For 

example, effect estimates for 

associations with mortality generally 

range from 0.5 to 5 percent increases per 

0.040 ppm increase in 1-hour maximum 

O3 or equivalent, whereas associations 

for hospitalization range up to 50 

percent increases per standardized O3

increment. However, the 2006 Criteria 

Document notes that there are large 

multicity studies that find small 

associations between short-term O3

exposure and mortality or morbidity 

and have done so with great precision 

due to the statistical power of the 

studies (p. 8–40). That is, the power of 

the studies allows the authors to reliably 

distinguish even weak relationships 

from the null hypothesis with statistical 

confidence. 

(2) In evaluating the robustness of 

associations, the 2006 Criteria 

Document (sections 7.1.3 and 8.4.4.3) 

and 2007 Staff Paper (section 3.4.2) have 

primarily considered the impact of 

exposure error, potential confounding 

by copollutants, and alternative models 

and model specifications. 

In time-series and panel studies, the 

temporal (e.g., daily or hourly) changes 

in ambient O3 concentrations measured 

at centrally-located ambient monitoring 

stations are generally used to represent 

a community’s exposure to ambient O3. 

In prospective cohort or cross-sectional 

studies, air quality data averaged over a 

period of months to years are used as 

indicators of a community’s long-term 

exposure to ambient O3 and other 

pollutants. In both types of analyses, 

exposure error is an important 

consideration, as actual exposures to 

individuals in the population will vary 

across the community. 

Ozone concentrations measured at 

central ambient monitoring sites may 

explain, at least partially, the variance 

in individual exposures to ambient O3; 

however, this relationship is influenced 

by various factors related to building 

ventilation practices and personal 

behaviors. Further, the pattern of 

exposure misclassification error and the 

influence of confounders may differ 

across the outcomes of interest as well 

as in susceptible populations. As 

discussed in the 2006 Criteria Document 


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(section 3.9), only a limited number of 

studies have examined the relationship 

between ambient O3 concentrations and 

personal exposures to ambient O3. One 

of the strongest predictors of the 

relationship between ambient 

concentrations and personal exposures 

appears to be time spent outdoors. The 

strongest relationships were observed in 

outdoor workers (Brauer and Brook, 

1995, 1997; O’Neill et al., 2004). 

Statistically significant correlations 

between ambient concentrations and 

personal exposures were also observed 

for children, who likely spend more 

time outdoors in the warm season (Linn 

et al., 1996; Xu et al., 2005). There is 

some concern about the extent to which 

ambient concentrations are 

representative of personal O3 exposures 

of another particularly susceptible 

group of individuals, the debilitated 

elderly, since those who suffer from 

chronic cardiovascular or respiratory 

conditions may tend to protect 

themselves more than healthy 

individuals from environmental threats 

by reducing their exposure to both O3

and its confounders, such as high 

temperature and PM. Studies by Sarnat 

et al. (2001, 2005) that included this 

susceptible group reported mixed 

results for associations between ambient 

O3 concentrations and personal 

exposures to O3. Collectively, these 

studies observed that the daily averaged 

personal O3 exposures tend to be well 

correlated with ambient O3

concentrations despite the substantial 

variability that existed among the 

personal measurements. These studies 

provide supportive evidence that 

ambient O3 concentrations from central 

monitors may serve as valid surrogate 

measures for mean personal exposures 

experienced by the population, which is 

of most relevance for time-series 

studies. A better understanding of the 

relationship between ambient 

concentrations and personal exposures, 

as well as of the other factors that affect 

relationship will improve the 

interpretation of concentrationpopulation health response associations 

observed. 

The 2006 Criteria Document (section 

7.1.3.1) also discusses the potential 

influence of exposure error on 

epidemiologic study results. Zeger et al. 

(2000) outlined the components to 

exposure measurement error, finding 

that ambient exposure can be assumed 

to be the product of the ambient 

concentration and an attenuation factor 

(i.e., building filter) and that panel 

studies and time-series studies that use 

ambient concentrations instead of 

personal exposure measurements will 

estimate a health risk that is attenuated 

by that factor. Navidi et al. (1999) used 

data from a children’s cohort study to 

compare effect estimates from a 

simulated ‘‘true’’ exposure level to 

results of analyses from O3 exposures 

determined by several methods, finding 

that O3 exposures based on the use of 

ambient monitoring data overestimate 

the individual’s O3 exposure and thus 

generally result in O3 effect estimates 

that are biased downward (EPA, 2006a, 

p. 7–8). Similarly, in a reanalysis of a 

study by Burnett et al. (1994) on the 

acute respiratory effects of ambient air 

pollution, Zidek et al. (1998) reported 

that accounting for measurement error, 

as well as making a few additional 

changes to the analysis, resulted in 

qualitatively similar conclusions, but 

the effects estimates were considerably 

larger in magnitude (EPA, 2006a, p. 7– 

8). A simulation study by Sheppard et 

al. (2005) also considered attenuation of 

the risk based on personal behavior, 

their microenvironment, and the 

qualities of the pollutant in time-series 

studies. Of particular interest is their 

finding that risk estimates were not 

further attenuated in time-series studies 

even when the correlations between 

personal exposures and ambient 

concentrations were weak. In addition 

to overestimation of exposure and the 

resulting underestimation of effects, the 

use of ambient O3 concentrations may 

obscure the presence of thresholds in 

epidemiologic studies (EPA, 2006a, p. 

7–9). 

As discussed in the 2006 Criteria 

Document (section 3.9), using ambient 

concentrations to determine exposure 

generally overestimates true personal O3

exposures by approximately 2- to 4-fold 

in available studies, resulting in 

attenuated risk estimates. The 

implication is that the effects being 

estimated occur at fairly low exposures 

and the potency of O3 is greater than 

these effects estimates indicate. As very 

few studies evaluating O3 health effects 

with personal O3 exposure 

measurements exist in the literature, 

effect estimates determined from 

ambient O3 concentrations must be 

evaluated and used with caution to 

assess the health risks of O3. In the 

absence of available data on personal O3

exposure, the use of routinely 

monitored ambient O3 concentrations as 

a surrogate for personal exposures is not 

generally expected to change the 

principal conclusions from O3

epidemiologic studies. Therefore, 

population health risk estimates derived 

using ambient O3 levels from currently 

available observational studies, with 

appropriate caveats about personal 

exposure considerations, remain useful. 

The 2006 Criteria Document 

recommends caution in the quantitative 

use of effect estimates calculated using 

ambient O3 concentrations as they may 

lead to underestimation of the potency 

of O3. However, the 2007 Staff Paper 

observes that the use of these risk 

estimates for comparing relative risk 

reductions between alternative ambient 

O3 standards considered in the risk 

assessment (discussed below in section 

II.B.2) is less likely to suffer from this 

concern. 

Confounding occurs when a health 

effect that is caused by one risk factor 

is attributed to another variable that is 

correlated with the causal risk factor; 

epidemiological analyses attempt to 

adjust or control for potential 

confounders. Copollutants (e.g., PM, 

CO, SO2 and NO2) can meet the criteria 

for potential confounding in O3-health 

associations if they are potential risk 

factors for the health effect under study 

and are correlated with O3. Effect 

modifiers include variables that may 

influence the health response to the 

pollutant exposure (e.g., co-pollutants, 

individual susceptibility, smoking or 

age). Both are important considerations 

for evaluating effects in a mixture of 

pollutants, but for confounding, the 

emphasis is on controlling or adjusting 

for potential confounders in estimating 

the effects of one pollutant, while the 

emphasis for effect modification is on 

identifying and assessing the effects for 

different modifiers. 

The 2006 Criteria Document (p. 

7–148) observes that O3 is generally not 

highly correlated with other criteria 

pollutants (e.g., PM10, CO, SO2 and 

NO2), but may be more highly correlated 

with secondary fine particles, especially 

during the summer months, and that the 

degree of correlation between O3 and 

other pollutants may vary across 

seasons. For example, positive 

associations are observed between O3

and pollutants such as fine particles 

during the warmer months, but negative 

correlations may be observed during the 

cooler months (EPA, 2006a, p. 7–17). 

Thus, the 2006 Criteria Document 

(section 7.6.4) pays particular attention 

to the results of season-specific analyses 

and studies that assess effects of PM in 

potential confounding of O3-health 

relationships. The 2006 Criteria 

Document also discussed the limitations 

of commonly used multipollutant 

models that include the difficulty in 

interpreting results where the 

copollutants are highly colinear, or 

where correlations between pollutants 

change by season (EPA, 2006a, p. 

7–150). This is particularly the situation 

where O3 and a copollutant, such as 


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sulfates, are formed under the same 

atmospheric condition; in such cases 

multipollutant models would produce 

unstable and possibly misleading results 

(EPA, 2006a, p. 7–152). 

For mortality, the results from 

numerous multicity and single-city 

studies indicate that O3-mortality 

associations do not appear to be 

substantially changed in multipollutant 

models including PM10 or PM2.5 (EPA, 

2006a, p. 7–101; Figure 7–22). Focusing 

on results of warm season analyses, 

effect estimates for O3-mortality 

associations are fairly robust to 

adjustment for PM in multipollutant 

models (EPA, 2006a, p. 7–102; Figure 

7–23). The 2006 Criteria Document 

concludes that in the few multipollutant 

analyses conducted for these endpoints, 

copollutants generally do not confound 

the relationship between O3 and 

respiratory hospitalization (EPA, 2006a, 

p. 7–79 to 7–80; Figure 7–12). 

Multipollutant models were not used as 

commonly in studies of relationships 

between respiratory symptoms or lung 

function with O3, but the 2006 Criteria 

Document reports that results of 

available analyses indicate that such 

associations generally were robust to 

adjustment for PM2.5 (p. 7–154). For 

example, in a large multicity study of 

asthmatic children (Mortimer et al., 

2002), the O3 effect was attenuated, but 

there was still a positive association; in 

Gent et al. (2003), effects of O3, but not 

PM2.5, remained statistically significant 

and even increased in magnitude in 

two-pollutant models (EPA, 2006a, p. 

7–53). Considering this body of studies, 

the 2006 Criteria Document (p. 7–154) 

concludes: ‘‘Multipollultant regression 

analyses indicated that O3 risk 

estimates, in general, were not sensitive 

to the inclusion of copollutants, 

including PM2.5 and sulfate. These 

results suggest that the effects of O3 on 

respiratory health outcomes appear to 

be robust and independent of the effects 

of other copollutants.’’ 

The 2006 Criteria Document (p. 7–14) 

observes that another challenge of timeseries epidemiological analysis is 

assessing the relationship between O3

and health outcomes while avoiding 

bias due to confounding by other timevarying factors, particularly seasonal 

trends and weather variables. These 

variables are of particular interest 

because O3 concentrations have a wellcharacterized seasonal pattern and are 

also highly correlated with changes in 

temperature, such that it can be difficult 

to distinguish whether effects are 

associated with O3 or with seasonal or 

weather variables in statistical analyses. 

The 2006 Criteria Document (section 

7.1.3.4) discusses statistical modeling 

approaches that have been used to 

adjust for time-varying factors, 

highlighting a series of analyses that 

were done in a Health Effects Institutefunded reanalysis of numerous timeseries studies. While the focus of these 

reanalyses was on associations with PM, 

a number of investigators also examined 

the sensitivity of O3 coefficients to the 

extent of adjustment for temporal trends 

and weather factors. In addition, several 

recent studies, including U.S. multicity 

studies (Bell et al., 2005; Huang et al., 

2005; Schwartz et al., 2005) and a metaanalysis study (Ito et al., 2005), 

evaluated the effect of model 

specification on O3-mortality 

associations. As discussed in the 2006 

Criteria Document (section 7.6.3.1), 

these studies generally report that 

associations reported with O3 are not 

substantially changed with alternative 

modeling strategies for adjusting for 

temporal trends and meteorologic 

effects. In the meta-analysis by Ito et al. 

(2005), a separate multicity analysis was 

presented that found that alternative 

adjustments for weather resulted in up 

to 2-fold difference in the O3 effect 

estimate. Significant confounding can 

occur when strong seasonal cycles are 

present, suggesting that season-specific 

results are more generally robust than 

year-round results in such cases. A 

number of epidemiological studies have 

conducted season-specific analyses, and 

have generally reported stronger and 

more precise effect estimates for O3

associations in the warm season than in 

analyses conducted in the cool seasons 

or over the full year. 

(3) Consistency refers to the persistent 

finding of an association between 

exposure and outcome in multiple 

studies of adequate power in different 

persons, places, circumstances and 

times (CDC, 2004). In considering 

results from multicity studies and 

single-city studies in different areas, the 

2006 Criteria Document (p. 8–41) 

observes general consistency in effects 

of short-term O3 exposure on mortality, 

respiratory hospitalization and other 

respiratory health outcomes. The 

variations in effects that are observed 

may be attributable to differences in 

relative personal exposure to O3, as well 

as varying concentrations and 

composition of copollutants present in 

different regions. Thus, the 2006 Criteria 

Document (p. 8–41) concludes that 

‘‘consideration of consistency or 

heterogeneity of effects is appropriately 

understood as an evaluation of the 

similarity or general concordance of 

results, rather than an expectation of 

finding quantitative results with a very 

narrow range.’’ 

(4) The 2007 Staff Paper recognizes 

that it is likely that there are biological 

thresholds for different health effects in 

individuals or groups of individuals 

with similar innate characteristics and 

health status. For O3 exposure, 

individual thresholds would 

presumably vary substantially from 

person to person due to individual 

differences in genetic susceptibility, 

pre-existing disease conditions and 

possibly individual risk factors such as 

diet or exercise levels (and could even 

vary from one time to another for a 

given person). Thus, it would be 

difficult to detect a distinct threshold at 

the population level below which no 

individual would experience a given 

effect, especially if some members of a 

population are unusually sensitive even 

down to very low concentrations (EPA, 

2004, p. 9–43, 9–44). 

Some studies have tested associations 

between O3 and health outcomes after 

removal of days with higher O3 levels 

from the data set; such analyses do not 

necessarily indicate the presence or 

absence of a threshold, but provide 

some information on whether the 

relationship is found using only lowerconcentration data. For example, using 

data from 95 U.S. cities, Bell et al. 

(2004) found that the effect estimate for 

an association between short-term O3

exposure and mortality was little 

changed when days exceeding 0.060 

ppm (24-hour average) were excluded in 

the analysis. Using data from 8 U.S. 

cities, Mortimer and colleagues (2002) 

also reported that associations between 

O3 and both lung function and 

respiratory symptoms remained 

statistically significant and of the same 

or greater magnitude in effect size when 

concentrations greater than 0.080 ppm 

(8-hour average) were excluded (EPA, 

2006a, p. 7–46). Several single-city 

studies also report similar findings of 

associations that remain or are increased 

in magnitude and statistical significance 

when data at the upper end of the 

concentration range are removed (EPA, 

2006a, section 7.6.5). 

Other time-series epidemiological 

studies have used statistical modeling 

approaches to evaluate whether 

thresholds exist in associations between 

short-term O3 exposure and mortality. 

As discussed in section 7.6.5 of the 2006 

Criteria Document, one European 

multicity study included evaluation of 

the shape of the concentration-response 

curve, and observed no deviation from 

a linear function across the range of O3

measurements from the study (Gryparis 

et al., 2004; EPA, 2006a p. 7–154). 

Several single-city studies also observed 

a monotonic increase in associations 

between O3 and morbidity that suggest 


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that no population threshold exists 

(EPA, 2006a, p. 7–159). 

On the other hand, a study in Korea 

used several different modeling 

approaches and reported that a 

threshold model provided the best fit for 

the data. The results suggested a 

potential threshold level of about 0.045 

ppm (1-hour maximum concentration; 

< 0.035 ppm, 8-hour average) for an 

association between mortality and shortterm O3 exposure during the summer 

months (Kim et al., 2004; EPA, 2006a, 

p. 8–43). The authors reported larger 

effect estimates for the association for 

data above the potential threshold level, 

suggesting that an O3-mortality 

association might be underestimated in 

the non-threshold model. A threshold 

analysis recently reported by Bell et al. 

(2006) for 98 U.S. communities, 

including the same 95 communities in 

Bell et al. (2004), indicated that if a 

population threshold existed for 

mortality, it would likely fall below a 

24-hour average O3 concentration of 

0.015 ppm (< 0.025 ppm, 8-hour 

average). In addition, Burnett and 

colleagues (1997a,b) plotted the 

relationships between air pollutant 

concentrations and both respiratory and 

cardiovascular hospitalization, and it 

appears in these results that the 

associations with O3 are found in the 

concentration range above about 0.030 

ppm (1-hour maximum; < 0.025 ppm, 8- 

hour average). Vedal and colleagues 

(2003) reported a significant association 

between O3 and mortality in British 

Columbia where O3 concentrations were 

quite low (mean 1-hour maximum 

concentration of 0.0273 ppm). The 

authors did not specifically test for 

threshold levels, but the fact that the 

association was found in an area with 

such low O3 concentrations suggests 

that any potential threshold level would 

be quite low in this data set. 

In summary, the 2006 Criteria 

Document finds that, taken together, the 

available evidence from controlled 

human exposure and epidemiological 

studies suggests that no clear conclusion 

can now be reached with regard to 

possible threshold levels for O3-related 

effects (EPA, 2006a, p. 8–44). Thus, the 

available epidemiological evidence 

neither supports nor refutes the 

existence of thresholds at the 

population level for effects such as 

increased hospital admissions and 

premature mortality. There are 

limitations in epidemiological studies 

that make discerning thresholds in 

populations difficult, including low 

data density in the lower concentration 

ranges, the possible influence of 

exposure measurement error, and 

interindividual differences in 

susceptibility to O3-related effects in 

populations. There is the possibility that 

thresholds for individuals may exist in 

reported associations at fairly low levels 

within the range of air quality observed 

in the studies but not be detectable as 

population thresholds in 

epidemiological analyses. 

b. Biological Plausibility and Coherence 

of Evidence 

The body of epidemiological studies 

discussed in the 2007 Staff Paper 

emphasizes the role of O3 in association 

with a variety of adverse respiratory and 

cardiovascular effects. While 

recognizing a variety of plausible 

mechanisms, there exists a general 

consensus suggesting that O3, could 

either directly or through initiation, 

interfere with basic cellular oxidation 

processes responsible for inflammation, 

reduced antioxidant capacity, 

atherosclerosis and other effects. 

Reasoning that O3 influences cellular 

chemistry through basic oxidative 

properties (as opposed to a unique 

chemical interaction), other reactive 

oxidizing species (ROS) in the 

atmosphere acting either independently 

or in combination with O3 may also 

contribute to a number of adverse 

respiratory and cardiovascular health 

effects. Consequently, the role of O3

should be considered more broadly as 

O3 behaves as a generator of numerous 

oxidative species in the atmosphere. 

In considering the biological 

plausibility of reported O3-related 

effects, the 2007 Staff Paper (section 

3.4.6) considers this broader question of 

health effects of pollutant mixtures 

containing O3. The potential for O3- 

related enhancements of PM formation, 

particle uptake, and exacerbation of PMinduced cardiovascular effects 

underscores the importance of 

considering contributions of O3

interactions with other often cooccurring air pollutants to health effects 

due to O3-containing pollutant mixes. 

The 2007 Staff Paper summarizes some 

examples of important pollutant 

mixture effects from studies that 

evaluate interactions of O3 with other 

co-occurring pollutants, as discussed in 

chapters 4, 5, and 6 of the 2006 Criteria 

Document. 

All of the types of interactive effects 

of O3 with other co-occurring gaseous 

and nongaseous viable and nonviable 

PM components of ambient air mixes 

noted above argue that O3 acts not only 

alone but that O3 also is a surrogate 

indicator for air pollution mixes which 

may enhance the risk of adverse effects 

due to O3 acting in combination with 

other pollutants. Viewed from this 

perspective, those epidemiologic 

findings of morbidity and mortality 

associations, with ambient O3

concentrations extending to quite low 

levels in many cases, become more 

understandable and plausible. 

The 2006 Criteria Document 

integrates epidemiological studies with 

mechanistic information from 

controlled human exposure studies and 

animal toxicological studies to draw 

conclusions regarding the coherence of 

evidence and biological plausibility of 

O3-related health effects to reach 

judgments about the causal nature of 

observed associations. As summarized 

below, coherence and biological 

plausibility is discussed for each of the 

following types of O3-related effects: 

Short-term effects on the respiratory 

system, effects on the cardiovascular 

system, effects related to long-term O3

exposure, and short-term mortalityrelated health endpoints. 

i. Coherence and Plausibility of ShortTerm Effects on the Respiratory System 

Acute respiratory morbidity effects 

that have been associated with shortterm exposure to O3 include such health 

endpoints as decrements in lung 

function, increased respiratory 

symptoms, increased airway 

responsiveness, airway inflammation, 

increased permeability related to 

epithelial injury, immune system 

effects, emergency department visits for 

respiratory diseases, and hospitalization 

due to respiratory illness. 

Recent epidemiological studies have 

supported evidence available in the 

previous O3 NAAQS review on 

associations between ambient O3

exposure and decline in lung function 

for children. The 2006 Criteria 

Document (p. 8–34) concludes that 

exposure to ambient O3 has a significant 

effect on lung function and is associated 

with increased respiratory symptoms 

and medication use, particularly in 

asthmatics. Short-term exposure to O3

has also been associated with more 

severe morbidity endpoints, such as 

emergency department visits and 

hospital admissions for respiratory 

cases, including specific respiratory 

illness (e.g., asthma) (EPA, 2006a, 

sections 7.3.2 and 7.3.3). In addition, a 

few epidemiological studies have 

reported positive associations between 

short-term O3 exposure and respiratory 

mortality, though the associations are 

not generally statistically significant 

(EPA, 2006a, p. 7–108). 

Considering the evidence from 

epidemiological studies, the results 

described above provide evidence for 

coherence in O3-related effects on the 

respiratory system. Effect estimates from 

U.S. and Canadian studies are shown in 


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23Results for studies of respiratory symptoms are 

presented as odds ratios; an odds ratio of 1.0 is 

equivalent to no effect, and thus is presented as 

equivalent to the zero effect estimate line. 

Figure 1, where it can be seen that 

mostly positive associations have been 

reported with respiratory effects ranging 

from respiratory symptoms, such as 

cough or wheeze, to hospitalization for 

various respiratory diseases, and there is 

suggestive evidence for associations 

with respiratory mortality. Many of the 

reported associations are statistically 

significant, particularly in the warm 

season. In Figure 1, the central effect 

estimate is indicated by a square for 

each result, with the vertical bar 

representing the 95 percent confidence 

interval around the estimate. In the 

discussions that follow, an individual 

study result is considered to be 

statistically significant if the 95 percent 

confidence interval does not include 

zero.23 Positive effect estimates indicate 

increases in the health outcome with O3

exposure. In considering these results as 

a whole, it is important to consider not 

only whether statistical significance at 

the 95 percent confidence level is 

reported in individual studies but also 

the general pattern of results, focusing 

in particular on studies with greater 

statistical power that report relatively 

more precise results. 

BILLING CODE 6560–50–P 


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BILLING CODE 6560–50–C 

Considering also evidence from 

toxicological, controlled human 

exposure, and field studies, the 2006 

Criteria Document (section 8.6) 

discusses biological plausibility and 

coherence of evidence for acute O3- 

induced respiratory health effects. 

Inhalation of O3 for several hours while 

subjects are physically active can elicit 

both acute adverse pathophysiological 

changes and subjective respiratory tract 

symptoms (EPA, 2006a, section 8.4.2). 

Acute pulmonary responses observed in 

healthy humans exposed to O3 at 

ambient concentrations include: 

decreased inspiratory capacity; mild 

bronchoconstriction; rapid, shallow 

breathing during exercise; subjective 

symptoms of tracheobronchial airway 

irritation, including cough and pain on 

deep inspiration; decreases in measures 

of lung function; and increased airway 

resistance. The severity of symptoms 

and magnitude of response depends on 

inhaled dose, individual O3 sensitivity, 

and the degree of attenuation or 

enhancement of response resulting from 

previous O3 exposures. Lung function 

studies of several animal species acutely 

exposed to relatively low O3 levels from 

a toxicological perspective (i.e., 0.25 to 

0.4 ppm) show responses similar to 

those observed in humans, including 

increased breathing frequency, 

decreased tidal volume, increased 

resistance, and decreased FVC. 

Alterations in breathing pattern return 

to normal within hours of exposure, and 


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attenuation in functional responses 

following repeated O3 exposures is 

similar to those observed in humans. 

Physiological and biochemical 

alterations investigated in controlled 

human exposure and animal toxicology 

studies tend to support certain 

hypotheses of underlying pathological 

mechanisms which lead to the 

development of respiratory-related 

effects reported in epidemiology studies 

(e.g., increased hospitalization and 

medication use). Some of these are: (a) 

Decrements in lung function, (b) 

bronchoconstriction, (c) increased 

airway responsiveness, (d) airway 

inflammation, (e) epithelial injury, (f) 

immune system activation, (g) host 

defense impairment, and (h) sensitivity 

of individuals, which depends on at 

least a person’s age, disease status, 

genetic susceptibility, and the degree of 

attenuation present due to prior 

exposures. The time sequence, 

magnitude, and overlap of these 

complex events, both in terms of 

development and recovery, illustrate the 

inherent difficulty of interpreting the 

biological plausibility of O3-induced 

cardiopulmonary health effects (EPA, 

2006a, p. 8–48). 

The interaction of O3 with airway 

epithelial cell membranes and ELF to 

form lipid ozonation products and ROS 

is supported by numerous human, 

animal and in vitro studies. Ozonation 

products and ROS initiate a cascade of 

events that lead to oxidative stress, 

injury, inflammation, airway epithelial 

damage and increased epithelial damage 

and increased alveolar permeability to 

vascular fluids. Repeated respiratory 

inflammation can lead to a chronic 

inflammatory state with altered lung 

structure and lung function and may 

lead to chronic respiratory diseases such 

as fibrosis and emphysema (EPA, 2006a, 

section 8.6.2). Continued respiratory 

inflammation also can alter the ability to 

respond to infectious agents, allergens 

and toxins. Acute inflammatory 

responses to O3 are well documented, 

and lung injury appears within 3 hours 

after exposure in humans. 

Taken together, the 2006 Criteria 

Document concludes that the evidence 

from experimental human and animal 

toxicology studies indicates that acute 

O3 exposure is causally associated with 

respiratory system effects. These effects 

include O3-induced pulmonary function 

decrements; respiratory symptoms; lung 

inflammation and increased lung 

permeability; airway 

hyperresponsiveness; increased uptake 

of nonviable and viable particles; and 

consequent increased susceptibility to 

PM-related toxic effects and respiratory 

infections (EPA, 2006a, p. 8–48). 

ii. Coherence and Plausibility of Effects 

on the Cardiovascular System 

There is very limited experimental 

evidence of animals and humans that 

has evaluated possible mechanisms or 

physiological pathways by which acute 

O3 exposures may induce 

cardiovascular system effects. Ozone 

induces lung injury, inflammation, and 

impaired mucociliary clearance, with a 

host of associated biochemical changes 

all leading to increased lung epithelial 

permeability. As noted above in section 

II.A.2.a, the generation of lipid 

ozonation products and ROS in lung 

tissues can influence pulmonary 

hemodynamics, and ultimately the 

cardiovascular system. Other potential 

mechanisms by which O3 exposure may 

be associated with cardiovascular 

disease outcomes have been described. 

Laboratory animals exposed to relatively 

high O3 concentrations (≥ 0.5 ppm) 

demonstrate tissue edema in the heart 

and lungs. Ozone-induced changes in 

heart rate, edema of heart tissue, and 

increased tissue and serum levels of 

ANF found with 8-hour 0.5 ppm O3

exposure in animal toxicology studies 

(Vesely et al., 1994a,b,c) also raise the 

possibility of potential cardiovascular 

effects of acute ambient O3 exposures. 

Animal toxicology studies have found 

both transient and persistent ventilatory 

responses with and without progressive 

decreases in heart rate (Arito et al., 

1997). Observations of O3-induced 

vasoconstriction in a controlled human 

exposure study by Brook et al. (2002) 

suggests another possible mechanism 

for O3-related exacerbations of 

preexisting cardiovascular disease. One 

controlled human study (Gong et al., 

1998) evaluated potential cardiovascular 

health effects of O3 exposure. The 

overall results did not indicate acute 

cardiovascular effects of O3 in either the 

hypertensive or control subjects. The 

authors observed an increase in ratepressure product and heart rate, a 

decrement for FEV1, and a > 10 mm Hg 

increase in the alveolar/arterial pressure 

difference for O2 following O3 exposure. 

Foster et al. (1993) demonstrated that 

even in relatively young healthy adults, 

O3 exposure can cause ventilation to 

shift away from the well-perfused basal 

lung. This effect of O3 on ventilation 

distribution may persist beyond 24- 

hours post-exposure (Foster et al., 

1997). These findings suggest that O3

may exert cardiovascular effects 

indirectly by impairing alveolar-arterial 

O2 transfer and potentially reducing O2

supply to the myocardium. Ozone 

exposure may increase myocardial work 

and impair pulmonary gas exchange to 

a degree that could perhaps be clinically 

important in persons with significant 

preexisting cardiovascular impairment. 

As noted above in section II.A.2.a, a 

limited number of new epidemiological 

studies have reported associations 

between short-term O3 exposure and 

effects on the cardiovascular system. 

Among these studies, three were 

population-based and involved 

relatively large cohorts; two of these 

studies evaluated associations between 

O3 and HRV and the other study 

evaluated the association between O3

levels and the relative risk of MI or heart 

attack. Such studies may offer more 

informative results based on their large 

subject-pool and design. Results from 

these three studies were suggestive of an 

association between O3 exposure and 

the cardiovascular endpoints studied. In 

other recent studies on the incidence of 

heart attacks and some more subtle 

cardiovascular health endpoints, such 

as changes in HRV or cardiac 

arrhythmia, some but not all studies 

reported associations with short-term 

exposure to O3 (EPA, 2006a, section 

7.2.7.1). From these studies, the 2006 

Criteria Document concludes that the 

‘‘current evidence is rather limited but 

suggestive of a potential effect on HRV, 

ventricular arrhythmias, and MI 

incidence’’ (EPA, 2006a, p. 7–65). 

An increasing number of studies have 

evaluated the association between O3

exposure and cardiovascular hospital 

admissions. As discussed in section 

7.3.4 of the 2006 Criteria Document, 

many reported negative or inconsistent 

associations, whereas other studies, 

especially those that examined the 

relationship when O3 exposures were 

higher, have found positive and robust 

associations between O3 and 

cardiovascular hospital admissions. The 

2006 Criteria Document (p. 7–83) finds 

that the overall evidence from these 

studies remains inconclusive regarding 

the effect of O3 on cardiovascular 

hospitalizations. The 2006 Criteria 

Document notes that the suggestive 

positive epidemiologic findings of O3

exposure on cardiac autonomic control, 

including effects on HRV, ventricular 

arrhythmias and heart attacks, and 

reported associations between O3

exposure and cardiovascular 

hospitalizations generally in the warm 

season gain credibility and scientific 

support from the results of experimental 

animal toxicology and controlled 

human exposure studies, which are 

indicative of plausible pathways by 

which O3 may exert cardiovascular 

effects (EPA, 2006a, section 8.6.1). 


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iii. Coherence and Plausibility of Effects 

Related to Long-Term O3 Exposure 

Controlled human exposure studies 

cannot evaluate effects of long-term 

exposures to O3; there is some evidence 

available from toxicological studies. 

While early animal toxicology studies of 

long-term O3 exposures were conducted 

using continuous exposures, more 

recent studies have focused on 

exposures which mimic diurnal and 

seasonal patterns and more realistic O3

exposure levels (EPA, 2006a, p. 8–50). 

Studies of monkeys that compared these 

two exposure scenarios found increased 

airway pathology only with the latter 

design. Persistent and irreversible 

effects reported in chronic animal 

toxicology studies suggest that 

additional complementary human data 

are needed from epidemiologic studies 

(EPA, 2006a, p. 8–50). 

There is limited evidence from human 

studies for long-term O3-induced effects 

on lung function. As discussed in 

section 8.6.2 of the 2006 Criteria 

Document, previous epidemiological 

studies have provided only inconclusive 

evidence for either mortality or 

morbidity effects of long-term O3

exposure. The 2006 Criteria Document 

(p. 8–50) observes that the inconsistency 

in findings may be due to a lack of 

precise exposure information, the 

possibility of selection bias, and the 

difficulty of controlling for confounders. 

Several new longitudinal epidemiology 

studies have evaluated associations 

between long-term O3 exposures and 

morbidity and mortality and suggest 

that these long-term exposures may be 

related to changes in lung function in 

children; however, little evidence is 

available to support a relationship 

between chronic O3 exposure and 

mortality or lung cancer incidence 

(EPA, 2006a, p. 8–50). 

The 2006 Criteria Document (p. 8–51) 

concludes that evidence from animal 

toxicology studies strongly suggests that 

chronic O3 exposure is capable of 

damaging the distal airways and 

proximal alveoli, resulting in lung tissue 

remodeling leading to apparent 

irreversible changes. Such structural 

changes and compromised lung 

function caused by persistent 

inflammation may exacerbate the 

progression and development of chronic 

lung disease. Together with the limited 

evidence available from epidemiological 

studies, these findings offer some 

insight into potential biological 

mechanisms for suggested associations 

between long-term or seasonal 

exposures to O3 and reduced lung 

function development in children 

which have been observed in 

epidemiologic studies (EPA, 2006a, p. 

8–51). 

iv. Coherence and Plausibility of ShortTerm Mortality-Related Health 

Endpoints 

An extensive epidemiological 

literature on air pollution related 

mortality risk estimates from the U.S., 

Canada, and Europe is discussed in the 

2006 Criteria Document (sections 7.4 

and 8.6.3). These single- and multicity 

mortality studies coupled with results 

from meta-analyses generally indicate 

associations between acute O3 exposure 

and elevated risk for all-cause mortality, 

even after adjustment for the influence 

of season and PM exposure. Several 

single-city studies that specifically 

evaluated the relationship between O3

exposure and cardiopulmonary 

mortality also reported results 

suggestive of a positive association 

(EPA, 2006a, p. 8–51). These mortality 

studies suggest a pattern of effects for 

causality that have biologically 

plausible explanations, but our 

knowledge regarding potential 

underlying mechanisms is very limited 

at this time and requires further 

research. Most of the physiological and 

biochemical parameters investigated in 

human and animal studies suggest that 

O3-induced biochemical effects are 

relatively transient and attenuate over 

time. The 2006 Criteria Document (p. 

8–52) hypothesizes a generic pathway of 

O3-induced lung damage, potentially 

involving oxidative lung damage with 

subsequent inflammation and/or decline 

in lung function leading to respiratory 

distress in some sensitive population 

groups (e.g., asthmatics), or other 

plausible pathways noted below that 

may lead to O3-related contributions to 

cardiovascular effects that ultimately 

increase risk of mortality. 

The third National Health and 

Nutrition Examination Survey follow-up 

data analysis indicates that about 20 

percent of the adult population has 

reduced FEV1 values, suggesting 

impaired lung function in a significant 

portion of the population. Most of these 

individuals have COPD, asthma or 

fibrotic lung disease (Manino et al., 

2003), which are associated with 

persistent low-grade inflammation. 

Furthermore, patients with COPD are at 

increased risk for cardiovascular 

disease. Also, lung disease with 

underlying inflammation may be linked 

to low-grade systemic inflammation 

associated with atherosclerosis, 

independent of cigarette smoking (EPA, 

2006a, p. 8–52). Lung function 

decrements in persons with 

cardiopulmonary disease have been 

associated with inflammatory markers, 

such as C-reactive protein (CRP) in the 

blood. At a population level it has been 

found that individuals with the lowest 

FEV1 values have the highest levels of 

CRP, and those with the highest FEV1

values have the lowest CRP levels 

(Manino et al., 2003; Sin and Man, 

2003). This complex series of 

physiological and biochemical reactions 

following O3 exposure may tilt the 

biological homeostasis mechanisms 

which could lead to adverse health 

effects in people with compromised 

cardiopulmonary systems. 

Several other types of newly available 

data also support reasonable hypotheses 

that may help to explain the findings of 

O3-related increases in cardiovascular 

mortality observed in some 

epidemiological studies. These include 

the direct effect of O3 on increasing PAF 

in lung tissue that can then enter the 

general circulation and possibly 

contribute to increased risk of blood clot 

formation and the consequent increased 

risk of heart attacks, cerebrovascular 

events (stroke), or associated 

cardiovascular-related mortality. Ozone 

reactions with cholesterol in lung 

surfactant to form epoxides and 

oxysterols that are cytotoxic to lung and 

heart muscles and that contribute to 

atherosclerotic plaque formation in 

arterial walls represent another 

potential pathway. Stimulation of 

airway irritant receptors may lead to 

increases in tissue and serum levels of 

ANF, changes in heart rate, and edema 

of heart tissue. A few new field and 

panel studies of human adults have 

reported associations between ambient 

O3 concentrations and changes in 

cardiac autonomic control (e.g., HRV, 

ventricular arrhythmias, and MI). These 

represent plausible pathways that may 

lead to O3-related contributions to 

cardiovascular effects that ultimately 

increase the risk of mortality. 

In addition, O3-induced increases in 

lung permeability allow more ready 

entry for inhaled PM into the blood 

stream, and thus O3 exposure may 

increase the risk of PM-related 

cardiovascular effects. Furthermore, 

increased ambient O3 levels contribute 

to ultrafine PM formation in the ambient 

air and indoor environments. Thus, the 

contributions of elevated ambient O3

concentrations to ultrafine PM 

formation and human exposure, along 

with the enhanced uptake of inhaled 

fine particles, consequently may 

contribute to exacerbation of PMinduced cardiovascular effects in 

addition to those more directly induced 

by O3 (EPA, 2006a, p. 8–53). 


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c. Summary 

Judgments concerning the extent to 

which relationships between various 

health endpoints and ambient O3

exposures are likely to be causal are 

informed by the conclusions and 

discussion in the 2006 Criteria 

Document as discussed above and 

summarized in section 3.7.5 of the 2007 

Staff Paper. These judgments reflect the 

nature of the evidence and the overall 

weight of the evidence, and are taken 

into consideration in the quantitative 

risk assessment discussed below in 

section II.B.2. 

For example, there is a very high level 

of confidence that O3 induces lung 

function decrements in healthy adults 

and children due in part to the dozens 

of controlled human exposure and 

epidemiological studies consistently 

showing such effects. The 2006 Criteria 

Document (p. 8–74) states that these 

studies provide clear evidence of 

causality for associations between shortterm O3 exposures and statistically 

significant declines in lung function in 

children, asthmatics and adults who 

exercise outdoors. An increase in 

respiratory symptoms (e.g., cough, 

shortness of breath) has been observed 

in controlled human exposure studies of 

short-term O3 exposures, and significant 

associations between ambient O3

exposures and a wide variety of 

respiratory symptoms have been 

reported in epidemiology studies (EPA, 

2006a, p. 8–75). Population time-series 

studies showing robust associations 

between O3 exposures and respiratory 

hospital admissions and emergency 

department visits are strongly supported 

by controlled human exposure, animal 

toxicological, and epidemiological 

evidence for O3-related lung function 

decrements, respiratory symptoms, 

airway inflammation, and airway 

hyperreactivity. The 2006 Criteria 

Document (p. 8–77) concludes that, 

taken together, the overall evidence 

supports the inference of a causal 

relationship between acute ambient O3

exposures and increased respiratory 

morbidity outcomes resulting in 

increased emergency department visits 

and hospitalizations during the warm 

season. Further, recent epidemiologic 

evidence has been characterized in the 

2006 Criteria Document (p. 8–78) as 

highly suggestive that O3 directly or 

indirectly contributes to non-accidental 

and cardiopulmonary-related mortality. 

4. O3-Related Impacts on Public Health 

The following discussion draws from 

chapters 6 and 7 and section 8.7 of the 

2006 Criteria Document and section 3.6 

of the 2007 Staff Paper to characterize 

factors which modify responsiveness to 

O3, populations potentially at risk for 

O3-related health effects, the adversity 

of O3-related effects, and the size of the 

at-risk populations in the U.S. These 

considerations are all important 

elements in characterizing the potential 

public health impacts associated with 

exposure to ambient O3.

a. Factors That Modify Responsiveness 

to Ozone 

There are numerous factors that can 

modify individual responsiveness to O3. 

These include: influence of physical 

activity; age; gender and hormonal 

influences; racial, ethnic and 

socioeconomic status (SES) factors; 

environmental factors; and oxidantantioxidant balance. These factors are 

discussed in more detail in section 6.5 

of the 2006 Criteria Document. 

It is well established that physical 

activity increases an individual’s 

minute ventilation and will thus 

increase the dose of O3 inhaled (EPA, 

2006a, section 6.5.4). Increased physical 

activity results in deeper penetration of 

O3 into more distal regions of the lungs, 

which are more sensitive to acute O3

response and injury. This will result in 

greater lung function decrements for 

acute exposures of individuals during 

increased physical activity. Research 

has shown that respiratory effects are 

observed at lower O3 concentrations if 

the level of exertion is increased and/or 

duration of exposure and exertion are 

extended. Predicted O3-induced 

decrements in lung function have been 

shown to be a function of exposure 

concentration, duration and exercise 

level for healthy, young adults 

(McDonnell et al., 1997). 

Most of the studies investigating the 

influence of age have used lung function 

decrements and symptoms as measures 

of response. For healthy adults, lung 

function and symptom responses to O3

decline as age increases. The rate of 

decline in O3 responsiveness appears 

greater in those 18 to 35 years old 

compared to those 35 to 55 years old, 

while there is very little change after age 

55. In one study (Seal et al., 1996) 

analyzing a large data set, a 5.4% 

decrement in FEV1 on average was 

estimated for 20-year-old individuals 

exposed to 0.12 ppm O3 for 2.3 hours, 

whereas similar exposure of 35-year-old 

individuals resulted in a 2.6% 

decrement on average. While healthy 

children tend not to report respiratory 

symptoms when exposed to low levels 

of O3, for subjects 18 to 36 years old 

symptom responses induced by O3 are 

observed but tend to decrease with 

increasing age within this range 

(McDonnell et al., 1999). 

Limited evidence of gender 

differences in response to O3 exposure 

has suggested that females may be 

predisposed to a greater susceptibility to 

O3. Lower plasma and NL fluid levels of 

the most prevalent antioxidant, uric 

acid, in females relative to males may be 

a contributing factor. Consequently, 

reduced removal of O3 in the upper 

airways may promote deeper 

penetration. However, most of the 

evidence on gender differences appears 

to be equivocal, with one study 

(Hazucha et al., 2003) suggesting that 

physiological responses of young 

healthy males and females may be 

comparable (EPA, 2006a, section 6.5.2). 

A few studies have suggested that 

ethnic minorities might be more 

responsive to O3 than Caucasian 

population groups (EPA, 2006a, section 

6.5.3). This may be more the result of a 

lack of adequate health care and 

socioeconomic status (SES) than any 

differences in sensitivity to O3. The 

limited data available, which have 

investigated the influence of race, ethnic 

or other related factors on 

responsiveness to O3, prevent drawing 

any clear conclusions at this time. 

Few human studies have examined 

the potential influence of environmental 

factors such as the sensitivity of 

individuals who voluntarily smoke 

tobacco (i.e., smokers) and the effect of 

high temperatures on O3

responsiveness. New controlled human 

exposure studies have confirmed that 

smokers are less responsive to O3 than 

nonsmokers; however, time course of 

development and recovery of these 

effects, as well as reproducibility, was 

not different from nonsmokers (EPA, 

2006a, section 6.5.5). Influence of 

ambient temperature on pulmonary 

effects induced by O3 has been studied 

very little, but additive effects of heat 

and O3 exposure have been reported. 

Antioxidants, which scavenge free 

radicals and limit lipid peroxidation in 

the ELF, are the first line of defense 

against oxidative stress. Ozone exposure 

leads to absorption of O3 in the ELF 

with subsequent depletion of 

antioxidant in the nasal ELF, but 

concentration and antioxidant enzyme 

activity in ELF or plasma do not appear 

related to O3 responsiveness (EPA 

2006a, section 6.5.6). Controlled studies 

of dietary antioxidant supplements have 

shown some protective effects on lung 

function decrements but not on 

symptoms and airway inflammatory 

responses. Dietary antioxidant 

supplements have provided some 

protection to asthmatics by attenuating 

post-exposure airway 

hyperresponsiveness. Animal studies 


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24 In the Staff Paper and documents from previous 

O3 NAAQS reviews, ‘‘at-risk’’ groups have also been 

called ‘‘sensitive’’ groups, to mean both groups with 

greater inherent susceptibility and those more likely 

to be exposed. 

have also supported the protective 

effects of ELF antioxidants. 

b. At-Risk Subgroups for O3-Related 

Effects 

Several characteristics may increase 

the extent to which a population group 

shows increased susceptibility or 

vulnerability. Information on potentially 

susceptible and vulnerable groups is 

summarized in section 8.7 of the 2006 

Criteria Document. As described there, 

the term susceptibility refers to innate 

(e.g., genetic or developmental) or 

acquired (e.g., personal risk factors, age) 

factors that make individuals more 

likely to experience effects with 

exposure to pollutants. A number of 

population groups have been identified 

as potentially susceptible to health 

effects as a result of O3 exposure, 

including people with existing lung 

diseases, including asthma, children 

and older adults, and people who have 

larger than normal lung function 

responses that may be due to genetic 

susceptibility. In addition, some 

population groups have been identified 

as having increased vulnerability to O3- 

related effects due to increased 

likelihood of exposure while at elevated 

ventilation rates, including healthy 

children and adults who are active 

outdoors, for example, outdoor workers 

and joggers. Taken together, the 

susceptible and vulnerable groups make 

up ‘‘at-risk’’ groups.24

i. Active People 

A large group of individuals at risk 

from O3 exposure consists of outdoor 

workers and children, adolescents, and 

adults who engage in outdoor activities 

involving exertion or exercise during 

summer daylight hours when ambient 

O3 concentrations tend to be higher. 

This conclusion is based on a large 

number of controlled-human exposure 

studies and several epidemiologic field/ 

panel studies which have been 

conducted with healthy children and 

adults and those with preexisting 

respiratory diseases (EPA 2006a, 

sections 6.2, 6.3, 7.2, and 8.4.4). The 

controlled human exposure studies 

show a clear O3 exposure-response 

relationship with increasing spirometric 

and symptomatic response as exercise 

level increases. Furthermore, O3- 

induced response increases as time of 

exposure increases. Studies of outdoor 

workers and others who participate in 

outdoor activities indicate that extended 

exposures to O3 at elevated exertion 

levels can produce marked effects on 

lung function, as discussed above in 

section IIA.2 (Brauer et al., 1996; Ho ̈ppe 

et al., 1995; Korrick et al., 1998; 

McConnell et al., 2002). 

These field studies with subjects at 

elevated exertion levels support the 

extensive evidence derived from 

controlled human exposure studies. The 

majority of controlled human exposure 

studies has examined the effects of O3

exposure in subjects performing 

continuous or intermittent exercise for 

variable periods of time and has 

reported significant O3-induced 

respiratory responses. The 

epidemiologic studies discussed above 

also indicate that prolonged exposure 

periods, combined with elevated levels 

of exertion or exercise, may magnify O3

effects on lung function. Thus, outdoor 

workers and others who participate in 

higher exertion activities outdoors 

during the time of day when high peak 

O3 concentrations occur appear to be 

particularly vulnerable to O3 effects on 

respiratory health. Although these 

studies show a wide variability of 

response and sensitivity among subjects 

and the factors contributing to this 

variability continue to be incompletely 

understood, the effect of increased 

exertion is consistent. It should be noted 

that this wide variability of response 

and sensitivity among subjects may be 

in part due to the wide range of other 

highly reactive photochemical oxidants 

coexisting with O3 in the ambient air. 

ii. People With Lung Disease 

People with preexisting pulmonary 

disease are among those at increased 

risk from O3 exposure. Altered 

physiological, morphological, and 

biochemical states typical of respiratory 

diseases like asthma, COPD, and 

chronic bronchitis may render people 

sensitive to additional oxidative burden 

induced by O3 exposure. At the time of 

the 1997 review, it was concluded that 

these groups were at greater risk because 

the impact of O3-induced responses on 

already-compromised respiratory 

systems would noticeably impair an 

individual’s ability to engage in normal 

activity or would be more likely to 

result in increased self-medication or 

medical treatment. At that time there 

was little evidence that people with preexisting disease were more responsive 

than healthy individuals in terms of the 

magnitude of lung function decrements 

or symptomatic responses. The new 

results from controlled exposure and 

epidemiologic studies continue to 

indicate that individuals with 

preexisting pulmonary disease are a 

sensitive population for O3-related 

health effects. 

Several controlled human exposure 

studies reviewed in the 1996 Criteria 

Document on atopic and asthmatic 

subjects have suggested but not clearly 

demonstrated enhanced responsiveness 

to acute O3 exposure compared to 

healthy subjects. The majority of the 

newer studies reviewed in Chapter 6 of 

the 2006 Criteria Document indicate 

that asthmatics are more sensitive than 

normal subjects in manifesting O3- 

induced lung function decrements. In 

one key study (Horstman et al., 1995), 

the FEV1 decrement observed in the 

asthmatics was significantly larger than 

in the healthy subjects (19% versus 

10%, respectively). There was also a 

notable tendency for a greater group 

mean O3-induced decrease in FEF25–75

in asthmatics relative to the healthy 

subjects (24% versus 15%, 

respectively). A significant positive 

correlation in asthmatics was also 

reported between the magnitude of O3- 

induced spirometric responses and 

baseline lung function, i.e., responses 

increased with severity of disease. 

Asthmatics present a differential 

response profile for cellular, molecular, 

and biochemical parameters (2006 

Criteria Document, Figure 8–1) that are 

altered in response to acute O3

exposure. Ozone-induced increases in 

neutrophils, IL–8 and protein were 

found to be significantly higher in the 

BAL fluid from asthmatics compared to 

healthy subjects, suggesting 

mechanisms for the increased 

sensitivity of asthmatics (Basha et al., 

1994; McBride et al., 1994; Scannell et 

al., 1996; Hiltermann et al., 1999; Holz 

et al., 1999; Bosson et al., 2003). 

Neutrophils, or PMNs, are the white 

blood cells most associated with 

inflammation. IL–8 is an inflammatory 

cytokine with a number of biological 

effects, primarily on neutrophils. The 

major role of this cytokine is to attract 

and activate neutrophils. Protein in the 

airways is leaked from the circulatory 

system, and is a marker for increased 

cellular permeability. 

Bronchial constriction following 

provocation with O3 and/or allergens 

presents a two-phase response. The 

early response is mediated by release of 

histamine and leukotrienes that leads to 

contraction of smooth muscle cells in 

the bronchi, narrowing the lumen and 

decreasing the airflow. In people with 

allergic airway disease, including 

people with rhinitis and asthma, these 

mediators also cause accumulation of 

eosinophils in the airways (Bascom et 

al., 1990; Jorres et al., 1996; Peden et al., 

1995 and 1997; Frampton et al., 1997; 

Michelson et al., 1999; Hiltermann et 

al., 1999; Holz et al., 2002; Vagaggini et 

al., 2002). In asthma, the eosinophil, 


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which increases inflammation and 

allergic responses, is the cell most 

frequently associated with exacerbations 

of the disease. A study by Bosson et al. 

(2003) evaluated the difference in O3- 

induced bronchial epithelial cytokine 

expression between healthy and 

asthmatic subjects. After O3 exposure 

the epithelial expression of IL–5 and 

GM–CSF increased significantly in 

asthmatics, compared to healthy 

subjects. Asthma is associated with Th2- 

related airway response (allergic 

response), and IL–5 is an important 

Th2-related cytokine. The O3-induced 

increase in IL–5, and also in GM–CSF, 

which affects the growth, activation and 

survival of eosinophils, may indicate an 

effect on the Th2-related airway 

response and on airway eosinophils. 

The authors reported that the O3- 

induced Th2-related cytokine responses 

that were found within the asthmatic 

group may indicate a worsening of their 

asthmatic airway inflammation and thus 

suggest a plausible link to 

epidemiological data indicating O3- 

associated increases in bronchial 

reactivity and hospital admissions. 

The accumulation of eosinophils in 

the airways of asthmatics is followed by 

production of mucus and a late-phase 

bronchial constriction and reduced 

airflow. In a study of 16 intermittent 

asthmatics, Hiltermann et al. (1999) 

found that there was a significant 

inverse correlation between the O3- 

induced change in the percentage of 

eosinophils in induced sputum and the 

change in PC20, the concentration of 

methacholine causing a 20% decrease in 

FEV1. Characteristic O3-induced 

inflammatory airway neutrophilia at one 

time was considered a leading 

mechanism of airway 

hyperresponsiveness. However, 

Hiltermann et al. (1999) determined that 

the O3-induced change in percentage 

neutrophils in sputum was not 

significantly related to the change in 

PC20. These results are consistent with 

the results of Zhang et al. (1995), which 

found neutrophilia in a murine model to 

be only coincidentally associated with 

airway hyperresponsiveness, i.e., there 

was no cause and effect relationship. 

(2006 Criteria Document, AX 6–26). 

Hiltermann et al. (1999) concluded that 

the results point to the role of 

eosinophils in O3-induced airway 

hyperresponsiveness. Increases in O3- 

induced nonspecific airway 

responsiveness incidence and duration 

could have important clinical 

implications for asthmatics. 

Two studies (Jo ̈rres et al., 1996; Holz 

et al., 2002) observed increased airway 

responsiveness to O3 exposure with 

bronchial allergen challenge in subjects 

with preexisting allergic airway disease. 

Jo ̈rres et al. (1996) found that O3 causes 

an increased response to bronchial 

allergen challenge in subjects with 

allergic rhinitis and mild allergic 

asthma. The subjects were exposed to 

0.25 ppm O3 for 3 hours with IE. Airway 

responsiveness to methacholine was 

determined 1 hour before and after 

exposure; responsiveness to allergen 

was determined 3 hours after exposure. 

Statistically significant decreases in 

FEV1 occurred in subjects with allergic 

rhinitis (13.8%) and allergic asthma 

(10.6%), and in healthy controls (7.3%). 

Methacholine responsiveness was 

statistically increased in asthmatics, but 

not in subjects with allergic rhinitis or 

healthy controls. Airway responsiveness 

to an individual’s historical allergen 

(either grass and birch pollen, house 

dust mite, or animal dander) was 

significantly increased after O3 exposure 

when compared to FA exposure. In 

subjects with asthma and allergic 

rhinitis, a maximum percent fall in 

FEV1 of 27.9% and 7.8%, respectively, 

occurred 3 days after O3 exposure when 

they were challenged with of the highest 

common dose of allergen. The authors 

concluded that subjects with asthma or 

allergic rhinitis, without asthma, could 

be at risk if a high O3 exposure is 

followed by a high dose of allergen. 

Holz et al. (2002) reported an early 

phase lung function response in subjects 

with rhinitis after a consecutive 4-day 

exposure to 0.125 ppm O3 that resulted 

in a clinically relevant (>20%) decrease 

in FEV1. Ozone-induced exacerbation of 

airway responsiveness persists longer 

and attenuates more slowly than O3- 

induced lung function decrements and 

respiratory symptom responses and can 

have important clinical implications for 

asthmatics. 

A small number of in vitro studies 

corroborate the differences in the 

responses of asthmatic and healthy 

subject generally found in controlled 

human exposure studies. In vitro 

studies (Schierhorn et al., 1999) of nasal 

mucosal biopsies from atopic and 

nonatopic subjects exposed to 0.1 ppm 

O3 found significant differences in 

release of IL–4, IL–6, IL–8, and TNF-a. 

Another study by Schierhorn et al. 

(2002) found significant differences in 

the O3-induced release of the 

neuropeptides neurokinin A and 

substance P for allergic patients in 

comparison to nonallergic controls, 

suggesting increased activation of 

sensory nerves by O3 in the allergic 

tissues. Another study by Bayram et al. 

(2002) using in vitro culture of 

bronchial epithelial cells recovered from 

atopic and nonatopic asthmatics also 

found significant increases in epithelial 

permeability in response to O3

exposure. 

The new data on airway 

responsiveness, inflammation, and 

various molecular markers of 

inflammation and bronchoconstriction 

indicate that people with asthma and 

allergic rhinitis (with or without 

asthma) comprise susceptible groups for 

O3-induced adverse effects. This body of 

evidence indicates that controlled 

human exposure and epidemiological 

panel studies of lung function 

decrements and respiratory symptoms 

that evaluate only healthy, nonasthmatic subjects likely underestimate 

the effects of O3 exposure on asthmatics 

and other susceptible populations. The 

effects of O3 on lung function, 

inflammation, and increased airway 

responsiveness demonstrated in subjects 

with asthma and other allergic airway 

diseases, provide plausible mechanisms 

underlying the more serious respiratory 

morbidity effects, such as emergency 

department visits and hospital 

admissions, and respiratory mortality 

effects. 

A number of epidemiological studies 

have been conducted using asthmatic 

study populations. The majority of 

epidemiological panel studies that 

evaluated respiratory symptoms and 

medication use related to O3 exposures 

focused on children. These studies 

suggest that O3 exposure is associated 

with increased respiratory symptoms 

and medication use in children with 

asthma. Other reported effects include 

respiratory symptoms, lung function 

decrements, and emergency department 

visits, as discussed in the 2006 Criteria 

Document (section 7.6.7.1). Strong 

evidence from a large multicity study 

(Mortimer et al., 2002), along with 

support from several single-city studies 

indicate that O3 exposure is associated 

with increased respiratory symptoms 

and medication use in children with 

asthma. With regard to ambient O3

levels and increased hospital 

admissions and emergency department 

visits for asthma and other respiratory 

causes, strong and consistent evidence 

establishes a correlation between O3

exposure and increased exacerbations of 

preexisting respiratory disease for 1- 

hour maximum O3 concentrations <0.12 

ppm. As discussed above and in the 

2006 Criteria Document, section 7.3, 

several hospital admission and 

emergency department visit studies in 

the U.S., Canada, and Europe have 

reported positive associations between 

increase in O3 and increased risk of 

emergency department visits and 

hospital admissions for asthma other 


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respiratory diseases, especially during 

the warm season. 

In summary, based on a substantial 

new body of evidence from animal, 

controlled human exposure and 

epidemiological studies the 2006 

Criteria Document (section x.x) 

concludes that people with asthma and 

other preexisting pulmonary diseases 

are among those at increased risk from 

O3 exposure. Evidence from controlled 

human exposure studies indicates that 

asthmatics may exhibit larger lung 

function decrements and can have larger 

inflammatory responses in response to 

O3 exposure than healthy controls. 

Asthmatics present a different response 

profile for cellular, molecular, and 

biochemical parameters that are altered 

in response to acute O3 exposure. 

Asthmatics, and people with allergic 

rhinitis, are more likely to mount an 

allergic-type response upon exposure to 

O3, as manifested by increases in white 

blood cells associated with allergy and 

related molecules, which increase 

inflammation in the airways. The 

increased inflammatory and allergic 

responses also may be associated with 

the larger late-phase responses that 

asthmatics can experience, which can 

include increased bronchoconstrictor 

responses to irritant substances or 

allergens and additional inflammation. 

Epidemiological studies have reported 

fairly robust associations between 

ambient O3 concentrations and 

measures of lung function and daily 

respiratory symptoms (e.g., chest 

tightness, wheeze, shortness of breath) 

in children with moderate to severe 

asthma and between O3 and increased 

asthma medication use. These more 

serious responses in asthmatics and 

others with lung disease provide 

biological plausibility for the respiratory 

morbidity effects observed in 

epidemiological studies, such as 

emergency department visits and 

hospital admissions. The body of 

evidence from controlled human 

exposure and epidemiological studies, 

which includes asthmatic as well as 

non-asthmatic subjects, indicates that 

controlled human exposure studies of 

lung function decrements and 

respiratory symptoms that evaluate only 

healthy, non-asthmatic subjects likely 

underestimate the effects of O3 exposure 

on asthmatics and other susceptible 

populations. 

Newly available reports from 

controlled human exposure studies (see 

chapter 6 in the 2006 Criteria 

Document) utilized subjects with 

preexisting cardiopulmonary diseases 

such as COPD, asthma, allergic rhinitis, 

and hypertension. The data generated 

from these studies that evaluated 

changes in spirometry did not find clear 

differences between filtered air and O3

exposure in COPD subjects. However, 

the new data on airway responsiveness, 

inflammation, and various molecular 

markers of inflammation and 

bronchoconstriction indicate that 

people with atopic asthma and allergic 

rhinitis comprise susceptible groups for 

O3-induced adverse health effects. 

Although controlled human exposure 

studies have not found evidence of 

larger spirometric responses to O3 in 

people with COPD relative to healthy 

subjects, this may be due to the fact that 

most people with COPD are older adults 

who would not be expected to be as 

responsive based on their age. However, 

in section 8.7.1, the 2006 Criteria 

Document notes that new 

epidemiological evidence indicates that 

people with COPD may be more likely 

to experience other effects, including 

emergency room visits, hospital 

admissions, or premature mortality. For 

example, results from an analysis of five 

European cities indicated strong and 

consistent O3 effects on unscheduled 

respiratory hospital admissions, 

including COPD (Anderson et al., 1997). 

Also, an analysis of a 9-year data set for 

the whole population of the Netherlands 

provided risk estimates for more 

specific causes of mortality, including 

COPD (Hoek et al., 2000, 2001; 

reanalysis Hoek, 2003); a positive, but 

nonsignificant, excess risk of COPDrelated mortality was found to be 

associated with short-term O3

concentrations. Moreover, as indicated 

by Gong et al. (1998), the effects of O3

exposure on alveolar-arterial oxygen 

gradients may be more pronounced in 

patients with preexisting obstructive 

lung diseases. Relative to healthy 

elderly subjects, COPD patients have 

reduced gas exchange and low SaO2.

Any inflammatory or edematous 

responses due to O3 delivered to the 

well-ventilated regions of the lung in 

COPD subjects could further inhibit gas 

exchange and reduce oxygen saturation. 

In addition, O3-induced 

vasoconstriction could also acutely 

induce pulmonary hypertension. 

Inducing pulmonary vasoconstriction 

and hypertension in these patients 

would perhaps worsen their condition, 

especially if their right ventricular 

function was already compromised 

(EPA, 2006a, section 6.10). These 

controlled human exposure and 

epidemiological studies indicate that 

people with pre-existing lung diseases 

other than asthma are also at greater risk 

from O3 exposure than people without 

lung disease. 

iii. Children and Older Adults 

Supporting evidence exists for 

heterogeneity in the effects of O3 by age. 

As discussed in section 6.5.1 of the 2006 

Criteria Document, children, 

adolescents, and young adults (<18 yrs 

of age) appear, on average, to have 

nearly equivalent spirometric responses 

to O3, but have greater responses than 

middle-aged and older adults when 

exposed to comparable O3 doses. 

Symptomatic responses to O3 exposure, 

however, do not appear to occur in 

healthy children, but are observed in 

asthmatic children, particularly those 

who use maintenance medications. For 

adults (>17 yrs of age) symptoms 

gradually decrease with increasing age. 

In contrast to young adults, the 

diminished symptomatic responses in 

children and the diminished 

symptomatic and spirometric responses 

in older adults increases the likelihood 

that these groups continue outdoor 

activities leading to greater O3 exposure 

and dose. 

As described in the section 7.6.7.2 of 

the 2006 Criteria Document, many 

epidemiological field studies focused on 

the effect of O3 on the respiratory health 

of school children. In general, children 

experienced decrements in lung 

function parameters, including PEF, 

FEV1, and FVC. Increases in respiratory 

symptoms and asthma medication use 

were also observed in asthmatic 

children. In one German study, children 

with and without asthma were found to 

be particularly susceptible to O3 effects 

on lung function. Approximately 20 

percent of the children, both with and 

without asthma, experienced a greater 

than 10 percent change in FEV1, 

compared to only 5 percent of the 

elderly population and athletes (Ho ̈ppe 

et al., 2003). 

The American Academy of Pediatrics 

(2004) notes that children and infants 

are among the population groups most 

susceptible to many air pollutants, 

including O3. This is in part because 

their lungs are still developing. For 

example, eighty percent of alveoli are 

formed after birth, and changes in lung 

development continue through 

adolescence (Dietert et al., 2000). 

Children are also likely to spend more 

time outdoors than adults, which results 

in increased exposure to air pollutants 

(Wiley et al., 1991a,b). Moreover, 

children have high minute ventilation 

rates and high levels of physical activity 

which also increases their dose 

(Plunkett et al., 1992). 

Several mortality studies have 

investigated age-related differences in 

O3 effects (EPA, 2006a, section 7.6.7.2). 

Older adults are also often classified as 


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25Similar to animal toxicology studies referred 

above, a polymorphism in a specific 

proinflammatory cytokine gene has been implicated 

in O3-induced lung function changes in healthy, 

mild asthmatics and individuals with rhinitis. 

These observations suggest a potential role for these 

markers in the innate susceptibility to O3, however, 

the validity of these markers and their relevance in 

the context of prediction to population studies 

requires additional research. 

26 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. 

being particularly susceptible to air 

pollution. The 2006 Criteria Document 

(p. 8–60) concludes that the basis for 

increased O3 sensitivity among the 

elderly is not known, but one 

hypothesis is that it may be related to 

changes in the respiratory tract lining 

fluid antioxidant defense network (Kelly 

et al., 2003). Older adults have lower 

baseline lung function than younger 

people, and are also more likely to have 

preexisting lung and heart disease. 

Increased susceptibility of older adults 

to O3 health effects is most clearly 

indicated in the newer mortality 

studies. Among the studies that 

observed positive associations between 

O3 and mortality, a comparison of all 

age or younger age (≤ 65 years of age) O3- 

mortality effect estimates to that of the 

elderly population (> 65 years) indicates 

that, in general, the elderly population 

is more susceptible to O3 mortality 

effects. The meta-analysis by Bell et al. 

(2005) found a larger mortality effect 

estimate for the elderly than for all ages. 

In the large U.S. 95 communities study 

(Bell et al., 2004), mortality effect 

estimates were slightly higher for those 

aged 65 to 74 years, compared to 

individuals less than 65 years and 75 

years or greater. The absolute effect of 

O3 on premature mortality may be 

substantially greater in the elderly 

population because of higher rates of 

preexisting respiratory and cardiac 

diseases. The 2006 Criteria Document 

(p. 7–177) concludes that the elderly 

population (>65 years of age) appear to 

be at greater risk of O3-related mortality 

and hospitalizations compared to all 

ages or younger populations. 

The 2006 Criteria Document notes 

that, collectively, there is supporting 

evidence of age-related differences in 

susceptibility to O3 lung function 

effects. The elderly population (> 65 

years of age) appear to be at increased 

risk of O3-related mortality and 

hospitalizations, and children (< 18 

years of age) experience other 

potentially adverse respiratory health 

outcomes with increased O3 exposure 

(EPA, 2006a, section 7.6.7.2). 

iv. People With Increased 

Responsiveness to Ozone 

New animal toxicology studies using 

various strains of mice and rats have 

identified O3-sensitive and resistant 

strains and illustrated the importance of 

genetic background in determining O3

susceptibility (EPA, 2006a, section 

8.7.4). Controlled human exposure 

studies have also indicated a high 

degree of variability in some of the 

pulmonary physiological parameters. 

The variable effects in individuals have 

been found to be reproducible, in other 

words, a person who has a large lung 

function response after exposure to O3

will likely have about the same response 

if exposed again to the same dose of O3. 

In controlled human exposure studies, 

group mean responses are not 

representative of this segment of the 

population that has much larger than 

average responses to O3. Recent studies 

of asthmatics by David et al. (2003) and 

Romieu et al. (2004) reported a role for 

genetic polymorphism in observed 

differences in antioxidant enzymes and 

genes involved in inflammation to 

modulate lung function and 

inflammatory responses to O3

exposure.25

Biochemical and molecular 

parameters extensively evaluated in 

these experiments were used to identify 

specific loci on chromosomes and, in 

some cases, to relate the differential 

expression of specific genes to 

biochemical and physiological 

differences observed among these 

species. Utilizing O3-sensitive and O3- 

resistant species, it has been possible to 

identify the involvement of increased 

airway reactivity and inflammation 

processes in O3 susceptibility. However, 

most of these studies were carried out 

using relatively high doses of O3, 

making the relevance of these studies 

questionable in human health effects 

assessment. The genes and genetic loci 

identified in these studies may serve as 

useful biomarkers in the future. 

v. Other Population Groups 

There is limited, new evidence 

supporting associations between shortterm O3 exposures and a range of effects 

on the cardiovascular system. Some but 

not all, epidemiological studies have 

reported associations between shortterm O3 exposures and the incidence of 

heart attacks and more subtle 

cardiovascular health endpoints, such 

as changes in HRV and cardiac 

arrhythmia. Others have reported 

associations with hospitalization or 

emergency department visits for 

cardiovascular diseases, although the 

results across the studies are not 

consistent. Studies also report 

associations between short-term O3

exposure and mortality from 

cardiovascular or cardiopulmonary 

causes. The 2006 Criteria Document (p. 

7–65) concludes that current 

cardiovascular effects evidence from 

some field studies is rather limited but 

supportive of a potential effect of shortterm O3 exposure and HRV, cardiac 

arrhythmia, and heart attack incidence. 

In the 2006 Criteria Document’s 

evaluation of studies of hospital 

admissions for cardiovascular disease 

(EPA 2006a, section 7.3.4), it is 

concluded that evidence from this 

growing group of studies is generally 

inconclusive regarding an association 

with O3 in studies conducted during the 

warm season (EPA 2006a, p. 7–83). This 

body of evidence suggests that people 

with heart disease may be at increased 

risk from short-term exposures to O3 ́

however, more evidence is needed to 

conclude that people with heart disease 

are a susceptible population. 

Other groups that might have 

enhanced sensitivity to O3, but for 

which there is currently very little 

evidence, include groups based on race, 

gender and SES, and those with 

nutritional deficiencies, which presents 

factors which modify responsiveness to 

O3. 

c. Adversity of Effects 

In the 2008 rulemaking, in making 

judgments as to when various O3-related 

effects become regarded as adverse to 

the health of individuals, EPA looked to 

guidelines published by the American 

Thoracic Society (ATS) and the advice 

of CASAC. While recognizing that 

perceptions of ‘‘medical significance’’ 

and ‘‘normal activity’’ may differ among 

physicians, lung physiologists and 

experimental subjects, the ATS (1985) 26

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 ATSdefined categories, evidence of 

statistically significant associations from 

epidemiological studies for effects in the 

second and third categories, and 

evidence from animal toxicology 


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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 

studies, but have not been conclusively 

demonstrated still fall primarily into the 

last two categories. In the 1997 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 the 2006 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 multicity time-series 

epidemiology studies and meta-analyses 

of these epidemiological studies are 

highly suggestive of an association 

between short-term O3 exposure and 

mortality particularly in the warm 

season. 

While O3 has been associated with 

effects that are clearly adverse, 

application of these guidelines, in 

particular to the least serious category of 

effects related to ambient O3 exposures, 

involves judgments about which 

medical experts on the CASAC panel 

and public commenters have expressed 

diverse views in the past. To help frame 

such judgments, EPA staff have defined 

specific ranges of functional responses 

(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 2007 Staff Paper. 

For active healthy people, moderate 

levels of functional responses (e.g., FEV1

decrements of ≥ 10 percent but < 20 

percent, 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 

percent, 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 

percent but < 20 percent) 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 percent but < 20 

percent, 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 percent, lasting longer 

than 24 hours) and/or severe 

symptomatic responses (e.g., persistent 

uncontrollable cough, severe discomfort 

on exercise or deep breath, persistent 

wheeze accompanied by shortness of 

breath, lasting longer than 24 hours) 

would likely interfere with normal 

activity for most individuals and would 

increase the likelihood that these 

individuals would seek medical 

treatment. In the context of standard 

setting, the CASAC indicated 

(Henderson, 2006c) that a focus on the 

lower end of the range of moderate 

levels of functional responses (e.g., FEV1

decrements ≥ 10 percent) is most 

appropriate for estimating potentially 

adverse lung function decrements in 

people with lung disease. 

In judging the extent to which these 

impacts represent effects that should be 

regarded as adverse to the health status 

of individuals, an additional factor that 

has been considered in previous 

NAAQS reviews is whether such effects 

are experienced repeatedly during the 

course of a year or only on a single 

occasion. While some experts would 

judge single occurrences of moderate 

responses to be a ‘‘nuisance,’’ especially 

for healthy individuals, a more general 

consensus view of the adversity of such 

moderate responses emerges as the 

frequency of occurrence increases. 

The new guidance builds upon and 

expands the 1985 definition of adversity 

in several ways. There is an increased 

focus on quality of life measures as 

indicators of adversity. There is also a 

more specific consideration of 

population risk. Exposure to air 

pollution that increases the risk of an 

adverse effect to the entire population is 

adverse, even though it may not 

increase the risk of any individual to an 

unacceptable level. For example, a 

population of asthmatics could have a 

distribution of lung function such that 

no individual has a level associated 

with significant impairment. Exposure 

to air pollution could shift the 

distribution to lower levels that still do 

not bring any individual to a level that 

is associated with clinically relevant 

effects. However, this would be 

considered to be adverse because 

individuals within the population 

would have diminished reserve 

function, and therefore would be at 

increased risk if affected by another 

agent. 

Of the various effects of O3 exposure 

that have been studied, many would 

meet the ATS definition of adversity. 

Such effects include, for example, any 

detectible level of permanent lung 

function loss attributable to air 

pollution, including both reductions in 

lung growth or acceleration of the agerelated decline of lung function; 

exacerbations of disease in individuals 

with chronic cardiopulmonary diseases; 

reversible loss of lung function in 

combination with the presence of 

symptoms; as well as more serious 

effects such as those requiring medical 

care including hospitalization and, 

obviously, mortality. 


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27Modeling that projects whether and how areas 

might attain alternative standards in a future year 

is presented in the Regulatory Impact Analysis 

being prepared in connection with this rulemaking. 

28EPA made available corrected versions of the 

final 2007 Staff Paper, and human exposure and 

health risk assessment technical support documents 

in July 2007 on the EPA Web site listed in the 

Availability of Related Information section of this 

notice. 

29The 12 CSAs modeled are: Atlanta-Sandy 

Springs-Gainesville, GA–AL; Boston-WorcesterManchester, MA–NH; Chicago-Naperville-Michigan 

City, IL–IN–WI; Cleveland-Akron-Elyria, OH; 

Detroit-Warren-Flint, MI; Houston-BaytownHuntsville, TX; Los Angeles-Long Beach-Riverside, 

d. Size of At-Risk Populations 

Although O3-related health risk 

estimates may appear to be small, their 

significance from an overall public 

health perspective is determined by the 

large numbers of individuals in the 

population groups potentially at risk for 

O3-related health effects discussed 

above. For example, a population of 

concern includes people with 

respiratory disease, which includes 

approximately 11 percent of U.S. adults 

and 13 percent of children who have 

been diagnosed with asthma and 6 

percent of adults with chronic 

obstructive pulmonary disease (chronic 

bronchitis and/or emphysema) in 2002 

and 2003 (Table 8–4 in the 2006 Criteria 

Document, section 8.7.5.2). More 

broadly, individuals with preexisting 

cardiopulmonary disease may constitute 

an additional population of concern, 

with potentially tens of millions of 

people included in each disease 

category. In addition, populations based 

on age group also comprise substantial 

segments of the population that may be 

potentially at risk for O3-related health 

impacts. Based on U.S. census data from 

2003, about 26 percent of the U.S. 

population are under 18 years of age 

and 12 percent are 65 years of age or 

older. Hence, large proportions of the 

U.S. population are included in life 

stages that are most likely to have 

increased susceptibility to the health 

effects of O3 and/or those with the 

highest ambient O3 exposures. 

The 2006 Criteria Document (section 

8.7.5.2) notes that the health statistics 

data illustrate what is known as the 

‘‘pyramid’’ of effects. At the top of the 

pyramid, there are approximately 2.5 

millions deaths from all causes per year 

in the U.S. population, with about 

100,000 deaths from chronic lower 

respiratory diseases. For respiratory 

health diseases, there are nearly 4 

million hospital discharges per year, 14 

million emergency department visits, 

112 million ambulatory care visits, and 

an estimated 700 million restricted 

activity days per year due to respiratory 

conditions from all causes per year. 

Applying small risk estimates for the 

O3-related contribution to such health 

effects with relatively large baseline 

levels of health outcomes can result in 

quite large public health impacts related 

to ambient O3 exposure. Thus, even a 

small percentage reduction in O3 health 

impacts on cardiopulmonary diseases 

would reflect a large number of avoided 

cases. In considering this information 

together with the concentrationresponse relationships that have been 

observed between exposure to O3 and 

various health endpoints, the 2006 

Criteria Document (section 8.7.5.2) 

concludes that exposure to ambient O3

likely has a significant impact on public 

health in the U.S. 

B. Human Exposure and Health Risk 

Assessments 

To put judgments about health effects 

that are adverse for individuals into a 

broader public health context, EPA has 

developed and applied models to 

estimate human exposures and health 

risks. This broader context includes 

consideration of the size of particular 

population groups at risk for various 

effects, the likelihood that exposures of 

concern will occur for individuals in 

such groups under varying air quality 

scenarios, estimates of the number of 

people likely to experience O3-related 

effects, the variability in estimated 

exposures and risks, and the kind and 

degree of uncertainties inherent in 

assessing the exposures and risks 

involved. 

As discussed below there are a 

number of important uncertainties that 

affect the exposure and health risk 

estimates. It is also important to note 

that there have been significant 

improvements in both the exposure and 

health risk model. CASAC expressed the 

view that the exposure analysis 

represents a state-of-the-art modeling 

approach and that the health risk 

assessment was ‘‘well done, balanced 

and reasonably communicated 

(Henderson, 2006c). While recognizing 

and considering the kind and degree of 

uncertainties in both the exposure and 

health risk estimates, the 2007 Staff 

Paper (pp. 6–20 to 6–21) judged that the 

quality of the estimates is such that they 

are suitable to be used as an input to the 

Administrator’s decisions on the O3

primary standard. 

In modeling exposures and health 

risks associated with just meeting the 

current and alternative O3 standards, 

EPA has simulated air quality to 

represent conditions just meeting these 

standards based on O3 air quality 

patterns in several recent years and on 

how the shape of the O3 air quality 

distribution have changed over time 

based on historical trends in monitored 

O3 air quality data. As described in the 

2007 Staff Paper (EPA, 2007b, section 

4.5.8) and discussed below, recent O3

air quality distributions have been 

statistically adjusted to simulate just 

meeting the current and selected 

alternative standards. These simulations 

do not reflect any consideration of 

specific control programs or strategies 

designed to achieve the reductions in 

emissions required to meet the specified 

standards. Further, these simulations do 

not represent predictions of when, 

whether, or how areas might meet the 

specified standards.27

As noted in section I.C above, around 

the time of the release of the final 2007 

Staff Paper in January 2007, EPA 

discovered a small error in the exposure 

model that when corrected resulted in 

slight increases in the simulated 

exposures. Since the exposure estimates 

are an input to the lung function portion 

of the health risk assessment, this 

correction also resulted in slight 

increases in the lung function risk 

estimates as well. The exposure and risk 

estimates discussed in this notice reflect 

the corrected estimates, and thus are 

slightly different than the exposure and 

risk estimates cited in the January 31, 

2007 Staff Paper.28

1. Exposure Analyses 

a. Overview 

As part of the 2008 rulemaking, the 

EPA conducted exposure analyses using 

a simulation model to estimate O3

exposures for the general population, 

school age children (ages 5–18), and 

school age children with asthma living 

in 12 U.S. metropolitan areas 

representing different regions of the 

country where the then current 8-hour 

O3 standard is not met. The emphasis on 

children reflects the finding of the 1997 

O3 NAAQS review that children are an 

important at-risk group. The 12 modeled 

areas combined represent a significant 

fraction of the U.S. urban population, 89 

million people, including 18 million 

school age children of whom 

approximately 2.6 million have asthma. 

The selection of urban areas to include 

in the exposure analysis took into 

consideration the location of O3

epidemiological studies, the availability 

of ambient O3 data, and the desire to 

represent a range of geographic areas, 

population demographics, and O3

climatology. These selection criteria are 

discussed further in chapter 5 of the 

2007 Staff Paper (EPA, 2007b). The 

geographic extent of each modeled area 

consists of the census tracts in the 

combined statistical area (CSA) as 

defined by OMB (OMB, 2005).29


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CA; New York-Newark-Bridgeport, NY–NJ–CT–PA; 

Philadelphia-Camden-Vineland, PA–NJ–DE–MD; 

Sacramento—Arden-Arcade—Truckee, CA–NV; St. 

Louis-St. Charles-Farmington, MO–IL; WashingtonBaltimore-N. Virginia, DC–MD–VA–WV. 

30All 12 of the CSAs modeled did not meet the 

0.084 ppm O3 NAAQS for the three year period 

examined. 

31The general approach used in the human 

exposure assessment was described in the draft 

Health Assessment Plan (EPA, 2005d) that was 

released to the CASAC and general public in April 

2005 and was the subject of a consultation with the 

CASAC O3 Panel on May 5, 2005. In October 2005, 

OAQPS released the first draft of the Staff Paper 

containing a chapter discussing the exposure 

analyses and first draft of the Exposure Analyses 

TSD for CASAC consultation and public review on 

December 8, 2005. In July 2006, OAQPS released 

the second draft of the Staff Paper and second draft 

of the Exposure Analyses TSD for CASAC review 

and public comment which was held by the CASAC 

O3 Panel on August 24–25, 2006. 

Exposure estimates were developed 

using a probabilistic exposure model 

that is designed to explicitly model the 

numerous sources of variability that 

affect people’s exposures. As discussed 

below, the model estimates population 

exposures by simulating human activity 

patterns, air conditioning prevalence, 

air exchange rates, and other factors. 

The modeled exposure estimates were 

developed for three recent years of 

ambient O3 concentrations (2002, 2003, 

and 2004), as well as for O3

concentrations adjusted to simulate 

conditions associated with just meeting 

the then current NAAQS and various 

alternative 8-hour standards based on 

the three year period 2002–2004.30 This 

exposure assessment is more fully 

described and presented in the 2007 

Staff Paper and in a technical support 

document, Ozone Population Exposure 

Analysis for Selected Urban Areas (EPA, 

2007c; hereafter Exposure Analysis 

TSD). The scope and methodology for 

this exposure assessment were 

developed over the last few years with 

considerable input from the CASAC 

Ozone Panel and the public.31

The goals of the O3 exposure 

assessment were: (1) To provide 

estimates of the size of at-risk 

populations exposed to various levels 

associated with recent O3

concentrations, and with just meeting 

the current O3 NAAQS and alternative 

O3 standards, in specific urban areas; (2) 

to provide distributions of exposure 

estimates over the entire range of 

ambient O3 concentrations as an 

important input to the lung function 

risk assessment summarized below in 

section II.B.2; (3) to develop a better 

understanding of the influence of 

various inputs and assumptions on the 

exposure estimates; and (4) to gain 

insight into the distribution of 

exposures and patterns of exposure 

reductions associated with meeting 

alternative O3 standards. 

The EPA recognizes that there are 

many sources of variability and 

uncertainty inherent in the inputs to 

this assessment and that there is 

uncertainty in the resulting O3 exposure 

estimates. With respect to variability, 

the exposure modeling approach 

accounts for variability in ambient O3

levels, demographic characteristics, 

physiological attributes, activity 

patterns, and factors affecting 

microenvironmental (e.g., indoor) 

concentrations. In EPA’s judgment, the 

most important uncertainties affecting 

the exposure estimates are related to the 

modeling of human activity patterns 

over an O3 season, the modeling of 

variations in ambient concentrations 

near roadways, and the modeling of air 

exchange rates that affect the amount of 

O3 that penetrates indoors. Another 

important uncertainty that affects the 

estimation of how many exposures are 

associated with moderate or greater 

exertion is the characterization of 

energy expenditure for children engaged 

in various activities. As discussed in 

more detail in the 2007 Staff Paper 

(EPA, 2007b, section 4.3.4.7), the 

uncertainty in energy expenditure 

values carries over to the uncertainty of 

the modeled breathing rates, which are 

important since they are used to classify 

exposures occurring at moderate or 

greater exertion which are the relevant 

exposures since O3-related effects 

observed in controlled human exposure 

studies only are observed when 

individuals are engaged in some form of 

exercise. The uncertainties in the 

exposure model inputs and the 

estimated exposures have been assessed 

using quantitative uncertainty and 

sensitivity analyses. Details are 

discussed in the 2007 Staff Paper 

(section 4.6) and in a technical 

memorandum describing the exposure 

modeling uncertainty analysis 

(Langstaff, 2007). 

b. Scope and Key Components 

Population exposures to O3 are 

primarily driven by ambient outdoor 

concentrations, which vary by time of 

day, location, and peoples’ activities. 

Outdoor O3 concentration estimates 

used in the exposure assessment are 

provided by measurements and 

statistical adjustments to the measured 

concentrations. The current exposure 

analysis allows comparisons of 

population exposures to O3 within each 

urban area, associated with current O3

levels and with O3 levels just meeting 

several potential alternative air quality 

standards or scenarios. Human 

exposure, regardless of the pollutant, 

depends on where individuals are 

located and what they are doing. 

Inhalation exposure models are useful 

in realistically estimating personal 

exposures to O3 based on activityspecific breathing rates, particularly 

when recognizing that large scale 

population exposure measurement 

studies have not been conducted that 

are representative of the overall 

population or at risk subpopulations. 

The model EPA used to simulate O3

population exposure is the Air 

Pollutants Exposure Model (APEX), the 

human inhalation exposure model 

within the Total Risk Integrated 

Methodology (TRIM) framework (EPA, 

2006c,d). APEX is conceptually based 

on the probabilistic NAAQS exposure 

model for O3 (pNEM/O3) used in the last 

O3 NAAQS review. Since that time the 

model has been restructured, improved, 

and expanded to reflect conceptual 

advances in the science of exposure 

modeling and newer input data 

available for the model. Key 

improvements to algorithms include 

replacement of the cohort approach 

with a probabilistic sampling approach 

focused on individuals, accounting for 

fatigue and oxygen debt after exercise in 

the calculation of breathing rates, and a 

new approach for construction of 

longitudinal activity patterns for 

simulated persons. Major improvements 

to data input to the model include 

updated air exchange rates, more recent 

census and commuting data, and a 

greatly expanded daily time-activities 

database. 

APEX is a probabilistic model 

designed to explicitly model the 

numerous sources of variability that 

affect people’s exposures. APEX 

simulates the movement of individuals 

through time and space and estimates 

their exposures to O3 in indoor, outdoor, 

and in-vehicle microenvironments. The 

exposure model takes into account the 

most significant factors contributing to 

total human O3 exposure, including the 

temporal and spatial distribution of 

people and O3 concentrations 

throughout an urban area, the variation 

of O3 levels within each 

microenvironment, and the effects of 

exertion on breathing rate in exposed 

individuals. A more detailed 

description of APEX and its application 

is presented in chapter 4 of the 2007 

Staff Paper and associated technical 

documents (EPA, 2006b,c,d). 

Several methods have been used to 

evaluate the APEX model and to 

characterize the uncertainty of the 

model estimates. These include 

conducting model evaluation, 

sensitivity analyses, and a detailed 

uncertainty analysis for one urban area. 


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32The 8-hour O3 standard established in 1997 

was 0.08 ppm, but the rounding convention 

specified that the average of the 4th daily maximum 

8-hour average concentrations over a three-year 

period must be at 0.084 ppm or lower to be in 

attainment of this standard. When EPA staff 

selected alternative standards to analyze, it was 

presumed that the same type of rounding 

convention would be used, and thus alternative 

standards of 0.084, 0.074, 0.064 ppm were chosen. 

33A design value is a statistic that describes the 

air quality status of a given area relative to the level 

of the NAAQS. Design values are often based on 

multiple years of data, consistent with specification 

of the NAAQS in Part 50 of the CFR. For the 8-hour 

O3 NAAQS, the 3-year average of the annual 4thhighest daily maximum 8-hour average 

concentrations, based on the monitor within (or 

downwind of) an urban area yielding the highest 

3-year average, is the design value. 

34The quadratic rollback approach and 

evaluation of this approach are described by 

Johnson (1997), Duff et al. (1998) and Rizzo (2005, 

2006). 

35As discussed above in Section II.A, O3 health 

responses observed in controlled human exposure 

studies are associated with exposures while 

engaged in moderate or greater exertion and, 

therefore, these are the exposure measures of 

interest. The level of exertion of individuals 

engaged in particular activities is measured by an 

equivalent ventilation rate (EVR), ventilation 

normalized by body surface area (BSA, in m2), 

which is calculated as VE/BSA, where VE is the 

ventilation rate (liters/minute). Moderate and 

greater exertion levels were defined as EVR > 13 

liters/min-m2 (Whitfield et al., 1996) to correspond 

to the exertion levels measured in most subjects 

studied in the controlled human exposure studies 

that reported health effects associated with 6.6 hour 

O3 exposures. 

These are discussed fully in the 2007 

Staff Paper (section 4.6) and in Langstaff 

(2007). The uncertainty of model 

structure was judged to be of lesser 

importance than the uncertainties of the 

model inputs and parameters. Model 

structure refers to the algorithms in 

APEX designed to simulate the 

processes that result in people’s 

exposures, for example, the way that 

APEX models exposures to individuals 

when they are near roads. The 

uncertainties in the model input data 

(e.g., measurement error, ambient 

concentrations, air exchange rates, and 

activity pattern data) have been assessed 

individually, and their impact on the 

uncertainty in the modeled exposure 

estimates was assessed in a unified 

quantitative analysis with results 

expressed in the form of estimated 

confidence ranges around the estimated 

measures of exposure. This uncertainty 

analysis was conducted for one urban 

area (Boston) using the observed 2002 

O3 concentrations and 2002 

concentrations adjusted to simulate just 

meeting the current standard, with the 

expectation that the results would be 

similar for other cities and years. One 

significant source of uncertainty, due to 

limitations in the database used to 

model peoples’ daily activities, was not 

included in the unified analysis, and 

was assessed through separate 

sensitivity analyses. This analysis 

indicates that the uncertainty of the 

exposure results is relatively small. For 

example, 95 percent uncertainty 

intervals were calculated for the APEX 

estimates of the percent of children or 

asthmatic children with exposures 

above 0.060, 0.070, or 0.080 ppm under 

moderate exertion, for two air quality 

scenarios (current 2002 and 2002 

adjusted to simulate just meeting the 

current standard) in Boston (Langstaff, 

2007, Tables 26 and 27). The 95 percent 

uncertainty intervals for this set of 12 

exposure estimates indicate the 

possibility of underpredictions of the 

exposure estimates ranging from 3 to 25 

percent of the modeled estimates, and 

overpredictions ranging from 4 to 11 

percent of the estimates. For example, 

APEX estimates the percent of asthmatic 

children with exposures above 0.070 

ppm under moderate exertion to be 24 

percent, for Boston 2002 O3

concentrations adjusted to simulate just 

meeting the current standard. The 95 

percent uncertainty interval for this 

estimate is 23¥30 percent, or ¥4 to +25 

percent of the estimate. These 

uncertainty intervals do not include the 

uncertainty engendered by limitations 

of the activity database, which is in the 

range of one to ten percent. 

The exposure periods modeled here 

are the O3 seasons in 2002, 2003, and 

2004. The O3 season in each area 

includes the period of the year where 

elevated O3 levels tend to be observed 

and for which routine hourly O3

monitoring data are available. Typically 

this period spans from March or April 

through September or October, or in 

some areas, spanning the entire year. 

Three years were modeled to reflect the 

substantial year-to-year variability that 

occurs in O3 levels and related 

meteorological conditions, and because 

the standard is specified in terms of a 

three-year period. The year-to-year 

variability observed in O3 levels is due 

to a combination of different weather 

patterns and the variation in emissions 

of O3 precursors. Nationally, 2002 was 

a relatively high year with respect to the 

4th highest daily maximum 8-hour O3

levels observed in urban areas across the 

U.S. (EPA, 2007b, Figure 2–16), with the 

mean of the distribution of O3 levels for 

the urban monitors being in the upper 

third among the years 1990 through 

2006. In contrast, on a national basis, 

2004 is the lowest year on record 

through 2006 for this same air quality 

statistic, and 8-hour daily maximum O3

levels observed in most, but not all of 

the 12 urban areas included in the 

exposure and risk analyses were 

relatively low compared to other recent 

years. The 4th highest daily maximum 

8-hour O3 levels observed in 2003 in the 

12 urban areas and nationally generally 

were between those observed in 2002 

and 2004. 

Regulatory scenarios examined in the 

2008 rulemaking include the then 

current 0.08 ppm, average of the 4th 

daily maximum 8-hour averages over a 

three year period standard; standards 

with the same form but with alternative 

levels of 0.080, 0.074, 0.070, and 0.064 

ppm; standards specified as the average 

of the 3rd highest daily maximum 8- 

hour averages over a three year period 

with alternative levels of 0.084 and 

0.074 ppm; and a standard specified as 

the average of the 5th highest daily 

maximum 8-hour averages over a three 

year period with a level of 0.074 ppm.32

The then current standard used a 

rounding convention that allows areas 

to have an average of the 4th daily 

maximum 8-hour averages as high as 

0.084 ppm and still meet the standard. 

All alternative standards analyzed were 

intended to reflect improved precision 

in the measurement of ambient 

concentrations (in ppm), where the 

precision would extend to three instead 

of two decimal places. 

The then current standard and all 

alternative standards were modeled 

using a quadratic rollback approach to 

adjust the hourly concentrations 

observed in 2002–2004 to yield a design 

value 33 corresponding to the standard 

being analyzed. The quadratic rollback 

technique reduces higher concentrations 

more than lower concentrations near 

ambient background levels.34 This 

procedure was considered in a 

sensitivity analysis in the 1997 review 

of the O3 standard and has been shown 

to be more realistic than a linear, 

proportional rollback method, where all 

of the ambient concentrations are 

reduced by the same factor. 

c. Exposure Estimates and Key 

Observations 

The exposure assessment, which 

provides estimates of the number of 

people exposed to different levels of 

ambient O3 while at specified exertion 

levels,35 serve two purposes. First, the 

entire range of modeled personal 

exposures to ambient O3 is an essential 

input to the portion of the health risk 

assessment based on exposure-response 

functions from controlled human 

exposure studies, discussed in the next 

section. Second, estimates of personal 

exposures to ambient O3 concentrations 

at and above specific benchmark levels 

provide some perspective on the public 


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36The full range of quantitative exposure 

estimates associated with just meeting the 0.084 

ppm and alternative O3 standards are presented in 

chapter 4 and Appendix 4A of the 2007 Staff Paper. 

health impacts of health effects that 

cannot currently be evaluated in 

quantitative risk assessments that may 

occur at current air quality levels, and 

the extent to which such impacts might 

be reduced by meeting the current and 

alternative standards. This is especially 

true when there are exposure levels at 

which it is known or can reasonably be 

inferred that specific O3-related health 

effects are occurring. In this notice, 

exposures at and above these 

benchmark concentrations are referred 

to as ‘‘exposures of concern.’’ 

It is important to note that although 

the analysis of ‘‘exposures of concern’’ 

was conducted using three discrete 

benchmark levels (i.e., 0.080, 0.070, and 

0.060 ppm), the concept is more 

appropriately viewed as a continuum 

with greater confidence and less 

uncertainty about the existence of 

health effects at the upper end and less 

confidence and greater uncertainty as 

one considers increasingly lower O3

exposure levels. The EPA recognizes 

that there is no sharp breakpoint within 

the continuum ranging from at and 

above 0.080 ppm down to 0.060 ppm. In 

considering the concept of exposures of 

concern, it is important to balance 

concerns about the potential for health 

effects and their severity with the 

increasing uncertainty associated with 

our understanding of the likelihood of 

such effects at lower O3 levels. 

Within the context of this continuum, 

estimates of exposures of concern at 

discrete benchmark levels provide some 

perspective on the public health 

impacts of O3-related health effects that 

have been demonstrated in controlled 

human exposure and toxicological 

studies but cannot be evaluated in 

quantitative risk assessments, such as 

lung inflammation, increased airway 

responsiveness, and changes in host 

defenses. They also help in 

understanding the extent to which such 

impacts have the potential to be reduced 

by meeting the current and alternative 

standards. In the selection of specific 

benchmark concentrations for this 

analysis, staff first considered the 

exposure level of 0.080 ppm, at which 

there is a substantial amount of 

controlled human exposure evidence 

demonstrating a range of O3-related 

health effects including lung 

inflammation and airway 

responsiveness in healthy individuals. 

Thus, as in the 1997 review, this level 

was selected as a benchmark level for 

this assessment of exposures of concern. 

Evidence newly available in this review 

is the basis for identifying additional, 

lower benchmark levels of 0.070 and 

0.060 ppm for this assessment. 

More specifically, as discussed above 

in section II.A.2, evidence available 

from controlled human exposure and 

epidemiological studies indicates that 

people with asthma have larger and 

more serious effects than healthy 

individuals, including lung function, 

respiratory symptoms, increased airway 

responsiveness, and pulmonary 

inflammation, which has been shown to 

be a more sensitive marker than lung 

function responses. Further, a 

substantial new body of evidence from 

epidemiological studies shows 

associations with serious respiratory 

morbidity and cardiopulmonary 

mortality effects at O3 levels that extend 

below 0.080 ppm. Additional, but very 

limited new evidence from controlled 

human exposure studies shows lung 

function decrements and respiratory 

symptoms in healthy subjects at an O3

exposure level of 0.060 ppm. The 

selected benchmark level of 0.070 ppm 

reflects the new information that 

asthmatics have larger and more serious 

effects than healthy people and 

therefore controlled human exposure 

studies done with healthy subjects may 

underestimate effects in this group, as 

well as the substantial body of 

epidemiological evidence of 

associations with O3 levels below 0.080 

ppm. The selected benchmark level of 

0.060 ppm additionally reflects the very 

limited new evidence from controlled 

human exposure studies that show lung 

function decrements and respiratory 

symptoms in some healthy subjects at 

the 0.060 ppm exposure level, 

recognizing that asthmatics are likely to 

have more serious responses and that 

lung function is not likely to be as 

sensitive a marker for O3 effects as is 

lung inflammation. 

The estimates of exposures of concern 

were reported in terms of both ‘‘people 

exposed’’ (the number and percent of 

people who experience a given level of 

O3 concentrations, or higher, at least one 

time during the O3 season in a given 

year) and ‘‘occurrences of exposure’’ (the 

number of times a given level of 

pollution is experienced by the 

population of interest, expressed in 

terms of person-days of occurrences). 

Estimating exposures of concern is 

important because it provides some 

indication of the potential public health 

impacts of a range of O3-related health 

outcomes, such as lung inflammation, 

increased airway responsiveness, and 

changes in host defenses. These 

particular health effects have been 

demonstrated in controlled human 

exposure studies of healthy individuals 

to occur at levels as low as 0.080 ppm 

O3, but have not been evaluated at lower 

levels in controlled human exposure 

studies. The EPA did not include these 

effects in the quantitative risk 

assessment due to a lack of adequate 

information on the exposure-response 

relationships. 

The 1997 O3 NAAQS review 

estimated exposures associated with 

1-hour heavy exertion, 1-hour moderate 

exertion, and 8-hour moderate exertion 

for children, outdoor workers, and the 

general population. The EPA’s analysis 

in the 1997 Staff Paper showed that 

exposure estimates based on the 8-hour 

moderate exertion scenario for children 

yielded the largest number of children 

experiencing exposures at or above 

exposures of concern. Consequently, 

EPA chose to focus on the 8-hour 

moderate and greater exertion exposures 

in all and asthmatic school age children 

in the current exposure assessment. 

While outdoor workers and other adults 

who engage in moderate or greater 

exertion for prolonged durations while 

outdoors during the day in areas 

experiencing elevated O3 concentrations 

also are at risk for experiencing 

exposures associated with O3-related 

health effects, EPA did not focus on 

quantitative estimates for these 

populations due to the lack of 

information about the number of 

individuals who regularly work or 

exercise outdoors. Thus, the exposure 

estimates presented here and in the 

2007 Staff Paper are most useful for 

making relative comparisons across 

alternative air quality scenarios and do 

not represent the total exposures in all 

children or other groups within the 

general population associated with the 

air quality scenarios. 

Population exposures to O3 were 

estimated in 12 urban areas for 2002, 

2003, and 2004 air quality, and also 

using O3 concentrations adjusted to just 

meet the then current and several 

alternative standards. The estimates of 

8-hour exposures of concern at and 

above benchmark levels of 0.080, 0.070, 

and 0.060 ppm aggregated across all 12 

areas are shown in Table 1 for air 

quality scenarios just meeting the 

current and four alternative 8-hour 

average standards.36 Table 1 provides 

estimates of the number and percent of 

school age children and asthmatic 

school age children exposed, with daily 

8-hour maximum exposures at or above 

each O3 benchmark level of exposures of 

concern, while at intermittent moderate 

or greater exertion and based on O3

concentrations observed in 2002 and 


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2004. Table 1 summarizes estimates for 

2002 and 2004 because these years 

reflect years that bracket relatively 

higher and lower O3 levels, with year 

2003 generally containing O3 levels in 

between when considering the 12 urban 

areas modeled. This table also reports 

the percent change in the number of 

persons exposed when a given 

alternative standard is compared with 

the then current standard. 

Key observations important in 

comparing exposure estimates 

associated with just meeting the current 

NAAQS and alternative standards under 

consideration include: 

(1) As shown in Table 6–1 of the 2007 

Staff Paper, the patterns of exposure in 

terms of percentages of the population 

exceeding a given exposure level are 

very similar for the general population 

and for asthmatic and all school age 

(5–18) children, although children are 

about twice as likely to be exposed, 

based on the percent of the population 

exposed, at any given level. 

(2) As shown in Table 1 below, the 

number and percentage of asthmatic and 

all school-age children aggregated across 

the 12 urban areas estimated to 

experience one or more exposures of 

concern decline from simulations of just 

meeting the then current 0.084 ppm 

standard to simulations of alternative 8- 

hour standards by varying amounts 

depending on the benchmark level, the 

population subgroup considered, and 

the year chosen. For example, the 

estimated percentage of school age 

children experiencing one or more 

exposures ≥ 0.070 ppm, while engaged 

in moderate or greater exertion, during 

an O3 season is about 18 percent of this 

population when the 0.084 ppm 

standard is met using the 2002 

simulation; this is reduced to about 12, 

4, 1, and 0.2 percent of children upon 

meeting alternative standards of 0.080, 

0.074, 0.070, and 0.064 ppm, 

respectively (all specified in terms of 

the 4th highest daily maximum 8-hour 

average), using the 2002 simulation. 

TABLE 1—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN 12 URBAN AREAS ESTIMATED TO

EXPERIENCE 8-HOUR OZONE EXPOSURES ABOVE 0.080, 0.070, AND 0.060 PPM WHILE AT MODERATE OR GREATER

EXERTION, ONE OR MORE TIMES PER SEASON, AND THE NUMBER OF OCCURRENCES ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA1 2

Benchmark levels 

of exposures of 

concern (ppm) 

8–Hour air 

quality 

standards 3

(ppm) 

All children, ages 5–18 

Aggregate for 12 urban areas 

Number of children exposed (% of all) 

[% reduction from 0.084 ppm standard] 

Asthmatic children, ages 5–18 

Aggregate for 12 urban areas 

Number of children exposed (% of group) 

[% reduction from 0.084 ppm standard] 

2002 2004 2002 2004 

0.080 .................... 0.084 700,000 (4%) 30,000 (0%) 110,000 (4%) 0 (0%) 

0.080 290,000 (2%) [70%] 10,000 (0%) [67%] 50,000 (2%) [54%] 0 (0%) 

0.074 60,000 (0%) [91%] 0 (0%) [100%] 10,000 (0%) [91%] 0 (0%) 

0.070 10,000 (0%) [98%] 0 (0%) [100%] 0 (0%) [100%] 0 (0%) 

0.064 0 (0%) [100%] 0 (0%) [100%] 0 (0%) [100%] 0 (0%) 

0.070 .................... 0.084 3,340,000 (18%) 260,000 (1%) 520,000 (20%) 40,000 (1%) 

0.080 2,160,000 (12%) [35%] 100,000 (1%) [62%] 330,000 (13%) [36%] 10,000 (0%) [75%] 

0.074 770,000 (4%) [77%] 20,000 (0%) [92%] 120,000 (5%) [77% ] 0 (0%) [100%] 

0.070 270,000 (1%) [92%] 0 (0%) [100%] 50,000 (2%) [90%] 0 (0%) [100%] 

0.064 30,000 (0.2%) [99%] 0 (0%) [100%] 10,000 (0.2%) [98% ] 0 (0%) [100%] 

0.060 .................... 0.084 7,970,000 (44%) 1,800,000 (10%) 1,210,000 (47%) 270,000 (11%) 

0.080 6,730,000 (37%) [16%] 1,050,000 (6%) [42%] 1,020,000 (40%) [16%] 150,000 (6%) [44%] 

0.074 4,550,000 (25%) [43%] 350,000 (2%) [80%] 700,000 (27%) [42%] 50,000 (2%) [81%] 

0.070 3,000,000 (16%) [62%] 110,000 (1%) [94%] 460,000 (18%) [62%] 10,000 (1%) [96%] 

0.064 950,000 (5%) [88%] 10,000 (0%) [99%] 150,000 (6%) [88%] 0 (0%) [100%] 

1 Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate ≥ 13 l-min/m2. 2 Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston, 

Los Angeles and Sacramento and March or April to September or October for the remaining urban areas. 3 All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of 

the annual 4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the 

2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 

0.084 ppm standard and selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might 

meet the specified standards. 

(3) Substantial year-to-year variability 

in exposure estimates is observed over 

the three-year modeling period. For 

example, the estimated number of 

school age children experiencing one or 

more exposures ≥ 0.070 ppm during an 

O3 season when a 0.084 ppm standard 

is met in the 12 urban areas included in 

the analysis is 3.3, 1.0, or 0.3 million for 

the 2002, 2003, and 2004 simulations, 

respectively. 

(4) There is substantial variability 

observed across the 12 urban areas in 

the percent of the population subgroups 

estimated to experience exposures of 

concern. For example, when 2002 O3

concentrations are simulated to just 

meet a 0.084 ppm standard, the 

aggregate 12 urban area estimate is 18 

percent of all school age children are 

estimated to experience O3 exposures 

≥ 0.070 ppm (Table 1 below), while the 

range of exposure estimates in the 12 

urban areas considered separately for all 

children range from 1 to 38 percent 

(EPA, 2007b, p. 4–48, Exhibit 2). There 

was also variability in exposure 

estimates among the modeled areas 

when using the 2004 air quality 

simulation for the same scenario; 

however it was reduced and ranged 

from 0 to 7 percent in the 12 urban areas 

(EPA, 2007b, p. 4–60, Exhibit 8). 

(5) Of particular note, as discussed 

above in section II.A of this notice, high 

inter-individual variability in 

responsiveness means that only a subset 

of individuals in these groups who are 

exposed at and above a given 

benchmark level would actually be 

expected to experience such adverse 

health effects. 


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37The methodology, scope, and results from the 

risk assessment conducted in the last review are 

described in Chapter 6 of the 1996 Staff Paper (EPA, 

1996) and in several technical reports (Whitfield et 

al., 1996; Whitfield, 1997) and publication 

(Whitfield et al., 1998). 

38The 9 urban study areas included in the 

exposure and risk analyses conducted during the 

last review were: Chicago, Denver, Houston, Los 

Angeles, Miami, New York City, Philadelphia, St. 

Louis, and Washington, DC. 

39The general approach used in the health risk 

assessment was described in the draft Health 

Assessment Plan (EPA, 2005d) that was released to 

the CASAC and general public in April 2005 and 

was the subject of a consultation with the CASAC 

O3 Panel on May 5, 2005. In October 2005, OAQPS 

released the first draft of the Staff Paper containing 

a chapter discussing the risk assessment and first 

draft of the Risk Assessment TSD for CASAC 

consultation and public review on December 8, 

2005. In July 2006, OAQPS released the second 

draft of the Staff Paper and second draft of the Risk 

Assessment TSD for CASAC review and public 

comment which was held by the CASAC O3 Panel 

on August 24–25, 2006. 

(6) In considering these observations, 

it is important to take into account the 

variability, uncertainties, and 

limitations associated with this 

assessment, including the degree of 

uncertainty associated with a number of 

model inputs and uncertainty in the 

model itself, as discussed above. 

2. Quantitative Health Risk Assessment 

This section discusses the approach 

used to develop quantitative health risk 

estimates associated with exposures to 

O3 building upon a more limited risk 

assessment that was conducted during 

the last review.37 As part of the 1997 

review, EPA conducted a health risk 

assessment that produced risk estimates 

for the number and percent of children 

and outdoor workers experiencing lung 

function and respiratory symptoms 

associated with O3 exposures for 9 

urban areas.38 The risk assessment for 

the 1997 review also included risk 

estimates for excess respiratory-related 

hospital admissions related to O3

concentrations for New York City. In the 

last review, the risk estimates played a 

significant role in both the staff 

recommendations and in the proposed 

and final decisions to revise the O3

standards. The health risk assessment 

conducted for the current review builds 

upon the methodology and lessons 

learned from the prior review. 

a. Overview 

The updated health risk assessment 

conducted as part of the 2008 

rulemaking includes estimates of (1) 

risks of lung function decrements in all 

and asthmatic school age children, 

respiratory symptoms in asthmatic 

children, respiratory-related hospital 

admissions, and non-accidental and 

cardiorespiratory-related mortality 

associated with recent ambient O3

levels; (2) risk reductions and remaining 

risks associated with just meeting the 

then current 0.084 ppm 8-hour O3

NAAQS; and (3) risk reductions and 

remaining risks associated with just 

meeting various alternative 8-hour O3

NAAQS in a number of example urban 

areas. This risk assessment is more fully 

described and presented in chapter 5 of 

the 2007 Staff Paper and in a technical 

support document (TSD), Ozone Health 

Risk Assessment for Selected Urban 

Areas (Abt Associates, 2007a, hereafter 

referred to as ‘‘Risk Assessment TSD’’). 

The scope and methodology for this risk 

assessment were developed over the last 

few years with considerable input from 

the CASAC O3 Panel and the public.39

The information contained in these 

documents included specific criteria for 

the selection of health endpoints, 

studies, and locations to include in the 

assessment. In a peer review letter sent 

by CASAC to the Administrator 

documenting its advice in October 2006 

(Henderson, 2006c), the CASAC O3

Panel concluded that the risk 

assessment was ‘‘well done, balanced, 

and reasonably communicated’’ and that 

the selection of health endpoints for 

inclusion in the quantitative risk 

assessment was appropriate. 

The goals of the risk assessment are: 

(1) To provide estimates of the potential 

magnitude of several morbidity effects 

and mortality associated with current O3

levels, and with meeting the then 

current 0.084 ppm standard and 

alternative 8-hour O3 standards in 

specific urban areas; (2) to develop a 

better understanding of the influence of 

various inputs and assumptions on the 

risk estimates; and (3) to gain insights 

into the distribution of risks and 

patterns of risk reductions associated 

with meeting alternative O3 standards. 

The health risk assessment is intended 

to be dependent on and reflect the 

overall weight and nature of the health 

effects evidence discussed above in 

section II.A and in more detail in the 

2006 Criteria Document and 2007 Staff 

Paper. While not independent of the 

overall evaluation of the health effects 

evidence, the quantitative health risk 

assessment provides additional insights 

regarding the relative public health 

implications associated with just 

meeting a 0.084 ppm standard and 

several alternative 8-hour standards. 

The risk assessment covers a variety 

of health effects for which there is 

adequate information to develop 

quantitative risk estimates. However, as 

noted by CASAC (Henderson, 2007) and 

in the 2007 Staff Paper, there are a 

number of health endpoints (e.g., 

increased lung inflammation, increased 

airway responsiveness, impaired host 

defenses, increased medication usage 

for asthmatics, increased emergency 

department visits for respiratory causes, 

and increased school absences) for 

which there currently is insufficient 

information to develop quantitative risk 

estimates, but which are important to 

consider in assessing the overall public 

health impacts associated with 

exposures to O3. These additional health 

endpoints are discussed above in 

section II.A.2 and are also taken into 

account in considering the level of 

exposures of concern in populations 

particularly at risk, discussed above in 

this notice. 

There are two parts to the health risk 

assessment: One based on combining 

information from controlled human 

exposure studies with modeled 

population exposure and the other 

based on combining information from 

community epidemiological studies 

with either monitored or adjusted 

ambient concentrations levels. Both 

parts of the risk assessment were 

implemented within a new probabilistic 

version of TRIM.Risk, the component of 

EPA’s Total Risk Integrated 

Methodology (TRIM) model framework 

that estimates human health risks. 

The EPA recognizes that there are 

many sources of uncertainty and 

variability in the inputs to this 

assessment and that there is significant 

variability and uncertainty in the 

resulting O3 risk estimates. As discussed 

in chapters 2, 5, and 6 of the 2007 Staff 

Paper, there is significant year-to-year 

and city-to-city variability related to the 

air quality data that affects both the 

controlled human exposure studiesbased and epidemiological studiesbased parts of the risk assessment. There 

are also uncertainties associated with 

the air quality adjustment procedure 

used to simulate just meeting various 

alternative standards. In the prior 

review, different statistical approaches 

using alternative functional forms (i.e., 

quadratic, proportional, Weibull) were 

used to reflect how O3 air quality 

concentrations have historically 

changed. Based on sensitivity analyses 

conducted in the prior review, the 

choice of alternative air quality 

adjustment procedures had only a 

modest impact on the risk estimates 

(EPA, 2007b, p. 6–20). With respect to 

uncertainties about estimated 

background concentrations, as 

discussed below and in the 2007 Staff 

Paper (section 5.4.3), alternative 

assumptions about background levels 

have a variable impact depending on the 

location, standard, and health endpoint 

analyzed. 


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40The 12 urban areas are the same urban areas 

evaluated in the exposure analysis discussed in the 

prior section. However, for most of the health 

endpoints based on findings from epidemiological 

studies, the geographic areas and populations 

examined in the health risk assessment were 

limited to those counties included in the original 

epidemiological studies that served as the basis for 

the concentration-response relationships. 

41EPA notes that the estimated level of policyrelevant background O3 used in the prior risk 

assessment was a single concentration of 0.04 ppm, 

which was the midpoint of the range of levels for 

policy-relevant background that was provided in 

the 1996 Criteria Document. 

With respect to the lung function part 

of the health risk assessment, key 

uncertainties include uncertainties in 

the exposure estimates, discussed 

above, and uncertainties associated with 

the shape of the exposure-response 

relationship, especially at levels below 

0.08 ppm, 8-hour average, where only 

very limited data are available down to 

0.04 ppm and there is an absence of data 

below 0.04 ppm (EPA, 2007b, pp. 6–20 

to 6–21). Concerning the part of the risk 

assessment based on effects reported in 

epidemiological studies, important 

uncertainties include uncertainties (1) 

surrounding estimates of the O3

coefficients for concentration-response 

relationships used in the assessment, (2) 

involving the shape of the 

concentration-response relationship and 

whether or not a population threshold 

or non-linear relationship exists within 

the range of concentrations examined in 

the studies, (3) related to the extent to 

which concentration-response 

relationships derived from studies in a 

given location and time when O3 levels 

were higher or behavior and/or housing 

conditions were different provide 

accurate representations of the 

relationships for the same locations 

with lower air quality distributions and/ 

or different behavior and/or housing 

conditions, and (4) concerning the 

possible role of co-pollutants which also 

may have varied between the time of the 

studies and the current assessment 

period. An important additional 

uncertainty for the mortality risk 

estimates is the extent to which the 

associations reported between O3 and 

non-accidental and cardiorespiratory 

mortality actually reflect causal 

relationships. 

As discussed below, some of these 

uncertainties have been addressed 

quantitatively in the form of estimated 

confidence ranges around central risk 

estimates; others are addressed through 

separate sensitivity analyses (e.g., the 

influence of alternative estimates for 

policy-relevant background levels) or 

are characterized qualitatively. For both 

parts of the health risk assessment, 

statistical uncertainty due to sampling 

error has been characterized and is 

expressed in terms of 95 percent 

credible intervals. The EPA recognizes 

that these credible intervals do not 

reflect all of the uncertainties noted 

above. 

b. Scope and Key Components 

The health risk assessment is based 

on the information evaluated in the 

2006 Criteria Document. The risk 

assessment includes several categories 

of health effects and estimates risks 

associated with just meeting a 0.084 

ppm standard and alternative 8-hour O3

NAAQS and with several individual 

recent years of air quality (i.e., 2002, 

2003, and 2004). The risk assessment 

considers the same alternative air 

quality scenarios that were examined in 

the human exposure analyses described 

above. Risk estimates were developed 

for up to 12 urban areas selected to 

illustrate the public health impacts 

associated with these air quality 

scenarios.40 As discussed above in 

section II.B.1, the selection of urban 

areas was largely determined by 

identifying areas in the U.S. which 

represented a range of geographic areas, 

population demographics, and 

climatology; with an emphasis on areas 

that did not meet the then current 0.084 

ppm 8-hour O3 NAAQS and which 

included the largest areas with O3

nonattainment problems. The selection 

criteria also included whether or not 

there were acceptable epidemiological 

studies available that reported 

concentration-response relationships for 

the health endpoints selected for 

inclusion in the assessment. 

The short-term exposure related 

health endpoints selected for inclusion 

in the quantitative risk assessment 

include those for which the 2006 

Criteria Document or the 2007 Staff 

Paper concluded that the evidence as a 

whole supports the general conclusion 

that O3, acting alone and/or in 

combination with other components in 

the ambient air pollution mix, is either 

clearly causal or is judged to be likely 

causal. Some health effects met this 

criterion of likely causality, but were 

not included in the risk assessment for 

other reasons, such as insufficient 

exposure-response data or lack of 

baseline incidence data. 

As discussed in the section above 

describing the exposure analysis, in 

order to estimate the health risks 

associated with just meeting various 

alternative 8-hour O3 NAAQS, it is 

necessary to estimate the distribution of 

hourly O3 concentrations that would 

occur under any given standard. Since 

compliance is based on a 3-year average, 

the amount of control has been applied 

to each year of data (i.e., 2002 to 2004) 

to estimate risks for a single O3 season 

or single warm O3 season, depending on 

the health effect, based on a simulation 

that adjusted each of these individual 

years so that the three year period 

would just meet the specified standard. 

Consistent with the risk assessment 

approach used in the last review, the 

risk estimates developed for both recent 

air quality levels and just meeting the 

then current 0.084 ppm standard and 

selected alternative 8-hour standards 

represent risks associated with O3 levels 

attributable to anthropogenic sources 

and activities (i.e., risk associated with 

concentrations above ‘‘policy-relevant 

background’’). Policy-relevant 

background O3 concentrations used in 

the O3 risk assessment were defined in 

chapter 2 of the 2007 Staff Paper (pp. 

2–48—2–55) as the O3 concentrations 

that would be observed in the U.S. in 

the absence of anthropogenic emissions 

of precursors (e.g., VOC, NOX, and CO) 

in the U.S., Canada, and Mexico. The 

results of a global tropospheric O3

model (GEOS–CHEM) have been used to 

estimate monthly background daily 

diurnal profiles for each of the 12 urban 

areas for each month of the O3 season 

using meteorology for the year 2001. 

Based on the results of the GEOS–CHEM 

model, the Criteria Document indicates 

that background O3 concentrations are 

generally predicted to be in the range of 

0.015 to 0.035 ppm in the afternoon, 

and they are generally lower under 

conditions conducive to man-made O3

episodes.41

This approach of estimating risks in 

excess of background is judged to be 

more relevant to policy decisions 

regarding ambient air quality standards 

than risk estimates that include effects 

potentially attributable to 

uncontrollable background O3

concentrations. Sensitivity analyses 

examining the impact of alternative 

estimates for background on lung 

function and mortality risk estimates 

have been developed and are included 

in the 2007 Staff Paper and Risk 

Assessment TSD and key observations 

are discussed below. Further, CASAC 

noted the difficulties and complexities 

associated with available approaches to 

estimating policy-relevant background 

concentrations (Henderson, 2007). 

In the first part of the risk assessment, 

lung function decrement, as measured 

by FEV1, is the only health response that 

is based on data from controlled human 

exposure studies. As discussed above, 

there is clear evidence of a causal 

relationship between lung function 

decrements and O3 exposures for school 

age children engaged in moderate 


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42As discussed above in section II.B.1, the urban 

areas were defined using the consolidated statistical 

areas definition and the total population residing in 

the 12 urban areas was approximately 88.5 million 

people. 

43For 9 of the 12 urban areas, the O3 season is 

defined as a period running from March or April 

to September or October. In 3 of the urban areas 

(Houston, Los Angeles, and Sacramento), the O3

season is defined as the entire year. 

44The geographic boundaries for the urban areas 

included in this portion of the risk assessment were 

generally matched to the geographic boundaries 

used in the epidemiological studies that served as 

the basis for the concentration-response functions. 

In most cases, the urban areas were defined as 

Continued 

exertion based on numerous controlled 

human exposure and summer camp 

field studies conducted by various 

investigators. Risk estimates have been 

developed for O3-related lung function 

decrements (measured as changes in 

FEV1) for all school age children (ages 

5 to 18) and a subset of this group, 

asthmatic school age children (ages 5 to 

18), whose average exertion over an 

8-hour period was moderate or greater. 

The exposure period and exertion level 

were chosen to generally match the 

exposure period and exertion level used 

in the controlled human exposure 

studies that were the basis for the 

exposure-response relationships. A 

combined data set including individual 

level data from the Folinsbee et al. 

(1988), Horstman et al. (1990), and 

McDonnell et al. (1991) studies, used in 

the previous risk assessment, and more 

recent data from Adams (2002, 2003a, 

2006) have been used to estimate 

probabilistic exposure-response 

relationships for 8-hour exposures 

under different definitions of lung 

function response (i.e., ≥ 10, 15, and 20 

percent decrements in FEV1). As 

discussed in the 2007 Staff Paper (p. 

5–27), while these specific controlled 

human exposure studies only included 

healthy adults aged 18–35, findings 

from other controlled human exposure 

studies and summer camp field studies 

involving school age children in at least 

six different locations in the 

northeastern United States, Canada, and 

Southern California indicated changes 

in lung function in healthy children 

similar to those observed in healthy 

adults exposed to O3 under controlled 

chamber conditions. 

Consistent with advice from CASAC 

(Henderson, 2006c), EPA has considered 

both linear and logistic functional forms 

in estimating the probabilistic exposureresponse relationships for lung function 

responses. A Bayesian Markov Chain 

Monte Carlo approach, described in 

more detail in the Risk Assessment TSD, 

has been used that incorporates both 

model uncertainty and uncertainty due 

to sample size in the combined data set 

that served as the basis for the 

assessment. The 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 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). The EPA has 

conducted a sensitivity analysis which 

examines the impact on the lung 

function risk estimates of two 

alternative choices, an 80 percent 

logistic/20 percent linear split and a 50 

percent logistic/50 percent linear split. 

As noted above, risk estimates have 

been developed for three measures of 

lung function response (i.e., ≥ 10, 15, 

and 20 percent decrements in FEV1). 

However, the 2007 Staff Paper and risk 

estimates summarized below focus on 

FEV1 decrements ≥ 15 percent for all 

school age children and ≥ 10 percent for 

asthmatic school age children, 

consistent with the advice from CASAC 

(Henderson, 2006c) that these levels of 

response represent indicators of adverse 

health effects in these populations. The 

Risk Assessment TSD and 2007 Staff 

Paper present the broader range of risk 

estimates including all three measures 

of lung function response. 

Developing risk estimates for lung 

function decrements involved 

combining probabilistic exposureresponse relationships based on the 

combined data set from several 

controlled human exposure studies with 

population exposure distributions for all 

and asthmatic school age children 

associated with recent air quality and 

air quality simulated to just meet the 

then current 0.084 ppm standard and 

alternative 8-hour O3 NAAQS based on 

the results from the exposure analysis 

described in the previous section. The 

risk estimates have been developed for 

12 large urban areas for the O3 season.42

These 12 urban areas include 

approximately 18.3 million school age 

children, of which 2.6 million are 

asthmatic school age children.43

In addition to uncertainties arising 

from sample size considerations, which 

are quantitatively characterized and 

presented as 95 percentile credible 

intervals, there are additional 

uncertainties and caveats associated 

with the lung function risk estimates. 

These include uncertainties about the 

shape of the exposure-response 

relationship, particularly at levels below 

0.080 ppm, and about policy-relevant 

background levels, for which sensitivity 

analyses have been conducted. 

Additional important caveats and 

uncertainties concerning the lung 

function portion of the health risk 

assessment include: (1) The 

uncertainties and limitations associated 

with the exposure estimates discussed 

above and (2) the inability to account for 

some factors which are known to affect 

the exposure-response relationships 

(e.g., assigning healthy and asthmatic 

children the same responses as observed 

in healthy adult subjects and not 

adjusting response rates to reflect the 

increase and attenuation of responses 

that have been observed in studies of 

lung function responses upon repeated 

exposures). A more complete discussion 

of assumptions and uncertainties is 

contained in chapter 5 of the 2007 Staff 

Paper and in the Risk Assessment TSD. 

The second part of the risk assessment 

is based on health effects observed in 

epidemiological studies. Based on a 

review of the evidence evaluated in the 

2006 Criteria Document and 2007 Staff 

Paper, as well as the criteria discussed 

in chapter 5 of the 2007 Staff Paper, the 

following categories of health endpoints 

associated with short-term exposures to 

ambient O3 concentrations were 

included in the risk assessment: 

respiratory symptoms in moderate to 

severe asthmatic children, hospital 

admissions for respiratory causes, and 

non-accidental and cardiorespiratory 

mortality. As discussed above, there is 

strong evidence of a causal relationship 

for the respiratory morbidity endpoints 

included in the risk assessment. With 

respect to nonaccidental and 

cardiorespiratory mortality, the 2006 

Criteria Document concludes that there 

is strong evidence which is highly 

suggestive of a causal relationship 

between nonaccidental and 

cardiorespiratory-related mortality and 

O3 exposures during the warm O3

season. As discussed in the 2007 Staff 

Paper (chapter 5), EPA also recognizes 

that for some of the effects observed in 

epidemiological studies, such as 

increased respiratory-related hospital 

admissions and nonaccidental and 

cardiorespiratory mortality, O3 may be 

serving as an indicator for reactive 

oxidant species in the overall 

photochemical oxidant mix and that 

these other constituents may be 

responsible in whole or part for the 

observed effects. 

Risk estimates for each health 

endpoint category were only developed 

for areas that were the same or close to 

the location where at least one 

concentration-response function for the 

health endpoint had been estimated.44


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either a single county or a few counties for this 

portion of the risk assessment. 

Thus, for respiratory symptoms in 

moderate to severe asthmatic children 

only the Boston urban area was 

included and four urban areas were 

included for respiratory-related hospital 

admissions. Nonaccidental mortality 

risk estimates were developed for 12 

urban areas and 8 urban areas were 

included for cardiorespiratory mortality. 

The concentration-response 

relationships used in the assessment are 

based on findings from human 

epidemiological studies that have relied 

on fixed-site ambient monitors as a 

surrogate for actual ambient O3

exposures. In order to estimate the 

incidence of a particular health effect 

associated with recent air quality in a 

specific county or set of counties 

attributable to ambient O3 exposures in 

excess of background, as well as the 

change in incidence corresponding to a 

given change in O3 levels resulting from 

just meeting various 8-hour O3

standards, three elements are required 

for this part of the risk assessment. 

These elements are: (1) Air quality 

information (including recent air quality 

data for O3 from ambient monitors for 

the selected location, estimates of 

background O3 concentrations 

appropriate for that location, and a 

method for adjusting the recent data to 

reflect patterns of air quality estimated 

to occur when the area just meets a 

given O3 standard); (2) relative riskbased concentration-response functions 

that provide an estimate of the 

relationship between the health 

endpoints of interest and ambient O3

concentration; and (3) annual or 

seasonal baseline health effects 

incidence rates and population data, 

which are needed to provide an estimate 

of the seasonal baseline incidence of 

health effects in an area before any 

changes in O3 air quality. 

A key component in the portion of the 

risk assessment based on 

epidemiological studies is the set of 

concentration-response functions which 

provide estimates of the relationships 

between each health endpoint of 

interest and changes in ambient O3

concentrations. Studies often report 

more than one estimated concentrationresponse function for the same location 

and health endpoint. Sometimes models 

include different sets of co-pollutants 

and/or different lag periods between the 

ambient concentrations and reported 

health responses. For some health 

endpoints, there are studies that 

estimated multicity and single-city O3

concentration-response functions. While 

the Risk Assessment TSD and chapter 5 

of the 2007 Staff Paper present a more 

comprehensive set of risk estimates, 

EPA has focused on estimates based on 

multicity studies where available. As 

discussed in chapter 5 of the 2007 Staff 

Paper, the advantages of relying more 

heavily on concentration-response 

functions based on multicity 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. Where studies 

reported different effect estimates for 

varying lag periods, consistent with the 

2006 Criteria Document, single day lag 

periods of 0 to 1 days were used for 

associations with respiratory hospital 

admissions and mortality. For mortality 

associated with exposure to O3 which 

may result over a several day period 

after exposure, distributed lag models, 

which take into account the 

contribution to mortality effects over 

several days, were used where available 

One of the most important elements 

affecting uncertainties in the 

epidemiological-based portion of the 

risk assessment is the concentrationresponse relationships used in the 

assessment. The uncertainty resulting 

from the statistical uncertainty 

associated with the estimate of the O3

coefficient in the concentrationresponse function was characterized 

either by confidence intervals or by 

Bayesian credible intervals around the 

corresponding point estimates of risk. 

Confidence and credible intervals 

express the range within which the true 

risk is likely to fall if the only 

uncertainty surrounding the O3

coefficient involved sampling error. 

Other uncertainties, such as differences 

in study location, time period (i.e., the 

years in which the study was 

conducted), and model uncertainties are 

not represented by the confidence or 

credible intervals presented, but were 

addressed by presenting estimates for 

different urban areas, by including risk 

estimates based on studies using 

different time periods and models, 

where available, and/or are discussed 

throughout section 5.3 of the 2007 Staff 

Paper. Because O3 effects observed in 

the epidemiological studies have been 

more clearly and consistently shown for 

warm season analyses, all analyses for 

this portion of the risk assessment were 

carried out for the same time period, 

April through September. 

The 2006 Criteria Document (p. 8–44) 

finds that no definitive conclusion can 

be reached with regard to the existence 

of population thresholds in 

epidemiological studies. The EPA 

recognizes, however, the possibility that 

thresholds for individuals may exist for 

reported associations at fairly low levels 

within the range of air quality observed 

in the studies, but not be detectable as 

population thresholds in 

epidemiological analyses. Based on the 

2006 Criteria Document’s conclusions, 

EPA judged and CASAC concurred, that 

there is insufficient evidence to support 

use of potential population threshold 

levels in the quantitative risk 

assessment. However, EPA recognizes 

that there is increasing uncertainty 

about the concentration-response 

relationship at lower concentrations 

which is not captured by the 

characterization of the statistical 

uncertainty due to sampling error. 

Therefore, the risk estimates for 

respiratory symptoms in moderate to 

severe asthmatic children, respiratoryrelated hospital admissions, and 

premature mortality associated with 

exposure to O3 must be considered in 

light of uncertainties about whether or 

not these O3-related effects occur in 

these populations at very low O3

concentrations. 

With respect to variability within this 

portion of the risk assessment, there is 

variability among concentrationresponse functions describing the 

relation between O3 and both 

respiratory-related hospital admissions 

and nonaccidental and cardiorespiratory 

mortality across urban areas. This 

variability is likely due to differences in 

population (e.g., age distribution), 

population activities that affect 

exposure to O3 (e.g., use of air 

conditioning), levels and composition of 

co-pollutants, baseline incidence rates, 

and/or other factors that vary across 

urban areas. The risk assessment 

incorporates some of the variability in 

key inputs to the analysis by using 

location-specific inputs (e.g., locationspecific concentration-response 

functions, baseline incidence rates, and 

air quality data). Although spatial 

variability in these key inputs across all 

U.S. locations has not been fully 

characterized, variability across the 

selected locations is imbedded in the 

analysis by using, to the extent possible, 

inputs specific to each urban area. 

c. Risk Estimates and Key Observations 

The 2007 Staff Paper (chapter 5) and 

Risk Assessment TSD present risk 

estimates associated with just meeting 

the then current 0.084 ppm standard 

and several alternative 8-hour 

standards, as well as three recent years 

of air quality as represented by 2002, 


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45 Due to time constraints, lung function risk 

estimates for asthmatic school age children were 

developed for only 5 of the 12 urban areas, and the 

areas were selected to represent different 

geographic regions. The 5 areas were: Atlanta, 

Chicago, Houston, Los Angeles, and New York City. 

2003, and 2004 monitoring data. As 

discussed in the exposure analysis 

section above, there is considerable cityto-city and year-to-year variability in the 

O3 levels during this period, which 

results in significant variability in both 

portions of the health risk assessment. 

In the 1997 risk assessment, risks for 

lung function decrements associated 

with 1-hour heavy exertion, 1-hour 

moderate exertion, and 8-hour moderate 

exertion exposures were estimated. 

Since the 8-hour moderate exertion 

exposure scenario for children clearly 

resulted in the greatest health risks in 

terms of lung function decrements, EPA 

chose to include only the 8-hour 

moderate exertion exposures in the risk 

assessment for this health endpoint. 

Thus, the risk estimates presented here 

and in the 2007 Staff Paper are most 

useful for making relative comparisons 

across alternative air quality scenarios 

and do not represent the total risks for 

lung function decrements in children or 

other groups within the general 

population associated with any of the 

air quality scenarios. Thus, some 

outdoor workers and adults engaged in 

moderate exertion over multi-hour 

periods (e.g., 6–8 hour exposures) also 

would be expected to experience similar 

lung function decrements. However, the 

percentage of each of these other 

subpopulations expected to experience 

these effects is expected to be smaller 

than all school age children who tend to 

spend more hours outdoors while active 

based on the exposure analyses 

conducted during the prior review. 

Table 2 presents a summary of the 

risk estimates for lung function 

decrements for the 0.084 ppm standard 

set in 1997 and several alternative 8- 

hour standard levels with the same 

form. 

TABLE 2—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN SEVERAL URBAN AREAS ESTIMATED TO EXPERIENCE MODERATE OR GREATER LUNG FUNCTION RESPONSES ONE OR MORE TIMES PER SEASON

ASSOCIATED WITH 8-HOUR OZONE EXPOSURES ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS

BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA 1 2

8-Hour air quality 

standards 3

All children, ages 5–18 FEV1 ≥ 15 percent 

Aggregate for 12 urban areas 

Number of children affected (% of all) 

[% reduction from 0.084 ppm standard] 

Asthmatic Children, ages 5–18 FEV1 ≥ 10 percent 

Aggregate for 5 urban areas 

Number of children affected (% of group) 

[% reduction from 0.084 ppm standard] 

2002 2004 2002 2004 

0.084 ppm (Standard set in 

1997).

610,000 (3.3%) 230,000 (1.2%) 130,000 (7.8%) 70,000 (4.2%) 

0.080 ppm ......................... 490,000 (2.7%) [20% reduction] 180,000 (1.0%) [22% reduction] NA4 NA 

0.074 ppm ......................... 340,000 (1.9%) [44% reduction] 130,000 (0.7%) [43% reduction] 90,000 (5.0%) [31% reduction] 40,000 (2.7%) [43% reduction] 

0.070 ppm ......................... 260,000 (1.5%) [57% reduction] 100,000 (0.5%) [57% reduction] NA NA 

0.064 ppm ......................... 180,000 (1.0%) [70% reduction] 70,000 (0.4%) [70% reduction] 50,000 (3.0%) [62% reduction] 20,000 (1.5%) [71% reduction] 

1Associated with exposures while engaged in moderate or greater exertion, which is defined as having an 8-hour average equivalent ventilation rate ≥ 13 l-min/m 2. 2Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, 

Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, 

New York). Estimates are for the O3 season which is all year in Houston, Los Angeles and Sacramento and March or April to September or October for the remaining urban areas. 3All standards summarized here have the same form as the 8-hour standard set in 1997, which is specified as the 3-year average of the annual 4th highest daily maximum 8-hour average concentrations. As described in the 2007 Staff Paper (section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard set in 1997 and selected alternative standards. These 

simulations do not represent predictions of when, whether, or how areas might meet the specified standards 4 NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic school age children population. 

The estimates are for the aggregate 

number and percent of all school age 

children across 12 urban areas and the 

aggregate number and percent of 

asthmatic school age children across 5 

urban areas 45 who are estimated to have 

at least 1 moderate or greater lung 

function response (defined as FEV1 ≥ 15 

percent in all children and ≥ 10 percent 

in asthmatic children) associated with 

8-hour exposures to O3 while engaged in 

moderate or greater exertion on average 

over the 8-hour period. The lung 

function risk estimates summarized in 

Table 2 illustrate the year-to-year 

variability in both remaining risk 

associated with a relatively high year 

(i.e., based on adjusting 2002 O3 air 

quality data) and relatively low year 

(based on adjusting 2004 O3 air quality 

data) as well as the year-to-year 

variability in the risk reduction 

estimated to occur associated with 

various alternative standards relative to 

just meeting the then current 0.084 ppm 

standard. For example, it is estimated 

that about 610,000 school age children 

(3.2 percent of school age children) 

would experience 1 or more moderate 

lung function decrements for the 12 

urban areas associated with O3 levels 

just meeting a 0.084 ppm standard 

based on 2002 air quality data compared 

to 230,000 (1.2 percent of children) 

associated with just meeting a 0.084 

ppm standard based on 2004 air quality 

data. 

As discussed in the 2007 Staff Paper, 

a child may experience multiple 

occurrences of a lung function response 

during the O3 season. For example, 

upon meeting a 0.084 ppm 8-hour 

standard, the median estimates are that 

about 610,000 children would 

experience a moderate or greater lung 

function response 1 or more times for 

the aggregate of the 12 urban areas over 

a single O3 season (based on the 2002 

simulation), and that there would be 

almost 3.2 million total occurrences. 

Thus, on average it is estimated that 

there would be about 5 occurrences per 

O3 season per responding child for air 

quality just meeting a 0.084 ppm 8-hour 


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standard across the 12 urban areas. 

While the estimated number of 

occurrences per O3 season is lower 

when based on the 2004 simulation than 

for the 2002 simulation, the estimated 

number of occurrences per responding 

child is similar. The EPA recognizes 

that some children in the population 

might have only 1 or 2 occurrences 

while others may have 6 or more 

occurrences per O3 season. Risk 

estimates based on adjusting 2003 air 

quality to simulate just meeting the a 

0.084 ppm standard and alternative 

8-hour standards are intermediate to the 

estimates presented in Table 2 above in 

this notice and are presented in the 

2007 Staff Paper (chapter 5) and Risk 

Assessment TSD. 

For just meeting a 0.084 ppm 8-hour 

standard, Table 5–8 in the 2007 Staff 

Paper shows that median estimates 

across the 12 urban areas for all school 

age children experiencing 1 or more 

moderate lung function decrements 

ranges from 0.9 to 5.4 percent based on 

the 2002 simulation and from 0.8 to 2.2 

percent based on the 2004 simulation. 

Risk estimates for each urban area 

included in the assessment, for each of 

the three years analyzed, and for 

additional alternative standards are 

presented in chapter 5 of the 2007 Staff 

Paper and in the Risk Assessment TSD. 

For just meeting a 0.084 ppm 8-hour 

standard, the median estimates across 

the 5 urban areas for asthmatic school 

age children range from 3.4 to 10.9 

percent based on the 2002 simulation 

and from 3.2 to 6.9 percent based on the 

2004 simulation. 

Key observations important in 

comparing estimated lung function risks 

associated with just meeting the 0.084 

ppm NAAQS and alternative standards 

under consideration include: 

(1) As discussed above, there is 

significant year to year variability in the 

range of median estimates of the number 

of school age children (ages 5–18) 

estimated to experience at least one 

FEV1 decrement ≥ 15 percent due to 

8-hour O3 exposures across the 12 urban 

areas analyzed, and similarly across the 

5 urban areas analyzed for asthmatic 

school age children (ages 5–18) 

estimated to experience at least one 

FEV1 decrement ≥ 10 percent, when 

various 8-hour standards are just met. 

(2) For asthmatic school age children, 

the median estimates of occurrences of 

FEV1 decrements ≥ 10% range from 

52,000 to nearly 510,000 responses 

associated with just meeting a 0.084 

ppm standard (based on the 2002 

simulation) and range from 61,000 to 

about 240,000 occurrences (based on the 

2004 simulation). These risk estimates 

would be reduced to a range of 14,000 

to about 275,000 occurrences (2002 

simulation) and to about 18,000 to 

nearly 125,000 occurrences (2004 

simulation) upon just meeting the most 

stringent alternative 8-hour standard 

(0.064 ppm, 4th highest). The average 

number of occurrences per asthmatic 

child in an O3 season ranged from about 

6 to 11 associated with just meeting a 

0.084 ppm standard (2002 simulation). 

The average number of occurrences per 

asthmatic child ranged from 4 to 12 

upon meeting the most stringent 

alternative examined (0.064 ppm, 4thhighest) based on the 2002 simulation. 

The number of occurrences per 

asthmatic child is similar for the 

scenarios based on the 2004 simulation. 

As discussed above, several 

epidemiological studies have reported 

increased respiratory morbidity 

outcomes (e.g., respiratory symptoms in 

moderate to severe asthmatic children, 

respiratory-related hospital admissions) 

and increased nonaccidental and 

cardiorespiratory mortality associated 

with exposure to ambient O3

concentrations. The results and key 

observations from this portion of the 

risk assessment are presented below: 

(1) Estimates for increased respiratory 

symptoms (i.e., chest tightness, 

shortness of breath, and wheeze) in 

moderate/severe asthmatic children 

(ages 0–12) were developed for the 

Boston urban area only. The median 

estimated number of days involving 

chest tightness (using the concentrationresponse relationship with only O3 in 

the model) is about 6,100 (based on the 

2002 simulation) and about 4,500 (based 

on the 2004 simulation) upon meeting a 

0.084 ppm 8-hour standard and this is 

reduced to about 4,600 days (2002 

simulation) and 3,100 days (2004 

simulation) upon meeting the most 

stringent alternative examined (0.064 

ppm, 4th-highest daily maximum 8- 

hour average). This corresponds to 11 

percent (2002 simulation) and 8 percent 

(2004 simulation) of total incidence of 

chest tightness upon meeting a 0.084 

ppm 8-hour standard and to about 8 

percent (2002 simulation) and 5.5 

percent (2004 simulation) of total 

incidence of chest tightness upon 

meeting a 0.064 ppm, 4th-highest daily 

maximum 8-hour average standard. 

Similar patterns of effects and 

reductions in effects are observed for 

each of the respiratory symptoms 

examined. 

(2) The 2007 Staff Paper and Risk 

Assessment TSD present unscheduled 

hospital admission risk estimates for 

respiratory illness and asthma in New 

York City associated with short-term 

exposures to O3 concentrations in 

excess of background levels from April 

through September for several recent 

years (2002, 2003, and 2004) and upon 

just meeting a 0.084 ppm standard and 

alternative 8-hour standards based on 

simulating O3 levels using 2002–2004 

O3 air quality data. For total respiratory 

illness, EPA estimates about 6.4 cases 

per 100,000 relevant population (2002 

simulation) and about 4.6 cases per 

100,000 relevant population (2004 

simulation), which represents 1.5 

percent (2002 simulation) and 1.0 

percent (2004 simulation) of total 

incidence or about 510 cases (2002 

simulation) and about 370 cases (2004 

simulation) upon just meeting a 0.084 

ppm 8-hour standard. For asthmarelated hospital admissions, which are a 

subset of total respiratory illness 

admissions, the estimates are about 5.5 

cases per 100,000 relevant population 

(2002 simulation) and about 3.9 cases 

per 100,000 relevant population (2004 

simulation), which represents about 3.3 

percent (2002 simulation) and 2.4 

percent (2004 simulation) of total 

incidence or about 440 cases (2002) and 

about 310 cases (2004) for this same air 

quality scenario. 

For increasingly more stringent 

alternative 8-hour standards, there is a 

gradual reduction in respiratory illness 

cases per 100,000 relevant population 

from 6.4 cases per 100,000 upon just 

meeting a 0.084 ppm 8-hour standard to 

4.6 cases per 100,000 under the most 

stringent 8-hour standard (i.e., 0.064 

ppm, average 4th-highest daily 

maximum) analyzed based on the 2002 

simulation. Similarly, based on the 2004 

simulation there is a gradual reduction 

from 4.6 cases per 100,000 relevant 

population upon just meeting a 0.084 

ppm 8-hour standard to 3.0 cases per 

100,000 under a 0.064 ppm, average 4thhighest daily maximum standard. 

Additional respiratory-related 

hospital admission estimates for three 

other locations are provided in the Risk 

Assessment TSD. The EPA notes that 

the concentration-response functions for 

each of these locations examined 

different outcomes in different age 

groups (e.g., > age 30 in Los Angeles, 

> age 64 in Cleveland and Detroit, vs. all 

ages in New York City), making 

comparison of the risk estimates across 

the areas very difficult. 

(3) Based on the median estimates for 

incidence for nonaccidental mortality 

(based on the Bell et al. (2004) 95 cities 

concentration-response function), 

meeting the most stringent standard 

(0.064 ppm) is estimated to reduce 

mortality by 40 percent of what it would 

be associated with just meeting a 0.084 

ppm standard (based on the 2002 

simulation). The patterns for 

cardiorespiratory mortality are similar. 


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46For example, assuming lower background 

levels resulted in increased estimates of nonaccidental mortality incidence per 100,000 that 

were often 50 to 100 percent greater than the base 

case estimates; assuming higher background levels 

resulted in decreased estimates of non-accidental 

mortality incidence per 100,000 that were less than 

the base case estimates by 50 percent or more in 

many of the areas. 

The aggregate O3-related 

cardiorespiratory mortality upon just 

meeting the most stringent standard 

shown is estimated to be about 42 

percent of what it would be upon just 

meeting a 0.084 ppm standard, using 

simulated O3 concentrations that just 

meet a 0.084 ppm standard and 

alternative 8-hour standards based on 

the 2002 simulation. Using the 2004 

simulation, the corresponding 

reductions show a similar pattern but 

are somewhat greater. 

(4) Much of the contribution to the 

risk estimates for non-accidental and 

cardiorespiratory mortality upon just 

meeting a 0.084 ppm 8-hour standard is 

associated with 24-hour O3

concentrations between background and 

0.040 ppm. Based on examining 

relationships between 24-hour 

concentrations averaged across the 

monitors within an urban area and 

8-hour daily maximum concentrations, 

8-hour daily maximum levels at the 

highest monitor in an urban area 

associated with these averaged 24-hour 

levels are generally about twice as high 

as the 24-hour levels. Thus, most O3- 

related nonaccidental mortality is 

estimated to occur when O3

concentrations are between background 

and when the highest monitor in the 

urban area is at or below 0.080 ppm, 

8-hour average concentration. 

The discussion below highlights 

additional observations and insights 

from the O3 risk assessment, together 

with important uncertainties and 

limitations. 

(1) As discussed in the 2007 Staff 

Paper (section 5.4.5), EPA has greater 

confidence in relative comparisons in 

risk estimates between alternative 

standards than in the absolute 

magnitude of risk estimates associated 

with any particular standard. 

(2) Significant year-to-year variability 

in O3 concentrations combined with the 

use of a 3-year design value to 

determine the amount of air quality 

adjustment to be applied to each year 

analyzed, results in significant year-toyear variability in the annual health risk 

estimates upon just meeting various 8- 

hour standards. 

(3) There is noticeable city-to-city 

variability in estimated O3-related 

incidence of morbidity and mortality 

across the 12 urban areas analyzed for 

both recent years of air quality and for 

air quality adjusted to simulate just 

meeting a 0.084 ppm standard and 

selected potential alternative standards. 

This variability is likely due to 

differences in air quality distributions, 

differences in exposure related to many 

factors including varying activity 

patterns and air exchange rates, 

differences in baseline incidence rates, 

and differences in susceptible 

populations and age distributions across 

the 12 urban areas. 

(4) With respect to the uncertainties 

about estimated policy-relevant 

background concentrations, as 

discussed in the 2007 Staff Paper 

(section 5.4.3), alternative assumptions 

about background levels had a variable 

impact depending on the health effect 

considered and the location and 

standard analyzed in terms of the 

absolute magnitude and relative changes 

in the risk estimates. There was 

relatively little impact on either 

absolute magnitude or relative changes 

in lung function risk estimates due to 

alternative assumptions about 

background levels. With respect to O3- 

related non-accidental mortality, while 

notable differences (i.e., greater than 50 

percent) 46 were observed for 

nonaccidental mortality in some areas, 

particularly for more stringent 

standards, the overall pattern of 

estimated reductions, expressed in 

terms of percentage reduction relative to 

the 0.084 ppm standard, was 

significantly less impacted. 

C. Reconsideration of the Level of the 

Primary Standard 

1. Evidence and Exposure/Risk-Based 

Considerations 

The approach used in the 2007 Staff 

Paper as a basis for staff 

recommendations on standard levels 

builds upon and broadens the general 

approach used by EPA in the 1997 

review. This approach reflects the more 

extensive and stronger body of evidence 

available for the 2008 rulemaking on a 

broader range of health effects 

associated with exposure to O3, 

including: (1) Additional respiratoryrelated endpoints; (2) new information 

about the mechanisms underlying 

respiratory morbidity effects supporting 

a judgment that the link between O3

exposure and these effects is causal; (3) 

newly identified cardiovascular-related 

health endpoints from animal 

toxicology and controlled human 

exposures studies that are highly 

suggestive that O3 can directly or 

indirectly contribute to cardiovascular 

morbidity, and (4) new U.S. multicity 

time series studies, single city studies, 

and several meta-analyses of these 

studies that provide relatively strong 

evidence for associations between shortterm O3 exposures and all-cause 

(nonaccidental) mortality, at levels 

below the current primary standard: As 

well as (5) a substantial body of new 

evidence of increased susceptibility in 

people with asthma and other lung 

diseases. In evaluating evidence-based 

and exposure/risk-based considerations, 

the 2007 Staff Paper considered: (1) The 

ranges of levels of alternative standards 

that are supported by the evidence, and 

the uncertainties and limitations in that 

evidence and (2) the extent to which 

specific levels of alternative standards 

reduce the estimated exposures of 

concern and risks attributable to O3 and 

other photochemical oxidants, and the 

uncertainties associated with the 

estimated exposure and risk reductions. 

a. Evidence-Based Considerations 

In taking into account evidence-based 

considerations, the 2007 Staff Paper 

evaluated available evidence from 

controlled human exposure studies and 

epidemiological studies, as well as the 

uncertainties and limitations in that 

evidence. In particular, it focused on the 

extent to which controlled human 

exposure studies provide evidence of 

lowest-observed-effects levels and the 

extent to which epidemiological studies 

provide evidence of associations that 

extend down to the lower levels of O3

concentrations observed in the studies 

or some indication of potential effect 

thresholds in terms of 8-hour average O3

concentrations. 

The most certain evidence of adverse 

health effects from exposure to O3

comes from the controlled human 

exposure studies, as discussed above in 

section II.A.2, and the large bulk of this 

evidence derives from studies of 

exposures at levels of 0.080 ppm and 

above. At those levels, there is 

consistent evidence of lung function 

decrements and respiratory symptoms 

in healthy young adults, as well as 

evidence of inflammation and other 

medically significant airway responses. 

Two studies by Adams (2002, 2006), 

newly available for consideration in the 

2008 rulemaking, are the only available 

controlled human exposure studies that 

examine respiratory effects associated 

with prolonged O3 exposures at levels 

below 0.080 ppm, which was the lowest 

exposure level that had been examined 

in the 1997 review. As discussed above 

in section II.A.2.a.i.(a)(i), the Adams 

(2006) study investigated a range of 

exposure levels, including 0.060 and 

0.080 ppm O3, and analyzed hour-byhour changes in responses, including 

lung function (measured in term of 

decrements in FEV1) and respiratory 


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symptoms, to investigate the effects of 

different patterns of exposure. At the 

0.060 ppm exposure level, the author 

reported no statistically significant 

differences for lung function 

decrements; statistically significant 

responses were reported for total 

subjective respiratory symptoms toward 

the end of the exposure period for one 

exposure pattern. The EPA’s reanalysis 

(Brown, 2007) of the data from the 

Adams (2006) study addressed the more 

fundamental question of whether there 

were statistically significant changes in 

lung function from a 6.6-hour exposure 

to 0.060 ppm O3 versus filtered air and 

used a standard statistical method 

appropriate for a simple paired 

comparison. This reanalysis found small 

group mean lung function decrements 

in healthy adults at the 0.060 ppm 

exposure level to be statistically 

significantly different from responses 

associated with filtered air exposure. 

Moreover, the Adams’ studies also 

report a small percentage of subjects (7 

to 20 percent) experienced lung 

function decrements (> 10 percent) at 

the 0.060 ppm exposure level. This is a 

concern because, for active healthy 

people, moderate levels of functional 

responses (e.g., FEV1 decrements of 

> 10% but < 20%) and/or moderate 

respiratory symptom responses would 

likely interfere with normal activity for 

relatively few responsive individuals. 

However, for people with lung disease, 

even moderate functional or 

symptomatic responses would likely 

interfere with normal activity for many 

individuals, and would likely result in 

more frequent use of medication. 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. Therefore, the 

results of the Adams studies which 

indicate that a small percentage of 

healthy, non-asthmatic subjects are 

likely to experience FEV1 decrements 

≥ 10% when exposed to 0.060 ppm O3

have implications for setting a standard 

that protects public health, including 

the health of sensitive populations such 

as asthmatics, with an adequate margin 

of safety. 

In considering these most recent 

controlled human exposure studies, the 

2007 Staff Paper concluded that these 

studies provide evidence of a lowestobserved-effects level of 0.060 ppm for 

potentially adverse lung function 

decrements and respiratory symptoms 

in some healthy adults while at 

prolonged moderate exertion. It further 

concluded that since people with 

asthma, particularly children, have been 

found to be more sensitive and to 

experience larger decrements in lung 

function in response to O3 exposures 

than would healthy adults, the 0.060 

ppm exposure level also can be 

interpreted as representing a level likely 

to cause adverse lung function 

decrements and respiratory symptoms 

in children with asthma and more 

generally in people with respiratory 

disease. 

In considering controlled human 

exposure studies of pulmonary 

inflammation, airway responsiveness, 

and impaired host defense capabilities, 

discussed above in section II.A.2.a.i, the 

2007 Staff Paper noted that these studies 

provide evidence of a lowest-observedeffects level for such effects in healthy 

adults at prolonged moderate exertion of 

0.080 ppm, the lowest level tested. 

Moreover there is no evidence that the 

0.080 ppm level is a threshold for these 

effects. Studies reporting inflammatory 

responses and markers of lung injury 

have clearly demonstrated that there is 

significant variation in response of 

subjects exposed, even to O3 exposures 

at 0.080 ppm. One study showed 

notable interindividual variability in 

young healthy adult subjects in most of 

the inflammatory and cellular injury 

indicators analyzed at 0.080 ppm. This 

inter-individual variability suggests that 

some portion of the population would 

likely experience such effects at 

exposure levels extending well below 

0.080 ppm. 

As discussed above, these 

physiological effects have been linked to 

aggravation of asthma and increased 

susceptibility to respiratory infection, 

potentially leading to increased 

medication use, increased school and 

work absences, increased visits to 

doctors’ offices and emergency 

departments, and increased hospital 

admissions. Further, pulmonary 

inflammation is related to increased 

cellular permeability in the lung, which 

may be a mechanism by which O3

exposure can lead to cardiovascular 

system effects, and to potential chronic 

effects such as chronic bronchitis or 

long-term damage to the lungs that can 

lead to reduced quality of life. These are 

all indicators of adverse O3-related 

morbidity effects, which are consistent 

with and lend plausibility to the adverse 

morbidity effects and mortality effects 

observed in epidemiological studies. 

Significant associations between 

ambient O3 exposures and a wide 

variety of respiratory symptoms and 

other morbidity outcomes (e.g., asthma 

medication use, school absences, 

emergency department visits, and 

hospital admissions) have been reported 

in epidemiological studies, as discussed 

above in section II.A.2.a.i. Overall, the 

2006 Criteria Document concludes that 

positive and robust associations were 

found between ambient O3

concentrations and various respiratory 

disease hospitalization outcomes, when 

focusing particularly on results of 

warm-season analyses. Recent studies 

also generally indicate a positive 

association between O3 concentrations 

and emergency department visits for 

asthma during the warm season. These 

positive and robust associations are 

supported by the controlled human 

exposure, animal toxicological, and 

epidemiological evidence for lung 

function decrements, increased 

respiratory symptoms, airway 

inflammation, and increased airway 

responsiveness. Taken together, the 

overall evidence supports a causal 

relationship between acute ambient O3

exposures and increased respiratory 

morbidity outcomes resulting in 

increased emergency department visits 

and hospitalizations during the warm 

season (EPA, 2006a, p. 8–77). 

Moreover, many single- and multicity 

epidemiological studies observed 

positive associations of ambient O3

concentrations with total nonaccidental 

and cardiopulmonary mortality. As 

discussed above in section II.A.2.b.i, the 

2006 Criteria Document finds that the 

results from U.S. multicity 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 magnitude of risk. 

The 2006 Criteria Document concludes 

that the ‘‘positive O3 effects estimates, 

along with the sensitivity analyses in 

these three meta-analyses, provide 

evidence of a robust association 

between ambient O3 and mortality’’ 

(EPA, 2006a, p. 7–97). In summary, the 

2006 Criteria Document (p. 8–78) 

concludes that these findings are highly 

suggestive that short-term O3 exposure 

directly or indirectly contribute to nonaccidental and cardiopulmonary-related 

mortality, but additional research is 

needed to more fully establish 

underlying mechanisms by which such 

effects occur. 

The 2007 Staff Paper considered the 

epidemiological studies to evaluate 

evidence related to potential effects 

thresholds at the population level for 

morbidity and mortality effects. As 

discussed above in section II.A.3.a (and 

more fully in the 2007 Staff Paper in 

chapter 3 and the 2006 Criteria 


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47Bell et al. (2006) referred to this level as being 

approximately equivalent to 120 μg/m3, daily 8- 

hour maximum, the World Health Organization 

guideline and European Commission target value 

for O3.

Document in chapter 7), a number of 

time-series studies have used statistical 

modeling approaches to evaluate 

potential thresholds at the population 

level. A few such studies reported some 

suggestive evidence of possible 

thresholds for morbidity and mortality 

outcomes in terms of 24-hour, 8-hour, 

and 1-hour averaging times. These 

results, taken together, provide some 

indication of possible 8-hour average 

threshold levels from below about 0.025 

to 0.035 ppm (within the range of 

background concentrations) up to 

approximately 0.050 ppm. Other 

studies, however, observe linear 

concentration-response functions 

suggesting no effect threshold. The 2007 

Staff Paper (p.6–60) concluded that the 

statistically significant associations 

between ambient O3 concentrations and 

lung function decrements, respiratory 

symptoms, indicators of respiratory 

morbidity including increase emergency 

department visits and hospital 

admissions, and possibly mortality 

reported in a large number of studies 

likely extend down to ambient O3

concentrations that are well below the 

level of the then current standard (0.084 

ppm). These associations also extend 

well below the level of the standard set 

in 2008 (0.075 ppm) in that the highest 

level at which there is any indication of 

a threshold is approximately 0.050 ppm. 

Toward the lower end of the range of O3

concentrations observed in such studies, 

ranging down to background levels (i.e., 

0.035 to 0.015 ppm), however, the 2007 

Staff Paper stated that there is 

increasing uncertainty as to whether the 

observed associations remain plausibly 

related to exposures to ambient O3, 

rather than to the broader mix of air 

pollutants present in the ambient 

atmosphere. 

The 2007 Staff Paper also considered 

studies that did subset analyses, which 

included only days with ambient O3

concentrations below the level of the 

then current standard, or below even 

lower O3 concentrations, and continue 

to report statistically significant 

associations. Notably, as discussed 

above, Bell et al. (2006) conducted a 

subset analysis that continued to show 

statistically significant mortality 

associations even when only days with 

a maximum 8-hour average O3

concentration below a value of 

approximately 0.061 ppm were 

included.47 Also of note is the large 

multicity NCICAS (Mortimer et al., 

2002) that reported statistically 

significant associations between 

ambient O3 concentrations and lung 

function decrements even when days 

with 8-hour average O3 levels greater 

than 0.080 ppm were excluded (which 

consisted of less than 5 percent of the 

days in the eight urban areas in the 

study). 

Further, as discussed above in section 

II.A.3.a, there are limitations in 

epidemiological studies that make 

discerning thresholds in populations 

difficult, including low data density in 

the lower concentration ranges, the 

possible influence of exposure 

measurement error, and interindividual 

differences in susceptibility to O3- 

related effects in populations. There is 

the possibility that thresholds for 

individuals may exist in reported 

associations at fairly low levels within 

the range of air quality observed in the 

studies but not be detectable as 

population thresholds in 

epidemiological analyses. 

Based on the above considerations, 

the 2007 Staff Paper recognized that the 

available evidence neither supports nor 

refutes the existence of effect thresholds 

at the population level for morbidity 

and mortality effects, and that if a 

population threshold level does exist, it 

would likely be well below the level of 

the then current standard and possibly 

within the range of background levels. 

Taken together, these considerations 

also support the conclusion that if a 

population threshold level does exist, it 

would likely be well below the level of 

the 0.075 ppm, 8-hour average, standard 

set in 2008. 

In looking more broadly at evidence 

from animal toxicological, controlled 

human exposure, and epidemiological 

studies, the 2006 Criteria Document 

found substantial evidence, newly 

available in the 2008 rulemaking, that 

people with asthma and other 

preexisting pulmonary diseases are 

among those at increased risk from O3

exposure. Altered physiological, 

morphological, and biochemical states 

typical of respiratory diseases like 

asthma, COPD, and chronic bronchitis 

may render people sensitive to 

additional oxidative burden induced by 

O3 exposure (EPA, 2006a, section 8.7). 

Children and adults with asthma are the 

groups that have been studied most 

extensively. Evidence from controlled 

human exposure studies indicates that 

asthmatics may exhibit larger lung 

function decrements in response to O3

exposure than healthy controls. As 

discussed more fully in section II.A.4 

above, asthmatics present a different 

response profile for cellular, molecular, 

and biochemical parameters (EPA, 

2006a, Figure 8–1) that are altered in 

response to acute O3 exposure. They can 

have larger inflammatory responses, as 

manifested by larger increases in 

markers of inflammation such as white 

bloods cells (e.g., PMNs) or 

inflammatory cytokines. Asthmatics, 

and people with allergic rhinitis, are 

more likely to have an allergic-type 

response upon exposure to O3, as 

manifested by increases in white blood 

cells associated with allergy (i.e., 

eosinophils) and related molecules, 

which increase inflammation in the 

airways. The increased inflammatory 

and allergic responses also may be 

associated with the larger late-phase 

responses that asthmatics can 

experience, which can include 

increased bronchoconstrictor responses 

to irritant substances or allergens and 

additional inflammation. 

In addition to the experimental 

evidence of lung function decrements, 

respiratory symptoms, and other 

respiratory effects in asthmatic 

populations, two large U.S. 

epidemiological studies as well as 

several smaller U.S. and international 

studies, have reported fairly robust 

associations between ambient O3

concentrations and measures of lung 

function and daily respiratory 

symptoms (e.g., chest tightness, wheeze, 

shortness of breath) in children with 

moderate to severe asthma and between 

O3 and increased asthma medication use 

(EPA, 2007a, chapter 6). These more 

serious responses in asthmatics and 

others with lung disease provide 

biological plausibility for the respiratory 

morbidity effects observed in 

epidemiological studies, such as 

emergency department visits and 

hospital admissions. 

The body of evidence from controlled 

human exposure and epidemiological 

studies, which includes asthmatic as 

well as non-asthmatic subjects, 

indicates that controlled human 

exposure studies of lung function 

decrements and respiratory symptoms 

that evaluate only healthy, nonasthmatic subjects likely underestimate 

the effects of O3 exposure on asthmatics 

and other susceptible populations. 

Therefore, relative to the healthy, nonasthmatic subjects used in most 

controlled human exposure studies, 

including the Adams (2002, 2006) 

studies, a greater proportion of people 

with asthma may be affected, and those 

who are affected may have as large or 

larger lung function and symptomatic 

responses at ambient exposures to 0.060 

ppm O3. This indicates that the lowestobserved-effects levels demonstrated in 

controlled human exposure studies that 

use only healthy subjects may not 


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48As described in the 2007 Staff Paper (section 

4.5.8) and discussed above in section II.B, recent O3

air quality distributions have been statistically 

adjusted to simulate just meeting the then current 

0.084 ppm standard and selected alternative 

standards. These simulations do not represent 

predictions of when, whether, or how areas might 

meet the specified standards. Modeling that projects 

whether and how areas might attain alternative 

standards in a future year is presented in the 

Regulatory Impact Analysis being prepared in 

connection with this rulemaking. 

49The abbreviated notation used to identify the 

then current 0.084 ppm standard and alternative 

standards in this section and in the risk assessment 

section of the Staff Paper is in terms of ppm and 

the nth highest daily maximum 8-hour average. For 

example, the 8-hour standard established in 1997 is 

identified as ‘‘0.084/4.’’ 

reflect the lowest levels at which people 

with asthma or other lung diseases may 

respond. 

Being mindful of the uncertainties 

and limitations inherent in interpreting 

the available evidence, the 2007 Staff 

Paper stated the view that the range of 

alternative O3 standards for 

consideration should take into account 

information on lowest-observed-effects 

levels in controlled human exposure 

studies as well as indications of possible 

effects thresholds reported in some 

epidemiological studies and questions 

of biological plausibility in attributing 

associations observed down to 

background levels to O3 exposures 

alone. Based on the evidence and these 

considerations, it concluded that the 

upper end of the range of consideration 

should be somewhat below 0.080 ppm, 

the lowest-observed-effects level for 

effects such as pulmonary 

inflammation, increased airway 

responsiveness and impaired hostdefense capabilities in healthy adults 

while at prolonged moderate exertion. 

The 2007 Staff Paper also concluded 

that the lower end of the range of 

alternative O3 standards appropriate for 

consideration should be the lowestobserved-effects level for potentially 

adverse lung function decrements and 

respiratory symptoms in some healthy 

adults, 0.060 ppm. 

b. Exposure and Risk-Based 

Considerations 

In addition to the evidence-based 

considerations informing staff 

recommendations on alternative levels, 

as discussed above in section II.B, the 

2007 Staff Paper also evaluated 

quantitative exposures and health risks 

estimated to occur upon meeting the 

then current 0.084 ppm standard and 

alternative standards.48 In so doing, it 

presented the important uncertainties 

and limitations associated with these 

exposure and risk assessments 

(discussed above in section II.B and 

more fully in chapters 4 and 5 of the 

2007 Staff Paper). 

The 2007 Staff Paper (and the 

CASAC) also recognized that the 

exposure and risk analyses could not 

provide a full picture of the O3

exposures and O3-related health risks 

posed nationally. The EPA did not have 

sufficient information to evaluate all 

relevant at-risk groups (e.g., outdoor 

workers) or all O3-related health 

outcomes (e.g., increased medication 

use, school absences, and emergency 

department visits that are part of the 

broader pyramid of effects discussed 

above in section II.A.4.d), and the scope 

of the 2007 Staff Paper analyses was 

generally limited to estimating 

exposures and risks in 12 urban areas 

across the U.S., and to only five or just 

one area for some health effects 

included in the risk assessment. Thus, 

national-scale public health impacts of 

ambient O3 exposures are clearly much 

larger than the quantitative estimates of 

O3-related incidences of adverse health 

effects and the numbers of children 

likely to experience exposures of 

concern associated with meeting the 

0.084 ppm standard or alternative 

standards. On the other hand, interindividual variability in responsiveness 

means that only a subset of individuals 

in each group estimated to experience 

exposures exceeding a given benchmark 

exposure of concern level would 

actually be expected to experience such 

adverse health effects. 

The 2007 Staff Paper focused on 

alternative standards with the same 

form as the then current 0.084 ppm O3

standard (i.e. the 0.074/4, 0.070/4 and 

0.064/4 scenarios).49 Having concluded 

in the 2007 Staff Paper that it was 

appropriate to consider a range of 

standard levels from somewhat below 

0.080 ppm down to as low as 0.060 

ppm, the 2007 Staff Paper looked to 

results of the analyses of exposure and 

risk for the 0.074/4 scenario to represent 

the public health impacts of selecting a 

standard in the upper part of the range, 

the results of analyses of the 0.070/4 

scenario to represent the impacts in the 

middle part of the range, and the results 

of the analyses of the 0.064/4 scenario 

to represent the lower part of the range. 

As discussed in section II.B.1 of this 

notice, the exposure estimates presented 

in the 2007 Staff Paper are for the 

number and percent of all children and 

asthmatic children exposed, and the 

number of person-days (occurrences) of 

exposures, with daily 8-hour maximum 

exposures at or above several 

benchmark levels while at intermittent 

moderate or greater exertion. Exposures 

above selected benchmark levels 

provide some perspective on the public 

health impacts of health effects that 

cannot currently be evaluated in 

quantitative risk assessments but that 

may occur at existing air quality levels, 

and the extent to which such impacts 

might be reduced by meeting alternative 

standard levels. As described in section 

II.B.1.c above, the 2007 Staff Paper 

refers to exposures at and above these 

benchmark levels as ‘‘exposures of 

concern.’’ The 2007 Staff Paper notes 

that exposures of concern, and the 

health outcomes they represent, likely 

occur across a range of O3 exposure 

levels, such that there is no one 

exposure level that addresses all public 

health concerns. As noted above in 

section II.B., EPA also has 

acknowledged that the concept is more 

appropriately viewed as a continuum 

with greater confidence and less 

uncertainty about the existence of 

health effects at the upper end and less 

confidence and greater uncertainty as 

one considers increasingly lower O3

exposure levels. 

Consistent with advice from CASAC, 

the 2007 Staff Paper estimates exposures 

of concern not only at 0.080 ppm O3, a 

level at which there are clearly 

demonstrated effects, but also at 0.070 

and 0.060 ppm O3 levels where there is 

some evidence that health effects are 

likely to occur in some individuals. The 

2007 Staff Paper recognizes that there 

will be varying degrees of concern about 

exposures at each of these levels, based 

in part on the population groups 

experiencing them. Given that there is 

clear evidence of inflammation, 

increased airway responsiveness, and 

changes in host defenses in healthy 

people exposed to 0.080 ppm and 

reason to infer that such effects will 

continue at lower exposure levels, but 

with increasing uncertainty about the 

extent to which such effects occur at 

lower O3 concentrations, the 2007 Staff 

Paper and discussion below, focus on 

exposures of concern at or above 

benchmark levels of 0.070 and 0.060 

ppm O3 for purposes of evaluating 

alternative standards. The focus on 

these two benchmark levels reflects the 

following evidence-based 

considerations, discussed above in 

section II.C.1, that raise concerns about 

adverse health effects likely occurring at 

levels below 0.080 ppm: (1) That there 

is limited, but important, new evidence 

from controlled human exposure studies 

showing lung function decrements and 

respiratory symptoms in some healthy 

subjects at 0.060 ppm; (2) that 

asthmatics are likely to have more 

serious responses than healthy 

individuals; (3) that lung function is not 

likely to be as sensitive a marker for O3


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effects as lung inflammation; and (4) 

that there is epidemiological evidence 

which reports associations with O3

levels that extend well below 0.080 

ppm. 

Table 3 below summarizes the 

exposure estimates for all children and 

asthmatic children for the 0.060 and 

0.070 ppm health effect benchmark 

levels associated with O3 levels adjusted 

to just meet 0.074/4, 0.070/4, and 0.064/ 

4 alternative 8-hour standards based on 

a generally poorer year of air quality 

(2002) and based on a generally better 

year of air quality (2004). This table 

includes exposure estimates reflecting 

the aggregate estimate for the 12 urban 

areas as well as the range across these 

same 12 areas. As shown in Table 3 

below, the percent of population 

exposed over the selected benchmark 

levels is very similar for all and 

asthmatic school age children. Thus, the 

following discussion focuses primarily 

on the exposure estimates for asthmatic 

children, recognizing that the pattern of 

exposure estimates is similar for all 

children when expressed in terms of 

percentage of the population. 

As noted in section II.B.2 and shown 

in Tables 1 and 3 of this notice, 

substantial year-to-year variability is 

observed, ranging to over an order of 

magnitude at the higher alternative 

standard levels, in estimates of the 

number of children and the number of 

occurrences of exposures of concern at 

both the 0.060 and 0.070 ppm 

benchmark levels. As shown in Table 3, 

and discussed more fully below, 

aggregate estimates of exposures of 

concern for the 12 urban areas included 

in the assessment are considerably 

larger for the benchmark level of ≥ 0.060 

ppm O3, compared to the 0.070 ppm 

benchmark, while the pattern of year-toyear variability is fairly similar. 

As shown in Table 3, aggregate 

estimates of exposures of concern for a 

0.060 ppm benchmark level vary 

considerably among the three 

alternative standards included in this 

table, particularly for the 2002 

simulations (a year with generally 

poorer air quality in most, but not all 

areas). For air quality just meeting a 

0.074/4 standard approximately 27% of 

asthmatic children, based on the 2002 

simulation, and approximately 2% of 

asthmatic children based on the 2004 

simulation (a year with better air quality 

in most but not all areas), are estimated 

to experience one or more exposures of 

concern at the benchmark level of ≥ 

0.060 ppm O3. Considering a 0.070/4 

standard using the same benchmark 

level (0.060 ppm), about 18% of 

asthmatic children are estimated to 

experience one or more exposures of 

concern, in a year with poorer air 

quality (2002), and only about 1% in a 

year with better air quality (2004). For 

the most stringent standard examined (a 

0.064/4 standard), about 6% of 

asthmatic children are estimated to 

experience one or more exposures of 

concern in the simulation based on the 

year with poorer air quality (2002), and 

exposures of concern at the 0.060 ppm 

benchmark level are essentially 

eliminated based on a year with better 

air quality (2004). 

Table 3 also provides aggregate 

exposure estimates for the 12 urban 

areas where a benchmark level of 

≥ 0.070 ppm is used. Based on the year 

with poorer air quality (2002), the 

estimate of the percent of asthmatic 

children exposed one or more times is 

about 5% when a 0.074/4 standard is 

just met; based on a year with better air 

quality (2004), exposures of concern are 

essentially eliminated. For this same 

benchmark (0.070 ppm), when a 0.070/ 

4 standard is just met, estimates range 

from about 2% of asthmatic children 

exposed one or more times over this 

benchmark based on a year with poorer 

air quality (2002), and exposures of 

concern are essentially eliminated based 

on a year with better air quality (2004). 

At the 0.070 ppm benchmark, just 

meeting a 0.064/4 standard essentially 

eliminates exposures of concern 

regardless of the year that is used as the 

basis for the analysis. 

The 2007 Staff Paper also notes that 

there is substantial city-to-city 

variability in these estimates, and notes 

that it is appropriate to consider not just 

the aggregate estimates across all cities, 

but also to consider the public health 

impacts in cities that receive relatively 

less protection from the alternative 

standards. As shown in Table 3, in 

considering the benchmark level of 

≥ 0.060 ppm, while the aggregate 

percentage of asthmatic children 

estimated to experience one or more 

exposures of concern across all 12 cities 

for a 0.074/4 standard is about 27% 

based on the year with poorer air quality 

(2002), it ranges up to approximately 

51% for asthmatic children in the city 

with the least degree of protection from 

that alternative standard. Similarly, for 

air quality just meeting a 0.070/4 

standard, the aggregate percentage of 

asthmatic children estimated to 

experience one or more exposures of 

concern across all 12 cities is 18% based 

on the year with poorer air quality, but 

it ranges up to about 41% in the city 

with the least degree of protection 

associated with just meeting that 

alternative standard. For just meeting a 

0.064/4 standard, the aggregate estimate 

of asthmatic children experiencing 

exposures of concern for the 0.060 ppm 

benchmark is about 6% based on the 

year with poorer air quality and ranges 

up to 16% in the city with the least 

degree of protection. 

This pattern of city-to-city variability 

also occurs at the benchmark level of 

≥ 0.070 ppm associated with air quality 

just meeting these same three alternative 

standards (i.e., 0.074/4, 0.070/4, and 

0.064/4). While the aggregate percentage 

of asthmatic children estimated to 

experience such exposures of concern 

across all 12 cities is about 5% based on 

the year with poorer air quality for just 

meeting the 0.074/4 standard, it ranges 

up to 14% in the city with the least 

degree of protection associated with that 

alternative standard. For just meeting a 

0.070/4 standard the aggregate estimate 

is 2% of asthmatic children 

experiencing exposures of concern for 

the 0.070 ppm benchmark based on the 

year with poorer air quality and ranges 

up to 6% in the city with the least 

degree of protection. The aggregate 

estimate for exposures of concern is 

further reduced to 0.2% of asthmatic 

children for this same benchmark level 

for air quality just meeting a 0.064/4 

standard based on the year with poorer 

air quality and ranges up to 1% in the 

city with the least degree of protection. 

In addition to observing the fraction 

of the population estimated to 

experience exposures of concern 

associated with just meeting alternative 

standards, EPA also took into 

consideration in the 2007 Staff Paper 

the percent reduction in exposures of 

concern and health risks associated with 

alternative standards relative to just 

meeting the then current 0.084/4 

standards. For the current decision it is 

also informative to consider the 

incremental reductions in exposures of 

concern associated with more stringent 

alternative standards relative to the 

0.075 ppm standard. As shown in Table 

1 above, at the ≥ 0.060 ppm benchmark 

level based on a year with poorer air 

quality, the reduction in exposures of 

concern for asthmatic children in going 

from the 0.074/4 standard (which 

approximates the 0.075 ppm standard 

adopted in 2008) down to a 0.064/4 

standard is observed to be very similar 

to the reduction estimated to occur in 

going from then current 0.084/4 

standard down to a 0.074/4 standard. 

More specifically, the estimates for 

asthmatic children are reduced from 

47% (about 1.2 million children) 

associated with meeting a 0.084/4 

standard down to 27% (about 700,000 

children) for just meeting a 0.074/4 

standard and the estimates are reduced 

further to about 6% (about 150,000 

children) associated with just meeting a 


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0.064/4 standard in the 12 urban areas 

included in the assessment. In a year 

with better air quality (2004), exposures 

estimated to exceed the 0.060 ppm 

benchmark in asthmatic children one or 

more times in a year are reduced from 

11% associated with just meeting a 

0.084/4 standard down to about 2% for 

a 0.074/4 standard and are essentially 

eliminated when a 0.064/4 standard is 

just met. 

Turning to consideration of the risk 

assessment estimates, Table 2 above 

summarizes the risk estimates for 

moderate lung function decrements in 

both all school age children and 

asthmatic school age children associated 

with just meeting several alternative 

standards based on simulations 

involving a year with relatively poorer 

air quality (2002) and a year with 

relatively better air quality (2004). As 

shown in Table 2, for the 2002 

simulation the reduction in the number 

of asthmatic children estimated to 

experience one or more moderate lung 

function decrements going from a 0.074/ 

4 standard down to a 0.064/4 standard 

is roughly equivalent to the additional 

health protection afforded associated 

with just meeting a 0.074/4 standard 

relative to then current 0.084/4 

standard. More specifically, for just 5 

urban areas, it is estimated that nearly 

8% of asthmatic children (130,000 

children) would experience one or more 

occurrences of moderate lung function 

decrements per year at a 0.084/4 

standard and this would be reduced to 

about 5% (90,000 children) at a 0.074/ 

4 standard and further reduced down to 

about 3% (50,000 children) at a 0.064/ 

4 standard. Based on the 2002 

simulations, the percent reduction 

associated with just meeting a 0.064/4 

standard relative to then current 0.084/ 

4 standard is about 62% which is about 

twice the reduction in risk compared to 

the estimated 31% reduction associated 

with just meeting a 0.074/4 standard. As 

shown in Table 2 above, similar patterns 

were observed in reductions in lung 

function risk for all school age children 

in 12 urban areas associated with these 

alternative standards. 

Figures 6–5 and 6–6 in the 2007 Staff 

Paper (EPA, 2007b) show the percent 

reduction in non-accidental mortality 

risk estimates associated with just 

meeting the same alternative standards 

discussed above relative to just meeting 

the then current 0.084/4 standard for 12 

urban areas, based on adjusting 2002 

and 2004 air quality data. These figures 

also provide perspective on the extent to 

which the risks in these years (i.e., 2002 

and 2004) are greater than those 

estimated to occur upon meeting the 

then current 0.084/4 standard (in terms 

of a negative percent reduction relative 

to a 0.084/4 standard). Based on the 

2002 simulations (EPA, 2007b, Figure 

6–5), the estimated reduction in nonaccidental mortality is about 30 to 70% 

across the 12 urban areas for just 

meeting a 0.064/4 standard relative to 

the then current 0.084/4 standard. This 

reduction is roughly twice the 15 to 

30% estimated reduction across the 12 

urban areas associated with just meeting 

a 0.074/4 standard relative to a 0.084/4 

standard. While the estimated incidence 

is lower based on the 2004 simulations 

(EPA, 2007b, Figure 6–6), the pattern of 

risk reductions among alternative 

standards is roughly similar to that 

observed for the 2002 simulations. 

In addition to the risk estimates for 

lung function decrements in all school 

age children and non-accidental 

mortality that were estimated for 12 

urban areas and lung function 

decrements in asthmatic children for 5 

urban areas, a similar pattern of 

incremental reductions in health risks 

was shown for two health outcomes 

where risks were estimated in one city 

only for each of these outcomes. These 

included reductions in respiratory 

symptoms in asthmatic children (EPA, 

2007b; Boston, Table 6–9) and 

respiratory-related hospital admissions 

(EPA, 2007a; New York City, Table 

6–10) associated with just meeting 

alternative 8-hour standards set at 0.074 

ppm, 0.070 ppm, and 0.064 ppm 

relative to just meeting the then current 

0.084 ppm standard. Using the 2002 

simulation, a standard set at 0.074/4 is 

estimated to reduce the incidence of 

symptom days in children with 

moderate to severe asthma in the Boston 

area by about 15 percent relative to a 

0.084/4 standard. With this reduction, it 

is estimated that about 1 respiratory 

symptom day in 8 during the O3 season 

would be attributable to O3 exposure. A 

standard set at 0.064/4 is estimated, 

based on the 2002 simulation, to reduce 

the incidence of symptom days in 

children with moderate to severe 

asthma in the Boston area by about a 25 

to 30 percent reduction relative to a 

0.084 ppm standard, which is roughly 

twice the reduction compared to that 

provided by a 0.074/4 standard. But 

even with this reduction, it is estimated 

that 1 respiratory symptom day in 10 

during the O3 season is attributable to 

O3 exposure. 

As shown in Table 6–10 (EPA, 2007b) 

estimated incidence of respiratoryrelated hospital admissions in one 

urban area (New York City) was reduced 

by 14 to 17 percent by a standard set at 

0.074/4 relative to then current 0.084/4 

standard, in the year with relatively 

high and relatively low O3 air quality 

levels, respectively. Similar to the 

pattern observed for the other health 

outcomes discussed above, the 

reduction in incidence of respiratoryrelated hospital admissions for a 0.064/ 

4 standard relative to a 0.084/4 standard 

is about twice that associated with a 

0.074/4 standard relative to a 0.084/4 

standard. 

TABLE 3—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN 12 URBAN AREAS ESTIMATED TO

EXPERIENCE 8-HOUR OZONE EXPOSURES ABOVE 0.060 AND 0.070 PPM WHILE AT MODERATE OR GREATER EXERTION, ONE OR MORE TIMES PER SEASON ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS

BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA1 2

Benchmark levels of exposures of 

concern 

(ppm) 

8-Hour air quality 

standards 3

(ppm) 

All children, ages 5–18 

Aggregate for 12 urban areas 

Number of children exposed 

(% of all children) 

[Range across 12 cities, % of all children] 

Asthmatic children, ages 5–18 

Aggregate for 12 urban areas 

Number of children exposed 

(% of group) 

[Range across 12 cities, % of group] 

2002 2004 2002 2004 

0.070 ............................................ 0.074 770,000 (4%) 

[0–13%] 

20,000 (0%) 

[0–1%] 

120,000 (5%) 

[0–14%] 

0 (0%) 

[0–1%] 

0.070 270,000 (1%) 

[0–5%] 

0 (0%) 

[0%] 

50,000 (2%) 

[0–6%] 

0 (0%) 

[0%] 

0.064 30,000 (0.2%) 

[0–1%] 

0 (0%) 

[0%] 

10,000 (0.2%) 

[0–1% ] 

0 (0%) 

[0%] 


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TABLE 3—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN 12 URBAN AREAS ESTIMATED TO

EXPERIENCE 8-HOUR OZONE EXPOSURES ABOVE 0.060 AND 0.070 PPM WHILE AT MODERATE OR GREATER EXERTION, ONE OR MORE TIMES PER SEASON ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS

BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA1 2—Continued 

Benchmark levels of exposures of 

concern 

(ppm) 

8-Hour air quality 

standards 3

(ppm) 

All children, ages 5–18 

Aggregate for 12 urban areas 

Number of children exposed 

(% of all children) 

[Range across 12 cities, % of all children] 

Asthmatic children, ages 5–18 

Aggregate for 12 urban areas 

Number of children exposed 

(% of group) 

[Range across 12 cities, % of group] 

2002 2004 2002 2004 

0.060 ............................................ 0.074 4,550,000 (25%) 

[1–48%] 

350,000 (2%) 

[0–9%] 

700,000 (27%) 

[1–51%] 

50,000 (2%) 

[0–9%] 

0.070 3,000,000 (16%) 

[1–36%] 

110,000 (1%) 

[0–4%] 

460,000 (18%) 

[0–41%] 

10,000 (1%) 

[0–3%] 

0.064 950,000 (5%) 

[0–17%] 

10,000 (0%) 

[0–1%] 

150,000 (6%) 

[0–16%] 

0 (0%) 

[0–1%] 

1 Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate ≥ 13 1-min/m2. 2Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston, 

Los Angeles and Sacramento and March or April to September or October for the remaining urban areas. 3All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of 

the annual 4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the 

2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 

0.084 ppm standard and selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might 

meet the specified standards. 

2. CASAC Views Prior to 2008 Decision 

In comments on the second draft Staff 

Paper, CASAC stated in its letter to the 

Administrator, ‘‘the CASAC 

unanimously recommends that the 

current primary ozone NAAQS be 

revised and that the level that should be 

considered for the revised standard be 

from 0.060 to 0.070 ppm’’ (Henderson, 

2006c, p. 5). This recommendation 

followed from its more general 

recommendation that the 0.084 ppm 

standard needed to be substantially 

reduced to be protective of human 

health, particularly in at-risk 

subpopulations. 

The CASAC Panel noted that 

beneficial reductions in some adverse 

health effects were estimated to occur 

upon meeting the lowest standard level 

(0.064 ppm) considered in the risk 

assessment (Henderson, 2006c, p. 4). 

The lower end of this range reflects 

CASAC’s views that ‘‘[w]hile data exist 

that adverse health effects may occur at 

levels lower than 0.060 ppm, these data 

are less certain and achievable gains in 

protecting human health can be 

accomplished through lowering the 

ozone NAAQS to a level between 0.060 

and 0.070 ppm.’’ (id.). 

In a subsequent letter sent specifically 

to offer advice to aid the Administrator 

and Agency staff in developing the O3

proposal, the CASAC reiterated that the 

Panel members ‘‘were unanimous in 

recommending that the level of the 

current primary ozone standard should 

be lowered from 0.08 ppm to no greater 

than 0.070 ppm’’ (Henderson, 2007, p. 

2). Further, the CASAC Panel expressed 

the view that the 2006 Criteria 

Document and 2007 Staff Paper, 

together with the information in its 

earlier letter, provide ‘‘overwhelming 

scientific evidence for this 

recommendation,’’ and emphasized the 

Clean Air Act requirement that the 

primary standard must be set to protect 

the public health with an adequate 

margin of safety (id.). 

3. Basis for 2008 Decision on the 

Primary Standard 

This section presents the rationale for 

the 2008 final decision on the primary 

O3 standard as presented in the 2008 

final rule (73 FR 16475). The EPA’s 

conclusions on the level of the standard 

began by noting that, having carefully 

considered the public comments on the 

appropriate level of the O3 standard, 

EPA concluded that the fundamental 

scientific conclusions on the effects of 

O3 reached in the 2006 Criteria 

Document and 2007 Staff Paper 

remained valid. In considering the level 

at which the primary O3 standard 

should be set, EPA placed primary 

consideration on the body of scientific 

evidence available in the 2008 final 

rulemaking on the health effects 

associated with O3 exposure, while 

viewing the results of exposure and risk 

assessments as providing information in 

support of the decision. In considering 

the available scientific evidence, EPA 

concluded that a focus on the proposed 

range of 0.070 to 0.075 ppm was 

appropriate in light of the large body of 

controlled human exposure and 

epidemiological and other scientific 

evidence. The notice stated that this 

body of evidence did not support 

retaining the then current 0.084 ppm 

8-hour O3 standard, as suggested by 

some commenters, nor did it support 

setting a level just below 0.080 ppm, 

because, based on the entire body of 

evidence, such a level would not 

provide a significant increase in 

protection compared to the 0.084 ppm 

standard. Further, such a level would 

not be appreciably below the level in 

controlled human exposure studies at 

which adverse effects have been 

demonstrated (i.e., 0.080 ppm). The 

notice also stated that the body of 

evidence did not support setting a level 

of 0.060 ppm or below, as suggested by 

other commenters. In evaluating the 

information from the exposure 

assessment and the risk assessment, 

EPA judged that this information did 

not provide a clear enough basis for 

choosing a specific level within the 

range of 0.075 to 0.070 ppm. 

In making a final judgment about the 

level of the primary O3 standard, EPA 

noted that the level of 0.075 ppm is 

above the range recommended by the 

CASAC (i.e., 0.070 to 0.060 ppm). The 

notice stated that in placing great weight 

on the views of CASAC, careful 

consideration had been given to 

CASAC’s stated views and the scientific 

basis and policy views for the range it 

recommended. In so doing, EPA fully 

agreed that the scientific evidence 

supports the conclusion that the current 

standard was not adequate and must be 

revised. 


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With respect to CASAC’s 

recommended range of standard levels, 

EPA observed that the basis for 

CASAC’s recommendation appeared to 

be a mixture of scientific and policy 

considerations. While in general 

agreement with CASAC’s views 

concerning the interpretation of the 

scientific evidence, EPA noted that 

there was no bright line clearly directing 

the choice of level, and the choice of 

what was appropriate was clearly a 

public health policy judgment entrusted 

to the EPA 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 recommendation for the range of 

the O3 standard, EPA observed that it 

reached a different policy judgment 

than the CASAC Panel based on 

apparently placing different weight in 

two areas: The role of the evidence from 

the Adams studies and the relative 

weight placed on the results from the 

exposure and risk assessments. While 

EPA found the evidence reporting 

effects at the 0.060 ppm level from the 

Adams studies to be too limited to 

support a primary focus at this level, 

EPA observed that the CASAC Panel 

appeared to place greater weight on this 

evidence, as indicated by its 

recommendation of a range down to 

0.060 ppm. It was noted that while the 

CASAC Panel supported a level of 0.060 

ppm, they also supported a level above 

0.060, which indicated that they did not 

believe that the results of Adams studies 

meant that the level of the standard had 

to be set at 0.060 ppm. The EPA also 

observed that the CASAC Panel 

appeared to place greater weight on the 

results of the risk assessment as a basis 

for its recommended range. In referring 

to the risk assessment results for lung 

function, respiratory symptoms, 

hospital admissions and mortality, the 

CASAC Panel concluded that: 

‘‘beneficial effects in terms of reduction 

of adverse health effects were calculated 

to occur at the lowest concentration 

considered (i.e., 0.064 ppm)’’ 

(Henderson, 2006c, p. 4). However, EPA 

more heavily weighed the implications 

of the uncertainties associated with the 

Agency’s quantitative human exposure 

and health risk assessments. Given these 

uncertainties, EPA did not agree that 

these assessment results appropriately 

served as a primary basis for concluding 

that levels at or below 0.070 ppm were 

required for the 8-hour O3 standard. 

The notice stated that after carefully 

taking the above comments and 

considerations into account, and fully 

considering the scientific and policy 

views of the CASAC, EPA decided to 

revise the level of the primary 8-hour O3

standard to 0.075 ppm. The EPA judged, 

based on the available evidence, that a 

standard set at this level would be 

requisite to protect public health with 

an adequate margin of safety, including 

the health of sensitive subpopulations, 

from serious health effects including 

respiratory morbidity, that were judged 

to be causally associated with shortterm and prolonged exposures to O3, 

and premature mortality. The EPA also 

judged that a standard set at this level 

provides a significant increase in 

protection compared to the 0.084 ppm 

standard, and is appreciably below 

0.080 ppm, the level in controlled 

human exposure studies at which 

adverse effects have been demonstrated. 

At a level of 0.075 ppm, exposures at 

and above the benchmark of 0.080 ppm 

are essentially eliminated, and 

exposures at and above the benchmark 

of 0.070 are substantially reduced or 

eliminated for the vast majority of 

people in at-risk groups. A standard set 

at a level lower than 0.075 would only 

result in significant further public 

health protection if, in fact, there is a 

continuum of health risks in areas with 

8-hour average O3 concentrations that 

are well below the concentrations 

observed in the key controlled human 

exposure studies and if the reported 

associations observed in 

epidemiological studies are, in fact, 

causally related to O3 at those lower 

levels. Based on the available evidence, 

EPA was not prepared to make these 

assumptions. Taking into account the 

uncertainties that remained in 

interpreting the evidence from available 

controlled human exposure and 

epidemiological studies at very low 

levels, EPA noted that the likelihood of 

obtaining benefits to public health 

decreased with a standard set below 

0.075 ppm O3, while the likelihood of 

requiring reductions in ambient 

concentrations that go beyond those that 

are needed to protect public health 

increased. The EPA judged that the 

appropriate balance to be drawn, based 

on the entire body of evidence and 

information available in the 2008 final 

rulemaking, was to set the 8-hour 

primary standard at 0.075 ppm. The 

EPA expressed the belief that a standard 

set at 0.075 ppm would be sufficient to 

protect public health with an adequate 

margin of safety, and did not believe 

that a lower standard was needed to 

provide this degree of protection. The 

EPA further asserted that this judgment 

appropriately considered the 

requirement for a standard that was 

neither more nor less stringent than 

necessary for this purpose and 

recognized that the CAA does not 

require that primary standards be set at 

a zero-risk level, but rather at a level 

that reduces risk sufficiently so as to 

protect public health with an adequate 

margin of safety. 

4. CASAC Advice Following 2008 

Decision 

Following the 2008 decision on the O3

standard, serious questions were raised 

as to whether the standard met the 

requirements of the CAA. In April 2008, 

the members of the CASAC Ozone 

Review Panel sent a letter to EPA stating 

‘‘In our most-recent letters to you on this 

subject—dated October 2006 and March 

2007—the CASAC unanimously 

recommended selection of an 8-hour 

average Ozone NAAQS within the range 

of 0.060 to 0.070 parts per million for 

the primary (human health-based) 

Ozone NAAQS’’ (Henderson, 2008). The 

letter continued: ‘‘The CASAC now 

wishes to convey, by means of this 

letter, its additional, unsolicited advice 

with regard to the primary and 

secondary Ozone NAAQS. In doing so, 

the participating members of the 

CASAC Ozone Review Panel are 

unanimous in strongly urging you or 

your successor as EPA Administrator to 

ensure that these recommendations be 

considered during the next review cycle 

for the Ozone NAAQS that will begin 

next year’’ (id.). Moreover, the CASAC 

Panel noted that ‘‘numerous medical 

organizations and public health groups 

have also expressed their support of 

these CASAC recommendations.’’ (id.) 

The letter further stated the following 

strong, unanimous view: 

[the CASAC did] ‘‘not endorse the 

new primary ozone standard as being 

sufficient protective of public health. 

The CASAC—as the Agency’s 

statutorily-established science advisory 

committee for advising you on the 

national ambient air quality standards— 

unanimously recommended decreasing 

the primary standard to within the range 

of 0.060–0.070 ppm. It is the 

Committee’s consensus scientific 

opinion that your decision to set the 

primary ozone standard above this range 

fails to satisfy the explicit stipulations 

of the Clean Air Act that you ensure an 

adequate margin of safety for all 

individuals, including sensitive 

populations’’ (Henderson, 2008). 

5. Administrator’s Proposed 

Conclusions 

For the reasons discussed below, the 

Administrator proposes to set a new 

level for the 8-hour primary O3 within 


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50As discussed above at the beginning of section 

II, the Administrator has focused her 

reconsideration of the primary O3 standard set in 

the 2008 final rule on the level of the standard, 

having decided not to reopen the 2008 final rule 

with regard to the need to revise the 1997 primary 

O3 standard to provide increased public health 

protection nor with regard to the indicator, 

averaging period, and form of the 2008 standard. 

51The EPA responded to these comments in the 

2008 final rule (73 FR 16454–5). 

the range from 0.060 to 0.070 ppm.50 In 

reaching this proposed decision, the 

Administrator has considered: the 

evidence-based considerations from the 

2006 Criteria Document and the 2007 

Staff Paper; the results of the exposure 

and risk assessments discussed above 

and in the 2007 Staff Paper; CASAC 

advice and recommendations provided 

in CASAC’s letters to the Administrator 

both during and following the 2008 

rulemaking; EPA staff 

recommendations; and public 

comments received in conjunction with 

review of drafts of these documents and 

on the 2007 proposed rule. In 

considering what level of an 8-hour O3

standard is requisite to protect public 

health with an adequate margin of 

safety, the Administrator is mindful that 

this choice requires judgments based on 

an interpretation of the evidence and 

other information that neither overstates 

nor understates the strength and 

limitations of the evidence and 

information. 

The Administrator notes that the most 

certain evidence of adverse health 

effects from exposure to O3 comes from 

the controlled human exposure studies, 

and that the large bulk of this evidence 

derives from studies of exposures at 

levels of 0.080 ppm and above. At those 

levels, there is consistent evidence of 

lung function decrements and 

respiratory symptoms in healthy young 

adults, as well as evidence of O3- 

induced pulmonary inflammation, 

airway responsiveness, impaired host 

defense capabilities, and other 

medically significant airway responses. 

Moreover, there is no evidence that the 

0.080 ppm exposure level is a threshold 

for any of these types of respiratory 

effects. Rather, there is now controlled 

human exposure evidence, including 

studies of lung function decrements and 

respiratory symptoms at the 0.060 ppm 

exposure level, that strengthens our 

previous understanding that this array 

of respiratory responses are likely to 

occur in some healthy adults at such 

lower levels. 

In particular, the Administrator notes 

two studies by Adams (2002, 2006), 

newly available in the 2008 rulemaking, 

that examined lung function and 

respiratory symptom effects associated 

with prolonged O3 exposures at levels 

below 0.080 ppm, as well as EPA’s 

reanalysis of the data from the Adams 

(2006) study at a 0.060 ppm exposure 

level. As discussed above, while the 

author’s analysis focused on hour-byhour comparisons of effects, for the 

purpose of exploring responses 

associated with different patterns of 

exposure, EPA’s reanalysis focused on 

addressing the more fundamental 

question of whether the pre- to postexposure change in lung function 

differed between a 6.6-hour exposure to 

0.060 ppm O3 versus a 6.6 hour 

exposure to clean filtered air. The 

Administrator notes that this reanalysis 

found small, but statistically significant 

group mean differences in lung function 

decrements in healthy adults at the 

0.060 ppm exposure level, which is now 

the lowest-observed-effects level for 

these effects. Moreover, these studies 

also report a small percentage of 

subjects (7 to 20 percent) experienced 

moderate lung function decrements 

(≥ 10 percent) at the 0.060 ppm exposure 

level. While for active healthy people, 

moderate levels of functional responses 

(e.g., FEV1 decrements of ≥ 10% but 

< 20%) and/or moderate respiratory 

symptom responses would likely 

interfere with normal activity for 

relatively few responsive individuals, 

the Administrator notes that for people 

with lung disease, even moderate 

functional or symptomatic responses 

would likely interfere with normal 

activity for many individuals, and 

would likely result in more frequent use 

of medication. Further, she notes that 

CASAC indicated 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 (Henderson, 2006c). 

The Administrator also notes that 

many public commenters on the 2007 

proposed rule raised a number of 

questions about the weight that should 

be placed on the Adams studies and 

EPA’s reanalysis of data from the Adams 

(2006) study. Some commenters 

expressed the view that the results of 

these studies and EPA’s reanalysis 

provided support for setting a standard 

level below the proposed range, while 

others raised questions about EPA’s 

reanalysis and generally expressed the 

view that the study results were not 

robust enough to reach conclusions 

about respiratory effects at the 0.060 

ppm exposure level.51

Based on all the above considerations, 

the Administrator concludes that the 

Adams studies provide limited but 

important evidence which adds to the 

overall body of evidence that informs 

her proposed decision on the range of 

levels within which a standard could be 

set that would be requisite to protect 

public health with an adequate margin 

of safety, including the health of at-risk 

populations such as people with lung 

disease. 

In considering controlled human 

exposure studies reporting O3-induced 

pulmonary inflammation, airway 

responsiveness, and impaired host 

defense capabilities at exposure levels 

down to 0.080 ppm, the lowest level at 

which these effects have been tested, the 

Administrator notes that these 

physiological effects have been linked to 

aggravation of asthma and increased 

susceptibility to respiratory infection, 

potentially leading to increased 

medication use, increased school and 

work absences, increased visits to 

doctors’ offices and emergency 

departments, and increased hospital 

admissions, especially in people with 

lung disease. These physiological effects 

are all indicators of potential adverse 

O3-related morbidity effects, which are 

consistent with and lend plausibility to 

the associations observed between O3

and adverse morbidity effects and 

mortality effects in epidemiological 

studies. 

With regard to epidemiological 

studies, the Administrator observes that 

statistically significant associations 

between ambient O3 levels and a wide 

array of respiratory symptoms and other 

morbidity outcomes including school 

absences, emergency department visits, 

and hospital admissions have been 

reported in a large number of studies. 

More specifically, positive and robust 

associations were found between 

ambient O3 concentrations and 

respiratory hospital admissions and 

emergency department visits, when 

focusing particularly on the results of 

warm season analyses. Taken together, 

the overall body of evidence from 

controlled human exposure, 

toxicological, and epidemiological 

studies supports the inference of a 

causal relationship between acute 

ambient O3 exposures and increased 

respiratory morbidity outcomes 

resulting in increased emergency 

department visits and hospitalizations 

during the warm season. Further, the 

Administrator notes that recent 

epidemiological evidence is highly 

suggestive that O3 directly or indirectly 

contributes to non-accidental and 

cardiopulmonary-related mortality. 

The Administrator also considered 

the epidemiological evidence with 

regard to considering potential effects 

thresholds at the population level for 


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52As noted in section II.C.1.b.above, the 

Administrator focused on alternative standards 

with different levels but the same form and 

averaging time as the primary standard set in 2008. 

morbidity and mortality effects. As 

discussed above, while some studies 

provide some indication of possible 8- 

hour average threshold levels from 

below about 0.025 to 0.035 ppm (within 

the range of background concentrations) 

up to approximately 0.050 ppm, other 

studies observe linear concentrationresponse functions suggesting that there 

may be no effects thresholds at the 

population level above background 

concentrations. In addition, other 

studies conducted subset analyses that 

included only days with ambient O3

concentrations below the level of the 

then current standard, or below even 

lower O3 concentrations, including a 

level as low as 0.061 ppm, and continue 

to report statistically significant 

associations. The Administrator notes 

that the relationships between ambient 

O3 concentrations and lung function 

decrements, respiratory symptoms, 

indicators of respiratory morbidity 

including increased respiratory-related 

emergency department visits and 

hospital admissions, and possibly 

mortality reported in a large number of 

studies likely extend down to ambient 

O3 concentrations well below the level 

of the standard set in 2008 (0.075 ppm), 

in that the highest level at which there 

is any indication of a threshold is 

approximately 0.050 ppm. The 

Administrator notes as well that toward 

the lower end of the range of O3

concentrations observed in such studies, 

ranging down to background levels (i.e., 

0.035 to 0.015 ppm), 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. She also 

notes that there are limitations in 

epidemiological studies that make 

discerning population thresholds 

difficult, as discussed above, such that 

there is the possibility that thresholds 

for individuals may exist in reported 

associations at fairly low levels within 

the range of air quality observed in the 

studies but not be detectable as 

population thresholds in 

epidemiological analyses. 

In looking more broadly at evidence 

from animal toxicological, controlled 

human exposure, and epidemiological 

studies, the Administrator finds 

substantial evidence, newly available 

for consideration in the 2008 

rulemaking, that people with asthma 

and other preexisting pulmonary 

diseases are among those at increased 

risk from O3 exposure. As discussed 

above, altered physiological, 

morphological, and biochemical states 

typical of respiratory diseases like 

asthma, COPD, and chronic bronchitis 

may render people sensitive to 

additional oxidative burden induced by 

O3 exposure. Children and adults with 

asthma are the group that has been 

studied most extensively. Evidence from 

controlled human exposure studies 

indicates that asthmatics and people 

with allergic rhinitis may exhibit larger 

lung function decrements in response to 

O3 exposure than healthy subjects and 

that they can have larger inflammatory 

responses. The Administrator also notes 

that two large U.S. epidemiological 

studies, as well as several smaller U.S. 

and international studies, have reported 

fairly robust associations between 

ambient O3 concentrations and 

measures of lung function and daily 

symptoms (e.g., chest tightness, wheeze, 

shortness of breath) in children with 

moderate to severe asthma and between 

O3 and increased asthma medication 

use. These more serious responses in 

asthmatics and others with lung disease 

provide biological plausibility for the 

respiratory morbidity effects observed in 

epidemiological studies, such as 

respiratory-related emergency 

department visits and hospital 

admissions. 

The Administrator also observes that 

a substantial body of evidence from 

controlled human exposure and 

epidemiological studies indicates that 

relative to the healthy, non-asthmatic 

subjects used in most controlled human 

exposure studies, a greater proportion of 

people with asthma may be affected, 

and those who are affected may have as 

large or larger lung function and 

symptomatic responses to O3 exposures. 

Thus, the Administrator concludes that 

controlled human exposure studies of 

lung function decrements and 

respiratory symptoms that evaluate only 

healthy, non-asthmatic subjects likely 

underestimate the effects of O3 exposure 

on asthmatics and other susceptible 

populations. 

In addition to the evidence-based 

considerations discussed above, the 

Administrator also considered 

quantitative exposures and health risks 

estimated to occur associated with air 

quality simulated to just meet various 

standard levels to help inform 

judgments about a range of standard 

levels for consideration that could 

provide an appropriate degree of public 

health protection. In so doing, she is 

mindful of the important uncertainties 

and limitations that are associated with 

the exposure and risk assessments, as 

discussed in more detail in the 2007 

Staff Paper, and above in sections II.B 

and II.C.1.b. Beyond these uncertainties, 

the Administrator also recognized 

important limitations related to the 

exposure and risk analyses. For 

example, EPA did not have sufficient 

information to evaluate all relevant atrisk groups (e.g., outdoor workers) or all 

O3-related health outcomes (e.g., 

increased medication use, school 

absences, emergency department visits), 

and the scope of the analyses was 

generally limited to estimating 

exposures and risks in 12 urban areas 

across the U.S., and to only five or just 

one area for some health effects. Thus, 

it is clear that national-scale public 

health impacts of ambient O3 exposures 

are much larger than the quantitative 

estimates of O3-related incidences of 

adverse health effects and the numbers 

of children likely to experience 

exposures of concern associated with 

meeting the then current standard or 

alternative standards. Taking these 

limitations into account, the CASAC 

advised EPA not to rely solely on the 

results of the exposure and risk 

assessments in considering alternative 

standards, but also to place significant 

weight on the body of evidence of O3- 

related health effects in drawing 

conclusions about an appropriate range 

of levels for consideration. The 

Administrator agrees with this advice. 

Turning first to the results of the 

exposure assessment, the Administrator 

focused on the extent to which 

alternative standard levels, 

approximately at and below the 0.075 

ppm O3 standard set in the 2008 final 

rule, are estimated to reduce exposures 

over the 0.060 and 0.070 ppm health 

effects benchmark levels, for all and 

asthmatic school age children in the 12 

urban areas included in the 

assessment.52 The Administrator also 

took note that the lowest standard level 

included in the exposure and health risk 

assessments was 0.064 ppm and that 

additional reductions in exposures over 

the selected health benchmark levels 

would be anticipated for just meeting a 

0.060 ppm standard. 

As an initial matter, the Administrator 

recognized that the concept of 

‘‘exposures of concern’’ is more 

appropriately viewed as a continuum, 

with greater confidence and less 

uncertainty about the existence of 

health effects at the upper end and less 

confidence and greater uncertainty as 

one considers increasingly lower O3

exposure levels. In considering the 

concept of exposures of concern, the 

Administrator also noted that it is 

important to balance concerns about the 

potential for health effects and their 


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severity with the increasing uncertainty 

associated with our understanding of 

the likelihood of such effects at lower 

O3 levels. Within the context of this 

continuum, estimates of exposures of 

concern at discrete benchmark levels 

provide some perspective on the public 

health impacts of O3-related 

physiological effects that have been 

demonstrated in controlled human 

exposure and toxicological studies but 

cannot be evaluated in quantitative risk 

assessments, such as lung inflammation, 

increased airway responsiveness, and 

changes in host defenses. They also help 

in understanding the extent to which 

such impacts have the potential to be 

reduced by meeting alternative 

standards. As discussed in II.C.1.a 

above, these O3-related physiological 

effects are plausibly linked to the 

increased morbidity seen in 

epidemiological studies (e.g., as 

indicated by increased medication use 

in asthmatics, school absences in all 

children, and emergency department 

visits and hospital admissions in people 

with lung disease). 

Estimates of the number of people 

likely to experience exposures of 

concern cannot be directly translated 

into quantitative estimates of the 

number of people likely to experience 

specific health effects, since sufficient 

information to draw such comparisons 

is not available—if such information 

were available, these health outcomes 

would have been included in the 

quantitative risk assessment. Due to 

individual variability in responsiveness, 

only a subset of individuals who have 

exposures at and above a specific 

benchmark level are expected to 

experience such adverse health effects, 

and susceptible population groups such 

as those with asthma are expected to be 

affected more by such exposures than 

healthy individuals. 

For the reasons discussed in section 

II.C.1.b above, the Administrator has 

concluded that it is appropriate to focus 

on both the 0.060 and 0.070 ppm health 

effect benchmarks for her decision on 

the primary standard. In summary, the 

focus on these two benchmark levels 

reflects the following evidence-based 

considerations, discussed above in 

section II.C.1.a, that raise concerns 

about adverse health effects likely 

occurring at levels below 0.080 ppm: (1) 

That there is limited, but important, 

new evidence from controlled human 

exposure studies showing lung function 

decrements and respiratory symptoms 

in some healthy subjects at 0.060 ppm; 

(2) that asthmatics are likely to have 

more serious responses than healthy 

individuals; (3) that lung function is not 

likely to be as sensitive a marker for O3

effects as lung inflammation; and (4) 

that there is epidemiological evidence 

which reports associations between 

ambient O3 concentrations and 

respiratory symptoms, ED visits, 

hospital admissions, and premature 

mortality in areas with O3 levels that 

extend well below 0.080 ppm. 

Based on the exposure and risk 

considerations discussed in detail in the 

2007 Staff Paper and presented in 

sections II.B and II.C.1.b above, the 

Administrator notes the following 

important observations from these 

assessments: (1) There is a similar 

pattern for all children and asthmatic 

school age children in terms of 

exposures of concern over selected 

benchmark levels when estimates are 

expressed in terms of percentage of the 

population; (2) the aggregate estimates 

of exposures of concern reflecting 

estimates for the 12 urban areas 

included in the assessment are 

considerably larger for the benchmark 

level of 0.060 ppm compared to the 

0.070 ppm benchmark; (3) there is 

notable year-to-year variability in 

exposure and risk estimates with higher 

exposure and risk estimates occurring in 

simulations involving a year with 

generally poorer air quality in most 

areas (2002) compared to a year with 

generally better air quality (2004); and 

(4) there is significant city-to-city 

variability in exposure and risk 

estimates, with some cities receiving 

considerably less protection associated 

with air quality just meeting the same 

standard. As discussed above, the 

Administrator believes that it is 

appropriate to consider not just the 

aggregate estimates across all cities, but 

also to consider the public health 

impacts in cities that receive relatively 

less protection from alternative 

standards under consideration. 

Similarly, the Administrator believes 

that year-to-year variability should also 

be considered in making judgments 

about which standards will protect 

public health with an adequate margin 

of safety. 

In addition, significant reductions in 

exposures of concern and risk have been 

estimated to occur across standard 

levels analyzed. The magnitudes of 

exposure and risk reductions estimated 

to occur in going from a 0.074 ppm 

standard to a 0.064 ppm standard are as 

large as those estimated to occur in 

going from the then current 0.084 ppm 

standard to a 0.074 ppm standard. 

Consequently, the reduction in risk that 

can be achieved by going from a 

standard of 0.074 ppm to a standard of 

0.064 ppm is comparable to the risk 

reduction that can be achieved by 

moving from the 1997 O3 standard, 

effectively a 0.084 ppm standard, to a 

standard very close to the 2008 standard 

of 0.075 ppm. 

The Administrator also observes that 

estimates of exposures of concern 

associated with air quality just meeting 

the alternative standards below 0.080 

ppm (i.e., 0.074, 0.070, and 0.064 ppm, 

the levels included in the assessment) 

are notably lower than estimates for 

alternative standards set at and above 

0.080 ppm. As shown in Table 6–8 in 

the 2007 Staff Paper, just meeting a 

0.080 ppm standard is associated with 

an aggregate estimate of exposures of 

concern of about 13% of asthmatic 

children at the 0.070 ppm benchmark 

level, ranging up to 31% in the city with 

the least degree of protection in a year 

with generally poorer air quality, and an 

aggregate estimate of exposures of 

concern of about 40% of asthmatic 

children, ranging up to 63% in the city 

with the least degree of protection at the 

0.060 ppm benchmark level. Based on 

the exposure estimates presented in 

Table 3 in this notice, she observes that 

standards included in the assessment 

below 0.080 ppm (i.e., 0.074, 0.070, and 

0.064 ppm), are estimated to have 

substantially lower estimates of 

exposures of concern at the 0.070 ppm 

benchmark level. Similarly, she notes 

that exposures of concern at the 0.060 

ppm benchmark associated with 

alternative standards below 0.080 ppm 

are appreciably lower than exposures 

associated with standards at or above 

0.080 ppm, especially for standards set 

at 0.064 and 0.070 ppm. 

As noted previously, the 

Administrator also recognizes that the 

risk estimates for health outcomes 

included in the risk assessment are 

limited and that the overall health 

effects evidence is indicative of a much 

broader array of O3-related health effects 

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, 

doctor’s visits, and emergency 

department visits), some of which have 

a greater impact on at-risk groups. 

Consideration of such unquantified 

risks for this array of health effects, 

taken together with the estimates of 

exposures of concern and the quantified 

health risks discussed above, supports 

the Administrator’s evidence-based 

conclusion that revising the standard 

level to a level well below 0.080 ppm 

will provide important increased public 

health protection, especially for at-risk 

groups such as people with asthma or 

other lung disease, as well as children 

and older adults, particularly those 

active outdoors, and outdoor workers. 


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Based on the evidence- and exposure/ 

risk-based considerations discussed 

above, the Administrator concludes that 

it is appropriate to set the level of the 

primary O3 standard to a level well 

below 0.080 ppm, a level at which the 

evidence provides a high degree of 

certainty about the adverse effects of O3

exposure in healthy people, to provide 

an adequate margin of safety for at-risk 

groups. In selecting a proposed range of 

levels, the Administrator believes it is 

appropriate to consider the following 

information: (1) The strong body of 

evidence from controlled human 

exposure studies evaluating healthy 

people at exposure levels of 0.080 ppm 

and above that demonstrated lung 

function decrements, respiratory 

symptoms, pulmonary inflammation, 

and other medically significant airway 

responses, as well as limited but 

important evidence of lung function 

decrements and respiratory symptoms 

in healthy people down to O3 exposure 

levels of 0.060 ppm; (2) the substantial 

body of evidence from controlled 

human exposure and epidemiological 

studies indicating that people with 

asthma are likely to experience larger 

and more serious effects than healthy 

people; (3) the body of epidemiological 

evidence indicating associations are 

observed for a wide range of serious 

health effects, including respiratoryrelated emergency department visits and 

hospital admissions and premature 

mortality, across distributions of 

ambient O3 concentrations that extend 

below the current standard level of 

0.075 ppm, as well as questions of 

biological plausibility in attributing the 

observed effects to O3 alone at the lower 

end of the concentration ranges 

extending down to background levels; 

and (4) the estimates of exposures of 

concern and risks for a range of health 

effects that indicate that important 

improvements in public health are very 

likely associated with O3 levels just 

meeting alternative standards, 

especially for standards set at 0.070 and 

0.064 ppm (the lowest levels included 

in the assessment), relative to standards 

set at and above 0.080 ppm. 

The Administrator next considered 

what standard level well below 0.080 

ppm would be requisite to protect 

public health, including the health of atrisk groups, with an adequate margin of 

safety that is sufficient but not more 

than necessary to achieve that result. 

The assessment of a standard level calls 

for consideration of both the degree of 

risk to public health at alternative levels 

of the standard as well as the certainty 

that such risk will occur at any specific 

level. Based on the information 

available in the 2008 rulemaking, there 

is no evidence-based bright line that 

indicates a single appropriate level. 

Instead there is a combination of 

scientific evidence and other 

information that needs to be considered 

as a whole in making this public health 

policy judgment, and selecting a 

standard level from a range of 

potentially reasonable values. 

As an initial matter, the Administrator 

considered whether the standard level 

of 0.075 ppm set in the 2008 final rule 

is sufficiently below 0.080 ppm to be 

requisite to protect public health with 

an adequate margin of safety. In 

considering this standard level, the 

Administrator looked to the rationale for 

selecting this level presented in the 

2008 final rule, as summarized above in 

section II.C.3. In that rationale, EPA 

observed that a level of 0.075 ppm is 

above the range of 0.060 to 0.070 ppm 

recommended by CASAC, and that the 

CASAC Panel appeared to place greater 

weight on the evidence from the Adams 

studies and on the results of the 

exposure and risk assessments, whereas 

EPA placed greater weight on the 

limitations and uncertainties associated 

with that evidence and the quantitative 

exposure and risk assessments. 

Additionally, EPA’s rationale did not 

discuss and thus placed no weight on 

exposures of concern relative to the 

0.060 ppm benchmark. Further, EPA 

concluded that ‘‘[a] standard set at a 

lower level than 0.075 ppm would only 

result in significant further public 

health protection if, in fact, there is a 

continuum of health risks in areas with 

8-hour average O3 concentrations that 

are well below the concentrations 

observed in the key controlled human 

exposure studies and if the reported 

associations observed in 

epidemiological studies are, in fact, 

causally related to O3 at those lower 

levels. Based on the available evidence, 

[EPA] is not prepared to make these 

assumptions’’ (73 FR 16483). 

In reconsidering the entire body of 

evidence available in the 2008 

rulemaking, including the Agency’s own 

assessment of the epidemiological 

evidence in the 2006 Criteria Document, 

and placing significant weight on the 

views of CASAC, the Administrator now 

concludes that important and significant 

risks to public health are likely to occur 

at a standard level of 0.075 ppm. She 

judges that a standard level of 0.075 

ppm is not sufficient to provide 

protection with an adequate margin of 

safety. In support of this conclusion, the 

Administrator finds that setting a 

standard that would protect public 

health, including the health of at-risk 

populations, with an adequate margin of 

safety should reasonably depend upon 

giving some weight to the results of the 

Adams studies and EPA’s reanalysis of 

the Adams’s data, and to how effectively 

alternative standard levels would serve 

to limit exposures of concern relative to 

the 0.060 ppm benchmark level as well 

as to the 0.070 ppm benchmark level. 

The Administrator notes that EPA’s risk 

assessment estimates comparable risk 

reductions in going from a 0.074 ppm 

standard to a 0.064 ppm standard as 

were estimated in going from the then 

current 0.084 ppm standard down to a 

0.074 ppm standard for an array of 

health effects analyzed. These estimates 

include reductions in risk for lung 

function decrements in all and 

asthmatic school age children, 

respiratory symptoms in asthmatic 

children, respiratory-related hospital 

admissions, and non-accidental 

mortality. 

Further, based on the exposure 

assessment estimates discussed above, 

the Administrator notes that for air 

quality just meeting a 0.074 ppm 

standard, approximately 27% of 

asthmatic school age children and 25% 

of all school age children are estimated 

to experience one or more exposures of 

concern over the 0.060 ppm benchmark 

level based on simulations for a year 

with generally poorer air quality; this 

estimate increases to about 50% of 

asthmatic and all children in the city 

with the least degree of protection. The 

Administrator judges that these 

estimates are large and strongly suggest 

significant public health impacts would 

likely remain in many areas with air 

quality just meeting a 0.075 ppm O3

standard. 

In light of these estimates and the 

available evidence, the Administrator 

agrees with CASAC’s conclusion that 

important public health protections can 

be achieved by a standard set below 

0.075 ppm, within the range of 0.060 to 

0.070 ppm. In addition, based on both 

the evidence- and exposure/risk-based 

considerations summarized above, the 

Administrator concludes that a standard 

set as high as 0.075 would not be 

considered requisite to protect public 

health with an adequate margin of 

safety, and that consideration of lower 

levels is warranted. In considering such 

lower levels, the Administrator 

recognizes that the CAA requires her to 

reach a public health policy judgment as 

to what standard would be requisite to 

protect public health with an adequate 

margin of safety, based on scientific 

evidence and technical assessments that 

have inherent uncertainties and 

limitations. This judgment requires 

making reasoned decisions as to what 

weight to place on various types of 


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evidence and assessments and on the 

related uncertainties and limitations. 

In selecting a level below 0.075 ppm 

that would serve as an appropriate 

upper end for a range of levels to 

propose, the Administrator has 

considered a more cautious approach to 

interpreting the available evidence and 

exposure/risk-based information—that 

is, an approach that places significant 

weight on uncertainties and limitations 

in the information so as to avoid 

potentially overestimating public health 

risks and protection likely to be 

associated with just meeting a particular 

standard level. In so doing, she notes 

that the most certain evidence of 

adverse health effects from exposure to 

O3 comes from the controlled human 

exposure studies, and that the large bulk 

of this evidence derives from studies of 

exposures at levels of 0.080 ppm and 

above. At those levels, there is 

consistent evidence of lung function 

decrements and respiratory symptoms 

in healthy young adults, as well as 

evidence of inflammation and other 

medically significant airway responses. 

Further, she takes note of the limited 

but important evidence from controlled 

human exposure studies indicating that 

lung function decrements and 

symptoms can occur in healthy people 

at levels as low as 0.060 ppm, while also 

recognizing the limitations in that 

evidence, as discussed above in sections 

II.A.1 and II.C.1.a. She also notes that 

some people with asthma are likely to 

experience larger and more serious 

effects than the healthy subjects 

evaluated in the controlled exposure 

studies, while recognizing that there is 

uncertainty about the magnitude of such 

differences. In considering the available 

epidemiological studies, she recognizes 

that they provide evidence of serious 

respiratory morbidity effects, including 

respiratory-related emergency 

department visits and hospital 

admissions, and non-accidental 

mortality at levels well below 0.080 

ppm, while also recognizing that there 

is increasing uncertainty associated 

with the likelihood that such effects 

occur at decreasing O3 levels down to 

background levels. Considering the 

exposure/risk information, as shown in 

Table 3, the Administrator observes that 

a standard set at 0.070 ppm would 

likely substantially limit exposures of 

concern relative to the 0.070 ppm 

benchmark level, while affording far 

less protection against exposures of 

concern relative to the 0.060 ppm 

benchmark level. To the extent that 

more weight is placed on protection 

relative to the higher benchmark level, 

and more weight is placed on the 

uncertainties associated with the 

epidemiological evidence, a standard set 

at 0.070 ppm might be considered to be 

adequately protective. Taken together, 

this type of cautious approach to 

interpreting the evidence and the 

exposure/risk information serves as the 

basis for the Administrator’s conclusion 

that the upper end of the proposed 

range should be set at 0.070 ppm O3. 

In selecting a level that would serve 

as an appropriate lower end for a range 

of levels to propose, the Administrator 

has considered a more precautionary 

approach to interpreting the available 

evidence and exposure/risk-based 

information—that is, an approach that 

places less weight on uncertainties and 

limitations in the information so as to 

avoid potentially underestimating 

public health improvements likely to be 

associated with just meeting a particular 

standard level. In so doing, the 

Administrator notes the limited, but 

important evidence of a lowestobserved-effects level at 0.060 ppm O3

from controlled human exposure studies 

reporting lung function decrements and 

respiratory symptoms in healthy 

subjects. Notably, these studies also 

report that a small percentage of 

subjects (7 to 20 percent) experienced 

moderate lung function decrements 

(≥ 10 percent) at the 0.060 ppm 

exposure level, recognizing that for 

people with lung disease, such 

moderate functional or symptomatic 

responses would likely interfere with 

normal activity for many individuals, 

and would likely result in more frequent 

use of medication. In addition, a 

substantial body of evidence indicates 

that people with asthma are likely to 

experience larger and more serious 

effects than healthy people and 

therefore controlled human exposure 

studies done with healthy subjects 

likely underestimate effects in this atrisk population. 

Moreover, epidemiological studies 

provide evidence of serious respiratory 

morbidity effects, including respiratoryrelated emergency department visits and 

hospital admissions, and non-accidental 

mortality at O3 levels that may plausibly 

extend down to at least 0.060 ppm even 

when considering the uncertainties 

inherent in such studies. The 

Administrator notes that the controlled 

human exposure studies conducted at 

0.060 ppm provide some biological 

plausibility for associations between 

respiratory morbidity and mortality 

effects found in epidemiological studies 

and O3 exposures down to 0.060 ppm. 

Considering the exposure information, 

as shown in Table 3, the Administrator 

observes that a standard set at 0.064 

ppm would likely essentially eliminate 

exposures of concern relative to the 

0.070 ppm benchmark level, while 

appreciably limiting exposures of 

concern relative to the 0.060 ppm 

benchmark level to approximately 6 

percent of asthmatic children in the 

aggregate across 12 cities and up to 16 

percent in the city that would receive 

the least protection. While not 

addressed in the exposure assessment 

done as part of the 2008 rulemaking, a 

standard set at 0.060 ppm would be 

expected to provide somewhat greater 

protection from such exposures, which 

is important to the extent that more 

weight is placed on providing 

protection relative to the lower 

benchmark level. Taken together, the 

Administrator concludes that this 

precautionary approach to interpreting 

the evidence and the exposure/risk 

information supports a level of 0.060 

ppm as the lower end of the proposed 

range. 

The Administrator has also concluded 

that the lower end of the proposed range 

should not extend below 0.060 ppm O3. 

In reaching this conclusion, she gives 

significant weight to the 

recommendation of the CASAC panel 

that 0.060 ppm should be the lower end 

of the range for consideration 

(Henderson, 2006c). In the 

Administrator’s view, the evidence from 

controlled human exposure studies at 

the 0.060 ppm exposure level, the 

lowest level tested, is not robust enough 

to support consideration of a lower 

level. While some epidemiological 

studies provide evidence of serious 

respiratory morbidity effects and nonaccidental mortality with no evidence of 

a threshold, the Administrator notes 

that other studies provide evidence of a 

potential threshold somewhat below 

0.060 ppm. Moreover, there are 

limitations in epidemiological studies 

that make discerning population 

thresholds difficult, including fewer 

observations in the range of lower 

concentrations, concerns related to 

exposure measurement error, the 

possible role of copollutants and effects 

modifiers, and interindividual 

differences in susceptibility to O3- 

related effects. In the Administrator’s 

judgment, these limitations in 

epidemiological studies, including the 

limitations in judging the causality of 

observed associations at lower O3 levels, 

and the lack of robust controlled human 

exposure data at 0.060 ppm make it 

difficult to interpret this evidence as a 

basis for a standard level set below 

0.060 ppm. Thus, in selecting 0.060 

ppm as the lower end of the range for 

the proposed level of the O3 standard, 

the Administrator has taken into 


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account information on the lowestobserved-effects levels in controlled 

human exposure studies, indications of 

possible thresholds reported in some 

epidemiological studies, the increasing 

uncertainty in the epidemiological 

evidence at even lower levels, as well as 

evidence about increased susceptibility 

of people with asthma and also other 

lung diseases. In so doing, she 

concludes that a primary O3 standard 

set below 0.060 ppm would be more 

than is necessary to protect public 

health with an adequate margin of safety 

for at-risk groups. 

In reaching her proposed decision, the 

Administrator has also considered the 

public comments that were received on 

the 2007 proposed rule (72 FR 37818). 

The Administrator notes that there were 

sharply divergent views expressed by 

two general sets of commenters with 

regard to considering the health effects 

evidence, results of exposure and risk 

assessments, and the advice of the 

CASAC panel. On one hand, medical 

groups, health effects researchers, 

public health organizations, 

environmental groups, and some state, 

tribal and local air pollution control 

agencies strongly supported a standard 

set within the range recommended by 

the CASAC. These commenters 

generally placed significant weight on 

the more recent evidence from 

controlled human exposure studies, 

down to the 0.060 ppm exposure level, 

as well as on the epidemiological 

studies and the results of the exposure 

and risk assessment conducted for the 

2008 rulemaking. Many of these 

commenters took a more precautionary 

view and supported a standard set at 

0.060 ppm O3, the lower end of the 

CASAC recommended range. The 

Administrator notes that these views are 

generally consistent with her proposed 

conclusions. On the other hand, another 

group of commenters primarily 

representing industry associations and 

businesses and some state 

environmental agencies, primarily 

expressed the view that the more recent 

evidence from controlled human 

exposure, the epidemiological studies, 

and the results of exposure and human 

health risk assessments were so 

uncertain that they did not provide a 

basis for making any changes to the then 

current 0.084 ppm O3 standard set in 

1997. This group of commenters 

generally argued that the health effects 

evidence newly available in the 2008 

rulemaking, the results of the exposure 

and health risk assessments, and the 

advice of the CASAC were flawed. For 

the reasons discussed above, the 

Administrator does not agree with the 

later group of commenters that 

essentially no weight should be placed 

on any of the new evidence or 

assessments that were available for 

consideration in the 2008 rulemaking. 

Based on consideration of the entire 

body of evidence and information 

available in the 2008 rulemaking, 

including exposure and risk estimates, 

as well as the recommendations of 

CASAC, the Administrator proposes to 

set the level of the primary 8-hour O3

standard to a level within the range of 

0.060 to 0.070 ppm. A standard level 

within this range would reduce the risk 

of a variety of health effects associated 

with exposure to O3, including the 

respiratory symptoms and lung function 

effects demonstrated in the controlled 

human exposure studies, and the 

respiratory-related emergency 

department visits, hospital admissions 

and mortality effects observed in the 

epidemiological studies. All of these 

effects are indicative of a much broader 

array of O3-related health endpoints, 

such as school absences and increased 

medication use, that are plausibly 

linked to these observed effects. 

Depending on the weight placed on the 

evidence and information available in 

the 2008 rulemaking, as well as the 

uncertainties and limitations in the 

evidence and information, a standard 

could be set within this range at a level 

that would be requisite to protect public 

health with an adequate margin of 

safety. 

In reaching this proposed decision, as 

discussed above, the Administrator has 

focused on the nature of the increased 

public health protection that would be 

afforded by a standard set within the 

proposed range of levels relative to the 

protection afforded by the standard set 

in 2008. Having considered the public 

comments received on the 2007 

proposed rule in reaching this proposed 

decision that reconsiders the 2008 final 

rule, the Administrator is interested in 

again receiving public comment on the 

benefits to public health associated with 

a standard set at specific levels within 

the proposed range relative to the 

benefits associated with the standard set 

in 2008. 

D. Proposed Decision on the Level of the 

Primary Standard 

For the reasons discussed above, and 

taking into account information and 

assessments presented in the 2006 

Criteria Document and 2007 Staff Paper, 

the advice and recommendations of 

CASAC, and public comments received 

during the 2008 rulemaking, the 

Administrator proposes to set a new 

level for the 8-hour primary O3

standard. Specifically, the 

Administrator proposes to set the level 

of the 8-hour primary O3 standard to 

within a range of 0.060 to 0.070 ppm. 

The proposed 8-hour primary standard 

would be met at an ambient air 

monitoring site when the 3-year average 

of the annual fourth-highest daily 

maximum 8-hour average O3

concentration is less than or equal to the 

level of the standard that is 

promulgated. Thus, the Administrator 

proposes to set a standard with a level 

within this range. She solicits comment 

on this range and on the appropriate 

weight to place on the various types of 

available evidence, the exposure and 

risk assessment results, and the 

uncertainties and limitations related to 

this information, as well as on the 

benefits to public health associated with 

a standard set within this range relative 

to the benefits associated with the 

standard set in 2008. 

III. Communication of Public Health 

Information 

Information on the public health 

implications of ambient concentrations 

of criteria pollutants is currently made 

available primarily through EPA’s Air 

Quality Index (AQI) program. The 

current Air Quality Index has been in 

use since its inception in 1999 (64 FR 

42530). It provides accurate, timely, and 

easily understandable information about 

daily levels of pollution (40 CFR 58.50). 

The AQI establishes a nationally 

uniform system of indexing pollution 

levels for O3, carbon monoxide, nitrogen 

dioxide, particulate matter and sulfur 

dioxide. The AQI converts pollutant 

concentrations in a community’s air to 

a number on a scale from 0 to 500. 

Reported AQI values enable the public 

to know whether air pollution levels in 

a particular location are characterized as 

good (0–50), moderate (51–100), 

unhealthy for sensitive groups (101– 

150), unhealthy (151–200), very 

unhealthy (201–300), or hazardous 

(300–500). The AQI index value of 100 

typically corresponds to the level of the 

short-term NAAQS for each pollutant. 

An AQI value greater than 100 means 

that a pollutant is in one of the 

unhealthy categories (i.e., unhealthy for 

sensitive groups, unhealthy, very 

unhealthy, or hazardous) on a given 

day; whereas an AQI value at or below 

100 means that a pollutant 

concentration is in one of the 

satisfactory categories (i.e., moderate or 

good). Decisions about the pollutant 

concentrations at which to set the 

various AQI breakpoints, that delineate 

the various AQI categories, draw 

directly from the underlying health 

information that supports the NAAQS 

review. 


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In the 2008 rulemaking, the AQI for 

O3 was revised by setting an AQI value 

of 100 equal to 0.075 ppm, 8-hour 

average, the level of the revised primary 

O3 standard. The other AQI breakpoints 

were also revised as follows: An AQI 

value of 50 is set at 0.059 ppm; an AQI 

value of 150 was set at 0.095 ppm; and 

an AQI value of 200 was set at 0.115 

ppm. All these levels are averaged over 

8 hours. These levels were developed by 

making proportional adjustments to the 

other AQI breakpoints (i.e., AQI values 

of 50, 150 and 200). 

The Agency recognizes the 

importance of revising the AQI in a 

timely manner to be consistent with any 

revisions to the NAAQS. Therefore, 

having proposed to set a new level for 

the 2008 primary 8-hour O3 standard in 

this action, EPA also proposes to 

finalize conforming changes to the AQI 

in connection with the Agency’s final 

decision on the level of the primary O3

standard. These conforming changes 

would include setting the 100 level of 

the AQI at the same level as that set for 

the primary O3 standard resulting from 

this rulemaking, and also making 

proportional adjustments to AQI 

breakpoints at the lower end of the 

range (i.e., AQI values of 50, 150 and 

200). EPA does not propose to change 

breakpoints at the higher end of the 

range (from 300 to 500), which would 

apply to state contingency plans or the 

Significant Harm Level (40 CFR 51.16), 

because the information from this 

reconsideration of the 2008 final rule 

does not inform decisions about 

breakpoints at those higher levels. 

With respect to reporting 

requirements (40 CFR Part 58, § 58.50), 

EPA proposes to require that the AQI be 

reported in all metropolitan and 

micropolitan statistical areas where O3

monitoring is required, as discussed 

below in section VI. The Agency solicits 

comments on our proposed approach to 

AQI reporting requirements. We are also 

revising 40 CFR Part 58, § 58.50(c) to 

require the reporting requirements to be 

based on the latest available census 

figures, rather than the most recent 

decennial U.S. census. This change is 

consistent with our current practice of 

using the latest population figures to 

make monitoring requirements more 

responsive to changes in population. 

IV. Rationale for Proposed Decision on 

the Secondary Standard 

As an initial matter, the Administrator 

notes that the 2008 final rule concluded 

that (1) the protection afforded by the 

1997 secondary O3 standard was ‘‘not 

sufficient and that the standard needs to 

be revised to provide additional 

protection from known and anticipated 

adverse effects on sensitive natural 

vegetation and sensitive ecosystems, 

and that such a revised standard could 

also be expected to provide additional 

protection to sensitive ornamental 

vegetation’’ and (2) ‘‘that there is not 

adequate information to establish a 

separate secondary standard based on 

other effects of O3 on public welfare’’ (73 

FR 16497). The Administrator is not 

reconsidering these aspects of the 2008 

decision, which are based on the 

reasons discussed in section IV.B of the 

2008 final rule (73 FR 16489–16497). 

The Administrator also notes that the 

2008 final rule concluded that it was 

appropriate to retain the O3 indicator for 

the secondary O3 standard. The 

Administrator is not reconsidering this 

aspect of the 2008 decision, which was 

based on the reasons discussed in 

sections IV.B and IV.C of the 2008 final 

rule (73 FR 16489–16497). For these 

reasons, the Administrator is not 

reopening the 2008 decision with regard 

to the need to revise the 1997 secondary 

O3 standard to provide additional 

protection from known and anticipated 

adverse effects on sensitive natural 

vegetation and sensitive ecosystems, nor 

with regard to the appropriate indicator 

for the secondary standard. Thus, the 

information that follows in this section 

specifically focuses on a reconsideration 

of the 8-hour secondary O3 standard set 

in the 2008 final rule for the purpose of 

determining whether and, if so, how to 

revise the form, averaging time, and 

level of the standard to provide 

appropriate protection from known and 

anticipated adverse effects on sensitive 

natural vegetation and sensitive 

ecosystems. 

This section presents the rationale for 

the Administrator’s proposed decision 

that the secondary O3 standard, which 

was set identical to the revised primary 

standard in the 2008 final rule, should 

instead be a new cumulative, seasonal 

standard. This standard is expressed in 

terms of a concentration-weighted form 

commonly called W126, which uses a 

sigmoidal weighting function to assign a 

weight to each hourly O3 concentration 

within the 12-hour daylight period (8 

am to 8 pm). This daily ozone index is 

defined as follows: 

daily W w C where C = hourly O at hour i, and w = ci i 3 c i 126 1

1 = , + ⋅ −

<

∑ 4403 126

8

8

e C

i= am

i pm

The daily index values are then 

summed over each month within the O3

season, and the annual highest 

consecutive three month sum is 

determined. The proposed standard 

consists of the three-year average of this 

highest three-month statistic, set at a 

level within the range of 7 to 15 ppmhours. 

As discussed more fully below, the 

rationale for this proposed new standard 

is based on a thorough review, in the 

2006 Criteria Document, of the latest 

scientific information on vegetation, 

ecological and other public welfare 

effects associated with the presence of 

O3 in the ambient air. This rationale also 

takes into account and is consistent 

with: (1) Staff assessments of the most 

policy-relevant information in the 2006 

Criteria Document and staff analyses of 

air quality, vegetation effects evidence, 

exposure, and risks, presented in the 

2007 Staff Paper, upon which staff 

recommendations for revisions to the 

secondary O3 standard are based; (2) 

CASAC advice and recommendations as 

reflected in discussions of drafts of the 

2006 Criteria Document and 2007 Staff 

Paper at public meetings, in separate 

written comments, and in CASAC’s 

letters to the Administrator, both before 

and after the 2008 rulemaking, and (3) 

public comments received during 

development of these documents, either 

in conjunction with CASAC meetings or 

separately; and on the 2007 proposed 

rule, and (4) consideration of the degree 

of protection to vegetation potentially 

afforded by the 2008 8-hour standard. 

In developing this rationale, the 

Administrator has again focused on 

direct O3 effects on vegetation, 

specifically drawing upon an integrative 

synthesis of the entire body of evidence 

(EPA, 2006a, chapter 9), published 

through early 2006, on the broad array 

of vegetation effects associated with the 

presence of O3 in the ambient air. In 

addition, because O3 can also indirectly 

affect other ecosystem components such 

as soils, water, and wildlife, and their 

associated ecosystem goods and 

services, through its effects on 

vegetation, a qualitative discussion of 

these other indirect impacts is also 


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53 In its assessment of the evidence judged to be 

most relevant to making decisions on the level of 

the O3 secondary standard, however, EPA has 

placed greater weight on U.S. studies, due to the 

often species-, site- and climate-specific nature of 

O3-related vegetation response. 

included, though these effects were not 

quantifiable at the time of the 2008 

rulemaking. As discussed below in 

section IV.A, the peer-reviewed 

literature includes studies conducted in 

the U.S., Canada, Europe, and many 

other countries around the world.53 In 

reconsidering this evidence, as was 

concluded in the 2008 rulemaking, and 

based on the body of scientific literature 

assessed in the 2006 Criteria Document, 

the Administrator continues to believe 

that it is reasonable to conclude that a 

secondary standard protecting the 

public welfare from known or 

anticipated adverse effects to trees and 

native vegetation would also afford 

increased protection from adverse 

effects to other environmental 

components relevant to the public 

welfare, including ecosystem services 

and function. Section IV.B focuses on 

considerations related to biologically 

relevant exposure indices. This 

rationale also draws upon the results of 

quantitative exposure and risk 

assessments, discussed below in section 

IV.C. Section IV.D focuses on the 

considerations upon which the 

Administrator’s proposed conclusions 

are based. Considerations regarding a 

cumulative seasonal standard as well as 

an 8-hour standard are discussed, and 

the rationale for the 2008 decision on 

the secondary standard and CASAC 

advice, given both prior to the 

development of the 2007 proposed rule 

and following the 2008 final rule, are 

summarized. Finally, the 

Administrator’s proposed conclusions 

on the secondary standard are 

presented. Section IV.E summarizes the 

proposed decision on the secondary O3

standard and the solicitation of public 

comments. 

As with virtually any policy-relevant 

vegetation effects research, there is 

uncertainty in the characterization of 

vegetation effects attributable to 

exposure to ambient O3. As discussed 

below, however, research conducted 

since the 1997 review provides 

important information coming from 

field-based exposure studies, including 

free air, gradient, and biomonitoring 

surveys, in addition to the more 

traditional open top chamber (OTC) 

studies. Moreover, the newly available 

studies evaluated in the 2006 Criteria 

Document have undergone intensive 

scrutiny through multiple layers of peer 

review and many opportunities for 

public review and comment. While 

important uncertainties remain, the 

review of the vegetation effects 

information has been extensive and 

deliberate. In the judgment of the 

Administrator, the intensive evaluation 

of the scientific evidence that has 

occurred provides an adequate basis for 

this reconsideration of the 2008 

rulemaking. 

A. Vegetation Effects Information 

This section outlines key information 

contained in the 2006 Criteria 

Document (chapter 9) and in the 2007 

Staff Paper (chapter 7) on known or 

anticipated effects on public welfare 

associated with the presence of O3 in 

ambient air. The information 

highlighted here summarizes: (1) New 

information available in the 2008 

rulemaking on potential mechanisms for 

vegetation effects associated with 

exposure to O3; (2) the nature of effects 

on vegetation that have been associated 

with exposure to O3 and consequent 

potential impacts on ecosystems; and (3) 

considerations in characterizing what 

constitutes an adverse welfare impact of 

O3. 

Exposures to O3 have been associated 

quantitatively and qualitatively with a 

wide range of vegetation effects. The 

decision in the 1997 review to set a 

more protective secondary standard 

primarily reflected consideration of the 

quantitative information on vegetation 

effects available at that time, 

particularly growth impairment (e.g., 

biomass loss) in sensitive forest tree 

species during the seedling growth stage 

and yield loss in important commercial 

crops. This information, derived mainly 

using the open top chamber (OTC) 

exposure method, found cumulative, 

seasonal O3 exposures were most 

strongly associated with observed 

vegetation response. The 2006 Criteria 

Document discusses a number of 

additional studies that support and 

strengthen key conclusions regarding O3

effects on vegetation and ecosystems 

found in the previous Criteria Document 

(EPA, 1996a, 2006a), including further 

clarification of the underlying 

mechanistic and physiological processes 

at the sub-cellular, cellular, and whole 

system levels within the plant. More 

importantly, however, in the context of 

this review, new quantitative 

information is now available across a 

broader array of vegetation effects (e.g., 

growth impairment during seedlings, 

saplings and mature tree growth stages, 

visible foliar injury, and yield loss in 

annual crops) and across a more diverse 

set of exposure methods, including 

chamber, free air, gradient, model, and 

field-based observation. The nonchambered, field-based study results 

begin to address one of the key data 

gaps cited by EPA in the 1997 review. 

The following discussion of the 

policy-relevant science regarding 

vegetation effects associated with 

cumulative, seasonal exposures to 

ambient levels of O3 integrates 

information from the 2006 Criteria 

Document (chapter 9) and the 2007 Staff 

Paper (chapter 7). 

1. Mechanisms 

Scientific understanding regarding O3

impacts at the genetic, physiological, 

and mechanistic levels helps to explain 

the biological plausibility and 

coherence of the evidence for O3- 

induced vegetation effects and informs 

the interpretation of predictions of risk 

associated with vegetation response at 

ambient O3 exposure levels. In most 

cases, the mechanisms of response are 

similar regardless of the degree of 

sensitivity of the species. The evidence 

assessed in the 2006 Criteria Document 

(EPA, 2006a) regarding the O3-induced 

changes in physiology continues to 

support the information discussed in 

the 1997 review (EPA, 1996a, 2006a). In 

addition, during the last decade 

understanding of the cellular processes 

within plants has been further clarified 

and enhanced. This section reviews the 

key scientific conclusions identified in 

1996 Criteria Document (EPA, 1996a), 

and incorporates recent information 

from the Criteria Document (EPA, 

2006a). This section describes: (1) Plant 

uptake of O3, (2) O3-induced cellular to 

systemic response, (3) plant 

compensation and detoxification 

mechanisms, (4) O3-induced changes to 

plant metabolism, and (5) plant 

response to chronic O3 exposures. 

a. Plant Uptake of Ozone 

To cause injury, O3 must first enter 

the plant through openings in the leaves 

called stomata. Leaves exist in a three 

dimensional environment called the 

plant canopy, where each leaf has a 

unique orientation and receives a 

different exposure to ambient air, 

microclimatological conditions, and 

sunlight. In addition, a plant may be 

located within a stand of other plants 

which further modifies ambient air 

exchange with individual leaves. Not all 

O3 entering a plant canopy is absorbed 

into the leaf stomata, but may be 

adsorbed to other surfaces e.g., leaf 

cuticles, stems, and soil (termed nonstomatal deposition) or scavenged by 

reactions with intra-canopy biogenic 

VOCs and naturally occurring NOx 

emissions from soils. Because O3 does 

not typically penetrate the leaf’s cuticle, 

it must reach the stomatal openings in 

the leaf for absorption to occur. The 


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movement of O3 and other gases such as 

CO2 into and out of leaves is controlled 

by stomatal guard cells that regulate the 

size of the stomatal apertures. These 

guard cells respond to a variety of 

internal species-specific factors as well 

as external site specific environmental 

factors such as light, temperature, 

humidity, CO2 concentration, soil 

fertility, water status, and in some cases, 

the presence of air pollutants, including 

O3. These modifying factors produce 

stomatal conductances that vary 

between leaves of the same plant, 

individuals and genotypes within a 

species as well as diurnally and 

seasonally. 

b. Cellular to Systemic Response 

Once inside the leaf, O3 can react with 

a variety of biochemical compounds 

that are exposed to the air spaces within 

the leaf or it can be dissolved into the 

water lining the cell wall of the air 

spaces. Once in the aqueous phase, O3

can be rapidly altered to form oxidative 

products that can diffuse more readily 

into and through the cell and react with 

many biochemical compounds. Early 

steps in a series of O3-induced events 

that can lead to leaf injury seems to 

involve alteration in cell membrane 

function, including membrane transport 

properties (EPA, 2006a) and/or reactions 

with organic molecules that in certain 

circumstances result in the generation of 

signaling compounds. The generation of 

such signaling compounds can lead to a 

cascade of events. One such signaling 

molecule is hydrogen peroxide (H2O2). 

The presence of higher-than-normal 

levels of H2O2 within the leaf is a 

potential trigger for a set of metabolic 

reactions that include those typical of 

the well documented ‘‘wounding’’ 

response or pathogen defense pathway 

generated by cutting of the leaf or by 

pathogen/insect attack. Ethylene is 

another compound produced when 

plants are subjected to biotic or abiotic 

stressors. Increased ethylene production 

by plants exposed to O3 stress was 

identified as a consistent marker for O3

exposure in studies conducted decades 

ago (Tingey et al., 1976). 

c. Compensation and Detoxification 

Ozone injury will not occur if (1) the 

rate and amount of O3 uptake is small 

enough for the plant to detoxify or 

metabolize O3 or its metabolites or (2) 

the plant is able to repair or compensate 

for the O3 impacts (Tingey and Taylor, 

1982; U.S. EPA, 1996a). With regard to 

the first, a few studies have documented 

direct stomatal closure or restriction in 

the presence of O3 in some species, 

which limits O3 uptake and potential 

subsequent injury. This response may 

be initiated ranging from within 

minutes to hours or days of exposure 

(Moldau et al., 1990; Dann and Pell, 

1989; Weber et al., 1993). However, 

exclusion of O3 simultaneously restricts 

the uptake of CO2, which also limits 

photosynthesis and growth. In addition, 

antioxidants present in plants can 

effectively protect tissue against damage 

from low levels of oxidants by 

dissipating excess oxidizing power. 

Since 1996, the role of detoxification in 

providing a level of resistance to O3 has 

been further investigated. A number of 

antioxidants have been found in plants. 

However, the pattern of changes in the 

amounts of these antioxidants varies 

greatly among different species and 

conditions. Most recent reports indicate 

that ascorbate within the cell wall 

provides the first significant 

opportunity for detoxification to occur. 

In spite of the new research, however, 

it is still not clear as to what extent 

detoxification protects against O3 injury. 

Specifically, data are needed on 

potential rates of antioxidant 

production, sub-cellular location(s) of 

antioxidants, and whether generation of 

these antioxidants in response to O3- 

induced stress potentially diverts 

resources and energy away from other 

vital uses. Thus, the 2006 Criteria 

Document concludes that scientific 

understanding of the detoxification 

mechanisms is not yet complete and 

requires further investigation (EPA, 

2006a). 

Regarding the second, once O3 injury 

has occurred in leaf tissue, some plants 

are able to repair or compensate for the 

impacts. In general, plants have a 

variety of compensatory mechanisms for 

low levels of stress including 

reallocation of resources, changes in 

root/shoot ratio, production of new 

tissue, and/or biochemical shifts, such 

as increased photosynthetic capacity in 

new foliage and changes in respiration 

rates, indicating possible repair or 

replacement of damaged membranes or 

enzymes. Since these mechanisms are 

genetically determined, not all plants 

have the same complement of 

compensatory mechanisms or degree of 

tolerance, and these may vary over the 

life of the plant as not all stages of a 

plant’s development are equally 

sensitive to O3. At higher levels or over 

longer periods of O3 stress, some of 

these compensatory mechanisms, such 

as a reallocation of resources away from 

storage in the roots in favor of leaves or 

shoots, could occur at a cost to the 

overall health of the plant. However, it 

is not yet clear to what degree or how 

the use of plant resources for repair or 

compensatory processes affects the 

overall carbohydrate budget or 

subsequent plant response to O3 or other 

stresses (EPA, 1996a, EPA, 2006a). 

d. Changes to Plant Metabolism 

Ozone inhibits photosynthesis, the 

process by which plants produce energy 

rich compounds (e.g., carbohydrates) in 

the leaves. This impairment can result 

from direct impact to chloroplast 

function and/or O3-induced stomatal 

closure resulting in reduced uptake of 

CO2. A large body of literature 

published since 1996 has further 

elucidated the mechanism of effect of O3

within the chloroplast. Pell et al. (1997) 

showed that O3 exposure results in a 

loss of the central carboxylating enzyme 

that plays an important role in the 

production of carbohydrates. Due to its 

central importance, any decrease in this 

enzyme may have severe consequences 

for the plant’s productivity. Several 

recent studies have found that O3 has a 

greater effect as leaves age, with the 

greatest impact of O3 occurring on the 

oldest leaves (Fiscus et al., 1997; Reid 

and Fiscus, 1998; Noormets et al., 2001; 

Morgan et al., 2004). The loss of this key 

enzyme as a function of increasing O3

exposure is also linked to an early 

senescence or a speeding up of normal 

development leading to senescence. If 

total plant photosynthesis is sufficiently 

reduced, the plant will respond by 

reallocating the remaining carbohydrate 

at the level of the whole organism (EPA, 

1996a, 2006a). This reallocation of 

carbohydrate away from the roots into 

above ground vegetative components 

can have serious implications for 

perennial species, as discussed below. 

e. Plant Response to Chronic Ozone 

Exposures 

Though many changes that occur with 

O3 exposure can be observed within 

hours, or perhaps days, of the exposure, 

including those connected with 

wounding, other effects take longer to 

occur and tend to become most obvious 

after chronic seasonal exposures to low 

O3 concentrations. These lower chronic 

exposures have been linked to 

senescence or some other physiological 

response very closely linked to 

senescence. In perennial plant species, 

a reduction in carbohydrate storage in 

one year may result in the limitation of 

growth the following year (Andersen et 

al., 1997). Such ‘‘carry-over’’ effects have 

been documented in the growth of tree 

seedlings (Hogsett et al., 1989; Sasek et 

al., 1991; Temple et al., 1993; EPA, 

1996a) and in roots (Andersen et al., 

1991; EPA, 1996a). Though it is not 

fully understood how chronic seasonal 

O3 exposure affects long-term growth 

and resistance to other biotic and abiotic 


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insults in long-lived trees, accumulation 

of these carry-over effects over time 

could affect survival and reproduction. 

2. Nature of Effects 

Ozone injury at the cellular level can 

accumulate sufficiently to induce effects 

at the level of a whole leaf or plant. 

These larger scale effects can include: 

Reduced carbohydrate production and/ 

or reallocation; reduced growth and/or 

reproduction; visible foliar injury and/ 

or premature senescence; and reduced 

plant vigor. Much of what is now 

known about these O3-related effects, as 

summarized below, is based on research 

that was available in the 1997 review. 

Studies available in the 2008 

rulemaking continue to support and 

expand this knowledge (EPA, 2006a). 

a. Carbohydrate Production and 

Allocation 

When total plant photosynthesis is 

sufficiently reduced, the plant will 

respond by reallocating the remaining 

carbohydrate at the level of the whole 

organism. Many studies have 

demonstrated that root growth is more 

sensitive to O3 exposure than stem or 

leaf growth (EPA, 2006a). When fewer 

carbohydrates are present in the roots, 

less energy is available for root-related 

functions such as acquisition of water 

and nutrients. In addition, by inhibiting 

photosynthesis and the amount of 

carbohydrates available for transfer to 

the roots, O3 can disrupt the association 

between soil fungi and host plants. 

Fungi in the soil form a symbiotic 

relationship with many terrestrial 

plants. For host plants, these fungi 

improve the uptake of nutrients, protect 

the roots against pathogens, produce 

plant growth hormones, and may 

transport carbohydrates from one plant 

to another (EPA, 1996a). These below 

ground effects have recently been 

documented in the field (Grulke et al., 

1998; Grulke and Balduman, 1999). Data 

from a long-studied pollution gradient 

in the San Bernardino Mountains of 

southern California suggest that O3

substantially reduces root growth in 

natural stands of Ponderosa pine (Pinus 

ponderosa). Root growth in mature trees 

was decreased at least 87 percent in a 

high-pollution site as compared to a 

low-pollution site (Grulke et al., 1998), 

and a similar pattern was found in a 

separate study with whole-tree harvest 

along this gradient (Grulke and 

Balduman, 1999). Though effects on 

other ecosystem components were not 

examined, a reduction of root growth of 

this magnitude could have significant 

implications for the below-ground 

communities at those sites. Because 

effects on leaf and needle carbohydrate 

content under O3 stress can range from 

a reduction (Barnes et al., 1990; Miller 

et al., 1989), to no effect (Alscher et al., 

1989), to an increase (Luethy-Krause 

and Landolt, 1990), studies that 

examine only above-ground vegetative 

components may miss important O3- 

induced changes below ground. These 

below-ground changes could signal a 

shift in nutrient cycling with 

significance at the ecosystem level 

(Young and Sanzone, 2002). 

b. Growth Effects on Trees 

Studies comparing the O3-related 

growth response of different vegetation 

types (coniferous and deciduous) and 

growth stages (e.g., seedling and mature) 

have established that on average, 

individual coniferous trees are less 

sensitive than deciduous trees, and 

deciduous trees are generally less 

sensitive to O3 than most annual plants, 

with the exception of a few fast growing 

deciduous tree species (e.g., quaking 

aspen, black cherry, and cottonwood), 

which are highly sensitive and, in some 

cases, as much or more sensitive to O3

than sensitive annual plants. In 

addition, studies have shown that the 

relationship between O3 sensitivity in 

seedling and mature growth stages of 

trees can vary widely, with seedling 

growth being more sensitive to O3

exposures in some species, while in 

others, the mature growth stage is the 

more O3 sensitive. In general, mature 

deciduous trees are likely to be more 

sensitive to O3 than deciduous 

seedlings, and mature evergreen trees 

are likely to be less sensitive to O3 than 

their seedling counterparts. Based on 

these results, stomatal conductance, O3

uptake, and O3 effects cannot be 

assumed to be equivalent in seedlings 

and mature trees. 

In the 1997 review (EPA, 1996b), 

analyses of the effects of O3 on trees 

were limited to 11 tree species for 

which concentration-response (C–R) 

functions for the seedling growth stage 

had been developed from OTC studies 

conducted by the National Health and 

Environmental Effects Research Lab, 

Western Ecology Division (NHEERL– 

WED). A number of replicate studies 

were conducted on these species, 

leading to a total of 49 experimental 

cases. The 2007 Staff Paper presented a 

graph of the composite regression 

equation that combines the results of the 

C–R functions developed for each of the 

49 cases. The NHEERL–WED study 

predicted relative biomass loss at 

various exposure levels in terms of a 12- 

hour W126. For example, 50 percent of 

the tree seedling cases would be 

protected from greater than 10 percent 

biomass loss at a 3-month, 12-hour 

W126 of approximately 24 ppm-hour, 

while 75 percent of cases would be 

protected from 10 percent biomass loss 

at a 3-month, 12-hour W126 level of 

approximately 16 ppm-hour. 

Since the 1997 review, only a few 

studies have developed C–R functions 

for additional tree seedling species 

(EPA, 2006a). One such study is of 

particular importance because it 

documented growth effects in the field 

of a similar magnitude as those 

previously seen in OTC studies but 

without the use of chambers or other 

fumigation methods (Gregg et al., 2003). 

This study placed eastern cottonwood 

(Populus deltoides) saplings at sites 

along a continuum of ambient O3

exposures that gradually increased from 

urban to rural areas in the New York 

City area (Gregg et al., 2003). Eastern 

cottonwood is a fast growing O3

sensitive tree species that is important 

ecologically along streams and 

commercially for pulpwood, furniture 

manufacturing, and as a possible new 

source for energy biomass (Burns and 

Hankola, 1990). Gregg et al. (2003) 

found that the cottonwood saplings 

grown in urban New York City grew 

faster than saplings grown in downwind 

rural areas. Because these saplings were 

grown in pots with carefully controlled 

soil nutrient and moisture levels, the 

authors were able to control for most of 

the differences between sites. After 

carefully considering these and other 

factors, the authors concluded the 

primary explanation for the difference 

in growth was the gradient of 

cumulative O3 exposures that increased 

as one moved downwind from urban to 

less urban and more rural sites. It was 

determined that the lower O3 exposure 

within the city center was due to NOX

titration reactions which removed O3

from the ambient air. The authors were 

able to reproduce the growth responses 

observed in the field in a companion 

OTC experiment, confirming O3 as the 

stressor inducing the growth loss 

response (Gregg et al., 2003). 

Another recent set of studies 

employed a modified Free Air CO2

Enrichment (FACE) methodology to 

expose vegetation to elevated O3

without the use of chambers. This 

exposure method was originally 

developed to expose vegetation to 

elevated levels of CO2, but was later 

modified to include O3 exposure in 

Illinois (SoyFACE) and Wisconsin 

(AspenFACE) for soybean and 

deciduous trees, respectively (Dickson 

et al., 2000; Morgan et al., 2004). The 

FACE method releases gas (e.g., CO2, O3) 

from a series of orifices placed along the 

length of the vertical pipes surrounding 

a circular field plot and uses the 


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prevailing wind to distribute it. This 

exposure method has many 

characteristics that differ from those 

associated with the OTC. Most 

significantly, this exposure method 

more closely replicates conditions in the 

field than do OTCs. This is because, 

except for O3 levels which are varied 

across co-located plots, plants are 

exposed to the same ambient growing 

conditions that occur naturally in the 

field (e.g., location-specific pollutant 

mixtures; climate conditions such as 

light, temperature and precipitation; 

insect pests, pathogens). By using one of 

several co-located plots as a control 

(e.g., receives no additional O3), and by 

exposing the other rings to differing 

levels of elevated O3, the growth 

response signal that is due solely to the 

change in O3 exposure can be clearly 

determined. Furthermore, the FACE 

system can expand vertically with the 

growth of trees, allowing for exposure 

experiments to span numerous years, an 

especially useful capability in forest 

research. 

On the other hand, the FACE 

methodology also has the undesirable 

characteristic of potentially creating 

hotspots near O3 gas release orifices or 

gradients of exposure in the outer ring 

of trees within the plots, such that 

averaging results across the entire ring 

potentially overestimates the response. 

In recognition of this possibility, 

researchers at the AspenFACE 

experimental site only measured trees in 

the center core of each ring, (e.g., at least 

5–6 meters away from the emission sites 

of O3) (Dickson et al., 2000, Karnosky et 

al., 2005). By taking this precaution, it 

is unlikely that their measurements 

were influenced by any potential 

hotspots or gradients of exposure within 

the FACE rings. Taking all of the above 

into account, results from the Wisconsin 

FACE site on quaking aspen appear to 

demonstrate that the detrimental effects 

of O3 exposure seen on tree growth and 

symptom expression in OTCs can be 

observed in the field using this exposure 

method (Karnosky et al., 1999; 2005). 

The 2007 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 of the 

weight of evidence available in this 

review and provide additional evidence 

that O3-induced effects observed in 

chambers also occur in the field. 

Trees and other perennials, in 

addition to cumulating the effects of O3

exposures over the annual growing 

season, can also cumulate effects across 

multiple years. It has been reported that 

effects can ‘‘carry over’’ from one year to 

another (EPA, 2006a). Growth affected 

by a reduction in carbohydrate storage 

in one year may result in the limitation 

of growth in the following year 

(Andersen et al., 1997). Carry-over 

effects have been documented in the 

growth of some tree seedlings (Hogsett 

et al., 1989; Simini et al., 1992; Temple 

et al., 1993) and in roots (Andersen et 

al., 1991; EPA, 1996a). On the basis of 

past and recent OTC and field study 

data, ambient O3 exposures that occur 

during the growing season in the United 

States are sufficient to potentially affect 

the annual growth of a number of 

sensitive seedling tree species. 

However, because most studies do not 

take into account the possibility of carry 

over effects on growth in subsequent 

years, the true implication of these 

annual biomass losses may be missed. It 

is likely that under ambient exposure 

conditions, some sensitive trees and 

perennial plants could experience 

compounded impacts that result from 

multiple year exposures. 

c. Visible Foliar Injury 

Cellular injury to leaves due to 

exposure to O3 can and often does 

become visible. Acute injury usually 

appears within 24 hours after exposure 

to O3 and, depending on species, can 

occur under a range of exposures and 

durations from 0.040 ppm for a period 

of 4 hours to 0.410 ppm for 0.5 hours 

for crops and 0.060 ppm for 4 hours to 

0.510 ppm for 1 hour for trees and 

shrubs (Jacobson, 1977). Chronic injury 

may be mild to severe. In some cases, 

cell death or premature leaf senescence 

may occur. The significance of O3 injury 

at the leaf and whole plant levels 

depends on how much of the total leaf 

area of the plant has been affected, as 

well as the plant’s age, size, 

developmental stage, and degree of 

functional redundancy among the 

existing leaf area. As a result, it is not 

presently possible to determine, with 

consistency across species and 

environments, what degree of injury at 

the leaf level has significance to the 

vigor of the whole plant. 

The presence of visible symptoms due 

to O3 exposures can, however, by itself, 

represent an adverse impact to the 

public welfare. Specifically, it can 

reduce the market value of certain leafy 

crops (such as spinach, lettuce), impact 

the aesthetic value of ornamentals (such 

as petunia, geranium, and poinsettia) in 

urban landscapes, and affect the 

aesthetic value of scenic vistas in 

protected natural areas such as national 

parks and wilderness areas. Many 

businesses rely on healthy looking 

vegetation for their livelihoods (e.g., 

horticulturalists, landscapers, Christmas 

tree growers, farmers of leafy crops) and 

a variety of ornamental species have 

been listed as sensitive to O3 (Abt 

Associates Inc., 1995). Though not 

quantified, there is likely some level of 

economic impact to businesses and 

homeowners from O3-related injury on 

sensitive ornamental species due to the 

cost associated with more frequent 

replacement and/or increased 

maintenance (fertilizer or pesticide 

application). In addition, because O3 not 

only results in discoloration of leaves 

but can lead to more rapid senescence 

(early shedding of leaves) there 

potentially could be some lost tourist 

dollars at sites where fall foliage is less 

available or attractive. 

The use of sensitive plants as 

biological indicators to detect 

phytotoxic levels of O3 is a longstanding 

and effective methodology (Chappelka 

and Samuelson, 1998; Manning and 

Krupa, 1992). Each bioindicator exhibits 

typical O3 injury symptoms when 

exposed under appropriate conditions. 

These symptoms are considered 

diagnostic as they have been verified in 

exposure-response studies under 

experimental conditions. In recent 

years, field surveys of visible foliar 

injury symptoms have become more 

common, with greater attention to the 

standardization of methods and the use 

of reliable indicator species (Campbell 

et al., 2000; Smith et al., 2003). 

Specifically, the United States Forest 

Service (USFS) through the Forest 

Health Monitoring Program (FHM) 

(1990–2001) and currently the Forest 

Inventory and Analysis (FIA) Program 

collects data regarding the incidence 

and severity of visible foliar injury on a 

variety of O3 sensitive plant species 

throughout the U.S. (Coulston et al., 

2003, 2004; Smith et al., 2003). 

Since the conclusion of the 1997 

review, the FIA monitoring program 

network and database has continued to 

expand. This network continues to 

document foliar injury symptoms in the 

field under ambient exposure 

conditions. Recent survey results show 

that O3-induced foliar injury incidence 

is widespread across the country. The 

visible foliar injury indicator has been 

identified as a means to track O3

exposure stress trends in the nation’s 

natural plant communities as 

highlighted in EPA’s most recent Report 

on the Environment (EPA, 2003a; http:// 

www.epa.gov/indicators/roe). 


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Previous Criteria Documents have 

noted the difficulty in relating visible 

foliar injury symptoms to other 

vegetation effects such as individual 

tree growth, stand growth, or ecosystem 

characteristics (EPA, 1996a) and this 

difficulty remains to the present day 

(EPA, 2006a). It is important to note that 

direct links between O3 induced visible 

foliar injury symptoms and other 

adverse effects are not always found. 

Therefore, visible foliar injury cannot 

serve as a reliable surrogate measure for 

other O3-related vegetation effects 

because other effects (e.g., biomass loss) 

have been reported with and without 

visible injury. In some cases, visible 

foliar symptoms have been correlated 

with decreased vegetative growth 

(Karnosky et al., 1996; Peterson et al., 

1987; Somers et al., 1998) and with 

impaired reproductive function (Black 

et al., 2000; Chappelka, 2002). 

Therefore, the lack of visible injury 

should not be construed to indicate a 

lack of phytotoxic concentrations of O3

nor absence of other non-visible O3

effects. 

d. Reduced Plant Vigor 

Though O3 levels over most of the 

U.S. are not high enough to kill 

vegetation directly, current levels have 

been shown to reduce the ability of 

many sensitive species and genotypes 

within species to adapt to or withstand 

other environmental stresses. These O3

effects may include increased 

susceptibility to freezing temperatures, 

increased vulnerability to pest 

infestations and/or root disease, and 

compromised ability to compete for 

available resources. As an example of 

the latter, when species with differing 

O3-sensitivities occur together, O3- 

sensitive species may experience a 

greater reduction in growth than more 

O3-tolerant species, which then can 

better compete for available resources. 

The result of such above effects can 

produce a loss in plant vigor in O3- 

sensitive species that over time may 

lead to premature plant death. 

e. Ecosystems 

Ecosystems are comprised of complex 

assemblages of organisms and the 

physical environment with which they 

interact. Each level of organization 

within an ecosystem has functional and 

structural characteristics. At the 

ecosystem level, functional 

characteristics include, but are not 

limited to, energy flow; nutrient, 

hydrologic, and biogeochemical cycling; 

and maintenance of food chains. The 

sum of the functions carried out by 

ecosystem components provides many 

benefits to humankind, as in the case of 

forest ecosystems (Smith, 1992). Some 

of these benefits, also termed 

‘‘ecosystem goods and services’’, include 

food, fiber production, aesthetics, 

genetic diversity, maintenance of water 

quality, air quality, and climate, and 

energy exchange. A conceptual 

framework for discussing the effects of 

stressors, including air pollutants such 

as O3, on ecosystems was developed by 

the EPA Science Advisory Board (Young 

and Sanzone, 2002). In this report, the 

authors identify six essential ecological 

attributes (EEAs) of ecosystems 

including landscape condition, biotic 

condition, chemical/physical condition, 

ecological processes, hydrology/ 

geomorphology, and natural disturbance 

regime. Each EEA is depicted as one of 

six triangles that together build a 

hexagon. On the outside of each triangle 

is a list of stressors that can act on the 

EEA. Tropospheric O3 is listed as a 

stressor of both biotic condition and the 

chemical/physical condition of 

ecosystems. As each EEA is linked to all 

the others, it is clearly envisioned in 

this framework that O3 could either 

directly or indirectly impact all of the 

EEAs associated with an ecosystem that 

is being stressed by O3. 

Vegetation often plays an influential 

role in defining the structure and 

function of an ecosystem, as evidenced 

by the use of dominant vegetation forms 

to classify many types of natural 

ecosystems, e.g., tundra, wetland, 

deciduous forest, and conifer forest. 

Plants simultaneously inhabit both 

above-and below-ground environments, 

integrating and influencing key 

ecosystem cycles of energy, water, and 

nutrients. When a sufficient number of 

individual plants within a community 

have been affected, O3-related effects 

can be propagated up to ecosystem-level 

effects. Thus, through its impact on 

vegetation, O3 can be an important 

ecosystem stressor. 

i. Potential Ozone Alteration of 

Ecosystem Structure and Function 

The 2006 Criteria Document outlines 

seven case studies where O3 effects on 

ecosystems have either been 

documented or are suspected. The 

oldest and clearest example involves the 

San Bernardino Mountain forest 

ecosystem in California. This system 

experienced chronic high O3 exposures 

over a period of 50 or more years. The 

O3-sensitive and co-dominant species of 

ponderosa and Jeffrey pine 

demonstrated severe levels of foliar 

injury, premature senescence, and 

needle fall that decreased the 

photosynthetic capacity of stressed 

pines and reduced the production of 

carbohydrates resulting in a decrease in 

radial growth and in the height of 

stressed trees. It was also observed that 

ponderosa and Jeffrey pines with slight 

to severe crown injury lost basal area in 

relation to competing species that are 

more tolerant to O3. Due to a loss of 

vigor, these trees eventually succumbed 

to the bark beetle, leading to elevated 

levels of tree death. Increased mortality 

of susceptible trees shifted the 

community composition towards white 

fir and incense cedar, effectively 

reversing the development of the normal 

fire climax mixture dominated by 

ponderosa and Jeffrey pines, and 

leading to increased fire susceptibility. 

At the same time, numerous other 

organisms and processes were also 

affected either directly or indirectly, 

including successional patterns of 

fungal microflora and their relationship 

to the decomposer community. Nutrient 

availability was influenced by the heavy 

litter and thick needle layer under 

stands with the most severe needle 

injury and defoliation. In this example, 

O3 appeared to be a predisposing factor 

that led to increased drought stress, 

windthrow, root diseases, and insect 

infestation (Takemoto et al., 2001). 

Thus, through its effects on tree water 

balance, cold hardiness, tolerance to 

wind, and susceptibility to insect and 

disease pests, O3 potentially impacted 

the ecosystem-related EEA of natural 

disturbance regime (e.g., fire, erosion). 

Although the role of O3 was extremely 

difficult to separate from other 

confounding factors, such as high 

nitrogen deposition, there is evidence 

that this shift in species composition 

has altered the structure and dynamics 

of associated food webs (Pronos et al., 

1999) and carbon (C) and nitrogen (N) 

cycling (Arbaugh et al., 2003). Ongoing 

and new research in this important 

ecosystem is needed to reveal the extent 

to which ecosystem services have been 

affected and to what extent strong 

causal linkages between historic and/or 

current ambient O3 exposures and 

observed ecosystem-level effects can be 

made. 

Ozone has also been reported to be a 

selective pressure among sensitive tree 

species (e.g., eastern white pine) in the 

east. The nature of community 

dynamics in eastern forests is different, 

however, than in the west, consisting of 

a wider diversity of species and uneven 

aged stands, and the O3 levels are less 

severe. Therefore, lower level chronic 

O3 stress in the east is more likely to 

produce subtle long-term forest 

responses such as shifts in species 

composition, rather than wide-spread 

community degradation. 

Some of the best-documented studies 

of population and community response 


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to O3 effects are the long-term studies of 

common plantain (Plantago major) in 

native plant communities in the United 

Kingdom (Davison and Reiling, 1995; 

Lyons et al., 1997; Reiling and Davison, 

1992c). Elevated O3 significantly 

decreased the growth of sensitive 

populations of common plantain 

(Pearson et al., 1996; Reiling and 

Davison, 1992a, b; Whitfield et al., 

1997) and reduced its fitness as 

determined by decreased reproductive 

success (Pearson et al., 1996; Reiling 

and Davison, 1992a). While spatial 

comparisons of population responses to 

O3 are complicated by other 

environmental factors, rapid changes in 

O3 resistance were imposed by ambient 

levels and variations in O3 exposure 

(Davison and Reiling, 1995). 

Specifically, in this case study, it 

appeared that O3-sensitive individuals 

are being removed by O3 stress and the 

genetic variation represented in the 

population could be declining. If genetic 

diversity and variation is lost in 

ecosystems, there may be increased 

vulnerability of the system to other 

biotic and abiotic stressors, and 

ultimately a change in the EEAs and 

associated services provided by those 

ecosystems. 

Recent free-air exposure experiments 

have also provided new insight into 

how O3 may be altering ecosystem 

structure and function (Karnosky et al., 

2005). For example, a field O3 exposure 

experiment at the AspenFACE site in 

Wisconsin (described in section 

IV.A.2.b. above) was designed to 

examine the effects of both elevated CO2

and O3 on mixed stands of aspen 

(Populus tremuloides), birch (Betula 

papyrifera), and sugar maple (Acer 

saccharum) that are characteristic of 

Great Lakes aspen-dominated forests 

(Karnosky et al., 2003; Karnosky et al., 

1999). They found evidence that the 

effects on above- and below-ground 

growth and physiological processes 

have cascaded through the ecosystem, 

even affecting microbial communities 

(Larson et al., 2002; Phillips et al., 

2002). This study also confirmed earlier 

observations of O3-induced changes in 

trophic interactions involving keystone 

tree species, as well as important insect 

pests and their natural enemies 

(Awmack et al., 2004; Holton et al., 

2003; Percy et al., 2002). 

Collectively these examples suggest 

that O3 is an important stressor in 

natural ecosystems, but it is difficult to 

quantify the contribution of O3 due to 

the combination of other stresses 

present in ecosystems. In most cases, 

because only a few components in each 

of these ecosystems have been examined 

and characterized for O3 effects, the full 

extent of ecosystem changes in these 

example ecosystems is not fully 

understood. Clearly, there is a need for 

highly integrated ecosystem studies that 

specifically investigate the effect of O3

on ecosystem structure and function in 

order to fully determine the extent to 

which O3 is altering ecosystem services. 

Continued research, employing new 

approaches, will be necessary to fully 

understand the extent to which O3 is 

affecting ecosystem services. 

ii. Effects on Ecosystem Services and 

Carbon Sequestration 

Since it has been established that O3

affects photosynthesis and growth of 

plants, O3 is most likely affecting the 

productivity of forest ecosystems. 

Therefore, it is desirable to link effects 

on growth and productivity to essential 

ecosystem services. However, it is very 

difficult to quantify ecosystem-level 

productivity losses because of the 

amount of complexity in scaling from 

the leaf-level or individual plant to the 

ecosystem level, and because not all 

organisms in an ecosystem are equally 

affected by O3. 

Terrestrial ecosystems are important 

in the Earth’s carbon (C) balance and 

could help offset emissions of CO2 by 

humans if anthropogenic C is 

sequestered in vegetation and soils. The 

annual increase in atmospheric CO2 is 

less than the total inputs from fossil fuel 

burning and land use changes (Prentice 

et al., 2001), and much of this 

discrepancy is thought to be attributable 

to CO2 uptake by plant photosynthesis 

(Tans & White, 1998). Temperate forests 

of the northern hemisphere have been 

estimated to be a net sink of about 0.6 

to 0.7 petagrams (Pg) C per year 

(Goodale et al. 2002). Ozone interferes 

with photosynthesis, causes some plants 

to senesce leaves prematurely, and in 

some cases, reduces allocation to stem 

and root tissue. Thus, O3 decreases the 

potential for C sequestration. For the 

purposes of this discussion, C 

sequestration is defined as the net 

exchange of carbon by the terrestrial 

biosphere. However, long-term storage 

in the soil organic matter is considered 

to be the most stable form of C storage 

in ecosystems. 

In a study including all ecosystem 

types, Felzer et al. (2004), estimated that 

U.S. net primary production (net flux of 

C into an ecosystem) was decreased by 

2.6–6.8 percent due to O3 pollution in 

the late 1980s to early 1990s. Ozone not 

only reduces C sequestration in existing 

forests, it can also affect reforestation 

projects (Beedlow et al. 2004). This 

effect, in turn, has been found to 

ultimately inhibit C sequestration in 

forest soils which act as long-term C 

storage (Loya et al., 2003; Beedlow et al. 

2004). The interaction of rising O3

pollution and rising CO2 concentrations 

in the coming decades complicates 

predictions of future sequestration 

potential. Models generally predict that, 

in the future, C sequestration will 

increase with increasing CO2, but often 

do not account for the decrease in 

productivity due to the local effects of 

current or potentially increasing levels 

of tropospheric O3. In the presence of 

high O3 levels, the stimulatory effect of 

rising CO2 concentrations on forest 

productivity has been estimated to be 

reduced by more that 20 percent (Tingey 

et al., 2001; Ollinger et al. 2002; 

Karnosky et al., 2003). 

In summary, it would be anticipated 

that meeting lower O3 standards would 

increase the amount of CO2 uptake by 

many ecosystems in the U.S. However, 

the amount of this improvement would 

be heavily dependent on the species 

composition of those ecosystems. Many 

ecosystems in the U.S. do have O3

sensitive plants. For example, forest 

ecosystems with dominant species such 

as aspen or ponderosa pine would be 

expected to increase CO2 uptake more 

with lower O3 than forests with more O3

tolerant species. 

A recent critique of the secondary 

NAAQS review process published in the 

report by the National Academy of 

Sciences on Air Quality Management in 

the United States (NRC, 2004) stated 

that ‘‘EPA’s current practice for setting 

secondary standards for most criteria 

pollutants does not appear to be 

sufficiently protective of sensitive crops 

and ecosystems * * *’’ This report 

made several specific recommendations 

for improving the secondary NAAQS 

process and concluded that ‘‘There is 

growing evidence that tighter standards 

to protect sensitive ecosystems in the 

United States are needed. * * *’’ An 

effort has been recently initiated within 

the Agency to identify indicators of 

ecological condition whose responses 

can be clearly linked to changes in air 

quality that are attributable to Agency 

environmental programs. Using a single 

indicator to represent the complex 

linkages and dynamic cycles that define 

ecosystem condition will always have 

limitations. With respect to O3-related 

impacts on ecosystem condition, only 

two candidate indicators, foliar injury 

(as described above) and radial growth 

in trees, have been suggested. Thus, 

while at the present time, most O3- 

related effects on ecosystems must be 

inferred from observed or predicted O3- 

related effects on individual plants, 

additional research at the ecosystem 

level could identify new indicators and/ 

or establish stronger causal linkages 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
3006 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

between O3-induced plant effects and 

ecosystem condition. 

f. Yield Reductions in Crops 

Ozone can interfere with carbon gain 

(photosynthesis) and allocation of 

carbon with or without the presence of 

visible foliar injury. As a result of 

decreased carbohydrate availability, 

fewer carbohydrates are available for 

plant growth, reproduction, and/or 

yield. Recent studies have further 

confirmed and demonstrated O3 effects 

on different stages of plant 

reproduction, including pollen 

germination, pollen tube growth, 

fertilization, and abortion of 

reproductive structures, as reviewed by 

Black et al. (2000). For seed-bearing 

plants, these reproductive effects will 

culminate in reduced seed production 

or yield. 

As described in the 1997 review and 

again in the 2006 Criteria Document and 

2007 Staff Paper, the National Crop Loss 

Assessment Network (NCLAN) studies 

undertaken in the early to mid-1980s 

provide the largest, most uniform 

database on the effects of O3 on 

agricultural crop yields. The NCLAN 

protocol was designed to produce crop 

exposure-response data representative 

of the areas in the U.S. where the crops 

were typically grown. In total, 15 

species (e.g., corn, soybean, winter 

wheat, tobacco, sorghum, cotton, barley, 

peanuts, dry beans, potato, lettuce, 

turnip, and hay [alfalfa, clover, and 

fescue]), accounting for greater than 85 

percent of U.S. agricultural acreage 

planted at that time, were studied. Of 

these 15 species, 13 species including 

38 different cultivars were combined in 

54 cases representing unique 

combinations of cultivars, sites, water 

regimes, and exposure conditions. Crops 

were grown under typical farm 

conditions and exposed in open-top 

chambers to ambient O3, sub-ambient 

O3, and above ambient O3. Robust C–R 

functions were developed for each of 

these crop species. These results 

showed that 50 percent of the studied 

cases would be protected from greater 

than 10 percent yield loss at a W126 

level of 21 ppm-hour, while a W126 of 

13 ppm-hour would provide protection 

for 75 percent of the cases studied from 

greater than 10 percent yield loss. 

Recent studies continue to find yield 

loss levels in crop species studied 

previously under NCLAN that reflect 

the earlier findings. In other words, 

there has been no evidence that crops 

are becoming more tolerant of O3 (EPA, 

2006a). For cotton, some newer varieties 

have been found to have higher yield 

loss due to O3 compared to older 

varieties (Olszyk et al., 1993, Grantz and 

McCool, 1992). In a meta-analysis of 53 

studies, Morgan et al. (2003) found 

consistent deleterious effects of O3

exposures on soybean from studies 

published between 1973 and 2001. 

Further, early results from the fieldbased exposure experiment SoyFACE in 

Illinois indicate a lack of any apparent 

difference in the O3 tolerance of old and 

recent cultivars of soybean in a study of 

22 soybean varieties (Long et al., 2002). 

Thus, the 2007 Staff Paper concluded 

that the recent scientific literature 

continues to support the conclusions of 

the 1996 Criteria Document that 

ambient O3 concentrations are reducing 

the yield of major crops in the U.S. 

In addition to the effects described on 

annual crop species, several studies 

published since the 1997 review have 

focused on perennial forage crops (EPA, 

2006a). These recent results confirm 

that O3 is also impacting yields and 

quality of multiple-year forage crops at 

sufficient magnitude to have nutritional 

and possibly economic implications to 

their use as ruminant animal feed at O3

exposures that occur in some years over 

large areas of the U.S. 

3. Adversity of Effects 

The 2007 Staff Paper recognized that 

the statute requires that a secondary 

standard be protective against ‘‘adverse’’ 

O3 effects, not all identifiable O3- 

induced effects. In considering what 

constitutes a vegetation effect that is 

adverse to the public welfare, the 2007 

Staff Paper recognizes that O3 can cause 

a variety of vegetation effects, beginning 

at the level of the individual cell and 

accumulating up to the level of whole 

leaves, plants, plant populations, 

communities and whole ecosystems, not 

all of which have been classified in past 

reviews as ‘‘adverse’’ to public welfare. 

Previous reviews have classified O3

vegetation effects as either ‘‘injury’’ or 

‘‘damage’’ to help in determining 

adversity. Specifically, ‘‘injury’’ is 

defined as encompassing all plant 

reactions, including reversible changes 

or changes in plant metabolism (e.g., 

altered photosynthetic rate), altered 

plant quality, or reduced growth, that 

does not impair the intended use or 

value of the plant (Guderian, 1977). In 

contrast, ‘‘damage’’ has been defined to 

include those injury effects that reach 

sufficient magnitude as to also reduce or 

impair the intended use or value of the 

plant. Examples of effects that are 

classified as damage include reductions 

in aesthetic values (e.g., foliar injury in 

ornamental species) as well as losses in 

terms of weight, number, or size of the 

plant part that is harvested (reduced 

yield or biomass production). Yield loss 

also may include changes in crop 

quality, i.e., physical appearance, 

chemical composition, or the ability to 

withstand storage, while biomass loss 

includes slower growth in species 

harvested for timber or other fiber uses. 

While this construct has proved useful 

in the past, it appears to be most useful 

in the context of evaluating effects on 

single plants or species grown in 

monocultures such as agricultural crops 

or managed forests. It is less clear how 

it might apply to potential effects on 

natural forests or entire ecosystems 

when O3-induced species level impacts 

lead to shifts in species composition 

and/or associated ecosystem services 

such as nutrient cycling or hydrologic 

cycles, where the intended use or value 

of the system has not been specifically 

identified. 

A more recent construct for assessing 

risks to forests described in Hogsett et 

al. (1997) suggests that ‘‘adverse effects 

could be classified into one or more of 

the following categories: (1) Economic 

production, (2) ecological structure, (3) 

genetic resources, and (4) cultural 

values.’’ This approach expands the 

context for evaluating the adversity of 

O3-related effects beyond the species 

level. Another recent publication, A 

Framework for Assessing and Reporting 

on Ecological Condition: An SAB report 

(Young and Sanzone, 2002), provides 

additional support for expanding the 

consideration of adversity beyond the 

species level by making explicit the 

linkages between stress-related effects 

(e.g., O3 exposure) at the species level 

and at higher levels within an 

ecosystem hierarchy. Taking this recent 

literature into account, the 2007 Staff 

Paper concludes that a determination of 

what constitutes an ‘‘adverse’’ welfare 

effect in the context of the secondary 

NAAQS review can appropriately occur 

within this broader paradigm. 

B. Biologically Relevant Exposure 

Indices 

The 2006 Criteria Document 

concluded that O3 exposure indices that 

cumulate differentially weighted hourly 

concentrations are the best candidates 

for relating exposure to plant growth 

responses. This conclusion follows from 

the extensive evaluation of the relevant 

studies in the 1996 Criteria Document 

(EPA, 1996a) and the recent evaluation 

of studies that have been published 

since that time. The following 

selections, taken from the 1996 Criteria 

Document (EPA, 1996a, section 5.5), 

further elucidate the depth and strength 

of these conclusions. Specifically, with 

respect to the importance of taking into 

account exposure duration, the 1996 

Criteria Document stated, ‘‘when O3

effects are the primary cause of variation 


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54The SUM06 index is defined as the sum of all 

hourly O3 concentrations greater or equal to 0.06 

ppm over a specified time. 

in plant response, plants from replicate 

studies of varying duration showed 

greater reductions in yield or growth 

when exposed for the longer duration’’ 

and ‘‘the mean exposure index of 

unspecified duration could not account 

for the year-to-year variation in 

response’’ (EPA, 1996a, pg. 5–96). 

Further, ‘‘because the mean exposure 

index treats all concentrations equally 

and does not specifically include an 

exposure duration component, the use 

of a mean exposure index for 

characterizing plant exposures appears 

inappropriate for relating exposure with 

vegetation effects’’ (EPA, 1996a, pg. 5– 

88). Regarding the relative importance 

of higher concentrations than lower in 

determining plant response, the 1996 

Criteria Document concluded that ‘‘the 

ultimate impact of long-term exposures 

to O3 on crops and seedling biomass 

response depends on the integration of 

repeated peak concentrations during the 

growth of the plant’’ (EPA, 1996a, pg. 5– 

104). Further, ‘‘at this time, exposure 

indices that weight the hourly O3

concentrations differentially appear to 

be the best candidates for relating 

exposure with predicted plant response’’ 

(EPA, 1996a, pgs. 5–136). 

At the conclusion of the 1997 review, 

the biological basis for a cumulative, 

seasonal form was not in dispute. There 

was general agreement between EPA 

and CASAC, based on their review of 

the air quality criteria, that a 

cumulative, seasonal form was more 

biologically based than the then current 

1-hour and newly proposed 8-hour 

average form. However, in selecting a 

specific form appropriate for a 

secondary standard, there was less 

agreement. An evaluation of the 

performance of several cumulative 

seasonal forms in predicting plant 

response data taken from OTC 

experiments had found that all 

performed about equally well and was 

unable to distinguish between them 

(EPA, 1996a). In selecting between two 

of these cumulative forms, the SUM06 54

and W126, in the absence of biological 

evidence to distinguish between them, 

EPA based its decision on both science 

and policy considerations. Specifically, 

these were: (1) All cumulative, peakweighted exposure indices considered, 

including W126 and SUM06, were 

about equally good as exposure 

measures to predict exposure-response 

relationships reported in the NCLAN 

crop studies; and (2) the SUM06 form 

would not be influenced by PRB O3

concentrations (defined at the time as 

0.03 to 0.05 ppm) under many typical 

air quality distributions. On the basis of 

these considerations, EPA chose the 

SUM06 as the most appropriate 

cumulative, seasonal form to consider 

when proposing an alternative 

secondary standard form (61 FR 65716). 

Though the scientific justification for 

a cumulative, seasonal form was 

generally accepted in the 1997 review, 

an analysis undertaken by EPA at that 

time had shown that there was 

considerable overlap between areas that 

would be expected not to meet the range 

of alternative 8-hour standards being 

considered for the primary NAAQS and 

those expected not to meet the range of 

values (expressed in terms of the 

seasonal SUM06 index) of concern for 

vegetation. This result suggested that 

improvements in national air quality 

expected to result from attaining an 8- 

hour primary standard within the 

recommended range of levels would 

also be expected to significantly reduce 

levels of concern for vegetation in those 

same areas. Thus, in the 1996 proposed 

rule, EPA proposed two alternatives for 

consideration: one alternative was to 

make the secondary standard equal in 

every way to the proposed 8-hour, 0.08 

ppm primary standard; and the second 

was to establish a cumulative, seasonal 

secondary standard in terms of a SUM06 

form as also appropriate to protect 

public welfare from known or 

anticipated adverse effects given the 

available scientific knowledge and that 

such a seasonal standard ‘‘* * * is more 

biologically relevant * * *’’ (61 FR 

65716). 

In the 1997 final rule, EPA decided to 

make the secondary standard identical 

to the primary standard. The EPA 

acknowledged, however, that ‘‘it 

remained uncertain as to the extent to 

which air quality improvements 

designed to reduce 8-hr average O3

concentrations averaged over a 3-year 

period would reduce O3 exposures 

measured by a seasonal SUM06 index.’’ 

(62 FR 38876) In other words, it was 

uncertain as to whether the 8-hour 

average form would, in practice, provide 

sufficient protection for vegetation from 

the cumulative, seasonal and 

concentration-weighted exposures 

described in the scientific literature as 

of concern. 

On the basis of that history, the 2007 

Staff Paper (chapter 7) revisited the 

issue of whether the SUM06 was still 

the most appropriate choice of 

cumulative, seasonal form for a 

secondary standard to protect the public 

welfare from known and anticipated 

adverse vegetation effects in light of the 

new information available in this 

review. Specifically, the 2007 Staff 

Paper considered: (1) The continued 

lack of evidence within the vegetation 

effects literature of a biological 

threshold for vegetation exposures of 

concern; and (2) new estimates of PRB 

that were lower than in the 1997 review. 

The W126 form, also evaluated in the 

1997 review, was again selected for 

comparison with the SUM06 form. 

Regarding the first consideration, the 

2007 Staff Paper noted that the W126 

form, by its incorporation of a 

continuous sigmoidal weighting 

scheme, does not create an artificially 

imposed concentration threshold, yet 

also gives proportionally more weight to 

the higher and typically more 

biologically potent concentrations, as 

supported by the scientific evidence. 

Second, the index value is not 

significantly influenced by O3

concentrations within the range of 

estimated PRB, as the weights assigned 

by the sigmoidal weighting scheme to 

concentrations in this range are near 

zero. Thus, it would also provide a more 

appropriate target for air quality 

management programs designed to 

reduce emissions from anthropogenic 

sources contributing to O3 formation. 

On the basis of these considerations, the 

2007 Staff Paper concluded that the 

W126 form was the most biologicallyrelevant cumulative, seasonal form 

appropriate to consider in the context of 

the 2008 rulemaking. 

C. Vegetation Exposure and Impact 

Assessment 

The vegetation exposure and impact 

assessment conducted for the 2008 

rulemaking and described in the 2007 

Staff paper, consisted of exposure, risk 

and benefits analyses and improved and 

built upon similar analyses performed 

in the 1997 review (EPA 1996b). The 

vegetation exposure assessment was 

performed using interpolation and 

included information from ambient 

monitoring networks and results from 

air quality modeling. The vegetation risk 

assessment included both tree and crop 

analyses. The tree risk analysis includes 

three distinct lines of evidence: (1) 

Observations of visible foliar injury in 

the field linked to monitored O3 air 

quality for the years 2001–2004; (2) 

estimates of seedling growth loss under 

then current and alternative O3

exposure conditions; and (3) simulated 

mature tree growth reductions using the 

TREGRO model to simulate the effect of 

meeting alternative air quality standards 

on the predicted annual growth of a 

single western species (ponderosa pine) 

and two eastern species (red maple and 

tulip poplar). The crop analysis 

includes estimates of the risks to crop 

yields from then current and alternative 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
3008 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

55The CMAQ model is a multi-pollutant, 

multiscale air quality model that contains state-ofthe-science techniques for simulating atmospheric 

and land processes that affect the transport, 

transformation, and deposition of atmospheric 

pollutants and/or their precursors on both regional 

and urban scales. It is designed as a science-based 

modeling tool for handling many major pollutants 

(including photochemical oxidants/O3, particulate 

matter, and nutrient deposition) holistically. The 

CMAQ model can generate estimates of hourly O3

concentrations for the contiguous U.S., making it 

possible to express model outputs in terms of a 

variety of exposure indices (e.g., W126, 8-hour 

average). 

O3 exposure conditions and the 

associated change in economic benefits 

expected to accrue in the agriculture 

sector upon meeting the levels of 

various alternative standards. Each 

element of the assessment is described 

below, including discussions of known 

sources and ranges of uncertainties 

associated with the elements of this 

assessment. 

1. Exposure Characterization 

Though numerous effects of O3 on 

vegetation have been documented as 

discussed above, it is important in 

considering risk to examine O3 air 

quality patterns in the U.S. relative to 

the location of O3 sensitive species that 

have a known concentration-response in 

order to predict whether adverse effects 

are occurring at current levels of air 

quality, and whether they are likely to 

occur under alternative standard forms 

and levels. 

The most important information about 

exposure to vegetation comes from the 

O3 monitoring data that are available 

from two national networks: (1) Air 

Quality System (AQS; http:// 

www.epa.gov/ttn/airs/airsaqs) and (2) 

Clean Air Status and Trends Network 

(CASTNET; http://www.epa.gov/ 

castnet/). The AQS monitoring network 

currently has over 1100 active O3

monitors which are generally sited near 

population centers. However, this 

network also includes approximately 36 

monitors located in national parks. 

CASTNET is the nation’s primary 

source for data on dry acidic deposition 

and rural, ground-level O3. It consists of 

over 80 sites across the eastern and 

western U.S. and is cooperatively 

operated and funded with the National 

Park Service. In the 1997 O3 NAAQS 

final rule, it was acknowledged that 

because the national air quality 

surveillance network for O3 was 

designed principally to monitor O3

exposure in populated areas, there was 

limited measured data available to 

characterize O3 air quality in rural and 

remote sites. Since the 1997 review, 

there has been a small increase in the 

number of CASTNET sites (from 

approximately 52 sites in 1992 to 84 

sites in 2004), however these monitors 

are not used for attainment 

designations. 

National parks represent areas of 

nationally recognized ecological and 

public welfare significance, which have 

been afforded a high level of protection 

by Congress. Two recent reports 

presented some discussion of O3 trends 

in a subset of national parks: The Ozone 

Report: Measuring Progress Through 

2003 (EPA, 2004), and 2005 Annual 

Performance and Progress Report: Air 

Quality in National Parks (NPS, 2005). 

Unfortunately, much of this information 

is presented only in terms of the current 

8-hr average form. The 2007 Staff Paper 

analyzed available air quality data in 

terms of the cumulative 12-hour W126 

form from 2001 to 2005 for a subset of 

national parks and other significant 

natural areas representing 4 general 

regions of the U.S. Many of these 

national parks and natural areas have 

monitored O3 levels above 

concentrations that have been shown to 

decrease plant growth and above the 

12-hour W126 levels analyzed in this 

review. For example, the Great Smokey 

Mountain, Rocky Mountain, Grand 

Canyon, Yosemite and Sequoia National 

Parks all had more than one year within 

the 2001–2005 period with a 12-hour 

W126 above 21 ppm-hour. This level of 

exposure has been associated with 

approximately no more than 10 percent 

biomass loss in 50 percent of the 49 tree 

seedling cases studied in the NHEERL– 

WED experiments (Lee and Hogsett, 

1996). Black cherry (Prunus serotina), 

an important O3-sensitive tree species in 

the eastern U.S., occurs in the Great 

Smoky Mountain National Park and is 

estimated to have O3-related seedling 

biomass loss of approximately 40 

percent when exposed to a 3 month, 

12-hour W126 O3 level greater than 21 

ppm-hour. Ponderosa pine (Pinus 

ponderosa) which occurs in the Grand 

Canyon, Yosemite and Sequoia National 

Parks has been reported to have 

approximately 10 percent biomass 

losses at 3 month, 12 hour W126 O3

levels as low as 17 ppm-hour (Lee and 

Hogsett, 1996). Impacts on seedlings 

may potentially affect long-term tree 

growth and survival, ultimately 

affecting the competitiveness of O3- 

sensitive tree species and genotypes 

within forest stands. 

In order to characterize exposures to 

vegetation at the national scale, 

however, the 2007 Staff Paper 

concluded that it could not rely solely 

on limited site-specific monitoring data, 

and that it was necessary to select an 

interpolation method that could be used 

to characterize O3 air quality over broad 

geographic areas. The 2007 Staff Paper 

therefore investigated the 

appropriateness of using the O3 outputs 

from the EPA/NOAA Community Multiscale Air Quality (CMAQ) 55 model 

system (http://www.epa.gov/asmdnerl/ 

CMAQ, Byun and Ching, 1999; Arnold 

et al. 2003, Eder and Yu, 2005) to 

improve spatial interpolations based 

solely on existing monitoring networks. 

Due to the significant resources required 

to run CMAQ, model outputs were only 

available for a limited number of years. 

For the 2008 rulemaking, the most 

recent outputs available at the time from 

CMAQ version 4.5 were for the year 

2001. 

Based on the significant difference in 

monitor network density between the 

eastern and western U.S., the 2007 Staff 

Paper concluded that it was appropriate 

to use separate interpolation techniques 

in these two regions. Only AQS and 

CASTNET monitoring data were used 

for the eastern interpolation, since it 

was determined that enhancing the 

interpolation with CMAQ data did not 

add much information to the eastern 

U.S. interpolation. In the western U.S., 

however, where rural monitoring is 

more sparse, O3 values generated by the 

CMAQ model were used to develop 

scaling factors to augment the 

interpolation. 

In order to characterize uncertainties 

associated with the interpolation 

method, monitored O3 concentrations 

were systematically compared to 

interpolated O3 concentrations in areas 

where monitors were located. In 

general, the interpolation method used 

in the current review performed well in 

many areas in the U.S., although it 

under-predicted higher 12-hour W126 

exposures in rural areas. Due to the 

important influence of higher exposures 

in determining risks to plants, this 

feature of the interpolated surface could 

result in an under-estimation of risks to 

vegetation in some areas. Taking these 

uncertainties into account, and given 

the absence of more complete rural 

monitoring data, this approach was used 

in developing national vegetation 

exposure and risk assessments that 

estimate relative changes in risk for the 

various alternative standards analyzed. 

To evaluate changing vegetation 

exposures and risks under selected air 

quality scenarios, the 2007 Staff Paper 

utilized 2001 base year O3 air quality 

distributions that had been adjusted 

with a rollback method (Horst and Duff, 

1995; Rizzo, 2005, 2006) to reflect 

meeting the then current and alternative 

secondary standard options. This 

technique combines both linear and 

quadratic elements to reduce higher O3


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56This analysis was updated using 2003–2005 air 

quality as it became available, finding similar 

results. 

concentrations more than lower ones. In 

this regard, the rollback method 

attempts to account for reductions in 

emissions without greatly affecting 

lower concentrations. The following O3

air quality scenarios were analyzed: (1) 

4th-highest daily maximum 8-hour 

average: 0.084 ppm (the effective level 

of the then current standard) and 0.070 

ppm levels; (2) 3-month, 12-hour. 

SUM06: 25 ppm-hour (proposed in the 

1997 review) and 15 ppm-hour levels; 

and (3) 3-month, 12-hour W126: 21 

ppm-hour and 13 ppm-hour levels. 

The two 8-hour average levels were 

chosen as possible alternatives of the 

then current form for comparison with 

the cumulative, seasonal alternative 

forms. The SUM06 scenarios were very 

similar to the W126 scenarios. Since the 

W126 was judged to be the more 

biologically-relevant cumulative, 

seasonal form, only the results for the 

W126 scenarios are summarized below. 

For the W126 form, the two levels were 

selected on the basis of the associated 

levels of tree seedling biomass loss and 

crop yield loss protection identified in 

the NHEERL–WED and NCLAN studies, 

respectively. Specifically, the upper 

level of W126 (21 ppm-hour) was 

associated with a level of tree and crop 

protection of approximately no more 

than 10 percent growth or yield loss in 

50 percent of cases studied. 

Alternatively, the lower level of W126 

(13 ppm-hour) was associated with a 

level of tree seedling and crop 

protection of approximately no more 

than 10 percent growth or yield loss in 

75 percent of studied cases. 

The following discussion highlights 

key observations drawn from comparing 

predicted changes in interpolated air 

quality under each alternative standard 

form and level scenario for the base 

year, 2001: 

(1) Under the base year (2001) ‘‘as is’’ 

air quality, a large portion of California 

had 12-hr W126 O3 levels above 31 

ppm-hour, which has been associated 

with approximately no more than 14 

percent biomass loss in 50 percent of 

tree seedling cases studies. Broader 

multi-state regions in the east (NC, TN, 

KY, IN, OH, PA, NJ, NY, DE, MD, VA) 

and west (CA, NV, AZ, OK, TX) are 

predicted to have levels of air quality 

above the W126 level of 21 ppm-hour, 

which is approximately equal to the 

secondary standard proposed in 1996 

and is associated with approximately no 

more than 10 percent biomass loss in 50 

percent of tree seedling cases studied. 

Much of the east and Arizona and 

California have 12-hour W126 O3 levels 

above 13 ppm-hour, which has been 

associated with approximately no more 

than 10 percent biomass loss in 75 

percent of tree seedling cases studied. 

The results of the exposure assessment 

indicate that current air quality levels 

could result in significant impacts to 

vegetation in some areas. 

(2) When 2001 air quality was rolled 

back to meet the then current 8-hour, 

0.084 ppm secondary standard, the 

overall 3-month 12-hour W126 O3 levels 

were somewhat improved, but not 

substantially. Under this scenario, there 

were still many areas in California with 

12-hour W126 O3 levels above 31 ppmhour. A broad multi-state region in the 

east (NC, TN, KY, IN, OH, PA, MD) and 

west (CA, NV, AZ, OK, TX) were still 

predicted to have O3 levels above the 

W126 level of 21 ppm-hour. 

(3) Exposures generated for just 

meeting a 0.070 ppm, 4th-highest 

maximum 8-hour average alternative 

standard showed substantially 

improved O3 air quality when compared 

to just meeting the then current 8-hour 

standard. Most areas were predicted to 

have O3 levels below the W126 level of 

21 ppm-hour, although some areas in 

the east (KY, TN, MI, AR, MO, IL) and 

west (CA, NV, AZ, UT, NM, CO, OK, 

TX) were still predicted to have O3

levels above the W126 level of 13 ppmhour. 

These results suggest that meeting a 

0.070 ppm, 8-hour secondary standard 

would provide substantially improved 

protection in some areas for vegetation 

from seasonal O3 exposures of concern. 

The 2007 Staff Paper recognizes, 

however, that some areas meeting a 

0.070 ppm 8-hour standard could 

continue to have elevated seasonal 

exposures, including forested park lands 

and other natural areas, and Class I 

areas which are federally mandated to 

preserve certain air quality related 

values. This is especially important in 

the high elevation forests in the Western 

U.S. where there are few O3 monitors. 

This is because the air quality patterns 

in remote areas can result in relatively 

low 8-hour averages while still 

experiencing relatively high cumulative 

exposures. 

To further characterize O3 air quality 

in terms of various secondary standard 

forms, an analysis was performed in the 

2007 Staff Paper to evaluate the extent 

to which county-level O3 air quality 

measured in terms of various levels of 

the current 8-hour average form 

overlapped with that measured in terms 

of various levels of the 12-hour W126 

cumulative, seasonal form. The 2007 

Staff Paper presented this analysis using 

2002–2004 56 county-level O3 air quality 

data from AQS sites and the subset of 

CASTNET sites having the highest O3

levels for the counties in which they are 

located. Since the current 8-hour 

average secondary form is a 3-year 

average, the analysis initially compared 

the 3-year averages of both the 8-hour 

and W126 forms. In addition, 

recognizing that some vegetation effects 

(e.g. crop yield loss and foliar injury) are 

driven solely by annual O3 exposures 

and are typically evaluated with respect 

to exposures within the annual growing 

season, the 2007 Staff Paper also 

presented a comparison of the current 

3-year average 8-hour form to the annual 

W126 form for the individual years, 

2002 and 2004. 

Results of the 3-year average 

comparisons showed that of the 

counties with air quality meeting the 3- 

year average form of a 0.084 ppm, 

8-hour average standard, 7 counties 

showed 3-year average W126 values 

above the 21 ppm-hour level. At the 

lower W126 level of 13 ppm-hour, 135 

counties with air quality meeting the 

3-year average form of a 0.084 ppm, 

8-hour average standard, would be 

above this W126 level. In addition, 

when the 3-year average of an 8-hour 

form was compared to annual W126 

values, further variability in the degree 

of overlap between the 8-hour form and 

W126 form became apparent. For 

example, the relatively high 2002 O3 air 

quality year showed a greater degree of 

overlap between those areas that would 

meet the levels analyzed for the current 

8-hour and alternative levels of the 

W126 form than did the relatively low 

O3 2004 air quality year. This lack of a 

consistent degree of overlap between the 

two forms in different air quality years 

demonstrates that annual vegetation 

would be expected to receive widely 

differing degrees of protection from 

cumulative seasonal exposures in some 

areas from year to year, even when the 

3-year average of the 8-hour form was 

consistently met. 

It is clear that this analysis is limited 

by the lack of monitoring in rural areas 

where important vegetation and 

ecosystems are located, especially at 

higher elevation sites. This is because 

O3 air quality distributions at high 

elevation sites often do not reflect the 

typical urban and near-urban pattern of 

low morning and evening O3

concentrations with a high mid-day 

peak, but instead maintain relatively flat 

patterns with many concentrations in 

the mid-range (e.g., 0.05–0.09 ppm) for 

extended periods. These conditions can 

lead to relatively low daily maximum 

8-hour averages concurrently with high 

cumulative values so that there is 

potentially less overlap between an 8- 


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hour average and a cumulative, seasonal 

form at these sites. The 2007 Staff Paper 

concluded that it is reasonable to 

anticipate that additional unmonitored 

rural high elevation areas important for 

vegetation may not be adequately 

protected even with a lower level of the 

8-hour form. 

The 2006 Criteria Document discusses 

policy relevant background (PRB) levels 

for high elevation sites and makes the 

following observations: (1) PRB 

concentrations of 0.04 to 0.05 ppm 

occur occasionally at high-elevation 

sites (e.g., > 1.5 km) in the spring due to 

the free-tropospheric influence, 

including some limited contribution 

from hemispheric pollution (O3

produced from anthropogenic emissions 

outside North America); and (2) while 

stratospheric intrusions might 

occasionally elevate O3 at high-altitude 

sites, these events are rare at surface 

sites. Therefore, the 2007 Staff Paper 

concluded that springtime PRB levels in 

the range identified above and rare 

stratospheric intrusions of O3 are 

unlikely to be a major influence on 

3-month cumulative seasonal W126 

values. 

It further remains uncertain as to the 

extent to which air quality 

improvements designed to reduce 

8-hour O3 average concentrations would 

reduce O3 exposures measured by a 

seasonal, cumulative W126 index. The 

2007 Staff Paper indicated this to be an 

important consideration because: (1) 

The biological database stresses the 

importance of cumulative, seasonal 

exposures in determining plant 

response; (2) plants have not been 

specifically tested for the importance of 

daily maximum 8-hour O3

concentrations in relation to plant 

response; and (3) the effects of 

attainment of a 8-hour standard in 

upwind urban areas on rural air quality 

distributions cannot be characterized 

with confidence due to the lack of 

monitoring data in rural and remote 

areas. These factors are important 

considerations in determining whether 

the current 8-hour form can 

appropriately provide requisite 

protection for vegetation. 

2. Assessment of Risks to Vegetation 

The 2007 Staff Paper presents results 

from quantitative and qualitative risk 

assessments of O3 risks to vegetation 

(EPA, 2007). In the 1997 review, crop 

yield and seedling biomass loss OTC 

data provided the basis for staff 

analyses, conclusions, and 

recommendations (EPA, 1996b). Since 

then, several additional lines of 

evidence have progressed sufficiently to 

provide staff with a more complete and 

coherent picture of the scope of O3- 

related vegetation risks, especially those 

faced by seedling, sapling and mature 

tree species growing in field settings, 

and indirectly, forested ecosystems. 

Specifically, research published after 

the 1997 review reflects an increased 

emphasis on field-based exposure 

methods (e.g., free air exposure and 

ambient gradient), improved field 

survey biomonitoring techniques, and 

mechanistic tree process models. 

Findings from each of these research 

areas are discussed separately below. In 

conducting these assessments, the Staff 

Paper analyses relied on both measured 

and modeled air quality information. 

For some effects, like visible foliar 

injury and modeled mature tree growth 

response, only monitored air quality 

information was used. For other effects 

categories (e.g., crop yield and tree 

seedling growth), staff relied on 

interpolated O3 exposures. 

a. Visible Foliar Injury 

As discussed above (section IV.A.2.c), 

systematic injury surveys have 

documented visible foliar injury 

symptoms diagnostic of phytotoxic O3

exposures on sensitive bioindicator 

plants. These surveys have produced 

more expansive evidence than that 

available at the time of the 1997 review 

that visible foliar injury is occurring in 

many areas of the U.S. under current 

ambient conditions. The 2007 Staff 

Paper presents an assessment combining 

recent U.S. Forest Service Forest 

Inventory and Analysis (FIA) 

biomonitoring site data with the county 

level air quality data for those counties 

containing the FIA biomonitoring sites. 

This assessment showed that incidence 

of visible foliar injury ranged from 21 to 

39 percent during the four-year period 

(2001–2004) across all counties with air 

quality levels at or below that of a 0.084 

ppm, 8-hour standard. Of the counties 

that met an 8-hour level of 0.070 ppm 

in those years, 11 to 30 percent still had 

incidence of visible foliar injury. The 

magnitude of these percentages suggests 

that phytotoxic exposures sufficient to 

induce visible foliar injury would still 

occur in many areas after meeting the 

level of a 0.084 ppm secondary standard 

or alternative 0.070 ppm 8-hour 

standard. Additionally, the data showed 

that visible foliar injury occurrence was 

geographically widespread and 

occurring on a variety of plant species 

in forested and other natural systems. 

Linking visible foliar injury to other 

plant effects is still problematic. 

However, its presence indicates that 

other O3-related vegetation effects could 

also be present. 

b. Seedling and Mature Tree Biomass 

Loss 

In the 1997 review, analyses of the 

effects of O3 on trees were limited to 11 

tree species for which C–R functions for 

the seedling growth stage had been 

developed from OTC studies conducted 

by the NHEERL–WED. Important tree 

species such as quaking aspen, 

ponderosa pine, black cherry, and tulip 

poplar were found to be sensitive to 

cumulative seasonal O3 exposures. 

Work done since the 1997 review at the 

AspenFACE site in Wisconsin on 

quaking aspen (Karnosky et al., 2005) 

and a gradient study performed in the 

New York City area (Gregg et al. 2003) 

has confirmed the detrimental effects of 

O3 exposure on tree growth in field 

studies without chambers and beyond 

the seedling stage (King et al. 2005). 

These field studies are discussed above 

in section IV.A. 

To update the seedling biomass loss 

risk analysis, C–R functions for biomass 

loss for available seedling tree species 

taken from the 2006 Criteria Document 

and information on tree growing regions 

derived from the U.S. Department of 

Agriculture’s Atlas of United States 

Trees were combined with projections 

of O3 air quality based on 2001 

interpolated exposures, to produce 

estimated biomass loss for each of the 

seedling tree species individually. Maps 

of these biomass loss projections are 

presented in the 2007 Staff Paper. For 

example, quaking aspen had a wide 

range of O3 exposures across its growing 

range and therefore, showed significant 

variability in percentages of projected 

seedling biomass loss across its range. 

Quaking aspen seedling biomass loss 

was projected to be greater than 4 

percent over much of its geographic 

range, though it can reach above 10 

percent in areas of Ohio, Pennsylvania, 

New York, New Jersey and California. 

Biomass loss for black cherry was 

projected to be greater than 20 percent 

in approximately half its range. Greater 

than 30 percent biomass loss for black 

cherry was projected in North Carolina, 

Tennessee, Indiana, Ohio, Pennsylvania, 

Arizona, Michigan, New York, New 

Jersey, Maryland and Delaware. For 

ponderosa pine, an important tree 

species in the western U.S., biomass 

loss was projected to be above 10 

percent in much of its range in 

California. Biomass loss still occurred in 

many tree species when O3 air quality 

was adjusted to meet the then current 8- 

hour standard of 0.084 ppm. For 

instance, black cherry, ponderosa pine, 

eastern white pine, and aspen had 

estimated median seedling biomass 

losses over portions of their growing 


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57Principal crops as defined by the USDA 

include corn, sorghum, oats, barley, winter wheat, 

rye, Durum wheat, other spring wheat, rice, 

soybeans, peanuts, sunflower, cotton, dry edible 

beans, potatoes, sugar beets, canola, proso millet, 

hay, tobacco, and sugarcane. Acreage data for the 

principal crops were taken from the USDA NASS 

2005 Acreage Report (http:// 

usda.mannlib.cornell.edu/reports/nassr/field/pcpbba/acrg0605.pdf). 

range as high as 24, 11, 6, and 6 percent, 

respectively, when O3 air quality was 

rolled back to just meet a 0.084 ppm, 

8-hour standard. The 2007 Staff Paper 

noted that these results are for tree 

seedlings and that mature trees of the 

same species may have more or less of 

a response to O3 exposure. Due to the 

potential for compounding effects over 

multiple years, experts at a consensus 

workshop on O3 vegetation effects and 

secondary standards, hereinafter 

referred to as the 1996 Consensus 

Workshop, reported in a subsequent 

1997 Workshop Report, that a biomass 

loss greater than 2 percent annually can 

be significant (Heck and Cowling, 1997). 

Decreased seedling root growth and 

survivability could affect overall stand 

health and composition in the long 

term. 

In addition to the estimation of O3

effects on seedling growth, recent work 

available in the 2008 rulemaking has 

enhanced our understanding of risks 

beyond the seedling stage. In order to 

better characterize the potential O3

effects on mature tree growth, a tree 

growth model (TREGRO) was used as a 

tool to evaluate the effect of changing O3

air quality under just meet scenarios for 

selected alternative O3 standards on the 

growth of mature trees. TREGRO is a 

process-based, individual tree growth 

simulation model (Weinstein et al, 

1991). This model has been used to 

evaluate the effects of a variety of O3

exposure scenarios on several species of 

trees by incorporating concurrent 

climate data in different regions of the 

U.S. to account for O3 and climate/ 

meteorology interactions (Tingey et al., 

2001; Weinstein et al., 1991; Retzlaff et 

al., 2000; Laurence et al., 1993; 

Laurence et al., 2001; Weinstein et al., 

2005). The model provides an analytical 

framework that accounts for the 

nonlinear relationship between O3

exposure and response. The interactions 

between O3 exposure, precipitation and 

temperature are integrated as they affect 

vegetation, thus providing an internal 

consistency for comparing effects in 

trees under different exposure scenarios 

and climatic conditions. An earlier 

assessment of the effectiveness of 

national ambient air quality standards 

in place since the early 1970s took 

advantage of 40 years of air quality and 

climate data for the Crestline site in the 

San Bernardino Mountains of California 

to simulate ponderosa pine growth over 

time with the improving air quality 

using TREGRO (Tingey et al., 2004). 

The TREGRO model was used to 

assess growth of Ponderosa pine in the 

San Bernardino Mountains of California 

(Crestline) and the growth of yellow 

poplar and red maple in the 

Appalachian mountains of Virginia and 

North Carolina, Shenandoah National 

Park (Big Meadows) and Linville Gorge 

Wilderness Area (Cranberry), 

respectively. Total tree growth 

associated with ‘‘as is’’ air quality, and 

air quality adjusted to just meet 

alternative O3 standards was assessed. 

Ponderosa pine is one of the most 

widely distributed pines in western 

North America, a major source of 

timber, important as wildlife habitat, 

and valued for aesthetics (Burns and 

Honkala, 1990). Red maple is one of the 

most abundant species in the eastern 

U.S. and is important for its brilliant fall 

foliage and highly desirable wildlife 

browse food (Burns and Honkala, 1990). 

Yellow poplar is an abundant species in 

the southern Appalachian forest. It is 10 

percent of the cove hardwood stands in 

southern Appalachians which are 

widely viewed as some of the country’s 

most treasured forests because the 

protected, rich, moist set of conditions 

permit trees to grow the largest in the 

eastern U.S. The wood has high 

commercial value because of its 

versatility and as a substitute for 

increasingly scarce softwoods in 

furniture and framing construction. 

Yellow poplar is also valued as a honey 

tree, a source of wildlife food, and a 

shade tree for large areas (Burns and 

Honkala, 1990). 

The 2007 Staff Paper analyses found 

that just meeting a 0.084 ppm standard 

would likely continue to allow O3- 

related reductions in annual net 

biomass gain in these species. This is 

based on model outputs that estimate 

that as O3 levels are reduced below 

those of a 0.084 ppm standard, 

significant improvements in growth 

would occur. For instance, estimated 

growth in red maple increased by 4 and 

3 percent at Big Meadows and Cranberry 

sites, respectively, when air quality was 

rolled back to just met a W126 value of 

13 ppm-hour. Yellow poplar was 

projected to have a growth increase 

between 0.6 and 8 percent under the 

same scenario at the two eastern sites. 

Though there is uncertainty 

associated with the above analyses, this 

information should be given careful 

consideration in light of several other 

pieces of evidence. Specifically, new 

evidence from experimental studies that 

go beyond the seedling growth stage 

continues to show decreased growth 

under elevated O3 (King et al. 2005). 

Some mature trees such as red oak have 

shown an even greater sensitivity of 

photosynthesis to O3 than seedlings of 

the same species (Hanson et al., 1994). 

As indicated above, smaller growth loss 

increments may be significant for 

perennial species. The potential for 

cumulative ‘‘carry over’’ effects as well 

as compounding also must be 

considered. The accumulation of such 

‘‘carry-over’’ effects over time may affect 

long-term survival and reproduction of 

individuals and ultimately the 

abundance of sensitive tree species in 

forest stands. 

c. Crops 

As discussed in the 2007 Staff Paper, 

risk of O3 exposure and associated 

monetized benefits were estimated for 

commodity crops, fruits and vegetables. 

Similar to the tree seedling analysis, this 

analysis combined C–R information on 

crops, crop growing regions and 

interpolated exposures during each crop 

growing season. NCLAN crop functions 

were used for commodity crops. 

According to USDA National 

Agricultural Statistical Survey (NASS) 

data, the 9 commodity crop species (e.g., 

cotton, field corn, grain sorghum, 

peanut, soybean, winter wheat, lettuce, 

kidney bean, potato) included in the 

2007 Staff Paper analysis accounted for 

69 percent of 2004 principal crop 

acreage planted in the U.S. in 2004.57

The C–R functions for six fruit and 

vegetable species (tomatoes-processing, 

grapes, onions, rice, cantaloupes, 

Valencia oranges) were identified from 

the California fruit and vegetable 

analysis from the 1997 review (Abt 

Associates Inc, 1995). The 2007 Staff 

Paper noted that fruit and vegetable 

studies were not part of the NCLAN 

program and C–R functions were 

available only in terms of seasonal 7- 

hour or 12-hour mean index. This index 

form is considered less effective in 

predicting plant response for a given 

change in air quality than the 

cumulative form used with other crops. 

Therefore, the fruit and vegetable C–R 

functions were considered more 

uncertain than those for commodity 

crops. 

Analyses in the 2007 Staff Paper 

showed that some of the most important 

commodity crops such as soybean, 

winter wheat and cotton had some 

projected losses under the 2001 base 

year air quality. Soybean yield losses 

were projected to be 2–4 percent in 

parts of Pennsylvania, New Jersey, 

Maryland and Texas. Winter wheat was 

projected to have yield losses of 2–6 

percent in parts of California. 


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58While the term ‘‘averaging time’’ is used, for the 

cumulative, seasonal standard the seasonal and 

Additionally, cotton was projected to 

have yield losses of above 6 percent in 

parts of California, Texas and North 

Carolina in 2001. The risk assessment 

estimated that just meeting the then 

current 0.084 ppm, 8-hour standard 

would still allow O3=related yield loss 

to occur in some commodity crop 

species and fruit and vegetable species 

currently grown in the U.S. For 

example, based on median C–R function 

response, in counties with the highest 

O3 levels, potatoes and cotton had 

estimated yield losses of 9–15 percent 

and 5–10 percent, respectively, when O3

air quality just met the level of a 0.084 

ppm, 8-hour standard. Estimated yield 

improved in these counties when the 

alternative W126 standard levels were 

met. The very important soybean crop 

had generally small yield losses 

throughout the country under just 

meeting the then current standard (0–4 

percent). 

The 2007 Staff Paper also presented 

estimates of monetized benefits for 

crops associated with a 0.084 ppm, 8- 

hour and alternative standards. The 

Agriculture Simulation Model (AGSIM) 

(Taylor, 1994; Taylor, 1993) was used to 

calculate annual average changes in 

total undiscounted economic surplus for 

commodity crops and fruits and 

vegetables when the then current and 

alternative standard levels were met. 

Meeting the various alternative 

standards did show some significant 

benefits beyond a 0.084 ppm, 8-hour 

standard. However, the 2007 Staff Paper 

recognized that the AGSIM economic 

benefits estimates also incorporate 

several sources of uncertainty, 

including: (1) Estimates of economic 

benefits derived from use of the more 

uncertain C–R relationships for fruits 

and vegetables; (2) uncertain 

assumptions about the treatment and 

effect of government farm payment 

programs; and (3) uncertain 

assumptions about near-term changes in 

the agriculture sector due to the 

increased use of crops as biofuels. 

Although the AGSIM model results 

provided a relative comparison of 

agricultural benefits between alternative 

standards, these uncertainties limited 

the utility of the absolute numbers. 

D. Reconsideration of Secondary 

Standard 

As discussed above at the beginning 

of section IV, this reconsideration of the 

secondary O3 standard set in the 2008 

rulemaking focuses on reconsidering 

certain elements of the standard, the 

form, averaging times, and level. The 

general approach for setting a secondary 

O3 standard used in the 2008 

rulemaking, and in the previous 1997 

rulemaking, was to consider two basic 

policy options: Setting a distinct 

secondary standard with a biologically 

relevant form and averaging times, or 

setting a secondary standard identical to 

the primary standard. In the 2007 

proposed rule, both such options were 

evaluated, commented on by CASAC 

and the public, and proposed, as 

discussed below in sections IV.D.1 and 

IV.D.2, respectively. In the 2008 final 

rule, EPA decided to set the secondary 

standard identical to the revised 8-hour 

primary standard, as discussed below in 

section IV.D.3. Section IV.D.4 

summarizes comments received from 

CASAC following the 2008 decision. 

The Administrator’s proposed 

conclusions based on this 

reconsideration are presented in section 

IV.D.5. 

1. Considerations Regarding the 2007 

Proposed Cumulative Seasonal Standard 

a. Form 

The 2006 Criteria Document and 2007 

Staff Paper concluded that the recent 

vegetation effects literature evaluated in 

the 2008 rulemaking strengthened and 

reaffirmed conclusions made in the 

1997 review that the use of a cumulative 

exposure index that differentially 

weights ambient concentrations is best 

able to relate ambient exposures to 

vegetation response at this time (EPA, 

2006a, b; see also discussion in IV.B 

above). The 1997 review focused in 

particular on two of these cumulative 

forms, the SUM06 and W126. In the 

2008 rulemaking, the 2007 Staff Paper 

again evaluated these two forms in light 

of two key pieces of then recent 

information: Estimates of PRB that were 

lower than in the 1997 review, and 

continued lack of evidence within the 

vegetation effects literature of a 

biological threshold for vegetation 

exposures of concern. On the basis of 

those policy and science-related 

considerations, the 2007 Staff Paper 

concluded that the W126 form was more 

appropriate in the context of the 2008 

rulemaking. Specifically, the W126 

form, by its incorporation of a sigmoidal 

weighting scheme, does not create an 

artificially imposed concentration 

threshold, gives proportionally more 

weight to the higher and typically more 

biologically potent concentrations, and 

is not significantly influenced by O3

concentrations within the range of 

estimated PRB. The Staff Paper further 

concluded that ‘‘it is not appropriate to 

continue to use an 8-hour averaging 

time for the secondary standard’’ and 

that ‘‘the 8-hour average form should be 

replaced with a cumulative, seasonal, 

concentration weighted form’’ (EPA, 

2007b; pg. 8–25). 

The CASAC, based on its assessment 

of the same vegetation effects science, 

agreed with the 2006 Criteria Document 

and 2007 Staff Paper and unanimously 

concluded that it is not appropriate to 

try to protect vegetation from the known 

or anticipated adverse effects of ambient 

O3 by continuing to promulgate 

identical primary and secondary 

standards for O3. Moreover, the 

members of the CASAC and a 

substantial majority of the CASAC O3

Panel agreed with 2007 Staff Paper 

conclusions and encouraged EPA to 

establish an alternative cumulative 

secondary standard for O3 and related 

photochemical oxidants that is 

distinctly different in averaging time, 

form and level from the current or 

potentially revised 8-hour primary 

standard. The CASAC also stated that 

‘‘the recommended metric for the 

secondary ozone standard is the 

(sigmoidally-weighted) W126 index’’ 

(Henderson, 2007). 

The EPA agreed with the conclusions 

drawn in the 2006 Criteria Document, 

2007 Staff Paper and by CASAC that the 

scientific evidence available in the 2008 

rulemaking continued to demonstrate 

the cumulative nature of O3-induced 

plant effects and the need to give greater 

weight to higher concentrations. Thus, 

EPA concluded that a cumulative 

exposure index that differentially 

weights O3 concentrations represents a 

reasonable policy choice for a seasonal 

secondary standard to protect against 

the effects of O3 on vegetation. The EPA 

further agreed with both the 2007 Staff 

Paper and CASAC that the most 

appropriate cumulative, concentrationweighted form to consider in the 2008 

rulemaking was the sigmoidally 

weighted W126 form, due to EPA’s 

recognition that there is no evidence in 

the literature for an exposure threshold 

that would be appropriate across all O3- 

sensitive vegetation and that this form is 

unlikely to be significantly influenced 

by O3 air quality within the range of 

PRB levels identified in this rulemaking. 

Thus, in 2007 EPA proposed as one 

option to replace the then current 0.084 

ppm, 8-hour average secondary standard 

with a standard defined in terms of the 

cumulative, seasonal W126 form. The 

EPA also proposed the option of making 

the secondary identical to the proposed 

revised primary standard. 

b. Averaging Times 58

The 2007 Staff Paper, in addition to 

form, also considered what exposure 


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diurnal time periods at issue are those over which 

exposures during a specified period of time are 

cumulated, not averaged. 

periods or durations are most relevant 

for vegetation, which, unlike people, is 

exposed to ambient air continuously 

throughout its lifespan. For annual 

species, this lifespan encompasses a 

period of only one year or less; while for 

perennials, lifespans can range from a 

few years to decades or centuries. 

However, because O3 levels are not 

continuously elevated and plants are 

not equally sensitive to O3 over the 

course of a day, season or lifetime, it 

becomes necessary to identify periods of 

exposure that have the most relevance 

for plant response. The 2007 Staff Paper 

discussed exposure periods relevant for 

vegetation in terms of a seasonal 

window and a diurnal window, and it 

also discussed defining the standard in 

terms of an annual index value versus 

a 3-year average of annual index values. 

The numbered paragraphs below 

present the 2007 Staff Paper discussions 

on these exposure periods, and the 

annual versus 3-year average index 

value, followed by a discussion of 

CASAC views and EPA proposed 

conclusions. 

(1) In considering an appropriate 

seasonal window, the 2007 Staff Paper 

recognized that, in general, many 

annual crops are grown for periods of a 

few months before being harvested. In 

contrast, other annual and perennial 

species may be photosynthetically 

active longer, and for some species and 

locations, throughout the entire year. In 

general, the period of maximum 

physiological activity and thus, 

maximum potential O3 uptake for 

annual crops, herbaceous species, and 

deciduous trees and shrubs coincides 

with some or all of the intra-annual 

period defined as the O3 season, which 

varies on a state-by-state basis. This is 

because the high temperature and high 

light conditions that promote the 

formation of tropospheric O3 also 

promote physiological activity in 

vegetation. 

The 2007 Staff Paper noted that the 

selection of any single seasonal 

exposure period for a national standard 

would represent a compromise, given 

the significant variability in growth 

patterns and lengths of growing seasons 

among the wide range of vegetation 

species occurring within the U.S. that 

may experience adverse effects 

associated with O3 exposures. However, 

the 2007 Staff Paper further concluded 

that the consecutive 3-month period 

within the O3 season with the highest 

W126 index value (e.g., maximum 

3-month period) would, in most cases, 

likely coincide with the period of 

greatest plant sensitivity on an annual 

basis. Therefore, the 2007 Staff Paper 

again concluded, as it did in the 1997 

review, that the annual maximum 

consecutive 3-month period is a 

reasonable seasonal time period, when 

combined with a cumulative, 

concentration weighted form, for 

protection of sensitive vegetation. 

(2) In considering an appropriate 

diurnal window, the Staff Paper 

recognized that over the course of the 

24-hour diurnal period, plant stomatal 

conductance varies in response to 

changes in light level, soil moisture and 

other environmentally and genetically 

controlled factors. In general, stomata 

are most open during daylight hours in 

order to allow sufficient CO2 uptake for 

use in carbohydrate production through 

the light-driven process of 

photosynthesis. At most locations, O3

concentrations are also highest during 

the daytime, and thus, most likely to 

coincide with maximum stomatal 

uptake. It is also known however, that 

in some species, stomata may remain 

open sufficiently at night to allow for 

some nocturnal uptake to occur. In 

addition, at some rural, high elevation 

sites, the O3 concentrations remain 

relatively flat over the course of the day, 

often at levels above estimated PRB. At 

these sites, nighttime W126 values can 

be of similar magnitude as daytime 

values, though the significance of these 

exposures is much less certain. This is 

because O3 uptake during daylight 

hours is known to impair the lightdriven process of photosynthesis, which 

can then lead to impacts on 

carbohydrate production, plant growth, 

reproduction (yield) and root function. 

It is less clear at this time to what extent 

and by what mechanisms O3 uptake at 

night adversely impacts plant function. 

In addition, many species have not been 

shown to take up O3 at night and/or do 

not occur in areas with elevated 

nighttime O3 concentrations. 

In reviewing the information on this 

topic that became available after the 

1997 review, the 2007 Staff Paper 

considered the information compiled in 

a summary report by Musselman and 

Minnick (2000). This work reported that 

some species take up O3 at night, but 

that the degree of nocturnal stomatal 

conductance varies widely between 

species and its relevance to overall O3- 

induced vegetation effects remain 

unclear. In considering this information, 

the 2007 Staff Paper concluded that for 

the vast majority of studied species, 

daytime exposures represent the 

majority of diurnal plant O3 uptake and 

are responsible for inducing the plant 

response of most significance to the 

health and productivity of the plant 

(e.g., reduced carbohydrate production). 

Until additional information is available 

about the extent to which co-occurrence 

of sensitive species and elevated 

nocturnal O3 exposures exists, and what 

levels of nighttime uptake are adverse to 

affected species, the 2007 Staff Paper 

concluded that this information 

continues to be preliminary, and does 

not provide a basis for reaching a 

different conclusion regarding the 

diurnal window at this time. The 2007 

Staff Paper further noted that additional 

research is needed to address the degree 

to which a 12-hour diurnal window may 

be under-protective in areas where 

elevated nighttime levels of O3 co-occur 

with sensitive species with a high 

degree of nocturnal stomatal 

conductance. Thus, as in the 1997 

review, the 2007 Staff Paper again 

concluded that based on the available 

science, the daytime 12-hour window (8 

a.m. to 8 p.m.) is the most appropriate 

period over which to cumulate diurnal 

O3 exposures, specifically those most 

relevant to plant growth and yield 

responses. 

(3) In considering whether the 

standard should be defined in terms of 

an annual index value or a 3-year 

average of annual index values, the 2007 

Staff Paper recognized that though most 

cumulative seasonal exposure levels of 

concern for vegetation have been 

expressed in terms of the annual 

timeframe, it may be appropriate to 

consider a 3-year average for purposes 

of standard stability. However, the 2007 

Staff Paper noted that for certain welfare 

effects of concern (e.g., foliar injury, 

yield loss for annual crops, growth 

effects on other annual vegetation and 

potentially tree seedlings), an annual 

time frame may be a more appropriate 

period in which to assess what level 

would provide the requisite degree of 

protection, while for other welfare 

effects (e.g., mature tree biomass loss), a 

3-year average may also be appropriate. 

Thus, the 2007 Staff Paper concluded 

that it is appropriate to consider both an 

annual and a 3-year average. Further, 

the 2007 Staff Paper concluded that 

should a 3-year average of the 12-hour 

W126 form be selected, a lower standard 

level should be considered to reduce the 

potential of adverse impacts to annual 

species from a single high O3 year that 

could still occur while attaining a 

standard on average over 3 years. 

The CASAC, in considering what 

seasonal, diurnal, and annual or 

multiyear time periods are most 

appropriate when combined with a 

cumulative, seasonal form to protect 

vegetation from exposures of concern, 

agreed that the 2007 Staff Paper 


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conclusion regarding the 3-month 

seasonal period and 12-hour daylight 

window was appropriate, with the 

distinction that both of these time 

periods likely represents the minimum 

time periods of importance. In 

particular, one O3 Panel member 

commented that for some species, 

additional O3 exposures of importance 

were occurring outside the 3-month 

seasonal and 12-hour diurnal windows. 

Further, the CASAC concluded that 

multi-year averaging to promote a 

‘‘stable’’ secondary standard is less 

appropriate for a cumulative, seasonal 

secondary standard than for a primary 

standard based on daily maximum 8- 

hour concentrations. The CASAC 

further concluded that if multi-year 

averaging is employed to afford greater 

stability of the secondary standard, the 

level of the standard should be revised 

downward to assure that the desired 

degree of protection is not exceeded in 

individual years. 

The EPA, in determining which 

seasonal and diurnal time periods are 

most appropriate to propose, took into 

account the 2007 Staff Paper and 

CASAC views. In being careful to 

consider what is needed to provide the 

requisite degree of protection, no more 

and no less, in 2007 EPA proposed that 

the 3-month seasonal period and 12- 

hour daylight period are appropriate. 

Based on the 2007 Staff Paper 

conclusions discussed above, EPA was 

mindful that there is the potential for 

under-protection with a 12-hour diurnal 

window in areas with sufficiently 

elevated nighttime levels of O3 where 

sensitive species with a high degree of 

nocturnal stomatal conductance occur. 

On the other hand, EPA also recognized 

that a longer diurnal window (e.g., 24- 

hour) has the possibility of overprotecting vegetation in areas where 

nighttime O3 levels remain relatively 

high but where no species having 

significant nocturnal uptake exist. In 

weighing these considerations, EPA 

agreed with the 2007 Staff Paper 

conclusion that until additional 

information is available about the extent 

to which this co-occurrence of sensitive 

species and elevated nocturnal O3

exposures exists, and what levels of 

nighttime uptake are adverse to affected 

species, this information does not 

provide a basis for reaching a different 

conclusion at this time. The EPA also 

considered to what extent the 3-month 

period within the O3 season was 

appropriate, recognizing that many 

species of vegetation have longer 

growing seasons. The EPA further 

proposed that the maximum 3-month 

period is sufficient and appropriate to 

characterize O3 exposure levels 

associated with known levels of plant 

response. Therefore, EPA proposed that 

the most appropriate exposure periods 

for a cumulative, seasonal form is the 

daytime 12-hour window (8 a.m. to 8 

p.m.) during the consecutive 3-month 

period within the O3 monitoring season 

with the maximum W126 index value. 

The EPA also proposed an annual 

rather than a multi-year cumulative, 

seasonal standard. In proposing this 

option, EPA also believed that it was 

appropriate to consider the benefits to 

the public welfare that would accrue 

from establishing a 3-year average 

secondary standard, and solicited 

comment on this alternative. In so 

doing, EPA also agreed with 2007 Staff 

Paper and CASAC conclusions that 

should a 3-year standard be finalized, 

the level of the standard should be set 

so as to provide the requisite degree of 

protection for those vegetation effects 

judged to be adverse to the public 

welfare within a single annual period. 

c. Level 

The 2007 Staff Paper, in identifying a 

range of levels for a 3-month, 12-hour 

W126 annual form appropriate to 

protect the public welfare from adverse 

impacts to vegetation from O3

exposures, considered what information 

from the array of vegetation effects 

evidence and exposure and risk 

assessment results was most useful. 

Regarding the vegetation effects 

evidence, the 2007 Staff Paper found 

stronger support than what was 

available at the time of the 1997 review 

for an increased level of protection for 

trees and ecosystems. Specifically, this 

expanded body of support includes: (1) 

Additional field based data from free 

air, gradient and biomonitoring surveys 

demonstrating adverse levels of O3- 

induced above and/or below-ground 

growth reductions on trees at the 

seedling, sapling and mature growth 

stages and incidence of visible foliar 

injury occurring at biomonitoring sites 

in the field at ambient levels of 

exposure; (2) qualitative support from 

free air (e.g., AspenFACE) and gradient 

studies on a limited number of tree 

species for the continued 

appropriateness of using OTC-derived 

C–R functions to predict tree seedling 

response in the field; (3) studies that 

continue to document below-ground 

effects on root growth and ‘‘carry-over’’ 

effects occurring in subsequent years 

from O3 exposures; and (4) increased 

recognition and understanding of the 

structure and function of ecosystems 

and the complex linkages through 

which O3, and other stressors, acting at 

the organism and species level can 

influence higher levels within the 

ecosystem hierarchy and disrupt 

essential ecological attributes critical to 

the maintenance of ecosystem goods 

and services important to the public 

welfare. 

Based on the above observations and 

on the vegetation effects and the results 

of the exposure and impact assessment 

summarized above, the 2007 Staff Paper 

concluded that just meeting the then 

current standard would still allow 

adverse levels of tree seedling biomass 

loss in sensitive commercially and 

ecologically important tree species in 

many regions of the country. Seedling 

risk assessment results showed that 

some tree seedling species are extremely 

sensitive (e.g., cottonwood, black cherry 

and aspen), with annual biomass losses 

occurring in the field of the same or 

greater magnitude that that of annual 

crops. Such information from the tree 

seedling risk assessment suggests that 

O3 levels would need to be substantially 

reduced to protect sensitive tree 

seedlings like black cherry from growth 

and foliar injury effects. 

In addition to the currently 

quantifiable risks to trees from ambient 

exposures, the 2007 Staff Paper also 

considered the more subtle impacts of 

O3 acting in synergy with other natural 

and man-made stressors to adversely 

affect individual plants, populations 

and whole systems. By disrupting the 

photosynthetic process, decreasing 

carbon storage in the roots, increasing 

early senescence of leaves and affecting 

water use efficiency in trees, O3

exposures could potentially disrupt or 

change the nutrient and water flow of an 

entire system. Weakened trees can 

become more susceptible to other 

environmental stresses such as pest and 

pathogen outbreaks or harsh weather 

conditions. Though it is not possible to 

quantify all the ecological and societal 

benefits associated with varying levels 

of alternative secondary standards, the 

2007 Staff Paper concluded that this 

information should be weighed in 

considering the extent to which a 

secondary standard should be set so as 

to provide potential protection against 

effects that are anticipated to occur. 

In addition, the 2007 Staff Paper also 

recognized that in the 1997 review, EPA 

took into account the results of a 1996 

Consensus Workshop. At this workshop, 

a group of independent scientists 

expressed their judgments on what 

standard form(s) and level(s) would 

provide vegetation with adequate 

protection from O3-related adverse 

effects. Consensus was reached with 

respect to selecting appropriate ranges 

of levels in terms of a cumulative, 

seasonal 3-month, 12-hr SUM06 


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standard for a number of vegetation 

effects endpoints. These ranges are 

identified below, with the estimated 

approximate equivalent W126 standard 

values shown in parentheses. For 

growth effects to tree seedlings in 

natural forest stands, a consensus was 

reached that a SUM06 range of 10 to 15 

(W126 range of 7 to 13) ppm-hour 

would be protective. For growth effects 

to tree seedlings and saplings in 

plantations, the consensus SUM06 range 

was 12 to 16 (W126 range of 9 to 14) 

ppm-hour. For visible foliar injury to 

natural ecosystems, the consensus 

SUM06 range was 8 to 12 (W126 range 

of 5 to 9) ppm-hour. 

Taking these consensus statements 

into account, EPA stated in the 1997 

final rule (62 FR 38856) that ‘‘the report 

lends important support to the view that 

the current secondary standard is not 

adequately protective of vegetation 

* * * [and] * * * foreshadows the 

direction of future scientific research in 

this area, the results of which could be 

important in future reviews of the O3

secondary standard’’ (62 FR 38856). 

Given the importance EPA put on the 

consensus report in the 1997 review, the 

2007 Staff Paper considered to what 

extent research published after 1997 

provided empirical support for the 

ranges of levels identified by the experts 

as protective of different types of O3- 

induced effects. With regard to O3- 

induced biomass loss in sensitive tree 

seedlings/saplings growing in natural 

forest stands, the information discussed 

in the 2007 Staff Paper, including the 

evidence from free air and gradient 

studies, provides additional direct 

support for the conclusion that the 1996 

Consensus Workshop approximate 

W126 range of 7–13 ppm-hour was an 

appropriate range to consider in 

selecting a protective level. With regard 

to visible foliar injury, the available 

evidence, including the 2007 Staff Paper 

analysis of incidence in counties with 

FIA monitoring sites and air quality 

data, showed significant levels of 

county-level visible foliar injury 

incidence at the W126 level of 13 ppmhour. However, because this analysis 

did not address risks of this effect at 

lower levels of O3 air quality, and 

because there is a significant 

uncertainty in predicting the degree of 

visible foliar injury symptoms expected 

for lower levels of O3 air quality, the 

evidence provides less certain but 

qualitative directional support for the 

1996 Consensus Workshop range of 5 to 

9 ppm-hour to protect against this effect. 

With regard to O3-induced effects on 

plantation trees, there is far less direct 

information available. Though some 

forest plantation trees are O3-sensitive, 

the monoculture nature of these stands 

makes uncertain the degree to which 

competition for resources might play a 

role and to what degree the variety of 

management practices applied would be 

expected to mitigate the O3-induced 

effects. Thus, it is difficult to 

distinguish a protective range of levels 

for plantation trees from a range of 

levels that would be protective of O3- 

sensitive tree seedlings and saplings in 

natural forest stands. Therefore, on the 

basis of the strength of the evidence 

available, the 2007 Staff Paper 

concluded that it was appropriate to 

consider a range for a 3-month, 12-hour, 

W126 standard that included the 1996 

consensus recommendations for growth 

effects in tree seedlings in natural forest 

stands (i.e., 7–13 ppm-hour in terms of 

a W126 form). 

In considering the available 

information on O3-related effects on 

crops in the 2008 rulemaking, the 2007 

Staff Paper observed the following 

regarding the strength of the underlying 

crop science: (1) Nothing in the recent 

literature points to a change in the 

relationship between O3 exposure and 

crop response across the range of 

species and/or cultivars of commodity 

crops currently grown in the U.S. that 

could be construed to make less 

appropriate the use of commodity crop 

C–R functions developed in the NCLAN 

program; (2) new field-based studies 

(e.g., SoyFACE) provide qualitative 

support in a few limited cases for the 

appropriateness of using OTC-derived 

C–R functions to predict crop response 

in the field; and (3) refinements in the 

exposure, risk and benefits assessments 

in this review reduce some of the 

uncertainties present in the 1997 

review. On the basis of these 

observations, the 2007 Staff Paper 

concluded that nothing in the newly 

assessed information called into 

question the strength of the underlying 

science upon which EPA based its 

proposed decision in the 1997 review to 

select a level of a cumulative, seasonal 

form associated with protecting 50 

percent of crop cases from no more than 

10 percent yield loss as providing the 

requisite degree of protection for 

commodity crops. 

The 2007 Staff Paper then considered 

whether any additional information is 

available to inform judgments as to the 

adversity of various O3-induced levels 

of crop yield loss to the public welfare. 

As noted above, the 2007 Staff Paper 

observed that agricultural systems are 

heavily managed, and that in addition to 

stress from O3, the annual productivity 

of agricultural systems is vulnerable to 

disruption from many other stressors 

(e.g., weather, insects, disease), whose 

impact in any given year can greatly 

outweigh the direct reduction in annual 

productivity resulting from elevated O3

exposures. On the other hand, O3 can 

also more subtly impact crop and forage 

nutritive quality and indirectly 

exacerbate the severity of the impact 

from other stressors. Though these latter 

effects currently cannot be quantified, 

they should be considered in judging to 

what extent a level of protection 

selected to protect commodity crops 

should be precautionary. 

Based on the above considerations, 

the 2007 Staff Paper concluded that the 

level of protection (no more than 10% 

yield or biomass loss in 50% of studied 

cases) judged requisite in the 1997 

review to protect the public welfare 

from adverse levels of O3-induced 

reductions in crop yields and tree 

seedling biomass loss, as provided by a 

W126 level of 21 ppm-hour, remains 

appropriate for consideration as an 

upper bound of a range of appropriate 

levels. 

Thus, the 2007 Staff Paper concluded, 

based on all the above considerations, 

that an appropriate range of 3-month, 

12-hour W126 levels was 7 to 21 ppmhour, recognizing that the level selected 

is largely a policy judgment as to the 

requisite level of protection needed. In 

determining the requisite level of 

protection for crops and trees, and 

indirectly, ecosystems, the 2007 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. 

The CASAC, in its final letter to the 

Administrator (Henderson, 2007), 

agreed with the 2007 Staff Paper 

recommendations that the lower bound 

of the range within which a seasonal 

W126 welfare-based (secondary) O3

standard should be considered is 

approximately 7 ppm-hour; however, it 

did not agree with staff’s 

recommendation that the upper bound 

of the range for consideration should be 

as high as 21 ppm-hour. Rather, CASAC 

recommended that the upper bound of 

the range considered should be no 

higher than 15 ppm-hour, which is just 

above the upper ends of the ranges 

identified in the 1996 Consensus 

Workshop as being protective of tree 

seedlings and saplings grown in natural 

forest stands and in plantations. The 

lower end of this range (7 ppm-hour) is 

the same as the lower end of the range 

identified in the 1996 Consensus 

Workshop as protective of tree seedlings 


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in natural forest stands from growth 

effects. 

In the 2007 proposed rule, taking 

2007 Staff Paper and CASAC views into 

account, EPA proposed a range of levels 

for a cumulative, seasonal secondary 

standard as expressed in terms of the 

maximum 3 month, 12-hour W126 form, 

in the range of 7 to 21 ppm-hour. This 

range encompasses the range of levels 

recommended by CASAC, and also 

includes a higher level as recommended 

for consideration in the 2007 Staff 

Paper. Given the uncertainty in 

determining the risk attributable to 

various levels of exposure to O3, EPA 

believed, as a public welfare policy 

judgment, that this was a reasonable 

range to propose. 

2. Considerations Regarding the 2007 

Proposed 8-Hour Standard 

In the 1997 review, the 1996 Staff 

Paper included an analysis to compare 

the degree of overlap between areas that 

would be expected not to meet the range 

of alternative 8-hour standards being 

considered for the primary NAAQS and 

those expected not to meet the range of 

values (expressed in terms of the 

seasonal SUM06 index) of concern for 

vegetation. This result suggested that 

improvements in national air quality 

expected to result from attaining an 8- 

hour primary standard within the 

recommended range of levels would 

also be expected to reduce levels of 

concern for vegetation in those same 

areas. In the 1997 final rule, the 

decision was made, on the basis of both 

science and policy considerations, to 

make the secondary identical to the 

primary standard. It acknowledged, 

however, that uncertainties remained 

‘‘as to the extent to which air quality 

improvements designed to reduce 8- 

hour average O3 concentrations 

averaged over a 3-year period would 

reduce O3 exposures measured by a 

seasonal SUM06 index’’ (62 FR 38876). 

On the basis of that history, the 2007 

Staff Paper analyzed the degree of 

overlap expected between alternative 8- 

hour and cumulative seasonal 

secondary standards (as discussed above 

in section IV.C.1) using then recent air 

quality. Based on the results, the 2007 

Staff Paper concluded that the degree to 

which the then current 8-hour standard 

form and level would overlap with areas 

of concern for vegetation expressed in 

terms of the 12-hour W126 standard is 

inconsistent from year to year and 

would depend greatly on the level of the 

12-hour W126 and 8-hour standards 

selected and the distribution of hourly 

O3 concentrations within the annual 

and/or 3-year average period. 

Thus, though the 2007 Staff Paper 

recognized again that meeting the 

current or alternative levels of the 8- 

hour average standard could result in air 

quality improvements that would 

potentially benefit vegetation in some 

areas, it urged caution be used in 

evaluating the likely vegetation impacts 

associated with a given level of air 

quality expressed in terms of the 8-hour 

average form in the absence of parallel 

W126 information. This caution was 

due to the concern that the analysis in 

the 2007 Staff Paper may not be an 

accurate reflection of the true situation 

in non-monitored, rural counties due to 

the lack of more complete monitor 

coverage in many rural areas. Further, of 

the counties that did not show overlap 

between the two standard forms, most 

were located in rural/remote high 

elevation areas which have O3 air 

quality patterns that are typically 

different from those associated with 

urban and near urban sites at lower 

elevations. Because the majority of such 

areas are currently not monitored, it is 

believed there are likely to be additional 

areas that have similar air quality 

distributions that would lead to the 

same disconnect between forms. Thus, 

the 2007 Staff Paper concluded that it 

remained problematic to determine the 

appropriate level of protection for 

vegetation using an 8-hour average form. 

The CASAC recognized that an 

important difference between the effects 

of acute exposures to O3 on human 

health and the effects of O3 exposures 

on welfare is that vegetation effects are 

more dependent on the cumulative 

exposure to, and uptake of, O3 over the 

course of the entire growing season 

(Henderson, 2006c). The CASAC O3

Panel members were unanimous in 

concluding the protection of natural 

terrestrial ecosystems and managed 

agricultural crops requires a secondary 

O3 standard that is substantially 

different from the primary O3 standard 

in averaging time, level, and form 

(Henderson, 2007). 

In considering the appropriateness of 

proposing a revised secondary standard 

that would be identical to the proposed 

primary standard, EPA took into 

account the approach used by the 

Agency in the 1997 review, the 

conclusions of the 2007 Staff Paper, 

CASAC advice, and the views of public 

commenters. The EPA first considered 

the 2007 Staff Paper analysis of the 

projected degree of overlap between 

counties with air quality expected to 

meet various alternative levels of an 8- 

hour standard and alternative levels of 

a W126 standard based on monitored air 

quality data. This analysis showed 

significant overlap within the proposed 

range of the primary 8-hour form and 

selected levels of the W126 standard 

form being considered, with the degree 

of overlap between these two forms 

depending greatly on the levels selected 

and the distribution of hourly O3

concentrations within the annual and/or 

3-year average period. On this basis, 

EPA concluded that a secondary 

standard set identical to the proposed 

primary standard would provide a 

significant degree of additional 

protection for vegetation as compared to 

that provided by the current secondary 

standard. The EPA also recognized that 

lack of rural monitoring data made 

uncertain the degree to which the 

proposed 8-hour or W126 alternatives 

would be protective, and that there 

would be the potential for not providing 

the appropriate degree of protection for 

vegetation in areas with air quality 

distributions that result in a high 

cumulative, seasonal exposure but do 

not result in high 8-hour average 

exposures. While this potential for 

under-protection using an 8-hour 

standard was clear, the number and size 

of areas at issue and the degree of risk 

was hard to determine. On the other 

hand, EPA also considered at that time 

that there was a potential risk of overprotection with a cumulative, seasonal 

standard given the inherent 

uncertainties associated with moving to 

a new form for the secondary standard, 

in particular those associated with 

predicting exposure and risk patterns 

based on a limited rural monitoring 

network. 

The EPA also considered the views 

and recommendations of CASAC, and 

agreed that a cumulative, seasonal 

standard is the most biologically 

relevant way to relate exposure to plant 

growth response. However, as reflected 

in the public comments, EPA also 

recognized that there remained 

significant uncertainties in determining 

or quantifying the degree of risk 

attributable to varying levels of O3

exposure, the degree of protection that 

any specific cumulative, seasonal 

standard would produce, and the 

associated potential for error in 

determining the standard that will 

provide a requisite degree of 

protection—i.e., sufficient but not more 

than what is necessary. Given this 

uncertainty, EPA also believed it was 

appropriate to consider the degree of 

protection that would be afforded by a 

secondary standard that was identical to 

the then proposed primary standard. 

Based on its consideration of the full 

range of views as described above, and 

in the 2007 proposed rule, EPA 

proposed as a second option to revise 


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59Prior to publication of the 2008 final rule, EPA 

did further analysis of the degree of overlap to 

extend the 2007 Staff Paper analyses, and that 

analysis was available in the docket. 

the secondary standard to be identical 

in every way to the then proposed 

primary standard. 

3. Basis for 2008 Decision on the 

Secondary Standard 

In the 2008 final rule, EPA noted that 

deciding on the appropriate secondary 

standard involved making a choice 

between two possible alternatives, each 

with their strengths and weaknesses. 

The 2008 final rule reported that within 

the Administration at that time there 

had been a robust discussion of the 

same strengths and weaknesses 

associated with each option that were 

identified earlier. The process by which 

EPA reached its final conclusion is 

described in the final rule (73 FR 

16497). The rationale for the 2008 

decision presented in the final rule (73 

FR 16499–16500) is described below. 

In considering the appropriateness of 

establishing a new standard defined in 

terms of a cumulative, seasonal form, or 

revising the then current secondary 

standard by making it identical to the 

revised primary standard, EPA took into 

account the approach used by the 

Agency in the 1997 review, the 

conclusions of the 2007 Staff Paper, 

CASAC advice, and the views of public 

commenters. In giving consideration to 

the approach taken in the 1997 review, 

EPA first considered the 2007 Staff 

Paper analysis of the projected degree of 

overlap between counties with air 

quality expected to meet the revised 8- 

hour primary standard, set at a level of 

0.075 ppm, and alternative levels of a 

W126 standard based on currently 

monitored air quality data. This analysis 

showed significant overlap between the 

revised 8-hour primary standard and 

selected levels of the W126 standard 

form being considered, with the degree 

of overlap between these alternative 

standards depending greatly on the 

W126 level selected and the distribution 

of hourly O3 concentrations within the 

annual and/or 3-year average period.59

On this basis, as an initial matter, EPA 

concluded that a secondary standard set 

identical to the proposed primary 

standard would provide a significant 

degree of additional protection for 

vegetation as compared to that provided 

by the then current 0.084 ppm 

secondary standard. In further 

considering the significant uncertainties 

that remain in the available body of 

evidence of O3-related vegetation effects 

and in the exposure and risk analyses 

conducted for the 2008 rulemaking, and 

the difficulty in determining at what 

point various types of vegetation effects 

become adverse for sensitive vegetation 

and ecosystems, EPA focused its 

consideration on a level for an 

alternative W126 standard at the upper 

end of the proposed range (i.e., 21 ppmhour). The 2007 Staff Paper analysis 

showed that at that W126 standard 

level, there would be essentially no 

counties with air quality that would be 

expected both to exceed such an 

alternative W126 standard and to meet 

the revised 8-hour primary standard— 

that is, based on this analysis of 

currently monitored counties, a W126 

standard would be unlikely to provide 

additional protection in any monitored 

areas beyond that likely to be provided 

by the revised primary standard. 

The EPA also recognized that the 

general lack of rural monitoring data 

made uncertain the degree to which the 

revised 8-hour standard or an 

alternative W126 standard would be 

protective in those areas, and that there 

would be the potential for not providing 

the appropriate degree of protection for 

vegetation in areas with air quality 

distributions that result in a high 

cumulative, seasonal exposure but do 

not result in high 8-hour average 

exposures. While this potential for 

under-protection using an 8-hour 

standard was clear, the number and size 

of areas at issue and the degree of risk 

was hard to determine. However, EPA 

concluded at that time that an 8-hour 

standard would also tend to avoid the 

potential for providing more protection 

than is necessary, a risk that EPA 

concluded would arise from moving to 

a new form for the secondary standard 

despite significant uncertainty in 

determining the degree of risk for any 

exposure level and the appropriate level 

of protection, as well as uncertainty in 

predicting exposure and risk patterns. 

The EPA also considered the views 

and recommendations of CASAC, and 

agreed that a cumulative, seasonal 

standard was the most biologically 

relevant way to relate exposure to plant 

growth response. However, as reflected 

in some public comments, EPA also 

judged that there remained significant 

uncertainties in determining or 

quantifying the degree of risk 

attributable to varying levels of O3

exposure, the degree of protection that 

any specific cumulative, seasonal 

standard would produce, and the 

associated potential for error in 

determining the standard that will 

provide a requisite degree of 

protection—i.e., sufficient but not more 

than what is necessary. Given these 

significant uncertainties, EPA 

concluded at that time that establishing 

a new secondary standard with a 

cumulative, seasonal form would result 

in uncertain benefits beyond those 

afforded by the revised primary 

standard and therefore may be more 

than necessary to provide the requisite 

degree of protection. 

Based on its consideration of the 

views discussed above, EPA judged in 

the 2008 rulemaking that the 

appropriate balance to be drawn was to 

revise the secondary standard to be 

identical in every way to the revised 

primary standard. The EPA believed 

that such a standard would be sufficient 

to protect public welfare from known or 

anticipated adverse effects, and did not 

believe that an alternative cumulative, 

seasonal standard was needed to 

provide this degree of protection. The 

EPA believed that this judgment 

appropriately considered the 

requirement for a standard that is 

neither more nor less stringent than 

necessary for this purpose. 

For the reasons discussed above, and 

taking into account information and 

assessments presented in the 2006 

Criteria Document and 2007 Staff Paper, 

the advice and recommendations of the 

CASAC Panel, and the public comments 

to date, EPA decided to revise the 

existing 8-hour secondary standard. 

Specifically, EPA revised the then 

current 8-hour average 0.084 ppm 

secondary standard by making it 

identical to the revised 8-hour primary 

standard set at a level of 0.075 ppm. 

4. CASAC Views Following 2008 

Decision 

Following the 2008 decision on the O3

standards, serious questions were raised 

as to whether the standards met the 

requirements of the CAA. In April 2008, 

the members of the CASAC Ozone 

Review Panel sent a letter to EPA stating 

‘‘In our most-recent letters to you on this 

subject—dated October 2006 and March 

2007—* * * the Committee 

recommended an alternative secondary 

standard of cumulative form that is 

substantially different from the primary 

Ozone NAAQS in averaging time, level 

and form—specifically, the W126 index 

within the range of 7 to 15 ppm-hour, 

accumulated over at least the 12 

‘‘daylight’’ hours and the three 

maximum ozone months of the summer 

growing season’’ (Henderson, 2008). The 

letter continued: ‘‘The CASAC now 

wishes to convey, by means of this 

letter, its additional, unsolicited advice 

with regard to the primary and 

secondary Ozone NAAQS. In doing so, 

the participating members of the 

CASAC Ozone Review Panel are 

unanimous in strongly urging you or 

your successor as EPA Administrator to 


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ensure that these recommendations be 

considered during the next review cycle 

for the Ozone NAAQS that will begin 

next year’’ (id.). The letter further stated 

the following views: 

The CASAC was * * * greatly 

disappointed that you failed to change the 

form of the secondary standard to make it 

different from the primary standard. As 

stated in the preamble to the Final Rule, even 

in the previous 1996 ozone review, ‘‘there 

was general agreement between the EPA staff, 

CASAC, and the Administrator, * * * that a 

cumulative, seasonal form was more 

biologically relevant than the previous 

1-hour and new 8-hour average forms (61 FR 

65716)’’ for the secondary standard. 

Therefore, in both the previous review and in 

this review, the Agency staff and its advisors 

agreed that a change in the form of the 

secondary standard was scientifically welljustified. 

* * * * * 

Unfortunately, this scientifically-sound 

approach of using a cumulative exposure 

index for welfare effects was not adopted, 

and the default position of using the primary 

standard for the secondary standard was once 

again instituted. Keeping the same form for 

the secondary Ozone NAAQS as for the 

primary standard is not supported by current 

scientific knowledge indicating that different 

indicator variables are needed to protect 

vegetation compared to public health. The 

CASAC was further disappointed that a 

secondary standard of the W126 form was 

not considered from within the Committee’s 

previously-recommended range of 7 to 15 

ppm-hour. The CASAC sincerely hopes that, 

in the next round of Ozone NAAQS review, 

the Agency will be able to support and 

establish a reasonable and scientificallydefensible cumulative form for the secondary 

standard. (Henderson, 2008) 

5. Administrator’s Proposed 

Conclusions 

For the reasons discussed below, the 

Administrator proposes to set a 

cumulative seasonal standard expressed 

as an annual index of the sum of 

weighted hourly concentrations (i.e., the 

W126 form), cumulated over 12 hours 

per day (8 am to 8 pm) during the 

consecutive 3-month period within the 

O3 season with the maximum index 

value, set at a level within the range of 

7 to 15 ppm-hour. This proposed 

decision takes into account the 

information and assessments presented 

in the 2006 Criteria Document and the 

2007 Staff Paper and related technical 

support documents, the advice and 

recommendations of CASAC both 

during and following the 2008 

rulemaking, and public comments 

received in conjunction with review of 

drafts of these documents and on the 

2007 proposed rule. 

a. Form 

As discussed above in section IV.B, 

the 2006 Criteria Document and 2007 

Staff Paper concluded that the recent 

vegetation effects literature evaluated in 

the 2008 rulemaking strengthens and 

reaffirms conclusions made in the 1997 

review that the use of a cumulative 

exposure index that differentially 

weights ambient concentrations is best 

able to relate ambient exposures to 

vegetation response. The 1997 review 

focused in particular on two of these 

cumulative forms, the SUM06 and 

W126 (EPA, 1996). Given that the data 

available at that time were unable to 

distinguish between these forms, the 

EPA, based on the policy consideration 

of not including O3 concentrations 

considered to be within the PRB, 

estimated at that time to be between 

0.03 and 0.05 ppm, concluded that the 

SUM06 form would be the more 

appropriate choice for a cumulative, 

exposure index for a secondary 

standard. 

In the 2008 rulemaking, the 2007 Staff 

Paper evaluated the continued 

appropriateness of the SUM06 form in 

light of new estimates of PRB that were 

lower than in the 1997 review, and the 

continued lack of evidence within the 

vegetation effects literature of a 

biological threshold for vegetation 

exposures of concern. On the basis of 

these policy and science-related 

considerations, the 2007 Staff Paper 

concluded that the W126 form was the 

more appropriate cumulative, 

concentration-weighted form. 

Specifically, the W126, by its 

incorporation of a sigmoidal weighting 

scheme, does not create an artificially 

imposed concentration threshold, gives 

proportionally more weight to the 

higher and typically more biologically 

potent concentrations, and is not 

significantly influenced by O3

concentrations within the range of 

estimated PRB. 

As discussed above, the CASAC, 

based on its assessment of the same 

vegetation effects science, agreed with 

the 2006 Criteria Document and 2007 

Staff Paper and unanimously concluded 

that protection of vegetation from the 

known or anticipated adverse effects of 

ambient O3 ‘‘requires a secondary 

standard that is substantially different 

from the primary standard in averaging 

time, level, and form,’’ i.e. not identical 

to the primary standard for O3

(Henderson, 2007). Moreover, the 

members of CASAC and a substantial 

majority of the other CASAC Panel 

members agreed with 2007 Staff Paper 

conclusions and encouraged EPA to 

establish an alternative cumulative 

secondary standard for O3 and related 

photochemical oxidants that is 

distinctly different in averaging time, 

form and level from the then current or 

potentially revised 8-hour primary 

standard (Henderson, 2006c). The 

CASAC Panel also stated that ‘‘the 

recommended metric for the secondary 

ozone standard is the (sigmoidally 

weighted) W126 index’’ (Henderson, 

2007). 

In reconsidering the 2008 final rule, 

the Administrator agrees with the 

conclusions drawn in the 2006 Criteria 

Document, 2007 Staff Paper and by 

CASAC that the scientific evidence 

available in the 2008 rulemaking 

continues to demonstrate the 

cumulative nature of O3-induced plant 

effects and the need to give greater 

weight to higher concentrations. Thus, 

the Administrator concludes that a 

cumulative exposure index that 

differentially weights O3 concentrations 

represents a reasonable policy choice for 

a secondary standard to protect against 

the effects of O3 on vegetation. The 

Administrator further agrees with both 

the 2007 Staff Paper and CASAC that 

the most appropriate cumulative, 

concentration-weighted form to 

consider is the sigmoidally weighted 

W126 form. 

The Administrator notes that in the 

2007 proposed rule, EPA proposed a 

second option of revising the then 

current 8-hour average secondary 

standard by making it identical to the 

proposed 8-hour primary standard. The 

2007 Staff Paper analyzed the degree of 

overlap expected between alternative 

8-hour and cumulative seasonal 

secondary standards using recent air 

quality monitoring data. Based on the 

results, the 2007 Staff Paper concluded 

that the degree to which the current 

8-hour standard form and level would 

overlap with areas of concern for 

vegetation expressed in terms of the 

12-hour W126 standard is inconsistent 

from year to year and would depend 

greatly on the level of the 12-hour W126 

and 8-hour standards selected and the 

distribution of hourly O3 concentrations 

within the annual and/or 3-year average 

period. The 2007 Staff Paper also 

recognized that meeting the then current 

or alternative levels of the 8-hour 

average standard could result in air 

quality improvements that would 

potentially benefit vegetation in some 

areas, but urged caution be used in 

evaluating the likely vegetation impacts 

associated with a given level of air 

quality expressed in terms of the 8-hour 

average form in the absence of parallel 

W126 information. This caution was 

due to the concern that the analysis in 

the 2007 Staff Paper may not be an 

accurate reflection of the true situation 

in non-monitored, rural counties due to 

the lack of more complete monitor 

coverage in many rural areas. Further, of 


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the counties that did not show overlap 

between the two standard forms, most 

were located in rural/remote high 

elevation areas which have O3 air 

quality patterns that are typically 

different from those associated with 

urban and near urban sites at lower 

elevations. Because the majority of such 

areas are currently not monitored, there 

are likely to be additional areas that 

have similar air quality distributions 

that would lead to the same disconnect 

between forms. Thus, the 2007 Staff 

Paper concluded that it remains 

problematic to determine the 

appropriate level of protection for 

vegetation using an 8-hour average form. 

The Administrator also notes that 

CASAC recognized that an important 

difference between the effects of acute 

exposures to O3 on human health and 

the effects of O3 exposures on welfare is 

that vegetation effects are more 

dependent on the cumulative exposure 

to, and uptake of, O3 over the course of 

the entire growing season (Henderson, 

2006c). The CASAC O3 Panel members 

were unanimous in concluding the 

protection of natural terrestrial 

ecosystems and managed agricultural 

crops requires a secondary O3 standard 

that is substantially different from the 

primary O3 standard in form, averaging 

time, and level (Henderson, 2007). 

In reaching her proposed decision in 

this reconsideration of the 2008 final 

rule, the Administrator has considered 

the comments received on the 2007 

proposed rule regarding revising the 

secondary standard either to reflect a 

new, cumulative form or by remaining 

equal to a revised primary standard. The 

commenters generally fell into two 

groups. 

One group of commenters, including 

environmental organizations, strongly 

supported the proposed option of 

moving to a cumulative, seasonal 

standard, generally based on the 

reasoning explained in the 2007 

proposal. Commenters in this group also 

expressed serious concerns with the 

other proposed option of setting a 

secondary O3 standard in terms of the 

same form and averaging time (i.e., daily 

maximum 8-hour average O3

concentration) as the primary standard. 

These commenters expressed the view 

that such a standard would fail to 

protect public welfare because the 

maximum daily 8-hour average O3

concentration failed to adequately 

characterize harmful O3 exposures to 

vegetation. This view was generally 

based on the observation that there is no 

consistent relationship in areas across 

the U.S. between 8-hour peak O3

concentrations and the longer-term 

cumulative exposures aggregated over a 

growing season that are biologically 

relevant in characterizing O3-related 

effects on sensitive vegetation. Thus, as 

EPA noted in the 2007 proposed rule, 

there is a lack of a rational connection 

between the level of an 8-hour standard 

and the requisite degree of protection 

required for a secondary O3 NAAQS. 

Another group of commenters, 

including industry organizations, agreed 

that a cumulative form of the standard 

may better match the underlying data, 

but expressed the view that remaining 

uncertainties associated with the 

vegetation effects evidence and/or EPA’s 

exposure, risk and benefits assessments 

were so great that the available 

information did not provide an adequate 

basis to adopt a standard with a level 

based on a cumulative, seasonal form. 

These commenters asserted that because 

of the substantial uncertainties 

remaining at the time of the 2008 

rulemaking, the benefits of changing to 

a W126 form were too uncertain to 

warrant revising the form of the 

standard at that time. 

The Administrator notes that in both 

the 1997 and the 2008 decisions, EPA 

recognized that the risk to vegetation 

from O3 exposures comes from 

cumulative exposures over a season or 

seasons. The CASAC has fully endorsed 

this view based on the available 

scientific evidence and assessments, 

and there is no significant disagreement 

on this issue by commenters. Thus, it is 

clear that the purpose of the secondary 

O3 NAAQS should be to provide an 

appropriate degree of protection against 

cumulative, seasonal exposures to O3

that are known or anticipated to harm 

sensitive vegetation or ecosystems. In 

reconsidering the 2008 final rule, the 

Administrator recognizes that the issue 

before the Agency is what form of the 

standard is most appropriate to perform 

that function. 

Within this framework, the 

Administrator recognizes that it is clear 

that a cumulative, seasonal form has a 

distinct advantage in protecting against 

cumulative, seasonal exposures. Such a 

form is specifically designed to measure 

directly the kind of O3 exposures that 

can cause harm to vegetation. In 

contrast, an 8-hour standard does not 

measure cumulative, seasonal exposures 

directly, and can only indirectly afford 

some degree of protection against such 

exposures. To the extent that clear 

relationships exist between 8-hour daily 

peak O3 concentrations and cumulative, 

seasonal exposures, the 8-hour form and 

averaging time would have the potential 

to be effective as an indirect surrogate. 

However, as discussed in the 2007 

proposed rule and the 2008 final rule, 

the evidence shows that there are 

known types of O3 air quality patterns 

that can lead to high levels of 

cumulative, seasonal O3 exposures 

without the occurrence of high daily 8- 

hour peak O3 concentrations. An 8-hour 

form and averaging time is an indirect 

way to measure biologically relevant 

exposure patterns, is poorly correlated 

with such exposure patterns, and 

therefore is less likely to identify and 

protect against the kind of cumulative, 

seasonal exposure patterns that have 

been determined to be harmful. 

Past arguments or reasons for not 

moving to a cumulative, seasonal form, 

with appropriate exposure periods, have 

not been based on disagreement over the 

biological relevance of the cumulative, 

seasonal form, or the recognized 

disadvantages of an 8-hour standard in 

measuring and identifying a specified 

cumulative, seasonal exposure pattern. 

The reasons for not moving to such a 

form have been based on concerns over 

whether EPA has an adequate basis to 

identify the nature and magnitude of 

cumulative, seasonal exposure patterns 

that the standard should be designed to 

protect against, given the various 

uncertainties in the evidence and the 

lack of rural O3 monitoring data. This 

most directly translates into a concern 

over whether EPA has an adequate basis 

to determine an appropriate level for a 

cumulative, seasonal secondary 

standard. 

The Administrator has also 

considered issues associated with 

selection of the W126 cumulative form, 

as reflected in the following assertions 

made by some commenters on the 2007 

proposed rule: (1) 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; (2) 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; (3) 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 (4) a 

second index that reflects the 

accumulation of peaks at or above 0.10 

ppm (called N100) should be added to 

a W126 index to achieve appropriate 

protection. 

With regard to whether the W126 

index lacks a biological basis, the 

Administrator finds no basis for 

reaching such a conclusion. As 

discussed above in section IV.B, the 


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60The 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. 

61While the term ‘‘averaging time’’ is used, for the 

cumulative, seasonal standard the seasonal and 

diurnal time periods at issue are those over which 

exposures during a specified period of time are 

cumulated, not averaged. 

vegetation effects science is clear that 

exposures of concern to plants are not 

based on one discrete 8-hour period 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 that plants in 

the U.S. are generally most biologically 

active during the warm season and are 

exposed to ambient O3 throughout this 

biologically active period. In addition, it 

has been shown in the scientific 

literature that all else being equal, 

plants respond more to higher O3

concentrations, with 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. 

With regard to whether a flux-based 

model would be a better choice, the 

2007 Staff Paper acknowledged that flux 

models may produce a more accurate 

calculation of dose to a specific plant 

species in a specific area. However, 

dose-response relationships have not 

been developed for these flux 

calculations for plants growing in the 

U.S. Further, flux calculations require 

large amounts of data for the physiology 

of each plant species and the local 

conditions for the growing range of each 

plant species. These exercises may be 

useful for limited small-scale risk 

assessments, but do not provide an 

appropriate basis for a national standard 

at this time. 

With regard to dissatisfaction with the 

performance of a particular cumulative 

index in use in Europe,60 and growing 

interest in development of flux-based 

models, the 2007 Staff Paper (Appendix 

7A) noted that ‘‘because of a lack of fluxresponse 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 semi-natural 

herbaceous vegetation (Ashmore et al., 

2004a).’’ Further, like the SUM06 index, 

the AOT40 index incorporates a 

threshold below which concentrations 

are not considered. Though the AOT40 

threshold is lower than the threshold 

value in SUM06, the 2007 Staff Paper 

concluded that the vegetation effects 

information does not provide evidence 

of an effects threshold that applies to all 

species. Thus, the Administrator 

concludes neither of these forms is as 

biologically relevant as the W126 form. 

With regard to consideration of 

coupling a W126 form with a separate 

N100 index, there was very little 

research on the N100 index or a coupled 

approach to be evaluated in the 2008 

rulemaking. The CASAC, after 

reviewing all the information in the 

2006 Criteria Document and the 2007 

Staff Paper, did not recommend an 

additional N100 index for 

consideration. Therefore, there is 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. Further, the W126 

form incorporates 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. 

In summary, having considered the 

scientific information and assessment 

results available in the 2008 rulemaking 

as discussed above in this proposal 

notice, as well as the recommendations 

of the staff and CASAC, and having 

taken into consideration issues raised in 

public comments received as part of the 

2008 rulemaking, and recognizing the 

determinations made below in section 

IV.D.5.c on level, the Administrator 

concludes that it is appropriate to set 

the secondary standard using a 

cumulative, seasonal form. The 

Administrator also concludes that the 

W126 form is best suited to reflect the 

biological impacts of O3 exposure on 

vegetation, and that there is adequate 

certainty in the information available in 

the 2008 rulemaking to support such a 

change in form. Thus, the Administrator 

proposes to set the secondary standard 

using a cumulative, seasonal W126 

form. 

b. Averaging Times 61

The Administrator, in addition to 

reconsidering what form of a secondary 

standard is most appropriate for 

protecting vegetation, is also 

reconsidering what exposure periods 

(e.g., seasonal window, diurnal 

window), and what standard index, in 

terms of an annual index value versus 

a 3-year average of annual index values, 

are most appropriate when used in 

conjunction with the W126 cumulative 

seasonal form. Based on the information 

set forth in the 2007 Staff Paper, as well 

as CASAC views, as discussed above in 

section IV.D.1.b, the Administrator has 

reached conclusions regarding exposure 

periods, and the annual versus 3-year 

average index, that have the most 

biological relevance for plant response, 

as discussed below. 

In considering an appropriate 

seasonal window, the Administrator 

notes that the 2007 Staff Paper 

concluded that the consecutive 3-month 

period within the O3 season with the 

highest W126 index value (e.g., 

maximum 3-month period) was a 

reasonable seasonal time period to 

consider. The Administrator further 

notes that the 2007 Staff Paper 

acknowledged that the selection of any 

single seasonal exposure period for a 

national standard would necessarily 

represent a compromise, given the 

significant variability in growth patterns 

and lengths of growing seasons among 

the wide range of sensitive vegetation 

species occurring within the U.S. 

However, the Administrator also 

considered the Staff Paper conclusion 

that the period of maximum potential 

plant uptake of O3 would also likely 

coincide with the period of highest O3

occurring within the intra-annual period 

defined as the O3 season, since the high 

temperature and light conditions 

conducive to O3 formation are also 

conducive for plant activity. The 

Administrator also observes that the 

CASAC panel was supportive of the 

Staff Paper views, while recognizing 

that 3 months likely represented the 

minimum timeframe appropriate to 

consider. Therefore, the Administrator 

concludes, on these bases, that the 

consecutive 3-month period within the 

O3 season with the highest W126 index 

value (e.g., maximum 3-month period) 

remains an appropriate seasonal 

window to propose for the protection of 

sensitive vegetation. 

With regard to consideration of an 

appropriate diurnal window, the 

Administrator has taken into account 

the 2007 Staff Paper conclusion that for 

the vast majority of studied species, 

daytime exposures represent the 

majority of diurnal plant O3 uptake and 

are responsible for inducing the plant 

response of most significance to the 

health and productivity of the plant 

(e.g., reduced carbohydrate production). 

The Administrator is also aware, based 

on discussions in the 2007 Staff Paper 

that there are some number of species 

that show non-negligible amounts of O3

uptake at night due to incomplete 

stomatal closure. In reaching her 

conclusion that the 2007 Staff Paper 

recommendation of a 12-hour daytime 


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window (8 a.m. to 8 p.m.) remains the 

most appropriate period over which to 

cumulate diurnal O3 exposures, 

specifically those most relevant to plant 

growth and yield responses, the 

Administrator places weight on the fact 

that the CASAC comments were also 

supportive of this diurnal window, 

recognizing again that it likely 

represents a minimum period over 

which plants can be vulnerable to O3

uptake. Therefore, the Administrator is 

again proposing the 12-hour daytime 

window (8 a.m. to 8 p.m.) as an 

appropriate diurnal window to protect 

against O3-induced plant effects. 

Lastly, in considering whether an 

annual or a 3-year average index is more 

appropriate, the Administrator notes 

that in addition to the available 

scientific evidence regarding plant 

effects that can be brought to bear, there 

are also other public welfare 

considerations that may be appropriate 

to consider. In taking this view, the 

Administrator notes that the 2007 Staff 

Paper recognized that though most 

cumulative seasonal exposure levels of 

concern for vegetation have been 

expressed in terms of the annual 

timeframe, it may be appropriate to 

consider a 3-year average for purposes 

of standard stability. The Administrator 

has considered that while the 2007 Staff 

Paper notes that for certain welfare 

effects of concern (e.g., foliar injury, 

yield loss for annual crops, growth 

effects on other annual vegetation and 

potentially tree seedlings), an annual 

time frame may be a more appropriate 

period in which to assess what level 

would provide the requisite degree of 

protection, for other welfare effects (e.g., 

mature tree biomass loss), it also points 

out that a 3-year average may also be 

appropriate. The Administrator further 

observes that in concluding that it was 

appropriate to consider both an annual 

and a 3-year average, the 2007 Staff 

Paper also concluded that should a 3- 

year average of the 3-month, 12-hour 

W126 form be selected, a potentially 

lower level should be considered to 

reduce the potential of adverse impacts 

to annual species from a single high O3

year that could still occur while 

attaining a standard on average over 

3-years. The Administrator also took 

note that the CASAC Panel, in 

addressing this issue of annual versus 3- 

year average concluded that multi-year 

averaging to promote a ‘‘stable’’ 

secondary standard is less appropriate 

for a cumulative, seasonal secondary 

standard than for a primary standard 

based on maximum 8-hour 

concentrations, and further concluded 

that if multi-year averaging is employed 

to increase the stability of the secondary 

standard, the level of the standard 

should be revised downward to assure 

that the desired degree of protection is 

not exceeded in individual years. The 

Administrator, in considering the merits 

of both the annual and 3-year average, 

and taking into account both the 2007 

Staff Paper and CASAC views, 

concludes that it is important to place 

more weight on the public welfare 

benefit in having a stable standard, and 

that appropriate protection for 

vegetation can be achieved using a 

3-year average form. The Administrator 

is thus proposing a 3-year average. 

However, given the uncertain nature of 

the evidence and potential concerns 

with using a 3-year average form, the 

Administrator is proposing to take 

comment on the appropriateness of the 

specific seasonal and diurnal exposure 

periods proposed, as well as the use of 

a 3-year average, and, as discussed 

below, the impact that selection of these 

proposed seasonal and diurnal exposure 

periods would have, in conjunction 

with a 3-year average form, on the 

appropriateness of the proposed range 

of levels. 

c. Level 

i. Considerations Regarding 2007 

Proposed Range of Levels 

The 2007 Staff Paper, in identifying a 

range of levels for a 3-month, 12-hour 

(daytime) W126 standard appropriate 

for the Administrator to consider in 

protecting the public welfare from 

known or anticipated adverse effects to 

vegetation from O3 exposures, 

considered what information from the 

array of vegetation effects evidence and 

exposure and risk assessment results 

was most useful. With respect to the 

vegetation effects evidence, the 2007 

Staff Paper found stronger support than 

what was available at the time of the 

1997 review for an increased level of 

protection for trees and forested 

ecosystems. Specifically, the expanded 

body of evidence included: (1) 

Additional field based data from free 

air, gradient and biomonitoring surveys 

demonstrating adverse levels of O3- 

induced growth reductions on trees at 

the seedling, sapling and mature growth 

stages and incidence of visible foliar 

injury occurring at biomonitoring sites 

in the field at ambient levels of 

exposure; (2) qualitative support from 

free air (e.g., AspenFACE) and gradient 

studies on a limited number of tree 

species for the continued 

appropriateness of using OTC-derived 

C–R functions to predict tree seedling 

response in the field; (3) studies that 

continued to document below-ground 

effects on root growth and ‘‘carry-over’’ 

effects occurring in subsequent years 

from O3 exposures; and (4) increased 

recognition and understanding of the 

structure and function of ecosystems 

and the complex linkages through 

which O3, and other stressors, acting at 

the organism and species level can 

influence higher levels within the 

ecosystem hierarchy and disrupt 

essential ecological attributes critical to 

the maintenance of ecosystem goods 

and services important to the public 

welfare. 

Based on the above sources of 

vegetation effects information and the 

results of the exposure and risk 

assessments summarized above, the 

2007 Staff Paper concluded that just 

meeting the then current 0.084 ppm, 

8-hour average standard would continue 

to allow adverse levels of O3-induced 

effects to occur in sensitive 

commercially and ecologically 

important tree species in many regions 

of the country. The 2007 Staff Paper 

further concluded that air quality levels 

would need to be substantially reduced 

to protect sensitive tree seedlings, such 

as black cherry, aspen, and cottonwood, 

from these growth and foliar injury 

effects. 

In addition to the currently 

quantifiable risks to trees from ambient 

exposures, the 2007 Staff Paper also 

considered the more subtle impacts of 

O3 acting in synergy with other natural 

and man-made stressors to adversely 

affect individual plants, populations 

and whole systems. By disrupting the 

photosynthetic process, decreasing 

carbon storage in the roots, increasing 

early senescence of leaves and affecting 

water use efficiency in trees, O3

exposures could potentially disrupt or 

change the nutrient and water flow of an 

entire system. Weakened trees can 

become more susceptible to other 

environmental stresses such as pest and 

pathogen outbreaks or harsh weather 

conditions. Though it is not possible to 

quantify all the ecological and societal 

benefits associated with varying levels 

of alternative secondary standards, the 

2007 Staff Paper concluded that this 

information should be weighed in 

considering the extent to which a 

secondary standard should be set so as 

to provide potential protection against 

effects that are anticipated to occur. 

The 2007 Staff Paper also recognized 

that in the 1997 review, EPA took into 

account the results of a 1996 Consensus 

Workshop. At this workshop, a group of 

independent scientists expressed their 

judgments on what standard form(s) and 

level(s) would provide vegetation with 

adequate protection from O3-related 

adverse effects. Consensus was reached 


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on protective ranges of levels in terms 

of a cumulative, seasonal 3-month, 12- 

hr SUM06 standard for a number of 

vegetation effects endpoints. These 

ranges are identified below, with the 

estimated approximate equivalent W126 

standard levels shown in parentheses. 

For growth effects to tree seedlings in 

natural forest stands, a consensus was 

reached that a SUM06 range of 10 to 15 

(W126 range of 7 to 13) ppm-hour 

would be protective. For growth effects 

to tree seedlings and saplings in 

plantations, the consensus SUM06 range 

was 12 to 16 (W126 range of 9 to 14) 

ppm-hour. For visible foliar injury to 

natural ecosystems, the consensus 

SUM06 range was 8 to 12 (W126 range 

of 5 to 9) ppm-hour. 

The 2007 Staff Paper then considered 

to what extent recent research provided 

empirical support for the ranges of 

levels identified by the experts as 

protective of different types of O3- 

induced effects. As discussed above in 

section IV.D.1.c, the 2007 Staff Paper 

concluded on the basis of the available 

evidence that it was appropriate to 

consider a range for a 3-month, 12-hour, 

W126 standard level that included the 

1996 Consensus Workshop 

recommendations regarding a range of 

levels protective against O3-induced 

growth effects in tree seedlings in 

natural forest stands (i.e., 7–13 ppmhour in terms of a W126 form). 

In considering the newly available 

information on O3-related effects on 

crops in this review, the 2007 Staff 

Paper observed the following regarding 

the strength of the underlying crop 

science: (1) Nothing in the recent 

literature points to a change in the 

relationship between O3 exposure and 

crop response across the range of 

species and/or cultivars of commodity 

crops currently grown in the U.S. that 

could be construed to make less 

appropriate the use of commodity crop 

C–R functions developed in the NCLAN 

program; (2) new field-based studies 

(e.g., SoyFACE) provide qualitative 

support in a few limited cases for the 

appropriateness of using OTC-derived 

C–R functions to predict crop response 

in the field; and (3) refinements in the 

exposure, risk and benefits assessments 

in this review reduce some of the 

uncertainties present in 1996. On the 

basis of these observations, the 2007 

Staff Paper concluded that nothing in 

the newly assessed information calls 

into question the strength of the 

underlying science upon which EPA 

based its proposed decision in the last 

review to select a level of a cumulative, 

seasonal form associated with protecting 

50 percent of crop cases from no more 

than 10 percent yield loss as providing 

the requisite degree of protection for 

commodity crops. 

The 2007 Staff Paper then considered 

whether any additional information was 

available to inform judgments as to the 

adversity of various O3-induced levels 

of crop yield loss to the public welfare. 

As noted above, the 2007 Staff Paper 

observed that agricultural systems are 

heavily managed, and that in addition to 

stress from O3, the annual productivity 

of agricultural systems is vulnerable to 

disruption from many other stressors 

(e.g., weather, insects, disease), whose 

impact in any given year can greatly 

outweigh the direct reduction in annual 

productivity resulting from elevated O3

exposures. On the other hand, O3 can 

also more subtly impact crop and forage 

nutritive quality and indirectly 

exacerbate the severity of the impact 

from other stressors. Since these latter 

effects could not be quantified at that 

time, they could only be considered 

qualitatively in reaching judgments 

about an appropriate degree of 

protection for commodity crops from 

O3-related effects. 

Based on the above considerations, 

the 2007 Staff Paper concluded that the 

level of protection judged requisite in 

the 1997 review to protect the public 

welfare from adverse levels of O3- 

induced reductions in crop yields and 

tree seedling biomass loss, as 

approximately provided by a W126 

level of 21 ppm-hour, remained 

appropriate for consideration as an 

upper bound of a range of appropriate 

levels. The 2007 Staff Paper also 

recognized that a standard set at this 

level would not protect the most 

sensitive species or individuals within a 

species from all potential effects related 

to O3 exposures and further, that this 

level derives from the extensive and 

quantitative historic and recent crop 

effects database, as well as current staff 

exposure and risk analyses (EPA, 2007, 

pg. 8–22). 

In identifying a lower bound for the 

range of alternative standard levels 

appropriate for consideration, staff 

concluded that several lines of evidence 

pointed to the need for greater 

protection for tree seedlings, mature 

trees, and associated forested 

ecosystems. Staff believed that tree 

growth was an important endpoint to 

consider because it is related to other 

aspects of societal welfare such as 

sustainable production of timber and 

related goods, recreation, and carbon 

(CO2) sequestration. Impacts on tree 

growth can also affect ecosystems 

through shifts in species composition 

and the loss of genetic diversity due to 

the loss of O3 sensitive individuals or 

species. In selecting an appropriate level 

of protection for trees, staff considered 

the results of the 1996 Consensus 

Workshop which identified the SUM06 

range of 10 to 15 (W126 of 7 to 13) ppmhour for growth effects to tree seedlings 

in natural forest stands. 

Because staff believed that O3-related 

effects on forest tree species are 

important public welfare effects of 

concern, it therefore concluded, based 

on the above, that it was appropriate to 

include 7 ppm-hour as the lower bound 

of the recommended range, the lower 

end of the approximate range 

recommended by CASAC (Henderson, 

2006c) and identified by the 1996 

Consensus Workshop participants as 

protective of forest trees. At this lower 

end of the range, staff anticipated, based 

on its analyses of risks of tree seedling 

biomass loss and mature tree growth 

reductions and on the basis of the 

scientific effects literature, that adverse 

effects of O3 on forested ecosystems 

would be substantially reduced. 

Further, staff anticipated that the lower 

end of this range would provide 

increased protection from the more 

subtle impacts of O3 acting in synergy 

with other natural and man-made 

stressors to adversely affect individual 

plants, populations and whole systems. 

Staff also noted that by disrupting the 

photosynthetic process, decreasing 

carbon storage in the roots, increasing 

early senescence of leaves and affecting 

water use efficiency in trees, O3

exposure could potentially disrupt or 

change the nutrient and water flow of an 

entire system. Such weakened trees can 

become more susceptible to other 

environmental stresses such as pest and 

pathogen outbreaks or harsh weather 

conditions. While recognizing that it is 

not possible to quantify all the 

ecological and societal benefits 

associated with varying levels of 

alternative secondary standards, staff 

believed that this information should be 

weighed in considering the extent to 

which a secondary standard should be 

precautionary in nature in protecting 

against effects that have not yet been 

adequately studied and evaluated. 

Thus, the 2007 Staff Paper concluded, 

based on all the above considerations, 

that an appropriate range of levels, for 

an annual standard using a 3-month, 

12-hour W126 form, for the 

Administrator to consider was 7 to 21 

ppm-hour, recognizing that the level 

selected is largely a policy judgment as 

to the requisite level of protection 

needed. In determining the requisite 

level of protection for crops and trees, 

the 2007 Staff Paper recognized that it 

was appropriate to weigh the 

importance of the predicted risks of 

these effects in the overall context of 


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62For example, the level of protection granted by 

Congress under the Wilderness Act of 1964 for 

designated ‘‘wilderness areas’’ requires that these 

areas ‘‘shall be administered for the use and 

enjoyment of the American people in such manner 

as will leave them unimpaired for future use as 

wilderness, and so as to provide for the protection 

of these areas, the preservation of their wilderness 

character’’ (The Wilderness Act, 1964). 

public welfare protection, along with a 

determination as to the appropriate 

weight to place on the associated 

uncertainties and limitations of this 

information. 

ii. CASAC and Public Comments Prior 

to 2008 Decision 

In considering the evidence described 

in both the 2006 Criteria Document and 

2006 draft Staff Paper, CASAC, in its 

October 24, 2006 letter to the 

Administrator, expressed its view 

regarding the appropriate form and 

range of levels for the Administrator to 

consider. The CASAC preferred a 

seasonal 3-month W126 standard in a 

range that is the approximate equivalent 

of the SUM06 at 10 to 20 ppm-hour. 

Following the 2007 proposal, EPA 

received additional CASAC and public 

comments regarding an appropriate 

range of levels of a W126 form for the 

Administrator to consider in finalizing a 

revised secondary NAAQS for O3. The 

CASAC, in its final letter to the 

Administrator (Henderson, 2007), 

agreed with the 2007 Staff Paper 

recommendations that the lower bound 

of the range within which a seasonal 

W126 secondary O3 standard should be 

considered is approximately 7 ppmhour; however, it did not agree with 

staff’s recommendation that the upper 

bound of the range should be as high as 

21 ppm-hour. Rather, as discussed 

above in section IV.D.1.c, the CASAC 

Panel recommended that the upper 

bound of the range considered should 

be no higher than a W126 of 15 ppmhour for an annual standard. 

The comments received from the 

public fell into two groups. One group 

of commenters supported the CASAC 

recommended range of 7–15 ppm-hour 

for a W126 standard. Many of these 

same commenters further emphasized 

the lower end of the proposed range as 

necessary to provide adequate 

protection for sensitive species. These 

commenters based their 

recommendation primarily on four 

sources of information: (1) Field-based 

evidence of foliar injury occurring on 

sensitive species at air quality levels 

well below that of the current standard; 

(2) the 1996 Consensus Workshop 

recommendations for protective levels 

in terms of cumulative exposures for 

different vegetation types; (3) CASAC 

advice and recommendations; and (4) 

studies published after the close of the 

2006 Criteria Document that potentially 

strengthen the link between species 

level impacts and ecosystem response. 

The other group of commenters did 

not support revising the current 

secondary standard. These commenters 

primarily focused on 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. These uncertainties 

included: (1) potential confounders, 

such as soil moisture, on visible foliar 

injury and the lack of a clear 

relationship between visible foliar 

injury symptoms and other vegetation 

effects; (2) lack of documentation of the 

basis for the recommendations from the 

1996 Consensus Workshop in selecting 

a range of levels, indicating that these 

recommendations should be used with 

great caution; (3) failure of CASAC and 

EPA to take into account the monitor 

height measurement gradient when 

making their recommendations 

concerning the level of the secondary 

standard; and (4) inability to 

quantitatively estimate ecosystem 

effects of O3 or to extrapolate 

meaningfully from effects on individual 

plants to ecosystem effects due to 

inadequate data. 

iii. Conclusions on Level 

The Administrator is proposing to set 

a cumulative, seasonal standard 

expressed in terms of the maximum 

3-month, 12-hour W126 form, in the 

range of 7 to 15 ppm-hour. In reaching 

this proposed decision about an 

appropriate range of levels for the 

secondary standard, the Administrator 

has considered the following: the 

evidence described in the 2006 Criteria 

Document and the 2007 Staff Paper; the 

results of the vegetation exposure and 

risk assessments discussed above and in 

the 2007 Staff Paper, giving weight to 

the assessments as judged appropriate; 

the CASAC Panel’s advice and 

recommendations in the CASAC’s 

letters to the Administrator; EPA staff 

recommendations; and public 

comments received during the 

development of these documents, either 

in connection with CASAC meetings or 

separately. In considering what range of 

levels of a cumulative 3-month standard 

to propose, the Administrator notes that 

this choice requires judgment as to what 

standard will protect the public welfare 

from any known or anticipated adverse 

effects. This choice must be based on an 

interpretation of the evidence and other 

information, such as the exposure and 

risk assessments, that neither overstates 

nor understates the strength and 

limitations of the evidence and 

information nor the appropriate 

inferences to be drawn. In taking all of 

the above into consideration, the 

Administrator also notes that there is no 

bright line clearly directing the choice 

of level for any of the effects of concern, 

and the choice of what is appropriate is 

clearly a public welfare policy judgment 

entrusted to the Administrator. 

In particular, the Administrator has 

given careful consideration to the 

following: (1) The nature and degree of 

effects of O3 to the public welfare, 

including what constitutes an adverse 

effect; (2) the strengths and limitations 

of the evidence that is available 

regarding known or anticipated adverse 

effects from cumulative, seasonal 

exposures, and its usefulness in 

informing selection of a proposed range; 

and (3) CASAC’s views regarding the 

strength of the evidence and its 

adequacy to inform a range of levels. 

Each of these topics is discussed in turn 

below. 

In determining the nature and degree 

of effects of O3 on the public welfare, 

the Administrator recognizes that the 

significance to the public welfare of O3- 

induced effects on sensitive vegetation 

growing within the U.S. can vary, 

depending on the nature of the effect, 

the intended use of the sensitive plants 

or ecosystems, and the types of 

environments in which the sensitive 

vegetation and ecosystems are located. 

Any given O3-related effect on 

vegetation and ecosystems (e.g., biomass 

loss, foliar injury), therefore, may be 

judged to have a different degree of 

impact on the public depending, for 

example, on whether that effect occurs 

in a Class I area, a city park, or 

commercial cropland. In her judgment, 

it is appropriate that this variation in 

the significance of O3-related vegetation 

effects should be taken into 

consideration in judging the level of 

ambient O3 that is requisite to protect 

the public welfare from any known or 

anticipated adverse effects. In this 

regard, the Administrator agrees with 

the definition of adversity as described 

above in section IV.A.3 and in the 2008 

rulemaking. As a result, the 

Administrator concludes that of those 

known and anticipated O3-related 

vegetation and ecosystem effects 

identified and discussed in this 

reconsideration, the highest priority and 

significance should be given to those 

that occur on sensitive species that are 

known to or are likely to occur in 

federally protected areas such as Class 

I areas 62 or on lands set aside by States, 

Tribes and public interest groups to 

provide similar benefits to the public 


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welfare, for residents on those lands, as 

well as visitors to those areas. 

Likewise, the Administrator also 

notes that the same known or 

anticipated O3-induced effects, 

occurring in other areas may call for less 

protection. For example, the 

maintenance of adequate agricultural 

crop yields is extremely important to 

the public welfare and is currently 

achieved through the application of 

intensive management practices, 

including in some cases, genetic 

engineering. These management 

practices, in conjunction with market 

forces and government programs, assure 

an appropriate balance is reached 

between costs of production and market 

availability. Thus, while research on 

agricultural crop species remains useful 

in illuminating mechanisms of action 

and physiological processes, 

information from this sector on O3- 

induced effects is considered less useful 

in informing judgments on what level(s) 

would be sufficient but not more than 

necessary to protect the public welfare. 

With respect to commercial production 

of commodities, the Administrator notes 

that judgments about the extent to 

which O3-related effects on 

commercially managed vegetation are 

adverse from a public welfare 

perspective are particularly difficult to 

reach, given that what is known about 

the relationship between O3 exposures 

and agricultural crop yield response 

derives largely from data generated 

almost 20 years ago. The Administrator 

recognizes that there is substantial 

uncertainty at this time as to whether 

these data remain relevant to the 

majority of species and cultivars of 

crops being grown in the field today. In 

addition, the extensive management of 

such vegetation may to some degree 

mitigate potential O3-related effects. The 

management practices used on these 

lands are highly variable and are 

designed to achieve optimal yields, 

taking into consideration various 

environmental conditions. Thus, the 

Administrator concludes there is no 

need for such additional protection for 

agricultural crops through the NAAQS. 

The Administrator also recognizes 

that O3-related effects on sensitive 

vegetation can occur in other areas that 

have not been afforded special Federal 

protections, ranging from effects on 

vegetation growing in residential or 

commercial settings, such as 

ornamentals used in urban/suburban 

landscaping, to vegetation grown in 

land use categories that are heavily 

managed for commercial production of 

commodities such as timber. For 

vegetation used for residential or 

commercial ornamental purposes, such 

as urban/suburban landscaping, the 

Administrator believes that there is not 

adequate information at this time to 

establish a secondary standard based 

specifically on impairment of urban/ 

suburban landscaping and other uses of 

ornamental vegetation, but notes that a 

secondary standard revised to provide 

protection for sensitive natural 

vegetation and ecosystems would likely 

also provide some degree of protection 

for such ornamental vegetation. 

Based on the above, the Administrator 

finds that the types of information most 

useful in informing the selection of an 

appropriate range of protective levels is 

appropriately focused on information 

regarding exposures and responses of 

sensitive trees and other native species 

known or anticipated to occur in 

protected areas such as Class I areas or 

on lands set aside by States, Tribes and 

public interest groups to provide similar 

benefits to the public welfare, for 

residents on those lands, as well as 

visitors to those areas. 

With regard to the available evidence, 

the Administrator finds the coherence 

and strength of the weight of evidence 

from the large body of available 

literature compelling. This evidence 

addresses a broad array of O3-induced 

effects on a variety of tree species across 

a range of growth stages (i.e., seedlings, 

saplings and mature trees) using diverse 

field-based (e.g. free air, gradient and 

ambient) and OTC exposure methods. It 

demonstrates that significant numbers 

of forest tree species are potentially 

experiencing O3-induced stress under 

levels of ambient air quality, both at and 

below the level of the 1997 standard. 

In particular, the Administrator notes 

the evidence from recent field-based 

studies and a gradient study of eastern 

cottonwood saplings (Gregg et al., 2003). 

She observes that this study found that 

cottonwood saplings grown in urban 

New York City grew faster than saplings 

grown in downwind rural areas where 

cumulative O3 exposures were higher, 

and the difference in biomass 

production between the urban site with 

the lowest cumulative exposure and the 

rural site with the highest cumulative 

exposure is dramatic (Figure 7–17 in the 

2007 Staff Paper). The Administrator 

further notes that cottonwood is one of 

the most sensitive tree species studied 

to date and it is also important both 

from an ecological and public welfare 

perspective, as discussed above in 

section IV.A.2.b and in the 2007 Staff 

Paper. 

The Administrator also notes the 

evidence related to the O3-induced 

effect of visible foliar injury. The 

Administrator observes that the visible 

foliar injury database created from the 

ambient field-based monitoring network 

managed by the Unites States Forest 

Service (USFS) Forest Inventory and 

Analysis (FIA) Program has continued 

to expand since the conclusion of the 

1997 review. In utilizing this dataset, 

EPA staff collaborated with FIA staff to 

compare the incidence of visible foliar 

injury at different levels of air quality by 

county throughout the U.S. in counties 

with FIA monitoring sites. In 

considering the results of this analysis, 

depicted in Table 7–4 of the 2007 Staff 

Paper, the Administrator notes that for 

the 2001–2004 period, the percent of 

counties with documented foliar injury 

at a level approximately equivalent to 

the W126 of 21 ppm-hour, was 26 to 49 

percent, while at the lower level 

approximately equivalent to a W126 of 

13 ppm-hour, incidence values ranged 

from 12 to 35 percent. The 

Administrator believes it likely that 

some sensitive species occurring in 

specially protected areas would also 

exhibit visible foliar injury symptoms to 

a similar degree at these exposure 

levels. She further notes that while 

direct links between O3 induced visible 

foliar injury symptoms and other 

adverse effects (e.g., biomass loss) are 

not always found, visible foliar injury in 

itself is considered by the National Park 

Service (NPS) to affect adversely air 

quality related values (AQRV) in Class 

I areas. 

The Administrator places significant 

weight on the judgments of CASAC. In 

so doing, the Administrator has 

carefully considered its stated views 

and the basis for the range of levels the 

CASAC O3 Panel recommended. In its 

2007 letter to the Administrator, the 

CASAC O3 Panel agreed with EPA staff 

recommendations that the lower bound 

of the range within which a seasonal 

W126 O3 standard should be considered 

is approximately 7 ppm-hour. However, 

‘‘it does not agree with Staff’s 

recommendations that the upper bound 

of the range should be as high as 21 

ppm-hour. Rather, the Panel 

recommends that the upper bound of 

the range considered should be no 

higher than 15 ppm-hour, which the 

Panel estimates is approximately 

equivalent to a seasonal 12-hour SUM06 

level of 20 ppm-hour’’ (Henderson, 

2007). The Administrator notes that 

CASAC views concerning an 

appropriate range of levels for the 

Administrator to consider were 

presented after CASAC had considered 

the entire body of evidence presented in 

both the 2006 Criteria Document and 

2007 Staff Paper, and are generally 

consistent with the 1996 Consensus 

Workshop recommendations. 


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In considering the issues raised by 

commenters on the 2007 proposed rule, 

the Administrator noted that many 

public commenters supported the range 

of levels recommended by CASAC. The 

Administrator also considered the views 

expressed by the NPS as to what range 

of levels it identified as useful in 

helping it achieve its mandate to protect 

AQRVs in national parks and 

wilderness areas and to provide a level 

of protection for its resources in keeping 

with the Congressional mandate set 

forth in The Wilderness Act of 1964. In 

so doing, the Administrator notes that 

the NPS supported the range 

recommended by CASAC, while 

emphasizing that the lower end of the 

range was more appropriate. The NPS 

notes that though some visible foliar 

injury would still be expected to occur 

above the lower end of the CASAC 

recommended range (i.e. 7 ppm-hour), 

the potential for growth impacts at that 

level would be very low. It further notes 

that most of these parks contain aspen, 

black cherry, or ponderosa pine, all 

sensitive species predicted to have 

significant growth effects at current 

W126 levels. 

The Administrator also considered 

those comments that highlighted 

sources of uncertainty in the evidence 

and risk assessments (summarized 

above in section IV.D.5.c.ii) to inform 

her judgments on how much weight to 

place on these associated uncertainties, 

as discussed below. 

With regard to the issue of possible 

confounders of foliar injury information, 

the Administrator recognizes that 

visible foliar injury, like other O3- 

induced plant effects, is moderated by 

environmental factors other than O3

exposure. However, the Administrator 

also notes that the O3-related visible 

foliar injury effect persisted across a 

four year period (2001–2004), despite 

year-to-year variability in meteorology 

and other environmental factors (see 

Table 7–4 in the 2007 Staff Paper). She 

also notes that approximately 26 to 49 

percent of counties had visible foliar 

injury incidence at the approximate 

W126 level of 21 ppm-hour, while at a 

W126 level of 13 ppm-hour, this range 

of percentages dropped to 

approximately 12 to 23 percent. In an 

area such as a national park, where 

visitors come in part for the aesthetic 

quality of the landscape, the 

Administrator recognizes that visible 

foliar injury incidence is an important 

welfare effect which should be 

considered in determining an 

appropriately protective standard level. 

With regard to the issues of what 

weight to place on the recommendations 

from the 1996 Consensus Workshop in 

selecting a range of levels, as the 1997 

Workshop Report did not clearly 

document the basis for its 

recommendations, the Administrator 

recognizes that the absence of such 

documentation does call for care in 

placing weight on such 

recommendations. However, the 

Administrator notes that the workshop 

participants were asked to review both 

the 1996 O3 Criteria Document and Staff 

Paper, representing the most up to date 

compilation of the state of the science 

available at that time, in order to ensure 

that their expert judgments made were 

also informed by the latest science. She 

also notes that another group of experts, 

the CASAC O3 Panel, reached a similar 

consensus based upon an expanded 

body of scientific evidence. In addition, 

the 2007 Staff Paper evaluated the same 

recommendations in the context of 

subsequent empirical evidence, and 

reached similar views, with the 

exception of the upper end of the 

recommended range, which in the 2007 

Staff Paper was based on effects on 

commercial crops that had been 

considered in the 1997 review. While it 

would always be more useful to have 

documentation of the reasoning and 

basis for an expert’s advice, in this case 

the Administrator judges that the 1996 

Consensus Workshop recommendations 

should be given substantial weight. 

With regard to other issues raised by 

some commenters related to 

uncertainties in the technical evidence 

and analyses, the Administrator notes 

that such issues had been addressed in 

the 2007 Staff Paper that reflected 

CASAC’s advice on such issues. For 

example, while the Administrator 

recognizes that 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, she believes that 

the potential for such anticipated effects 

should be considered in judging to what 

degree a standard should be 

precautionary. 

In considering all of the issues 

discussed above, the Administrator has 

decided to propose a range of 7–15 

ppm-hour. In selecting as an upper 

bound a level of 15 ppm-hour, the 

Administrator notes that this level was 

specifically supported by the CASAC O3

Panel and is just above the range 

identified in the 1996 Consensus 

Workshop report as needed to provide 

adequate protection for trees growing in 

natural areas. In addition, the NPS, 

along with many public commenters, 

were in support of the CASAC range, 

including the upper bound of 15 ppmhour, and indicated that lower values 

within this range would be more 

protective for sensitive trees in 

protected areas from biomass loss and 

visible foliar injury symptoms. 

While the upper end of this range is 

lower than the upper end of 21 ppmhour recommended in the 2007 Staff 

Paper, this upper level of 21 ppm-hour 

was originally put forward in the 1997 

review in terms of a SUM06 of 25 ppmhour (W126 of 21 ppm-hour) and was 

justified on the basis that it was 

predicted to allow up to 10% biomass 

loss annually in 50% of studied 

commercial crops and tree seedling 

species. Recognizing the significant 

uncertainties that are associated with 

evaluating effects on commercial crops 

from a public welfare perspective, the 

Administrator now concludes that 

commercial crop data are no longer 

useful for setting the upper level of the 

range for proposal. 

With regard to her selection of a 

proposed range, the Administrator has 

considered that the direction from 

Congress to provide a high degree of 

protection in Class I areas creates a 

clearer target for gauging what types and 

magnitudes of effects would be known 

or anticipated to affect the intended use 

of these and other similarly protected 

areas, that would thus be considered 

adverse to the public welfare. Such 

similar areas include lands set aside by 

States, Tribes and public interest groups 

to provide similar benefits to the public 

welfare, for residents on those lands, as 

well as visitors to those areas. The 

Administrator also believes that in order 

to preserve wilderness areas in an 

unimpaired state for future generations, 

she must consider a level that affords 

substantial protection from known 

adverse O3-related effects of biomass 

loss and foliar injury on sensitive tree 

species, as well as a level that takes into 

account potential ‘‘anticipated’’ adverse 

O3-related effects, including effects that 

result in continued impairment in the 

year following O3 exposure (i.e., carryover effects), below ground impacts, 

ecosystem level impacts, and reduced 

CO2 sequestration 

While the Administrator 

acknowledges that growth effects and 

visible foliar injury can still occur in 

sensitive species at levels below the 

upper bound of the proposed range, the 

Administrator also recognizes that some 

significant uncertainties remain 

regarding the risk of these effects, as 

discussed above. For example, the 

Administrator concludes that remaining 

uncertainties make it difficult to judge 

the point at which visible foliar injury 

becomes adverse to the public welfare 

in various types of specially protected 

areas. Uncertainties associated with 

monitoring ambient exposures must be 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
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considered in evaluating the strength of 

predictions regarding the degree of tree 

seedling growth impairment estimated 

to occur at varying ambient exposures. 

These uncertainties add to the challenge 

of judging which exposure levels are 

expected to be associated with levels of 

tree seedling growth effects considered 

adverse to public welfare The 

Administrator believes that it is 

important to consider these 

uncertainties, and the weight to place 

on such uncertainties, in selecting a 

range of standard levels to propose. 

Establishing 15 ppm-hour as the upper 

end of the proposed range reflects her 

judgment regarding the appropriate 

weight to place on these uncertainties in 

determining the degree of protection 

that is warranted for known and 

anticipated adverse effects. 

With regard to her selection of a lower 

bound for the proposed range, the 

Administrator believes that if weight is 

placed on taking a more precautionary 

approach, recognizing that the real 

world impacts on trees and ecosystems 

could, in some cases, be greater than 

predicted, then the lower end of the 

range of 7 ppm-hour could be 

warranted. There is clear evidence that 

higher cumulative exposures can occur 

in rural areas downwind of urban areas 

and potentially in Class I areas. 

Unmonitored high elevation sites would 

also likely have higher cumulative 

exposures than lower elevation sites 

that are currently monitored. All of 

these considerations lead the 

Administrator to propose 7 ppm-hour as 

the low end of the proposed range. 

As discussed above in section 

IV.D.5.a, the main opposition to 

changing to a secondary standard with 

a cumulative, seasonal form has been 

the view that EPA does not have an 

adequate basis to identify the kinds and 

types of cumulative, seasonal exposure 

patterns that the standard should be 

designed to protect against, given the 

various uncertainties in the evidence, 

and whether EPA has an adequate basis 

to determine an appropriate level for a 

cumulative, seasonal secondary 

standard. While EPA agreed with this 

position in the 1997 review, the 

Administrator believes that the evidence 

before her appropriately supports a 

secondary standard that is distinctly 

different in form and averaging time 

from the 8-hour primary standard, and 

that such a standard is necessary to 

provide sufficient protection from 

cumulative, seasonal exposures to O3. 

While a different conclusion on this 

issue was reached in the 1997 review, 

the current conclusion that an exposure 

index that is cumulative and seasonal in 

nature, and therefore that setting a 

standard based on such a form is 

necessary and appropriate, is based on 

information newly available in the 2008 

rulemaking, which strengthens the 

information available in the 1997 review 

and reduces remaining uncertainties. 

Such newly available information 

includes quantitative information for a 

broader array of vegetation effects 

(extending to sapling and mature tree 

growth stages) obtained using a more 

diverse set of field-based research study 

designs and improved analytical 

methods for assessing O3-related 

exposures and risks as discussed above 

in sections IV.A–C. 

These newly available studies also 

provide important support to the 

quantitative estimates of impaired tree 

growth based on earlier studies 

available in the 1997 review and 

address one of the key data gaps cited 

in the 1997 review. Additional 

qualitative information is also available 

regarding improved understanding of 

linkages between stress-related effects of 

O3 exposures at the species level and 

those at higher levels within 

ecosystems. Finally, this information 

includes the use of new analytical 

methods, including a new multipollutant, multi-scale air quality model 

used to characterize exposures of O3- 

sensitive tree and crop species further 

address uncertainties in the assessments 

done in the 1997 review. In total, this 

newly available information increases 

the Administrator’s confidence in 

important aspects of this rulemaking 

The decision in 2008 to set the 

secondary O3 standard identical to the 

8-hour primary standard largely 

mirrored the decision in 1997, but failed 

to account for this significant increase 

in the body of knowledge available to 

support the 2008 rulemaking. This body 

of knowledge, while continuing to 

reflect significant uncertainties, 

provides an appropriate basis for 

determining a level of a cumulative, 

seasonal standard that, in the judgment 

of the Administrator, provides sufficient 

but not more than necessary protection 

from cumulative, seasonal exposures to 

O3. This is clearly so when compared to 

a standard that uses an indirect form 

that is not biologically relevant, an 8- 

hour average standard aimed at peak 

daily exposures. This judgment is fully 

consistent with the advice provided by 

CASAC. 

After carefully taking the above 

considerations into account, and giving 

significant weight to the views of 

CASAC, the Administrator has decided 

to propose a range of levels of 7–15 

ppm-hour for a cumulative, seasonal 

secondary O3 standard expressed as an 

index of the annual sum of weighted 

hourly concentrations (i.e., the W126 

form), cumulated over 12 hours per day 

during the consecutive 3-month period 

within the O3 season with the maximum 

index value, averaged over three years. 

In the Administrator’s judgment, based 

on the information available in the 2008 

rulemaking, a standard could be set 

within this range that would be 

requisite to protect public welfare from 

known or anticipated adverse effects to 

O3-sensitive vegetation and ecosystems. 

In the Administrator’s judgment, a 

standard set at a level below the lower 

end of the range is not now supported 

by the weight of evidence and would 

not give sufficient weight to the 

important uncertainties and limitations 

inherent in the available scientific 

evidence and in the quantitative 

assessments conducted for the 2008 

rulemaking. A standard set at a level 

above the upper end of the range is also 

not now supported by the weight of 

evidence and would not give sufficient 

weight to the credible inferences that 

the Agency has drawn from the 

scientific evidence nor to the 

quantitative assessments conducted for 

the 2008 rulemaking. The Administrator 

judges that the appropriate balance to be 

drawn, based on the entire body of 

evidence and information available in 

the 2008 rulemaking, is a range between 

7 and 15 ppm-hour. On balance, the 

Administrator believes that a standard 

could be set within this range that 

would be sufficient but not more than 

necessary to protect public welfare from 

known or anticipated adverse effects 

due to O3. 

In reaching this proposed decision, as 

discussed above, the Administrator has 

focused on the nature of the benefits 

associated with setting a distinct 

secondary standard with a cumulative, 

seasonal form relative to a standard with 

a peak daily 8-hour average form, as 

well as on assessments that quantify the 

degree of protection likely to be afforded 

by such standards. In so doing, the 

Administrator has acknowledged 

limitations in quantifying the expected 

benefits associated with the proposed 

cumulative seasonal standard relative to 

the secondary standard set in 2008. 

Having considered the public comments 

received on the 2007 proposed rule in 

reaching this proposed decision, the 

Administrator is interested in again 

receiving public comment on the 

benefits to public welfare associated 

with the proposed cumulative seasonal 

standard set at specific levels within the 

proposed range relative to the standard 

set in 2008. 


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E. Proposed Decision on the Secondary 

O3 Standard 

For the reasons discussed above, and 

taking into account information and 

assessments presented in the 2006 

Criteria Document and 2007 Staff Paper, 

the advice and recommendations of 

CASAC, and the public comments 

received in conjunction with the 2008 

rulemaking, the Administrator has 

decided to propose to set a new 

cumulative, seasonal secondary O3

standard with a form expressed as an 

index of the annual sum of weighted 

hourly concentrations (i.e., the W126 

form), cumulated over 12 hours per day 

(8 a.m. to 8 p.m.) during the consecutive 

3-month period within the O3 season 

with the maximum index value, 

averaged over three years, set within a 

range of 7 to 15 ppm-hour. The 

Administrator solicits comment on the 

weight that is appropriately placed on 

the various types of evidence and 

analyses upon which this proposed 

standard is based, and on the 

appropriate weight to be placed on the 

uncertainties in this information, as 

well as on the benefits to public welfare 

associated with the proposed standard 

relative to the benefits associated with 

the standard set in 2008. 

Data handling conventions for the 

proposed new secondary O3 standard 

are specified in the proposed addition of 

a new section to 40 CFR 50 Appendix 

P, as discussed in section V below. 

Issues related to monitoring 

requirements for the proposed new 

secondary O3 standard are discussed 

below in section VI. 

V. Interpretation of the NAAQS for O3

and Proposed Revisions to the 

Exceptional Events Rule 

Appendix P to 40 CFR part 50, 

Interpretation of the Primary and 

Secondary National Ambient Air 

Quality Standards for Ozone, addresses 

data completeness requirements, data 

reporting, handling, and rounding 

conventions, and example calculations. 

The current Appendix P explains the 

computations necessary for determining 

when the current identical primary and 

secondary standards are met. The EPA 

is proposing to revise Appendix P to 

reflect the proposed revisions to the 

primary and secondary O3 NAAQS 

discussed above and to make other 

changes described below. 

As discussed below, the proposed 

revisions to Appendix P include the 

following: The addition of data 

interpretation procedures applicable to 

the proposed cumulative, seasonal 

secondary NAAQS (see section V.B); 

clarification of certain language in the 

current provisions applicable to the 

primary NAAQS to reduce potential 

confusion (section V.C); revisions to the 

provisions regarding the use of 

incomplete data sets for purposes of the 

primary NAAQS and the data 

completeness requirements across three 

years (sections V.D and V.E); the 

addition of a provision providing the 

Administrator discretion to use 

incomplete data as if it were complete, 

for the purpose of the primary NAAQS 

(section V.F); a change from truncation 

to rounding of multi-hour and multiyear average O3 concentrations for the 

purposes of the primary standard 

(section V.G); and the addition of 

provisions addressing data to be used in 

making comparisons to the NAAQS 

(section V.H). The proposed revisions 

also include changes in organization for 

greater clarity and consistency with 

other data interpretation appendices to 

40 CFR part 50, which are not further 

described in this preamble. 

The EPA is also proposing changes to 

the O3-specific deadlines, in 40 CFR 

50.14, by which states must flag ambient 

air data that they believe have been 

affected by exceptional events and 

submit initial descriptions of those 

events, and the deadlines by which 

states must submit detailed 

justifications to support the exclusion of 

that data from EPA determinations of 

attainment or nonattainment with the 

NAAQS. The O3-specific deadlines in 

the current 40 CFR 50.14 would not be 

appropriate given the anticipated 

schedule for the designations of areas 

under the proposed revised O3 NAAQS. 

A. Background 

The purpose of a data interpretation 

appendix in general is to provide the 

practical details on how to make a 

comparison between multi-day and 

possibly multi-monitor ambient air 

concentration data and the level of the 

NAAQS, so that determinations of 

compliance and violation are as 

objective as possible. Data interpretation 

guidelines also provide criteria for 

determining whether there are sufficient 

data to make a NAAQS level 

comparison at all. Appendix P was 

promulgated in March 2008 along with 

the most recent revisions to the primary 

and secondary O3 NAAQS. It is very 

similar to Appendix I, Interpretation of 

the 8-Hour Primary and Secondary 

National Ambient Air Quality Standards 

for Ozone, which was adopted in 1997 

when the O3 NAAQS were first revised 

to have an 8-hour averaging period 

rather than the earlier 1-hour averaging 

period, along with other changes in 

form and level. The only substantive 

difference between Appendix I and the 

current version of Appendix P is that 

Appendix P contains truncation 

procedures consistent with the 

additional decimal digit used to express 

the level of the 2008 NAAQS in parts 

per million (0.075 ppm) compared to 

the 1997 NAAQS (0.08 ppm). In July 

2007, EPA had also proposed to include 

in Appendix P data interpretation 

procedures for the proposed cumulative, 

seasonal secondary O3 NAAQS, but 

these procedures were not finalized 

given that the final secondary NAAQS 

was identical in all respects to the final 

primary NAAQS. 

An exceptional event is defined in 40 

CFR 50.1 as an event that affects air 

quality, is not reasonably controllable or 

preventable, is an event caused by 

human activity that is unlikely to recur 

at a particular location or a natural 

event, and is determined by the 

Administrator in accordance with 40 

CFR 50.14 to be an exceptional event. 

Air quality data that are determined to 

have been affected by an exceptional 

event under the procedural steps and 

substantive criteria specified in section 

50.14 may be excluded from 

consideration when EPA makes a 

determination that an area is meeting or 

violating the associated NAAQS. The 

key procedural deadlines in section 

50.14 are that a state must notify EPA 

that data have been affected by an event, 

i.e., ‘‘flag’’ the data in the Air Quality 

Systems (AQS) database, and provide an 

initial description of the event by July 

1 of the year after the data are collected, 

and that the State must submit the full 

justification for exclusion within 3 years 

after the quarter in which the data were 

collected. However, if a regulatory 

decision based on the data, for example 

a designation action, is anticipated, the 

schedule is shortened and all 

information must be submitted to EPA 

no later than a year before the decision 

is to be made. This generic schedule 

presents problems when a NAAQS has 

been recently revised, as discussed in 

section V.I below. On May 15, 2009, 

EPA finalized a set of O3-specific 

deadlines that corrected these problems 

at the time with respect to the 2008 

NAAQS revisions (74 FR 23307). 

However, because of the anticipated 

effect of the current reconsideration on 

the schedule for O3 designations, the 

schedule problems will resurface unless 

the deadlines are adjusted again. 

B. Interpretation of the Secondary O3

Standard 

The EPA is proposing data 

interpretation procedures for the 

proposed secondary O3 NAAQS, which 

is defined in terms of a specific 

cumulative, seasonal form, commonly 


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63Because only enough missing 1-hour ozone 

values would be substituted as needed to meet the 

75 percent completeness requirement, to avoid 

unreasonable underestimation of the true W126 

index, tying the the selection of the substitution 

value to the hour of the missing value, as is 

proposed for data substitution for the purpose of the 

primary standard (see section V.D), would 

introduce considerable complexity by requiring an 

algorithm for determining which specific missing 

values would be substituted. Therfore, EPA is 

proposing this simpler substitution approach for the 

secondary standard. 

64At present, EPA’s Air Quality System (AQS) for 

storing and reporting air quality data provides a 

completeness report that is based on yet a third 

approach, in which the period for reporting data 

completeness is the required monitoring season 

plus any extension needed to encompass any 

exceedances that may have occurred outside the 

required season. However, EPA’s practice for 

regulatory purposes has been to consider 

completeness only over the required ozone 

monitoring season. 

referred to as the W126 form, as 

described above in section IV. The 

proposed new section 4 of Appendix P 

on data interpretation for the secondary 

standard contains the following main 

features. 

The ‘‘design value’’ for the secondary 

standard, the statistic for a monitoring 

site which would be compared to the 

level of the secondary standard to 

determine if the site meets the standard, 

would be the average of the annual 

maximum values of the three-month 

index value from three calendar years. 

The new section would provide clear 

directions and examples for the 

calculation of the daily index value, the 

monthly cumulative index value, the 

annual maximum index value for a year, 

and the design value itself. 

Only the data from the required O3

monitoring season would be examined 

to determine the annual maximum 

index value; any additional period of 

monitoring undertaken voluntarily by a 

state would not be considered. The EPA 

believes that because of the recently 

proposed extension of the required 

monitoring seasons in many states (74 

FR 34525, July 16, 2009), as discussed 

below in section VI, such a period of 

voluntary monitoring would be unlikely 

to have such high index values as to 

affect the annual maximum index value. 

Moreover, the proposed required 

monitoring season may encompass the 

most active growing season in many 

areas. The EPA invites comment on 

whether instead the entire actual O3

monitoring period should be 

considered, to eliminate any possibility 

that the highest cumulative index value 

that can be determined with available 

data might be missed. 

For each month in a three-month 

period, O3 data would have to be 

available for at least 75 percent of 

daylight hours (defined for this purpose 

as 8 a.m.–7:59 p.m. LST). If data are 

available for at least 75 percent but 

fewer than 100 percent of these daylight 

hours in a month, the cumulative index 

value calculated from the available 

daylight hours in the month would be 

increased to compensate for the missing 

hours, based on an assumption that the 

missing hours would have the same 

distribution of O3 concentrations as the 

available hours. A substitution test is 

also proposed, by which months in 

which fewer than 75 percent of daylight 

hours have O3 concentration data might 

also be useable for calculating a valid 

cumulative index value. Such months 

would be used if the available O3

concentrations are so high that even 

substituting low concentration values 

for enough missing data to meet the 75 

percent requirement would result in a 

design value greater than the level of the 

standard. The low value that would be 

substituted would be the lowest 1-hour 

O3 concentration observed at the 

monitoring site during daylight hours 

during the required O3 monitoring 

season, in that calendar year, or one-half 

the method detection limit (MDL) of the 

ozone instrument, whichever is 

higher.63

The EPA notes that while this 

proposed approach to identifying the 

substitution value for the secondary 

standard is technically appropriate, it 

would necessitate data processing 

efforts during implementation that 

might be avoidable via some other 

approach that is also technically 

reasonable. We therefore invite 

comment on such alternative 

approaches, and we may adopt another 

approach in the final rule. For example, 

for simplicity the substituted 1-hour O3

concentration value could instead 

simply always be zero or one-half the 

MDL of the O3 instrument, noting that 

because of the sigmoidal weighting 

factor the exact magnitude of the low 

substitution value may typically make 

very little difference to the annual index 

value. Also, using the previous calendar 

year as the source of the substitution 

value instead of the current calendar 

year would have the advantage of 

allowing all parties to know early in 

each year what the substitution value 

will be. 

The EPA is proposing that all decimal 

digits be retained in intermediate steps 

of the calculation of the cumulative 

index, with the result rounded to have 

no decimal digits when expressed in 

ppm-hours before comparison the level 

of the secondary NAAQS. 

EPA expects that the three months 

over which the cumulative weighted 

index value is highest will generally 

occur in the middle of each year. 

Therefore, the proposed new section 4 

of Appendix P presumes this, and does 

not address a situation in which the 

three months of maximum cumulative 

index spans two calendar years, for 

example December to February. The 

EPA invites comment on whether a 

provision addressing such a remote 

possibility is needed and what its terms 

should be. For example, the process of 

checking each three month period in a 

calendar year to determine which gives 

the highest index value could include 

the combinations of December/January/ 

February and November/December/ 

January within one calendar year. 

C. Clarifications Related to the Primary 

Standard 

The EPA is proposing two clarifying 

changes to Appendix P to make 

unambiguous two aspects of data 

interpretation for the primary 8-hour 

standard. The first change clarifies that 

the standard data completeness 

requirement that valid daily maximum 

8-hour values exist for 75 percent of all 

days refers to days within the required 

O3 monitoring season only. The current 

wording of Appendix P is somewhat 

open to a reading that the requirement 

applies to all days in the actual 

monitoring record for the site in 

question, which could be longer than 

the required season if a state voluntarily 

monitors on additional days, or shorter 

than the required season if a monitor 

has started or ceased operation 

sometime during the required season. 

The O3 data completeness requirement 

is intended to avoid a determination 

that an area has met the NAAQS when 

in fact more than a reasonable number 

of days with high O3 potential were not 

successfully monitored. This purpose 

can be served if the data within the 

required O3 monitoring season only are 

reasonably complete, because as 

mentioned above EPA has proposed to 

revise the required O3 seasons so that 

they encompass all days with potential 

for an exceedance of even the lowest 

proposed level for the primary standard. 

Unsuccessful monitoring outside the 

required season should not be an 

obstacle to a finding of attainment. 

However, if an O3 monitor has missed 

more than 25 percent of the required O3

monitoring season, for example because 

it started or stopped operation midseason, this should prevent a finding of 

attainment based on a three-year period 

that includes that season. The proposed 

clarifying language reflects EPA’s actual 

intention and our past practice in 

applying Appendix P for regulatory 

purposes, and Appendix I as well.64


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65Actually, it is an interpretation of the text of 

Appendix P, section 2.1, that the average resulting 

from the data substitution is to be taken as the ‘‘8- 

hour’’ average, rather than the average of the 

available 5 or fewer hours of data, which would be 

higher. The text is not entirely clear on this point. 

66EPA also is proposing eliminate this 90 percent 

requirement, see section V.E. The point made in 

this paragraph applies with or without the 90 

percent requirement in place. 

The second proposed clarifying 

change would make it clear that when 

determining the fourth-highest daily 

maximum 8-hour O3 concentration for a 

year, all days with monitoring data are 

to be considered, not just days within 

the required O3 monitoring season. This 

proposed clarifying language also 

reflects EPA’s actual intention and our 

past practice in applying Appendix P, 

and Appendix I as well. While EPA 

believes it to be quite unlikely that an 

exceedance will occur outside the 

proposed revised required O3

monitoring seasons and have a high 

enough concentration to affect the 

selection of the fourth-highest 

concentration for the year, when and if 

such an occurrence does happen, the 

data should not be ignored. 

D. Revision to Exceptions From 

Standard Data Completeness 

Requirements for the Primary Standard 

The EPA is proposing to revise 

portions of Appendix P that describe 

certain exceptions to the standard data 

completeness requirements, under 

which a monitoring site can in some 

cases be determined to be meeting or 

violating the primary NAAQS despite 

not meeting the standard data 

completeness requirements. These 

changes would make Appendix P more 

logical in certain types of cases with 

incomplete data. While the particular 

types of cases whose outcome would be 

different with these changes have been 

rare historically, there may be more 

such affected cases in the future in 

conjunction with a primary O3 standard 

revised to a level within the range of 

levels proposed in this action. 

The standard data completeness 

requirements in Appendix P for the 

primary O3 NAAQS apply a 75 percent 

requirement at each of three stages of 

data completeness testing. As discussed 

below, for each stage, there is an 

existing exception to the 75 percent 

requirement. 

In the first stage, an 8-hour period can 

be considered to have a valid 8-hour 

average O3 concentration only if at least 

75 percent of the hours, i.e., 6 or more 

hours, have a valid hourly O3 value. The 

provided exception is that if there are 5 

or fewer hours but if substituting a very 

low value (specifically, one-half the 

MDL of the O3 instrument) for all the 

missing hours results in a hypothetical 

8-hour average that is above the level of 

the primary standard, the 8-hour period 

is considered valid and is assigned the 

hypothetical level resulting from the 

data substitution.65 For example, if the 

O3 concentration was 0.125 ppm for 5 

hours, substituting a typical MDL/2 

value of 0.0025 ppm for three missing 

hours would result in an 8-hour average 

of 0.079 ppm, which is an exceedance 

of the current primary standard, so the 

valid 8-hour average for the period 

would be taken to be 0.079 ppm. If this 

value is higher than one or more of the 

highest four daily maximum 8-hour 

concentrations otherwise calculated for 

the year, considering it to be valid 

affects the value identified as the fourthhighest for the year and thus also affects 

the final design value. The logical 

problem with this approach is that it is 

possible for a hypothetical 

8-hour average with such substitution to 

be below the level of the NAAQS, thus 

not meeting the current condition for 

the exception, but for it to still make a 

critical difference in making the threeyear design value be above the level of 

the NAAQS, because a three-year design 

value can include (and be sensitive to 

the exact value of) an annual fourthhighest daily maximum that is not 

above the level of the NAAQS. This 

could be the case if the hypothetical 8- 

hour average with substitution is the 

maximum concentration 8-hour period 

for its day, and the day is one of the 

highest four O3 days of the year. 

Whether it actually is the case would 

further depend on the value of the 

8-hour average itself, the values of the 

next highest daily maximum 8-hour 

average concentration in the year, and 

the values of the annual fourth-highest 

daily maximum 8-hour concentration 

from the other two years. If the 

substituted 8-hour average would make 

a critical difference, it should be treated 

as valid and used in the calculation of 

the three-year design value, even if it is 

not itself above the level of the standard. 

Another problem is that one-half of the 

MDL, which typically is about 0.0025 

ppm, is very likely to be considerably 

lower than the actual O3 concentrations 

that were not successfully measured. 

Thus, while the one-half-MDLsubstituted value is prevented from 

being an overestimate of the actual 

8-hour average concentration, it is an 

unreasonably low estimate of that 

concentration which may have the effect 

of allowing a site with actual O3 levels 

above the standard to be found to meet 

the standard. The condition in the 

exception requiring a one-half-MDLsubstituted ‘‘8-hour’’ average to be above 

the level of the NAAQS is therefore 

inappropriate. 

In the second stage of data 

completeness testing, 75 percent of the 

24 possible 8-hour time blocks, which is 

18 or more, must have valid 8-hour 

average concentrations values. The 

intent of this requirement is to make 

sure that most of the day was actually 

monitored, such that the highest 

concentration 8-hour period was likely 

to be captured in the data. When this is 

not the case, the day is not considered 

in selecting the annual fourth-highest 

daily maximum 8-hour concentration 

and no credit for the day’s monitoring 

is given towards the third stage of data 

interpretation (see below). The provided 

exception in the current Appendix P is 

that a day is considered valid if at least 

one 8-hour period has an average 

concentration above the level of the 

standard. However, as in the first stage, 

it is possible for an 8-hour period with 

an average concentration at or below the 

level of the NAAQS to play a critical 

role in whether the three-year design 

value meets the standard. Invalidating 

the day could have the effect of causing 

a lower value to be selected as the 

annual fourth-highest daily maximum 

8-hour concentration, leading to a threeyear design value that does not exceed 

the NAAQS while it would have 

exceeded if the day and the 8-hour 

average value had been treated as valid. 

The condition in the exception 

requiring at least one 8-hour average 

during the day to be above the level of 

the NAAQS is therefore inappropriate. 

In the third stage of data completeness 

testing, a completeness criterion is 

applied for the number of days in the 

required O3 season that have a valid 

maximum 8-hour average, i.e., days that 

have met the completeness conditions 

in the first two stages or have met the 

condition for an exception. Specifically, 

for each of the three years being used in 

the design value calculation, the 

number of valid days within the 

required O3 monitoring season (with no 

credit for extra days outside the season) 

must be at least 75 percent of the days 

in the required O3 season, and the 

number of valid days across all three 

years must be 90 percent of the days in 

the three seasons.66 The provided 

exception to the 75/90 percent 

requirement is that data from a year 

with less than 75 percent of seasonal 

days can nevertheless be used if during 

the year at least one day’s maximum 8- 

hour average O3 concentration was 


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3030 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

67EPA notes that in the current versions of 

Appendix I and P, it is not explicit that this 

provided exception also applies in the case of three 

years which each have 75 percent or more of days 

with valid data but less than 90 percent across three 

years. Because EPA is proposing to remove the 90 

percent requirement (see section V.E) this 

ambiguity does not need correction. 

68Appendix P now provides that in the event that 

only 6 or 7 hourly averages are available, the valid 

8-hour average shall be computed on the basis of 

the hours available, using 6 or 7 as the divisor. We 

are not proposing to change this provision. 

69The requirement that there be at least four days 

with at least one hourly measurement is actually 

redundant and is stated only for ease of 

understanding, since there would be no annual 

fourth-highest daily maximum 8-hour concentration 

unless there are at least four days with monitoring 

data, and a single hourly data point is necessary 

and sufficient (with the proposed substitution step) 

to generate a daily maximum 8-hour concentration. 

above the level of the standard and if 

the three-year design value is also above 

the standard.67 The problem with this 

exception, similar to the problems with 

the exceptions in the first and second 

stages of data completeness testing, is 

that a daily maximum 8-hour 

concentration that is at or below the 

level of the NAAQS can nevertheless 

make a critical difference in making the 

three-year design value be above the 

level of the NAAQS. When it does, an 

incorrect final result will be reached if 

the year of data is not granted an 

exception to the 75/90 percent 

requirement. Specifically, there would 

be no valid three-year design value and 

no conclusion would be reached as to 

attainment or nonattainment, despite it 

being clear that the actual situation is 

nonattainment, in the sense that 

successful collection of additional hours 

and days of monitoring data could not 

possibly have resulted in a passing 

three-year design value. Moreover, since 

the three-year design value is the 

average of the fourth-highest daily 

maximum 8-hour concentration from 

each year, there is no logical connection 

between the design value and the 

existence of a single daily maximum 

concentration greater than the level of 

the standard, which is the current 

condition for the exception for this stage 

of testing for data incompleteness. 

EPA proposes to remedy this situation 

by replacing the three separate 

statements of the exceptions to the three 

standard completeness requirements 

with a new data substitution step that 

addresses the root cause of the data 

incompleteness situation: missing 

hourly concentrations which make it 

doubtful whether actual maximum daily 

8-hour concentrations were measured 

on a reasonably large percentage of the 

days during the required O3 monitoring 

season of each year. In the event that 

only 1, 2, 3, 4, or 5 hourly averages are 

available for an 8-hour period, a 

partially substituted 8-hour average 

would be computed by substituting for 

all the hours without hourly averages a 

low hourly average value selected as 

follows, and then using 8 as the 

divisor.68 For days within the required 

O3 monitoring season, the substitution 

value would be the lowest hourly 

average O3 concentration observed for 

that hour of the day (local standard 

time) on any day during the required O3

monitoring season of that year, or onehalf the MDL, whichever is higher. 

Using this value makes it highly 

unlikely that the resulting partially 

substituted 8-hour average 

concentration is higher than the actual 

concentration. Therefore, using the 

partially substituted 8-hour average in 

the design value calculation procedure 

is highly unlikely to result in an 

incorrect finding that a site does not 

meet the standard, but it may lead to a 

correct finding that a site does not meet 

the standard in some cases in which 

there would be no finding possible or an 

incorrect finding under the current 

version of Appendix P. However, the 

use of the higher of the lowest observed 

same-hour concentration or one-half the 

MDL could be problematic if a robust 

set of hourly measurements is not 

available for the year, for example if a 

monitor began operation late in an 

ozone season. In such a case, the lowest 

observed same-hour concentration 

might not be low enough to eliminate all 

possibility that the value used for 

substitution is higher than the missing 

concentration value. To reduce this 

likelihood to essentially zero, we are 

proposing that if the number of samehour concentration values available for 

the required O3 monitoring season for 

the year is less than 50 percent of the 

number of days during the required O3

monitoring season, one-half the MDL of 

the O3 instrument would be used in the 

substitution instead of the lowest 

observed concentration. We invite 

comment on whether another 

percentage should be used for this 

purpose instead of 50 percent. 

The EPA notes that while this 

proposed approach to identifying the 

substitution value for the primary 

standard is technically appropriate, it 

would necessitate new data processing 

efforts during implementation that 

might be avoidable via some other 

approach that is also technically 

reasonable. There may also be 

approaches which are more technically 

appropriate. We therefore invite 

comment on such alternative 

approaches, and we may adopt another 

approach in the final rule. Examples of 

simpler approaches would be to identify 

in the final rule a fixed substitution 

value other than one-half the MDL, to 

accept as valid 8-hour periods with only 

five measured hourly concentrations, to 

interpret between two hourly 

concentrations to obtain a substitute for 

a single missing hourly concentration, 

or to use the previous calendar year as 

the source of the substitution value 

instead of the current calendar year 

(thereby allowing all parties to know 

early in each year what the substitution 

value will be). Examples of more 

complex approaches that might be more 

technically appropriate include 

selecting a low percentile of the 

available same-hour concentration data 

rather than the lowest value to be the 

substitution value, or selecting the 

lowest same-hour value from the same 

calendar quarter or month (of the 

current year or the most recent year) 

rather than from the entire required 

ozone monitoring season. We also invite 

comment on whether the proposed 

approach to substitution should be used 

at all and if not what other approach 

should be used to address the potential 

problem just described. 

We propose that for simplicity and to 

further reduce any risk of a false finding 

that a site does not meet the standard, 

for days outside the required O3

monitoring season, the substitution 

value would always be one-half the 

MDL of the O3 instrument. We similarly 

invite comment on this aspect. 

There would be no condition that a 

partially substituted 8-hour average 

exceed the level of the standard for it be 

used in calculating the design value, 

unlike is now the case. An 8-hour 

period with no available hourly 

averages at all would not have a valid 

8-hour average, as is now the case. 

In addition, to complete the solution 

to the problems described above, we are 

proposing that a design value that is 

greater than the level of the primary 

standard would be valid provided that 

in each year there were at least four 

days with at least one valid 8-hour 

concentration.69 One or more of these 

8-hour average concentrations could be 

the partially substituted 8-hour average 

concentration resulting from the above 

described substitution procedure. In 

such a case, there is essentially no 

possibility that more complete 

monitoring data would have shown the 

site to be meeting the NAAQS. It is 

appropriate to include all 8-hour 

averages including those involving 

substitution when testing for an 

exceedance of the standard, because 

those averages are extremely unlike to 


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70EPA has recently proposed to amend the 

completeness requirements for sulfur dioxide and 

nitrogen dioxide to add quarterly 75 percent 

completeness requirements in connection with 

proposals to establish 1-hour primary NAAQS for 

these pollutants, still with no requirement for 90 

percent completeness across three years. 

be overestimates of actual 

concentrations. 

Finally, a design value equal to or less 

than the level of the standard would be 

valid only if at least 75 percent of the 

days in the required O3 monitoring 

season of each year have daily 

maximum 8-hour concentrations that 

are based on at least 18 periods with at 

least 6 hourly concentrations. This 

ensures that a site will be found to meet 

the standard only when a reasonably 

high percentage of the days in the 

required O3 monitoring season have 

reasonably complete hourly data. In this 

situation, it would be inappropriate to 

count the 8-hour periods with five or 

fewer actual hourly measurement values 

towards the 75 percent requirement 

when testing for whether a site meets 

the standard, because those 8-hour 

averages will be based on substitution of 

low values and therefore will be 

underestimates of actual concentrations. 

The only way to be reasonably certain 

that no 8-hour period had a high enough 

concentration so as to contribute to a 

design value over the level of the 

standard is to have at least 18 periods 

in which substitution for missing O3

values was not needed. This provision 

has the same effect as several elements 

of the current Appendix P considered 

together, and thus is not a substantive 

change. 

E. Elimination of the Requirement for 90 

Percent Completeness of Daily Data 

Across Three Years 

As stated above in section VI.D, 

Appendix P currently requires that in 

order for a design value equal to or less 

than the standard to be valid, at least 75 

percent of days in each of three years 

must have a valid daily maximum 

8-hour average concentration value, i.e., 

that many days must have at least 18 

8-hour periods with at least 6 reported 

hourly concentrations each. Appendix P 

also requires that the average of the 

percentages from three consecutive 

years be at least 90 percent. The EPA is 

proposing to eliminate this 90 percent 

requirement for the average of three 

years and to retain only the requirement 

that each individual year have a 

percentage of at least 75 percent. 

The 90 percent requirement was 

incorporated into Appendix I (the data 

interpretation appendix for the 0.08 

ppm O3 NAAQS) in 1997 with an 

explanation that EPA had observed that 

90 percent of O3 monitoring sites 

routinely achieved 90 percent data 

capture. The EPA now notes, however, 

that while the majority of monitoring 

sites do achieve 90 percent or better 

data capture in any given year, there are 

exceptions every year. The 90 percent 

requirement applied to the average 

percentage over three years is quite 

unforgiving if there has been one year 

with relatively low data completeness. 

For example, if one year just met the 75 

percent requirement, the remaining two 

years would have to achieve a 97.5 

percent data capture rate in order for the 

three years to meet the 90 percent 

requirement. This would allow only 4 

missed hours of measurements per 

week, which would be challenging. The 

consequences for states could be 

important, under the current 

requirement. One possible result could 

be that an area actually in 

nonattainment with the NAAQS might 

have to be designated unclassifiable, 

although the substitution procedure 

proposed for cases of incomplete data, 

as described above in section VI.D, 

provides a path to an appropriate 

nonattainment finding in at least some 

cases. Another possible result is that a 

nonattainment area which had actually 

come into attainment could be unable to 

receive an attainment determination 

until three more years of sufficiently 

complete data are collected. This might, 

for example, result in an area which has 

achieved needed emissions reductions 

by its attainment deadline nevertheless 

being bumped up to a higher 

classification. 

The 90 percent requirement over three 

years has the potential to treat two areas 

disparately, for no obvious logical 

reason. Consider two areas with 

identical air quality. Suppose the first 

area has annual completeness 

percentages of 75, 95, and 95 percent 

(averaging to 85 percent and thus failing 

the 90 percent requirement) and the 

second area has annual completeness 

percentages of 75, 98, and 98 percent 

(averaging to 90 percent). Suppose that 

the three-year design values in both 

areas are below the level of the NAAQS. 

Practically speaking, the most important 

uncertainty about whether each area 

actually meets the NAAQS is the low 

data capture rate in the first year. There 

is no obvious logic why the fact that the 

second area achieves marginally better 

data capture in the second and third 

year should permit it to receive an 

attainment finding despite this 

uncertainty, while the first area may 

not. 

The EPA also notes that for the other 

gaseous criteria pollutants—sulfur 

dioxide, carbon monoxide and nitrogen 

dioxide—the completeness requirement 

is for 75 percent completeness of hourly 

measurements in an individual year.70

For these reasons, EPA proposes to 

eliminate the 90 percent requirement 

across three years of data but to retain 

the 75 percent requirement for 

individual years. The EPA notes that as 

a practical matter, the current 90 

percent requirement in effect requires a 

minimum data capture rate somewhat 

above 75 percent in each year, because 

if data capture in any one year were as 

low as 75 percent the required data 

capture in the other years would be very 

hard to achieve. The minimum annual 

data capture rate is effectively 

somewhere in the range of 80 percent 

(implying a requirement to achieve 95 

percent data capture in the two 

remaining years in order to meet the 90 

percent requirement across three years) 

and 85 percent (implying a requirement 

to achieve 92.5 percent data capture in 

the two remaining years). The EPA 

invites comment on whether instead of 

retaining the 75 percent completeness 

requirement in each individual year, the 

requirement should be 80 percent or 85 

percent. 

F. Administrator Discretion To Use 

Incomplete Data 

The EPA is proposing that the 

Administrator have general discretion to 

use incomplete data to calculate design 

values that would be treated as valid for 

comparison to the NAAQS despite the 

incompleteness, either at the request of 

a state or at her own initiative. Similar 

provisions exist already for the PM2.5

and lead NAAQS, and EPA has recently 

proposed such provisions to accompany 

the proposed 1-hour NO2 and SO2

primary NAAQS. The Administrator 

would consider monitoring site 

closures/moves, monitoring diligence, 

and nearby concentrations in 

determining whether to use such data. 

G. Truncation Versus Rounding 

Almost all State agencies now report 

hourly O3 concentrations in parts per 

million to three decimal places, since 

the typical incremental sensitivity of 

currently used O3 monitors is 0.001 

ppm. In the current Appendix P 

approach, in calculating 8-hour average 

O3 concentrations from such hourly data 

any calculated digits past the third 

decimal place are truncated rather than 

retained or rounded back to three 

decimal places. Also, in calculating 

3-year averages of the fourth-highest 

daily maximum 8-hour average 

concentrations, Appendix P currently 

requires the result to be reported to the 


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third decimal place with digits to the 

right of the third decimal place 

truncated. In this regard, Appendix P 

follows the precedent of Appendix I, 

except that Appendix P is based on a 

NAAQS level specified to three decimal 

places (0.075 ppm) while Appendix I 

addressed the case of a NAAQS level 

specified to only two decimal places 

(0.08 ppm). In the rulemaking that 

concluded in 2008 by establishing the 

0.075 ppm level, EPA noted that the 

2007 Staff Paper demonstrated that 

taking into account the precision and 

bias in 1-hour O3 measurements, the 

8-hour design value had an uncertainty 

of approximately 0.001 ppm. Thus, EPA 

considered any value less than 0.001 

ppm to be highly uncertain and, 

therefore, proposed and adopted 

truncation to the third decimal place for 

reporting 1-hour O3 concentrations and 

for both the individual 8-hour averages 

used to determine the annual fourth 

maximum and the 3-year average of the 

fourth maxima. 

The effect of this repeated truncation 

is that there is a consistent downward 

bias in the calculation of the three-year 

design value. The size of this bias can 

be notable. For example, seven hours 

with O3 concentrations of 0.076 ppm 

plus one hour of 0.075 ppm results in 

an 8-hour average of 0.075 ppm after 

truncation, nearly a full 0.001 ppm 

below the actual 8-hour average of 

0.075875 ppm. Seven hours with O3

concentrations of 0.077 ppm plus one 

hour of 0.076 ppm results in an 8-hour 

average of 0.076 ppm after truncation. 

One year with the first pattern plus two 

years with the second pattern would 

give a three-year design value of 0.075 

ppm, meeting the NAAQS, even though 

23 of the 24 individual 1-hour 

concentrations involved in the 

calculation of the design value were 

above 0.075 ppm. 

The EPA has decided to reconsider 

this aspect of O3 data interpretation. 

Specifically, we are proposing that (1) 

1-hour concentrations continue to be 

reported to only three decimal places, 

the same as is now specified in 

Appendix P, i.e., that the current 

practice of truncation of the 1-hour data 

to the nearest 0.001 ppm be retained; (2) 

all digits resulting from the calculation 

of 8-hour averages be retained; and (3) 

the three-year average of annual fourthhighest daily maximum 8-hour 

concentrations be rounded to three 

decimal places before comparison to the 

NAAQS. The EPA continues to believe 

that given the uncertainty in individual 

1-hour O3 concentration measurements 

it is appropriate to truncate those 

measurements at three decimal places 

(many O3 instruments are programmed 

to only report three digits anyway). 

However, the calculations of 8-hour 

averages and three-year averages are 

mathematical steps, not a measurement 

process subject to uncertainties, and 

EPA perceives no logic in having a 

consistent downward bias by truncating 

the results of these mathematical steps. 

The EPA notes that the O3 NAAQS is 

the only NAAQS for which multi-hour, 

multi-day, or multi-year averages of 

concentrations are truncated rather than 

rounded. The proposed change will 

make this aspect of O3 data 

interpretation consistent with data 

interpretation procedures for the other 

criteria pollutants. 

H. Data Selection 

The current version of Appendix P 

does not explicitly address the issue of 

what ambient monitoring data for O3

can and must be compared to the O3

NAAQS. The EPA proposes to add to 

Appendix P language addressing this 

issue. This language is similar to 

provisions recently proposed to be 

included in new data interpretation 

appendices for nitrogen dioxide and 

sulfur dioxide. The new section of 

Appendix P would clarify that all 

quality assured data collected with 

approved monitoring methods and 

known to EPA shall be compared to the 

NAAQS, even if not submitted to EPA’s 

Air Quality System. The section also 

addresses the question of what O3 data 

should be used when two or more O3

monitors have been operating and have 

reported data for the same period at one 

monitoring site. 

I. Exceptional Events Information 

Submission Schedule 

States are responsible for identifying 

air quality data that they believe warrant 

special consideration, including data 

affected by exceptional events. States 

identify such data by flagging (making a 

notation in a designated field in the 

electronic data record) specific values in 

the Air Quality System (AQS) database. 

States must flag the data and submit a 

justification that the data are affected by 

exceptional events if they wish EPA to 

consider excluding the data in 

determining whether or not an area is 

attaining the new O3 NAAQS. 

All states that include areas that could 

exceed the O3 NAAQS and could 

therefore be designated as 

nonattainment for the O3 NAAQS have 

the potential to be affected by this 

rulemaking. Therefore, this action 

applies to all states; to local air quality 

agencies to which a state has delegated 

relevant responsibilities for air quality 

management including air quality 

monitoring and data analysis; and to 

Tribal air quality agencies where 

appropriate. The Exceptional Events 

Rule preamble describes in greater 

detail to whom the rule applies (72 FR 

13562–13563, March 22, 2007). 

The CAA Section 319(b)(2) authorizes 

EPA to promulgate regulations that 

govern the review and handling of air 

quality monitoring data influenced by 

exceptional events. Under this 

authority, EPA promulgated the 

Exceptional Events Rule (Treatment of 

Data Influenced by Exceptional Events 

(72 FR 13560, March 22, 2007) which 

sets a schedule for states to flag 

monitored data affected by exceptional 

events in AQS and for them to submit 

documentation to demonstrate that the 

flagged data values were caused by an 

exceptional event. Under this schedule, 

a state must initially notify EPA that 

data have been affected by an 

exceptional event by July 1 of the year 

after the data are collected; this is 

accomplished by flagging the data in 

AQS. The state must also include an 

initial description of the event when 

flagging the data. In addition, the state 

is required to submit a full 

demonstration to justify exclusion of 

such data within three years after the 

quarter in which the data were 

collected, or if a regulatory decision 

based on the data (such as a designation 

action) is anticipated, the demonstration 

must be submitted to EPA no later than 

one year before the decision is to be 

made. 

The rule also authorizes EPA to revise 

data flagging and documentation 

schedules for data used in the initial 

designation of areas under a new 

NAAQS. The generic schedule, while 

appropriate for the period after initial 

designations have been made under a 

NAAQS, may need adjustment when a 

new NAAQS is promulgated because 

until the level and form of the NAAQS 

have been promulgated, a state would 

not have complete knowledge of the 

criteria for excluding data. In these 

cases, the generic schedule may 

preclude states from submitting timely 

flags and associated documentation for 

otherwise approvable exceptional 

events. This could, if not modified, 

result in some areas receiving a 

nonattainment designation when the 

NAAQS violations were legitimately 

due to exceptional events. 

As a result of the Administrator’s 

decision to reconsider the 2008 O3

NAAQS, EPA is proposing to revise the 

exceptional events flagging and 

documentation schedule to correspond 

to the designations schedules that EPA 

is considering for the proposed 

revisions to the primary and secondary 

O3 NAAQS. The designation schedules 


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under consideration are discussed in 

greater detail below in section VII.A and 

summarized here. The CAA requires 

EPA to promulgate the initial 

designations for all areas no later than 

2 years from the promulgation of a new 

NAAQS. Such period may be extended 

for up to one year if EPA has 

insufficient information. (See CAA 

section 107(d).) For a new primary O3

standard, EPA intends to issue 

designations on an accelerated 

schedule. For a new seasonal secondary 

O3 standard, EPA is considering two 

alternative schedules for initial area 

designations. 

Primary Standard: If, as a result of the 

reconsideration, EPA promulgates a new 

primary O3 standard on August 31, 

2010, EPA is proposing that state 

Governors would need to submit their 

initial designation recommendations to 

EPA by January 7, 2011. EPA would 

promulgate the final designations in 

July 2011 to allow sufficient time for the 

designations to be published and 

effective by August 31, 2011. EPA 

expects to base the final designations for 

the primary O3 standard on three 

consecutive years of certified air quality 

monitoring data from the years 2007– 

2009 or 2008–2010, if available. EPA is 

proposing that for exceptional event 

claims made for data years 2007–2009, 

states must flag and provide an initial 

description and detailed documentation 

by November 1, 2010. For data collected 

during data year 2010, EPA is proposing 

that exceptional event data that states 

want EPA to exclude from consideration 

in the designations process must be 

flagged with an initial description and 

fully documented by March 1, 2011 or 

60 days after the end of the quarter 

when the event occurred, whichever 

date is first. To meet this proposed 60- 

day deadline, a state would also have to 

submit the O3 concentration data to 

AQS sooner than the normal deadline 

for such submission, which is 90 days 

after the end of the calendar quarter. 

EPA believes this is a reasonable 

expectation given that most states 

currently submit O3 data earlier than the 

90-day deadline. 

Secondary Standard: If, as a result of 

the reconsideration, EPA promulgates a 

new seasonal secondary O3 standard by 

August 31, 2010, EPA is taking 

comment on two alternative 

designations schedules. Under the first 

alternative, EPA would designate areas 

for the secondary standard on the same 

accelerated schedule discussed above 

for the primary standard. Under the 

second alternative, EPA would 

designate areas for the secondary 

standard on the maximum 2-year 

schedule provided under the CAA. 

Accelerated Schedule: Under the 

accelerated schedule for a seasonal 

secondary O3 NAAQS, EPA is proposing 

that for exceptional event claims made 

for data years 2007–2009, states must 

flag and provide an initial description 

and detailed documentation by 

November 1, 2010. For data collected 

during data year 2010, EPA is proposing 

that exceptional event data that states 

want EPA to exclude from consideration 

in the designations process must be 

flagged with an initial description and 

fully documented by March 1, 2011 or 

60 days after the end of the quarter 

when the event occurred, whichever 

date is first. 

2-year Schedule: Under the 2-year 

schedule, states would have 1 year, or 

by August 2011, to submit their 

designations recommendations and EPA 

would finalize designations under the 

new secondary standard by August 

2012. EPA expects to base final 

designations for a new seasonal 

secondary standard on the most recent 

three years of certified air quality 

monitoring data, which would typically 

be from the years 2009–2011 in this 

case. Exceptional event data claims used 

from years 2008–2010 must be flagged 

with an initial description included in 

AQS and submitted with complete 

documentation supporting such claims 

by July 1, 2011. Exceptional event data 

claims from data year 2011 must be 

flagged with an initial description and 

submitted with complete 

documentation supporting such claims 

60 days after the end of the calendar 

quarter when the event occurred or 

March 1, 2012, whichever occurs first. 

Therefore, using the authority 

provided in CAA section 319(b)(2) and 

in the Exceptional Events Rule at 40 

CFR 50.14(c)(2)(vi), EPA is proposing to 

modify the schedule for data flagging 

and submission of demonstrations for 

exceptional events data considered for 

initial designations under the proposed 

reconsidered O3 primary and secondary 

NAAQS, as follows: 

TABLE 1—SCHEDULE FOR EXCEPTIONAL EVENT FLAGGING AND DOCUMENTATION SUBMISSION FOR DATA TO BE USED IN

DESIGNATIONS DECISIONS FOR NEW NAAQS 

NAAQS Pollutant/standard/(level)/ 

promulgation date 

Air quality data 

collected for 

calendar year 

Event flagging & initial description 

deadline 

Detailed documentation submission 

deadline 

Primary Ozone/8-Hr Standard (Level 

TBD)/promulgated by August 31, 2010.

2007–2009 November 1, 2010 b ................................ November 1, 2010.b

2010 60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b

60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b

Secondary Ozone/(Level TBD) Alternative 2-year Schedule—to be promulgated by August 31, 2010.2008 July 1, 2011b ........................................... July 1, 2011.a

2009–2010 July 1, 2011b ........................................... July 1, 2011.b

2011 60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2012, whichever occurs 

first.b

60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2012, whichever occurs 

first.b

Secondary Ozone/(Level TBD)—Alternative Accelerated Schedule—to be 

promulgated by August 31, 2010.

2007–2009 November 1, 2010 b ................................ November 1, 2010.b

2010 60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b

60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b

aThese dates are unchanged from those published in the original rulemaking. 


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71The requirements specified in Table D–2 of 

Appendix D to part 58, as noted in the third 

footnote of Table D–2, are applicable to the levels 

of the O3 NAAQS as defined in 40 CFR part 50. 

Accordingly, the 85 percent threshold for requiring 

higher minimum monitoring requirements within 

MSAs would apply to the proposed levels for the 

cumulative, seasonal secondary standard as well as 

to the proposed levels of the 8-hour primary 

standard. 

72These MSAs are not currently required to 

monitor for O3. 

b Indicates change from general schedule in 40 CFR 50.14. 

Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final initial designations for new NAAQS. 

The general schedule applies for all other purposes, most notably, for data used by EPA for redesignations to attainment. 

VI. Ambient Monitoring Related to 

Proposed O3 Standards 

Presently, States (including the 

District of Columbia, Puerto Rico, and 

the Virgin Islands, and including local 

agencies when so delegated by the State) 

are required to operate minimum 

numbers of EPA-approved O3 monitors 

based on the population of each of their 

Metropolitan Statistical Areas (MSA) 

and the most recently measured O3

levels in each area. Each State (or in 

some cases portions of a State) also has 

a required O3 monitoring season based 

on historical experience on when O3

levels are high enough to be of 

regulatory or public health concern. 

These requirements are contained in 40 

CFR part 58 Appendix D, Network 

Design Criteria for Ambient Air Quality 

Monitoring. See section 4.1, especially 

Tables D–2 and D–3. These 

requirements were last revised on 

October 17, 2006 as part of a 

comprehensive review of ambient 

monitoring requirements for all criteria 

pollutants (71 FR 61236). 

A. Background 

In the 2007 proposed rule for the O3

NAAQS (72 FR 37818), EPA did not 

propose specific changes to monitoring 

requirements to support the proposed 

NAAQS revisions, but instead solicited 

comment on several key matters that 

were expected to be important issues 

affecting the potential redesign of 

monitoring networks if revisions to the 

NAAQS were finalized. These matters 

included O3 monitoring requirements in 

urban areas, the potential need for 

monitoring to support multiple 

objectives important to characterization 

in non-urban areas including the 

support of the secondary O3 NAAQS, 

and the length of the required O3

monitoring seasons. Comments on these 

monitoring issues were received during 

the ensuing public comment period, and 

these comments were summarized in 

the 2008 final rule for the O3 NAAQS 

(73 FR 16501). As noted in that action, 

EPA stated its intention to propose, in 

a separate rulemaking, the specific 

changes to O3 monitoring requirements 

that were deemed necessary to support 

the revised 2008 O3 NAAQS which set 

the level of the primary 8-hour O3

standard to 0.075 ppm and set the 

secondary standard identical in all 

respects to the primary standard. EPA 

published these proposed changes to O3

monitoring requirements in a proposal 

dated July 16, 2009, Ambient Ozone 

Monitoring Regulations: Revisions to 

Network Design Requirements (74 FR 

34525). The EPA currently plans to 

finalize these changes in a final O3

monitoring rule in 2010, either before or 

in conjunction with the final rule on the 

O3 NAAQS. 

In the following sections, the specific 

provisions of the 2009 O3 monitoring 

proposal are briefly reviewed, and then 

discussed in the context of the proposed 

revisions of the 2008 O3 NAAQS that 

have been discussed earlier in this 

notice. 

B. Urban Monitoring Requirements 

As noted earlier, current O3

monitoring requirements for urban areas 

are based on two factors: MSA 

population and the most recent 3-year 

design value concentrations within each 

MSA. There are higher minimum 

monitoring requirements for areas that 

have most recent design values greater 

than or equal to 85 percent of the 

NAAQS (i.e., design value 

concentrations that are greater than or 

equal to 85 percent of the level of the 

NAAQS), and lower requirements for 

areas that have design values less than 

85 percent of the NAAQS. These 

minimum monitoring requirements for 

O3 were revised during the 2006 

monitoring rulemaking to ensure that 

additional monitors would be required 

in areas with higher design values and 

to also ensure that these requirements 

would remain applicable through future 

NAAQS reviews and potential revisions 

of the standards. Accordingly, these 

requirements do not need to be updated 

with the revisions of the O3 NAAQS 

proposed in this action since the 85 

percent threshold will be applied to the 

standard levels that are finalized for the 

primary and secondary standards.71 For 

example, given the range of levels of the 

primary standard being proposed, the 

level of the 85 percent threshold that 

requires greater minimum monitoring 

requirements ranges from 0.051 ppm (85 

percent of 0.060 ppm) to 0.060 ppm (85 

percent of 0.070 ppm). 

EPA did propose one change to urban 

monitoring requirements in the 2009 O3

monitoring proposal. Specifically, EPA 

proposed to modify the minimum O3

monitoring requirements to require one 

monitor to be placed in MSAs of 

populations ranging from 50,000 to less 

than 350,000 in situations where there 

is no current monitor and no history of 

O3 monitoring within the previous 5 

years indicating a design value of less 

than 85 percent of the revised 

NAAQS.72 Since this proposed change 

to minimum requirements is also 

subject to the 85 percent threshold, EPA 

believes that the proposed change 

remains appropriate to support the 

revisions to the primary and secondary 

O3 NAAQS proposed in this action. 

C. Non-Urban Monitoring Requirements 

In the 2007 proposed rule for the O3

NAAQS, EPA solicited comment on the 

status of monitoring requirements for 

non-urban areas, specifically whether 

non-urban areas with sensitive 

vegetation that are only currently 

sparsely monitored for O3 could 

experience undetected violations of the 

secondary NAAQS as a result of 

transport from urban areas with high 

precursor emissions and/or O3

concentrations or from formation of 

additional O3 from precursors emitted 

from sources outside urban areas. 

Comments that were received in 

response to the 2009 O3 NAAQS 

monitoring proposal noted the 

voluntary nature of most non-urban O3

monitoring and the resulting relative 

lack of non-urban O3 monitors in some 

areas. These commenters stated that 

EPA should consider adding monitoring 

requirements to support the secondary 

NAAQS by requiring O3 monitors in 

locations that contain O3-sensitive 

plants or ecosystems. These commenters 

also noted that the placement of current 

O3 monitors may not be appropriate for 

evaluating issues such as vegetation 

exposure since many of these monitors 

were likely located to meet other 

objectives. 

Based on these comments as well as 

analyses of O3 concentrations from 

discretionary non-urban monitors 

located across the U.S, EPA included 

new proposed non-urban O3 monitoring 

requirements in the 2009 O3 monitoring 

proposal. These proposed requirements 

are intended to satisfy several important 

objectives including: (1) Better 

characterization of O3 concentrations to 

which O3-sensitive vegetation and 


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73 Defined as areas having at least one urban 

cluster of at least 10,000 but less than a population 

of 50,000. 

ecosystems are exposed in rural/remote 

areas to ensure that potential secondary 

NAAQS violations are measured; (2) 

assessment of O3 concentrations in 

smaller communities located outside of 

the larger urban MSAs covered by urban 

monitoring requirements; and (3) the 

assessment of the location and severity 

of maximum O3 concentrations that 

occur in non-urban areas and may be 

attributable to upwind urban sources. 

For reasons noted below, EPA believes 

that these proposed O3 monitoring 

requirements are sufficient to support 

the revisions to the O3 NAAQS 

proposed in this action. 

With regard to the first objective, we 

note uncertainties will remain about the 

O3 concentrations to which sensitive 

natural vegetation and ecosystems are 

exposed until additional monitors are 

sited in National Parks, State and/or 

tribal areas, wilderness areas, and other 

similar locations with sensitive 

ecosystems that are set aside to provide 

similar public welfare benefits. These 

monitors would support evaluation of 

the secondary NAAQS with a more 

robust data set than is now available. As 

noted in the 2009 O3 monitoring 

proposal, EPA proposed that States 

operate at least one monitor to be 

located in areas such as some Federal, 

State, Tribal, or private lands, including 

wilderness areas that have O3-sensitive 

natural vegetation and/or ecosystems. If 

EPA finalizes a cumulative, seasonal 

secondary standard at the lower end of 

the proposed range, then it is plausible 

that additional O3 monitors, above the 

number required by the monitoring 

proposal, may be needed in such areas 

to provide adequate coverage of 

locations likely to experience violations 

of the revised secondary NAAQS. These 

additional monitors could be 

established through discretionary State 

initiatives to supplement minimum 

monitoring requirements, negotiated 

agreements between States and EPA 

Regional Administrators, or through a 

future rulemaking that addresses 

potential increased O3 monitoring 

requirements to specifically address the 

need for additional monitoring to ensure 

detection of secondary standard 

violations. 

With regard to the second objective of 

characterizing elevated ambient O3

levels to which people are exposed in 

smaller communities located outside of 

the larger urban MSAs, the likelihood of 

measuring concentrations that approach 

or exceed the levels of the NAAQS due 

to the transport of O3 from upwind areas 

and/or the formation of O3 due to 

precursor emissions from industrial 

sources outside of urban areas is clearly 

increased due to the revised NAAQS 

proposed in this action. Given that the 

analyses described in the 2009 O3

monitoring proposal demonstrated that 

50 percent of existing monitors located 

in such Micropolitan Statistical Areas 73

exceeded the current NAAQS and 

nearly all monitors recorded design 

values greater than or equal to 85 

percent of the current NAAQS, the 

potential for violations in such areas can 

only be increased with the NAAQS 

revisions proposed in this action. As 

noted for the first non-urban monitoring 

objective, it is plausible that additional 

O3 monitors, above the number required 

by the 2009 monitoring proposal may be 

needed in Micropolitan Statistical Areas 

to provide adequate coverage of 

locations likely to experience violations 

of the proposed lower primary NAAQS 

levels. These additional monitors could 

be established through discretionary 

State initiatives to supplement 

minimum monitoring requirements, 

negotiated requirements between States 

and EPA Regional Administrators, or 

through a future rulemaking that 

addresses potential increased O3

monitoring requirements to specifically 

address the need for additional 

monitoring to ensure detection of 

primary standard violations in smaller 

communities. 

The third proposed non-urban 

monitoring objective, requiring O3

monitors to be located in the area of 

expected maximum O3 concentration 

outside of any MSA, potentially 

including the far downwind transport 

zones of currently well-monitored urban 

areas, is not directly related to the level 

of the O3 NAAQS. It is instead intended 

to ensure that all parts of a State meet 

the NAAQS and that all necessary 

emission control strategies have been 

included in State Implementation Plans. 

Accordingly, this proposed monitoring 

objective remains applicable 

independent of revisions to the O3

NAAQS proposed in this action. 

D. Revisions to the Length of the 

Required O3 Monitoring Seasons 

Ozone monitoring is only required 

during the seasons of the year that are 

conducive to O3 formation. These 

seasons vary in length as the conditions 

that determine the likely O3 formation 

(i.e., seasonally-dependent factors such 

as ambient temperature, strength of 

solar insolation, and length of day) 

differ by location. In some locations, 

conditions conducive to O3 formation 

are limited to a few summer months of 

the year while in other locations these 

conditions occur year-round. As a 

result, the length of currently required 

O3 monitoring seasons can vary from a 

length of 4 months in colder climates to 

a length of 12 months in warmer 

climates. 

The 2009 O3 monitoring proposal also 

addressed the issue of whether in some 

areas the required O3 monitoring season 

should be made longer. The proposal 

also addressed the status of any 

currently effective Regional 

Administrator-granted waiver approvals 

to O3 monitoring seasons, and the 

impact of proposed changes to 

monitoring requirements on such 

waiver approvals. 

The EPA performed several analyses 

in support of proposed changes to the 

required O3 monitoring seasons. The 

first analysis determined the number of 

observed exceedances of the 0.075 ppm 

level of the current 8-hour NAAQS in 

the months falling outside the currently 

required local O3 monitoring season 

using monitors in areas that collected O3

data year-round in 2004–2006. The 

second analysis examined observed 

occurrences of daily maximum 8-hour 

O3 averages of at least 0.060 ppm. This 

threshold was chosen because it 

represented 80 percent of the current 

0.075 ppm NAAQS level and provides 

an indicator of ambient conditions that 

may be conducive to the formation of O3

concentrations that approach or exceed 

the NAAQS. While proposals for 

revising each State’s required 

monitoring season were based on 

observed data in and surrounding each 

State, statistically predicted 

exceedances were also used to validate 

conclusions for each State. 

The aforementioned analyses 

provided several results. The analysis of 

observed exceedances of the 0.075 ppm 

level of the current O3 NAAQS 

indicated occurrences in eight States 

during months outside of the current 

required monitoring season. The eight 

States were Maine, Massachusetts, New 

Hampshire, New Jersey, New York, 

South Carolina, Vermont, and 

Wyoming. With the exception of 

Wyoming, these exceedances occurred 

in a very limited manner and timeframe, 

just before the beginning of these States’ 

required O3 monitoring season 

(beginning in these States on April 1). 

The frequency of observed occurrences 

of maximum 8-hour average O3 levels of 

at least 0.060 ppm was quite high across 

the country in months outside of the 

current required monitoring season. A 

total of 32 States experienced such 

occurrences; 22 States had such levels 

only before the required monitoring 

season; 9 States had such levels both 

before and after the required monitoring 


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season; and 1 State had such levels only 

after the required monitoring season. In 

a number of cases, the frequency of such 

ambient concentrations was high, with 

some States experiencing between 31 to 

46 out-of-season days during 2004 to 

2006 at a high percentage of all 

operating year-round O3 monitors. 

Based on these analyses, EPA 

proposed a lengthening of the O3

monitoring season requirements in 

many areas. The 2009 proposed changes 

were based not only on the goal of 

monitoring out-of-season O3 NAAQS 

violations but also on the goal of 

ensuring monitoring when ambient O3

levels reach 80 percent of the NAAQS 

so that persons unusually sensitive to 

O3 would be alerted to potential 

NAAQS exceedances. 

The EPA believes that the factors used 

to support the 2009 proposed changes to 

O3 monitoring seasons are appropriate 

to support the revisions of the O3

NAAQS proposed in this action. With 

regard to the primary standard, we note 

that the lower end of the range being 

proposed is an 8-hour level of 0.060 

ppm, which is identical to the ambient 

O3 level that was utilized in one of the 

analyses discussed above. Although that 

level was chosen to provide an indicator 

of ambient levels that were below but 

approaching the level of the NAAQS 

and hence to serve as an alert to 

potential exceedances, we note that 

EPA’s traditional practice had been to 

base the length of required O3

monitoring seasons on the likelihood of 

measuring exceedances of the level of 

the NAAQS. Therefore, if EPA finalizes 

the level of the primary standard at the 

lower end of the proposed range, the O3

monitoring seasons that have been 

proposed as part of the 2009 O3

monitoring proposal would provide 

sufficient monitoring coverage to ensure 

the goal of measuring potential 

violations of the primary standard. 

One O3 monitoring season issue that 

was not considered in the 2009 O3

monitoring proposal was the question of 

whether analyses of ambient data based 

on 8-hour average statistics would also 

indicate whether the resulting proposed 

monitoring seasons would capture the 

cumulative maximum consecutive 3- 

month O3 levels necessary to compute 

design values based on the secondary 

NAAQS proposed in this action, which 

is defined in terms of a W126 

cumulative peak-weighted index, as 

discussed above in section IV. If areas 

experienced high cumulative index 

values during months outside of the 

required O3 monitoring seasons (based 

on 8-hour statistics), then further 

revisions to the required monitoring 

seasons might be necessary to ensure 

monitoring during all months important 

to the calculation of design values for 

the revised form proposed for the 

secondary NAAQS. A related issue is 

whether such high cumulative O3 values 

also occurred during time periods that 

are biologically relevant for O3-sensitive 

vegetation. 

The EPA is not proposing additional 

revisions to O3 monitoring seasons at 

this time. Additional analyses of the 

distribution of elevated cumulative 

W126 index values will be conducted, 

and the biologically relevant seasonal 

issue will be further reviewed. Based on 

the results of these analyses, EPA may 

consider proposing further revisions to 

the O3 monitoring season as related to 

the secondary O3 NAAQS. 

VII. Implementation of Proposed O3

Standards 

A. Designations 

After EPA establishes or revises a 

NAAQS, the CAA directs EPA and the 

states to take steps to ensure that the 

new or revised NAAQS are met. The 

first step is to identify areas of the 

country that do not meet the new or 

revised NAAQS. This step is known as 

the initial area designations. 

The CAA provides that, ‘‘By such date 

as the Administrator may reasonably 

require, but not later than 1 year after 

promulgation of a new or revised 

national ambient air quality standard for 

any pollutant under section 109, the 

Governor of each state shall * * * 

submit to the Administrator a list of all 

areas (or portions thereof) in the state’’ 

that designates those areas as 

nonattainment, attainment, or 

unclassifiable. The CAA specifies that, 

‘‘The Administrator may not require the 

Governor to submit the required list 

sooner than 120 days after promulgating 

a new or revised national ambient air 

quality standard.’’ The CAA defines an 

area as nonattainment if it is violating 

the NAAQS or if it is contributing to a 

violation in a nearby area. (See CAA 

section 107(d)(1).) 

The CAA further provides, ‘‘Upon 

promulgation or revision of a national 

ambient air quality standard, the 

Administrator shall promulgate the 

designations of all areas (or portions 

thereof) * * * as expeditiously as 

practicable, but in no case later than 2 

years from the date of promulgation of 

the new or revised national ambient air 

quality standard. Such period may be 

extended for up to one year in the event 

the Administrator has insufficient 

information to promulgate the 

designations.’’ EPA is required to notify 

states of any intended modifications to 

their recommendations that EPA may 

deem necessary no later than 120 days 

prior to promulgating designations. 

States then have an opportunity to 

demonstrate why any such proposed 

modification is inappropriate. Whether 

or not a state provides a 

recommendation, EPA must promulgate 

the designation that the Agency deems 

appropriate. (See CAA section 

107(d)(1)(B).) 

On September 16, 2009, when the 

Administrator announced her decision 

to reconsider the 2008 O3 NAAQS, she 

also indicated that the Agency would 

work with states to accelerate 

implementation of the standards 

adopted after reconsideration, including 

the initial area designations process. 

Acceleration of designations for the 

primary standard would help limit any 

delays in health protections associated 

with the reconsideration of the 

standards. If a secondary standard 

different from the primary standard is 

adopted, this would be the first time 

different primary and secondary 

standards would be in place for the O3

standards. While welfare protection is 

also important, for the reasons provided 

below, we are providing alternative 

schedules for designating areas for the 

secondary standard. 

If, as a result of the reconsideration, 

EPA determines that the record supports 

a primary standard different from that 

promulgated in 2008 and promulgates 

such different primary O3 NAAQS in 

2010, EPA intends to promulgate final 

designations on an accelerated schedule 

to allow the designations to be effective 

in 1 year. In order to meet such a 

schedule, EPA is proposing that the 

deadline for states to submit their 

designations recommendations for the 

revised 2010 primary standard be 129 

days after promulgation of that primary 

standard. EPA recognizes that the 

proposed deadline would be an 

ambitious schedule. Therefore, EPA 

intends to provide technical information 

and guidance for states as early as 

possible to facilitate the development of 

their recommendations. Many of the 

areas that would be violating the 

proposed primary ozone standard are 

also violating the 2008 ozone standards. 

State Governors have provided 

recommendations on these areas 

pursuant to the 2008 standards and 

recommendations may not need much 

further evaluation. 

Based on this proposed schedule, if 

EPA promulgates a new primary 

standard on August 31, 2010, state 

Governors would need to submit their 

initial designation recommendations to 

EPA by January 7, 2011. If the 

Administrator intends to modify any 

state recommendation, EPA would 


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notify the Governor no later than March 

2011, 120 days prior to promulgating 

the final designations. States would 

then have an opportunity to comment 

on EPA’s intended designations before 

EPA promulgates the final designations. 

EPA would promulgate the final 

designations in July 2011 to allow 

sufficient time for the designations to be 

published and effective by August 31, 

2011. EPA expects to base the final 

designations for the primary O3

standard on three consecutive years of 

certified air quality monitoring data 

from the years 2007–2009 or from 2008– 

2010, if available. 

If, as a result of the reconsideration, 

EPA promulgates a distinct secondary 

standard that differs from that 

promulgated in 2008 and also differs 

from the 2010 primary standard, as 

proposed above, EPA is proposing two 

alternative deadlines for states to submit 

their designations recommendations. 

Under the first alternative, EPA would 

designate areas for the secondary 

standard on the same accelerated 

schedule discussed above for the 

primary standard. In order to meet that 

schedule, EPA is proposing that states 

submit their recommendations for the 

revised 2010 secondary standard 129 

days after promulgation of that 

secondary standard. Accordingly, if EPA 

promulgates the new secondary 

standard on August 31, 2010, state 

Governors would need to submit their 

initial designation recommendations to 

EPA by January 7, 2011. 

Weighing in favor of designating areas 

for the secondary standard at the same 

time as designations for the primary 

standard is that planning for both 

standards would occur on the same 

schedule. Our examination of current 

air quality data from the existing 

monitoring network indicates that for 

levels of the primary and secondary 

standards proposed in this action, it is 

likely that the vast majority of areas 

violating the secondary standard would 

overlap with areas violating the primary 

standard. In this case, implementing 

requirements for the primary and 

secondary standards on different 

schedules could present resource 

challenges to state and local agencies by 

requiring duplication of effort and 

hindering consideration of all factors 

when deciding which control strategies 

to adopt for each standard. For example, 

if designations for the secondary 

standard were delayed by a certain 

period (e.g., a year) beyond the 

designations for the primary standard, 

then EPA would likely delay 

submission of attainment SIPs for the 

secondary standard for a similar period 

beyond the proposed date for 

submission of the attainment SIPs for 

the primary standard. In this case, the 

initial transportation conformity 

determination for the secondary 

standard would be required later than 

the initial determination for the primary 

standard by the difference in time 

between the effective dates of the two 

designations. 

Under the second alternative, EPA 

would designate areas for the secondary 

standard on the maximum 2-year 

schedule provided under the CAA. To 

meet that 2-year schedule, EPA is 

proposing that states submit their 

recommendations for the revised 

secondary standard no later than 1 year 

after promulgation of the 2010 

secondary standard. Accordingly, if EPA 

promulgates a secondary standard on 

August 31, 2010, that differs from the 

primary standard, as proposed, under 

the alternative 2-year designations 

schedule, state Governors would need to 

submit their initial designation 

recommendations to EPA by August 31, 

2011. If the Administrator intends to 

modify any state recommendation, EPA 

would notify the Governor no later than 

May 2012, 120 days prior to the 2-year 

deadline for promulgating the final 

designations. States would then have an 

opportunity to comment on EPA’s 

intended designations before EPA 

promulgates the final designations. EPA 

would promulgate the final designations 

for the secondary standard by August 

31, 2012. EPA expects to base the final 

designations in August 2012 for a 

different secondary standard on the 

most recent three consecutive years of 

certified air quality monitoring data, 

which would be from the years 2009– 

2011. 

In the past, EPA has always set the 

secondary O3 standard to be identical to 

the primary O3 standard and the 

standards have embodied relatively 

short-term average concentrations (e.g., 

1-hour or 8-hour). In this action, EPA is 

proposing a cumulative, seasonal 

secondary standard that differs from the 

proposed primary standard. EPA has not 

previously set a seasonal secondary 

standard for O3. Therefore, EPA and 

states do not have experience in 

implementing this type of secondary O3

standard or in determining what area 

boundaries would be appropriate. As we 

further explore implementation 

considerations for the secondary 

standard, we may encounter 

unanticipated issues that may require 

additional time to address. Thus, EPA is 

considering whether an accelerated 

schedule for a seasonal secondary 

standard would provide adequate time 

for resolving issues that we cannot now 

anticipate. If EPA designates areas for 

the secondary standard on a 2-year 

schedule, we note that we expect that 

accelerated implementation of the 

health-based primary standard would 

also result in accelerated welfare 

benefits. EPA requests comment on 

factors affecting the efficient and 

effective implementation of a secondary 

standard that differs from the primary 

standard in the context of establishing 

designations schedules. 

EPA notes, as discussed in greater 

detail above in section VI, that it has 

proposed a monitoring rule that would 

increase the density of monitoring in 

National Parks and other non-urban and 

lesser populated areas (July 16, 2009; 74 

FR 34525). The proposed requirements 

are intended to satisfy several important 

objectives, including better 

characterization of O3 exposures to O3- 

sensitive vegetation and ecosystems in 

rural/remote areas to ensure that 

potential secondary NAAQS violations 

are measured. As proposed, the new 

monitors would not be deployed until 

2012 or 2013. Therefore, data from these 

monitors would not be available for use 

within the statutory timeframe for EPA 

to complete designations for a 2010 

secondary standard regardless of which 

schedule EPA follows. 

While CAA section 107 specifically 

addresses states, EPA intends to follow 

the same process for tribes to the extent 

practicable, pursuant to section 301(d) 

of the CAA regarding tribal authority, 

and the Tribal Authority Rule (63 FR 

7254; February 12, 1998). 

In a separate notice elsewhere in 

today’s Federal Register, EPA is 

announcing that it is using its authority 

under the CAA to extend by 1 year the 

deadline for promulgating initial area 

designations for the O3 NAAQS that 

were promulgated in March 2008. The 

new deadline is March 12, 2011. That 

notice explains the basis for the 

deadline extension. As mentioned 

above, on September 16, 2009, EPA 

notified the Court of its decision to 

initiate a rulemaking to reconsider the 

primary and secondary O3 NAAQS set 

in March 2008 to ensure they satisfy the 

requirements of the CAA. In its notice 

to the Court, EPA stated that the final 

rule would be signed by August 31, 

2010. Extending the deadline for 

promulgating designations for the 2008 

O3 NAAQS until March 12, 2011 will 

allow EPA to complete the 

reconsideration rulemaking for the 2008 

O3 NAAQS before determining whether 

it is necessary to finalize designations 

for those NAAQS or, instead, whether it 

is necessary to begin the designation 

process for different NAAQS 

promulgated pursuant to the 

reconsideration. 


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B. State Implementation Plans 

The CAA section 110 provides the 

general requirements for SIPs. Within 3 

years after the promulgation of new or 

revised NAAQS (or such shorter period 

as the Administrator may prescribe) 

each State must adopt and submit 

‘‘infrastructure’’ SIPs to EPA to address 

the requirements of section 110(a)(1). 

Thus, States should submit these SIPs 

no later than August 21, 2013, three 

years after promulgation of the 

reconsidered ozone standard in 2010. 

These ‘‘infrastructure SIPs’’ provide 

assurances of State resources and 

authorities, and establish the basic State 

programs, to implement, maintain, and 

enforce new or revised standards. 

In addition to the infrastructure SIPs, 

which apply to all States, CAA title I, 

part D outlines the State requirements 

for achieving clean air in designated 

nonattainment areas. These 

requirements include timelines for 

when designated nonattainment areas 

must attain the standards, deadlines for 

developing SIPs that demonstrate how 

the State will ensure attainment of the 

standards, and specific emissions 

control requirements. EPA plans to 

address how these requirements, such 

as attainment demonstrations and 

attainment dates, reasonable further 

progress, new source review, 

conformity, and other implementation 

requirements, apply to the O3 NAAQS 

promulgated pursuant to the 

reconsideration in a subsequent 

rulemaking. Also in that rulemaking 

EPA will establish deadlines for 

submission of nonattainment area SIPs 

but anticipates that the deadlines will 

be no later than the end of December 

2013, or 28 months after final 

designations. 

C. Trans-Boundary Emissions 

Cross border O3 contributions from 

within North America (Canada and 

Mexico) entering the U.S. are generally 

thought to be small. Section 179B of the 

Clean Air Act allows designated 

nonattainment areas to petition EPA to 

consider whether such a locality might 

have met a clean air standard ‘‘but for’’ 

cross border contributions. To date, few 

areas have petitioned EPA under this 

authority. The impact of foreign 

emissions on domestic air quality in the 

United States is a challenging and 

complex problem to assess. EPA is 

engaged in a number of activities to 

improve our understanding of 

international transport. As work 

progresses on these activities, EPA will 

be able to better address the 

uncertainties associated with transboundary flows of air pollution and 

their impacts. 

VIII. Statutory and Executive Order 

Reviews 

A. Executive Order 12866: Regulatory 

Planning and Review 

Under section 3(f)(1) of Executive 

Order (EO) 12866 (58 FR 51735, October 

4, 1993), the O3 NAAQS action is an 

‘‘economically significant regulatory 

action’’ because it is likely to have an 

annual effect on the economy of $100 

million or more. Accordingly, EPA 

submitted this action to the Office of 

Management and Budget (OMB) for 

review under EO 12866 and any 

changes made in response to OMB 

recommendations have been 

documented in the docket for this 

action. In addition, EPA prepared this 

regulatory impact analysis (RIA) of the 

potential costs and benefits associated 

with this action. This analysis is 

contained in the Regulatory Impact 

Analysis for the Ozone NAAQS 

Reconsideration, October 2009 

(henceforth, ‘‘RIA’’). A copy of the 

analysis is available in the RIA docket 

(EPA–HQ–OAR–2007–0225) and the 

analysis is briefly summarized here. The 

RIA estimates the costs and monetized 

human health and welfare benefits of 

attaining five alternative O3 NAAQS 

nationwide. Specifically, the RIA 

examines the alternatives of 0.079 ppm, 

0.075 ppm, 0.070 ppm, 0.065 ppm, and 

0.060 ppm. The RIA contains 

illustrative analyses that consider a 

limited number of emissions control 

scenarios that States and Regional 

Planning Organizations might 

implement to achieve these alternative 

O3 NAAQS. However, the Clean Air Act 

(CAA) and judicial decisions make clear 

that the economic and technical 

feasibility of attaining ambient 

standards are not to be considered in 

setting or revising NAAQS, although 

such factors may be considered in the 

development of State plans to 

implement the standards. Accordingly, 

although an RIA has been prepared, the 

results of the RIA have not been 

considered in issuing this proposed 

rule. 

B. Paperwork Reduction Act 

This action does not impose an 

information collection burden under the 

provisions of the Paperwork Reduction 

Act, 44 U.S.C. 3501 et seq. There are no 

information collection requirements 

directly associated with the 

establishment of a NAAQS under 

section 109 of the CAA. 

Burden means the total time, effort, or 

financial resources expended by persons 

to generate, maintain, retain, or disclose 

or provide information to or for a 

Federal agency. This includes the time 

needed to review instructions; develop, 

acquire, install, and utilize technology 

and systems for the purposes of 

collecting, validating, and verifying 

information, processing and 

maintaining information, and disclosing 

and providing information; adjust the 

existing ways to comply with any 

previously applicable instructions and 

requirements; train personnel to be able 

to respond to a collection of 

information; search data sources; 

complete and review the collection of 

information; and transmit or otherwise 

disclose the information. 

An agency may not conduct or 

sponsor, and a person is not required to 

respond to a collection of information 

unless it displays a currently valid OMB 

control number. The OMB control 

numbers for EPA’s regulations in 40 

CFR are listed in 40 CFR part 9. 

C. Regulatory Flexibility Act 

The Regulatory Flexibility Act (RFA) 

generally requires an agency to prepare 

a regulatory flexibility analysis of any 

rule subject to notice and comment 

rulemaking requirements under the 

Administrative Procedure Act or any 

other statute unless the agency certifies 

that the rule will not have a significant 

economic impact on a substantial 

number of small entities. Small entities 

include small businesses, small 

organizations, and small governmental 

jurisdictions. 

For purposes of assessing the impacts 

of today’s proposed rule on small 

entities, small entity is defined as: (1) A 

small business that is a small industrial 

entity as defined by the Small Business 

Administration’s (SBA) regulations at 13 

CFR 121.201; (2) a small governmental 

jurisdiction that is a government of a 

city, county, town, school district or 

special district with a population of less 

than 50,000; and (3) a small 

organization that is any not-for-profit 

enterprise which is independently 

owned and operated and is not 

dominant in its field. 

After considering the economic 

impacts of today’s proposed rule on 

small entities, I certify that this action 

will not have a significant economic 

impact on a substantial number of small 

entities. This proposed rule will not 

impose any requirements on small 

entities. Rather, this rule establishes 

national standards for allowable 

concentrations of O3 in ambient air as 

required by section 109 of the CAA. See 

also American Trucking Associations v. 

EPA. 175 F. 3d at 1044–45 (NAAQS do 

not have significant impacts upon small 


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entities because NAAQS themselves 

impose no regulations upon small 

entities). We continue to be interested in 

the potential impacts of the proposed 

rule on small entities and welcome 

comments on issues related to such 

impacts 

D. Unfunded Mandates Reform Act 

Title II of the Unfunded Mandates 

Reform Act of 1995 (UMRA), Public 

Law 104–4, establishes requirements for 

Federal agencies to assess the effects of 

their regulatory actions on State, local, 

and Tribal governments and the private 

sector. Under section 202 of the UMRA, 

EPA generally must prepare a written 

statement, including a cost-benefit 

analysis, for proposed and final rules 

with ‘‘Federal mandates’’ that may result 

in expenditures to State, local, and 

Tribal governments, in the aggregate, or 

to the private sector, of $100 million or 

more in any 1 year. Before promulgating 

an EPA rule for which a written 

statement is needed, section 205 of the 

UMRA generally requires EPA to 

identify and consider a reasonable 

number of regulatory alternatives and to 

adopt the least costly, most costeffective or least burdensome alternative 

that achieves the objectives of the rule. 

The provisions of section 205 do not 

apply when they are inconsistent with 

applicable law. Moreover, section 205 

allows EPA to adopt an alternative other 

than the least costly, most cost-effective 

or least burdensome alternative if the 

Administrator publishes with the final 

rule an explanation why that alternative 

was not adopted. Before EPA establishes 

any regulatory requirements that may 

significantly or uniquely affect small 

governments, including Tribal 

governments, it must have developed 

under section 203 of the UMRA a small 

government agency plan. The plan must 

provide for notifying potentially 

affected small governments, enabling 

officials of affected small governments 

to have meaningful and timely input in 

the development of EPA regulatory 

proposals with significant Federal 

intergovernmental mandates, and 

informing, educating, and advising 

small governments on compliance with 

the regulatory requirements. 

Today’s proposed rule contains no 

Federal mandates (under the regulatory 

provisions of Title II of the UMRA) for 

State, local, or Tribal governments or 

the private sector. The proposed rule 

imposes no new expenditure or 

enforceable duty on any State, local or 

Tribal governments or the private sector, 

and EPA has determined that this 

proposed rule contains no regulatory 

requirements that might significantly or 

uniquely affect small governments. 

Furthermore, as indicated previously, in 

setting a NAAQS EPA cannot consider 

the economic or technological feasibility 

of attaining ambient air quality 

standards, although such factors may be 

considered to a degree in the 

development of State plans to 

implement the standards. See also 

American Trucking Associations v. 

EPA, 175 F. 3d at 1043 (noting that 

because EPA is precluded from 

considering costs of implementation in 

establishing NAAQS, preparation of a 

Regulatory Impact Analysis pursuant to 

the Unfunded Mandates Reform Act 

would not furnish any information 

which the court could consider in 

reviewing the NAAQS). Accordingly, 

EPA has determined that the provisions 

of sections 202, 203, and 205 of the 

UMRA do not apply to this proposed 

decision. The EPA acknowledges, 

however, that any corresponding 

revisions to associated SIP requirements 

and air quality surveillance 

requirements, 40 CFR part 51 and 40 

CFR part 58, respectively, might result 

in such effects. Accordingly, EPA will 

address, as appropriate, unfunded 

mandates if and when it proposes any 

revisions to 40 CFR parts 51 or 58. 

E. Executive Order 13132: Federalism 

Executive Order 13132, entitled 

‘‘Federalism’’ (64 FR 43255, August 10, 

1999), requires EPA to develop an 

accountable process to ensure 

‘‘meaningful and timely input by State 

and local officials in the development of 

regulatory policies that have federalism 

implications.’’ ‘‘Policies that have 

federalism implications’’ is defined in 

the Executive Order to include 

regulations that have ‘‘substantial direct 

effects on the States, on the relationship 

between the national government and 

the States, or on the distribution of 

power and responsibilities among the 

various levels of government.’’ 

This proposed rule does not have 

federalism implications. It will not have 

substantial direct effects on the States, 

on the relationship between the national 

government and the States, or on the 

distribution of power and 

responsibilities among the various 

levels of government, as specified in 

Executive Order 13132. The rule does 

not alter the relationship between the 

Federal government and the States 

regarding the establishment and 

implementation of air quality 

improvement programs as codified in 

the CAA. Under section 109 of the CAA, 

EPA is mandated to establish NAAQS; 

however, CAA section 116 preserves the 

rights of States to establish more 

stringent requirements if deemed 

necessary by a State. Furthermore, this 

proposed rule does not impact CAA 

section 107 which establishes that the 

States have primary responsibility for 

implementation of the NAAQS. Finally, 

as noted in section E (above) on UMRA, 

this rule does not impose significant 

costs on State, local, or Tribal 

governments or the private sector. Thus, 

Executive Order 13132 does not apply 

to this rule. 

However, as also noted in section D 

(above) on UMRA, EPA recognizes that 

States will have a substantial interest in 

this rule and any corresponding 

revisions to associated SIP requirements 

and air quality surveillance 

requirements, 40 CFR part 51 and 40 

CFR part 58, respectively. Therefore, in 

the spirit of Executive Order 13132, and 

consistent with EPA policy to promote 

communications between EPA and State 

and local governments, EPA specifically 

solicits comment on this proposed rule 

from State and local officials. 

F. Executive Order 13175: Consultation 

and Coordination With Indian Tribal 

Governments 

Executive Order 13175, entitled 

‘‘Consultation and Coordination with 

Indian Tribal Governments’’ (65 FR 

67249, November 9, 2000), requires EPA 

to develop an accountable process to 

ensure ‘‘meaningful and timely input by 

tribal officials in the development of 

regulatory policies that have tribal 

implications.’’ This rule concerns the 

establishment of O3 NAAQS. The Tribal 

Authority Rule gives Tribes the 

opportunity to develop and implement 

CAA programs such as the O3 NAAQS, 

but it leaves to the discretion of the 

Tribe whether to develop these 

programs and which programs, or 

appropriate elements of a program, they 

will adopt. 

This proposed rule does not have 

Tribal implications, as specified in 

Executive Order 13175. It does not have 

a substantial direct effect on one or 

more Indian Tribes, since Tribes are not 

obligated to adopt or implement any 

NAAQS. Thus, Executive Order 13175 

does not apply to this rule. 

Although Executive Order 13175 does 

not apply to this rule, EPA contacted 

tribal environmental professionals 

during the development of the March 

2008 rule. The EPA staff participated in 

the regularly scheduled Tribal Air call 

sponsored by the National Tribal Air 

Association during the spring of 2007 as 

the proposal was under development. 

EPA specifically solicits additional 

comment on this proposed rule from 

Tribal officials. 


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3040 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

G. Executive Order 13045: Protection of 

Children From Environmental Health 

and Safety Risks 

Executive Order 13045, ‘‘Protection of 

Children from Environmental Health 

Risks and Safety Risks’’ (62 FR 19885, 

April 23, 1997) applies to any rule that: 

(1) Is determined to be ‘‘economically 

significant’’ as defined under Executive 

Order 12866, and (2) concerns an 

environmental health or safety risk that 

EPA has reason to believe may have a 

disproportionate effect on children. If 

the regulatory action meets both criteria, 

the Agency must evaluate the 

environmental health or safety effects of 

the planned rule on children, and 

explain why the planned regulation is 

preferable to other potentially effective 

and reasonably feasible alternatives 

considered by the Agency. 

This proposed rule is subject to 

Executive Order 13045 because it is an 

economically significant regulatory 

action as defined by Executive Order 

12866, and we believe that the 

environmental health risk addressed by 

this action may have a disproportionate 

effect on children. The proposed rule 

will establish uniform national ambient 

air quality standards for O3; these 

standards are designed to protect public 

health with an adequate margin of 

safety, as required by CAA section 109. 

However, the protection offered by these 

standards may be especially important 

for children because children, especially 

children with asthma, along with other 

sensitive population subgroups such as 

all people with lung disease and people 

active outdoors, are potentially 

susceptible to health effects resulting 

from O3 exposure. Because children are 

considered a potentially susceptible 

population, we have carefully evaluated 

the environmental health effects of 

exposure to O3 pollution among 

children. Discussions of the results of 

the evaluation of the scientific evidence, 

policy considerations, and the exposure 

and risk assessments pertaining to 

children are contained in sections II.B 

and II.C of this preamble. A listing of 

the documents that contain the 

evaluation of scientific evidence, policy 

considerations, and exposure and risk 

assessments that pertain to children is 

found in the section on Children’s 

Environmental Health in the 

Supplementary Information section of 

this preamble, and a copy of all 

documents have been placed in the 

public docket for this action. The public 

is invited to submit comments or 

identify peer-reviewed studies and data 

that assess effects of early life exposure 

to O3. 

H. Executive Order 13211: Actions That 

Significantly Affect Energy Supply, 

Distribution or Use 

This proposed rule is not a 

‘‘significant energy action’’ as defined in 

Executive Order 13211, ‘‘Actions 

Concerning Regulations That 

Significantly Affect Energy Supply, 

Distribution, or Use’’ (66 FR 28355 (May 

22, 2001)) because in the Agency’s 

judgment it is not likely to have a 

significant adverse effect on the supply, 

distribution, or use of energy. The 

purpose of this rule is to establish 

revised NAAQS for O3. The rule does 

not prescribe specific pollution control 

strategies by which these ambient 

standards will be met. Such strategies 

will be developed by States on a caseby-case basis, and EPA cannot predict 

whether the control options selected by 

States will include regulations on 

energy suppliers, distributors, or users. 

Thus, EPA concludes that this rule is 

not likely to have any adverse energy 

effects and does not constitute a 

significant energy action as defined in 

Executive Order 13211. 

I. National Technology Transfer and 

Advancement Act 

Section 12(d) of the National 

Technology Transfer and Advancement 

Act of 1995 (NTTAA), Public Law 104– 

113, section 12(d) (15 U.S.C. 272 note) 

directs EPA to use voluntary consensus 

standards in its regulatory activities 

unless to do so would be inconsistent 

with applicable law or otherwise 

impractical. Voluntary consensus 

standards are technical standards (e.g., 

materials specifications, test methods, 

sampling procedures, and business 

practices) that are developed or adopted 

by voluntary consensus standards 

bodies. The NTTAA directs EPA to 

provide Congress, through OMB, 

explanations when the Agency decides 

not to use available and applicable 

voluntary consensus standards. 

This proposed rulemaking does not 

involve technical standards. Therefore, 

EPA is not considering the use of any 

voluntary consensus standards. 

J. Executive Order 12898: Federal 

Actions To Address Environmental 

Justice in Minority Populations and 

Low-Income Populations 

Executive Order 12898 (59 FR 7629 

(Feb. 16, 1994)) establishes federal 

executive policy on environmental 

justice. Its main provision directs 

federal agencies, to the greatest extent 

practicable and permitted by law, to 

make environmental justice part of their 

mission by identifying and addressing, 

as appropriate, disproportionately high 

and adverse human health or 

environmental effects of their programs, 

policies, and activities on minority 

populations and low-income 

populations in the United States. 

EPA has determined that this 

proposed rule will not have 

disproportionately high and adverse 

human health or environmental effects 

on minority or low-income populations 

because it increases the level of 

environmental protection for all affected 

populations without having any 

disproportionately high and adverse 

human health or environmental effects 

on any population, including any 

minority or low-income population. The 

proposed rule will establish uniform 

national standards for O3 air pollution. 

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Lippmann, M. (1992) A multi-year study 

of air pollution and respiratory hospital 

admissions in three New York State 

metropolitan areas: results for 1988 and 

1989 summers. J. Exposure Anal. 

Environ. Epidemiol. 2:429–450. 

Tingey, D. T.; Standley, C.; Field, R. W. 

(1976) Stress ethylene evolution: a 

measure of ozone effects on plants. 

Atmos. Environ. 10: 969–974. 

Tingey, D. T.; Taylor, G. E., Jr. (1982) 

Variation in plant response to ozone: a 

conceptual model of physiological 

events. In: Unsworth, M. H.; Ormrod, D. 

P., eds. Effects of gaseous air pollution in 

agriculture and horticulture. London, 

United Kingdom: Butterworth Scientific; 

pp. 113–138. 

Tingey, D. T.; Laurence, J. A.; Weber, J. A.; 

Greene, J.; Hogsett, W. E.; Brown, S.; Lee, 

E. H. (2001) Elevated CO2 and 

temperature alter the response of Pinus 

ponderosa to ozone: A simulation 

analysis. Ecol. Appl.11: 1412–1424. 

Tingey, D. T.; Hogsett, W. E.; Lee, E. H.; 

Laurence, J. A. (2004) Stricter ozone 

ambient air quality standard has 

beneficial effect on Ponderosa pine in 

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Touloumi, G.; Katsouyanni, K.; Zmirou, D.; 

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Bacharova, L.; Bisanti, L.; Vonk, J. M.; 

Ponka, A. (1997) Short-term effects of 

ambient oxidant exposure on mortality: 

a combined analysis within the APHEA 

project. Am. J. Epidemiol. 146: 177–185. 

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Carnevali, S.; Bartoli, M. L.; Bacci, E.; 

Dente, F. L.; Di Franco, A.; Giannini, D.; 

Paggiaro, P. L. (2002) Ozone exposure 

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3048 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

to the EPA Administrator, dated 

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(1995) Differential susceptibility to 

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115. 

List of Subjects in 40 CFR Parts 50 and 

58 

Environmental protection, Air 

pollution control, Carbon monoxide, 

Lead, Nitrogen dioxide, Ozone, 

Particulate matter, Sulfur oxides. 

Dated: January 6, 2010. 

Lisa P. Jackson, 

Administrator. 

For the reasons set forth in the 

preamble, parts 50 and 58 of chapter 1 

of title 40 of the code of Federal 

regulations are proposed to be amended 

as follows: 

PART 50—NATIONAL PRIMARY AND 

SECONDARY AMBIENT AIR QUALITY 

STANDARDS 

1. The authority citation for part 50 

continues to read as follows: 

Authority: 42 U.S.C. 7401 et seq. 

2. Section 50.15 is revised to read as 

follows: 

§ 50.15 National primary and secondary 

ambient air quality standards for ozone. 

(a) The level of the national 8-hour 

primary ambient air quality standard for 

O3 is (0.060–0.070) parts per million 

(ppm), daily maximum 8-hour average, 

measured by a reference method based 

on Appendix D to this part and 

designated in accordance with part 53 of 

this chapter or an equivalent method 

designated in accordance with part 53 of 

this chapter. 

(b) The 8-hour primary O3 ambient air 

quality standard is met at an ambient air 

quality monitoring site when the 

average of the annual fourth-highest 

daily maximum 8-hour average O3

concentration is less than or equal to 

(0.060–0.070) ppm, as determined in 

accordance with appendix P to this part. 

(c) The level of the national secondary 

ambient air quality standard for O3 is a 

cumulative index value of (7–15) ppmhours, measured by a reference method 

based on Appendix D to this part and 

designated in accordance with part 53 of 

this chapter or an equivalent method 

designated in accordance with part 53 of 

this chapter. 

(d) The secondary O3 ambient air 

quality standard is a seasonal standard 

expressed as a sum of weighted hourly 

concentrations, cumulated over the 12 

hour daylight period from 8 a.m. to 8 

p.m. local standard time, during the 

consecutive 3-month period within the 

O3 monitoring season with the 

maximum index value. The secondary 

O3 standard is met at an ambient air 

quality monitoring site when the annual 

maximum consecutive 3-month 

cumulative index value (W126) is less 

than or equal to (7–15) ppm-hours, as 

determined in accordance with 

appendix P to this part. 

3. Section 50.14 is amended by 

adding entries for primary and 

secondary ozone standards to the end of 

Table 1 in paragraph (c)(2)(vi) to read as 

follows: 

§ 50.14 Treatment of air quality monitoring 

data influenced by exceptional events. 

* * * * * 

(c) * * * 

(2) * * * 

(vi) * * * 

TABLE 1—SCHEDULE FOR EXCEPTIONAL EVENT FLAGGING AND DOCUMENTATION SUBMISSION FOR DATA TO BE USED IN

DESIGNATIONS DECISIONS FOR NEW NAAQS 

NAAQS pollutant/ 

standard/(level)/ 

promulgation date 

Air quality data 

collected for 

calendar year 

Event flagging & initial description 

deadline 

Detailed documentation submission 

deadline 

* * * * * * * 

Primary Ozone/8-Hr ................................. 2007–2009 November 1, 2010 b ................................ November 1, 2010.b

Standard (Level TBD)/promulgated by 

August 31, 2010.

2010 60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b

60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b

Secondary Ozone/(Level TBD) Alternative 2-year Schedule—to be Promulgated by August 31, 2010.2008 July 1, 2011 b ........................................... July 1, 2011.a

2009–2010 July 1, 2011 b ........................................... July 1, 2011.b

2011 60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2012, whichever occurs 

first.b

60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2012, whichever occurs 

first.b

Secondary Ozone/(Level TBD)—Alternative Accelerated Schedule—to be 

promulgated by August 31, 2010.

2007–2009 November 1, 2010 b ................................ November 1, 2010.b

2010 60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b

60 Days after the end of the calendar 

quarter in which the event occurred or 

March 1, 2011, whichever date occurs 

first.b


srobinson on DSKHWCL6B1PROD with PROPOSALS2
Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 3049 

TABLE 1—SCHEDULE FOR EXCEPTIONAL EVENT FLAGGING AND DOCUMENTATION SUBMISSION FOR DATA TO BE USED IN

DESIGNATIONS DECISIONS FOR NEW NAAQS—Continued 

NAAQS pollutant/ 

standard/(level)/ 

promulgation date 

Air quality data 

collected for 

calendar year 

Event flagging & initial description 

deadline 

Detailed documentation submission 

deadline 

* * * * * * * 

aThese dates are unchanged from those published in the original rulemaking. 

b Indicates change from general schedule in 40 CFR 50.14. 

Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final initial designations for new NAAQS. 

The general schedule applies for all other purposes, most notably, for data used by EPA for redesignations to attainment. 

4. Appendix P to part 50 is revised to 

read as follows: 

Appendix P to Part 50—Interpretation 

of the Primary and Secondary National 

Ambient Air Quality Standards for 

Ozone 

1. General 

(a) This appendix explains the data 

handling conventions and computations 

necessary for determining whether the 8-hour 

primary and secondary national ambient air 

quality standards for ozone specified in 

§ 50.15 are met at an ambient ozone air 

quality monitoring site. Ozone is measured in 

the ambient air by a reference method based 

on Appendix D of this part, as applicable, 

and designated in accordance with part 53 of 

this chapter, or by an equivalent method 

designated in accordance with part 53 of this 

chapter. Data reporting, data handling, and 

computation procedures to be used in 

making comparisons between reported ozone 

concentrations and the levels of the ozone 

standards are specified in the following 

sections. 

(b) Whether to exclude, retain, or make 

adjustments to the data affected by 

exceptional events, including stratospheric 

ozone intrusion and other natural events, is 

determined by the requirements under 

§§ 50.1, 50.14 and 51.930. 

(c) The terms used in this appendix are 

defined as follows: 

8-hour average is the rolling average of 

eight hourly ozone concentrations as 

explained in section 3 of this appendix. 

Annual fourth-highest daily maximum 

refers to the fourth-highest value measured at 

a monitoring site during a particular year. 

Annual Cumulative W126 Index is the 

maximum sum over three consecutive 

calendar months of the monthly W126 index 

in a year, as explained in section 4 of this 

appendix. 

Daily maximum 8-hour average 

concentration refers to the maximum 

calculated 8-hour average for a particular day 

as explained in section 3 of this appendix. 

Daily W126 Index is the sum of the 

sigmoidally weighted hourly ozone 

concentrations during the 12-hour daylight 

period, 8 a.m. to 7:59 p.m. local standard 

time (LST). 

Design values are the metrics (i.e., 

statistics) that are compared to the primary 

and secondary NAAQS levels to determine 

compliance, calculated as shown in sections 

3 and 4 of this appendix. 

Monthly W126 Index is the sum of the 

daily W126 index over one calendar month 

during the required ozone monitoring season, 

adjusted for incomplete data if appropriate, 

as explained in section 4 of this appendix. 

Required ozone monitoring season refers to 

the span of time within a calendar year when 

individual States are required to measure 

ambient ozone concentrations as listed in 

part 58 Appendix D to this chapter. 

Year refers to calendar year. 

2. Requirements for Data Used for 

Comparisons With the Ozone NAAQS 

(a) All valid FRM/FEM ozone data 

submitted to EPA’s Air Quality System 

(AQS), or otherwise available to EPA, 

meeting the requirements of part 58 of this 

chapter including appendices A, C, and E 

shall be used in design value calculations. 

(b) When two or more ozone monitors are 

operated at a site, the state may in advance 

designate one of them as the primary 

monitor. If the state has not made this 

designation, the Administrator will make the 

designation, either in advance or 

retrospectively. Design values will be 

developed using only the data from the 

primary monitor, if this results in a valid 

design value. If data from the primary 

monitor do not allow the development of a 

valid design value, data solely from the other 

monitor(s) will be used in turn to develop a 

valid design value, if this results in a valid 

design value. If there are three or more 

monitors, the order for such comparison of 

the other monitors will be determined by the 

Administrator. The Administrator may 

combine data from different monitors in 

different years for the purpose of developing 

a valid primary or secondary standard design 

value, if a valid design value cannot be 

developed solely with the data from a single 

monitor. However, data from two or more 

monitors in the same year at the same site 

will not be combined in an attempt to meet 

data completeness requirements, except if 

one monitor has physically replaced another 

instrument permanently, in which case the 

two instruments will be considered to be the 

same monitor, or if the state has switched the 

designation of the primary monitor from one 

instrument to another during the year. 

(c) Hourly average concentrations shall be 

reported in parts per million (ppm) to the 

third decimal place, with additional digits to 

the right of the third decimal place truncated. 

The start of each hour shall be identified in 

local standard time (LST). 

3. Comparison to the Primary Standard for 

Ozone 

(a) Computing 8-Hour Averages 

Running 8-hour averages shall be 

computed from the hourly ozone 

concentration data for each hour of the year 

and shall be stored in the first, or start, hour 

of the 8-hour period. In the event that only 

6 or 7 hourly averages are available, the valid 

8-hour average shall be computed on the 

basis of the hours available, using 6 or 7 as 

the divisor. In the event that only 1, 2, 3, 4, 

or 5 hourly averages are available, the 8-hour 

average shall be computed on the basis of 

substituting for all the hours without hourly 

averages a low hourly average value selected 

as follows, using 8 as the divisor. For days 

within the required ozone monitoring season, 

the substitution value shall be the lowest 

hourly average ozone concentration observed 

during the same hour (local standard time) of 

any day in the required ozone monitoring 

season of that year, or one-half of the method 

detection limit of the ozone instrument, 

whichever is higher. However, if the number 

of same-hour concentration values available 

for the required ozone monitoring season for 

the year, from which the lowest observed 

hourly concentration would be identified for 

purposes of this substitution, is less than 

50% of the number of days during the 

required ozone monitoring season, one-half 

the method detection limit of the ozone 

instrument shall be used in the substitution. 

For days outside the required ozone 

monitoring season, the substitution value 

shall be one-half the method detection limit 

of the ozone instrument. An 8-hour period 

with no available hourly averages does not 

have a valid 8-hour average. The computed 

8-hour average ozone concentrations are not 

rounded or truncated. 

(b) Daily Maximum 8-Hour Average 

Concentrations 

There are 24 8-hour periods in each 

calendar day. Some of these may not have 

valid 8-hour averages, under section 3(a). The 

daily maximum 8-hour concentration for a 

given calendar day is the highest of the valid 

8-hour average concentrations computed for 

that day. This process is repeated, yielding a 

daily maximum 8-hour average ozone 

concentration for each day with ambient 

ozone monitoring data, including days 

outside the required ozone monitoring season 

if data are available. The daily maximum 8- 

hour concentrations from two consecutive 

days may have some hourly concentrations 

in common. Generally, overlapping daily 

maximum 8-hour averages are not likely, 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
3050 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

except in those non-urban monitoring 

locations with less pronounced diurnal 

variation in hourly concentrations. In these 

cases, the maximum 8-hour average 

concentration from each day is used, even if 

the two averages have some hours in 

common. 

(c) Primary Standard Design Value 

The primary standard design value is the 

annual fourth-highest daily maximum 8-hour 

ozone concentration considering all days 

with monitoring data including any days 

outside the required ozone monitoring 

season, expressed in parts per million, 

averaged over three years. The 3-year average 

shall be computed using the three most 

recent, consecutive years of monitoring data 

that can yield a valid design value. For a 

design value to be valid for comparison to the 

standard, the monitoring data set on which 

it is based must meet the data completeness 

requirements described in section 3(d). The 

computed 3-year average of the annual 

fourth-highest daily maximum 8-hour 

average ozone concentrations shall be 

rounded to three decimal places. Values 

equal to or greater than 0.xxx5 ppm shall 

round up. 

(d) Data Completeness Requirements for a 

Valid Design Value 

(i) A design value greater than the standard 

is valid if in each of the three years there are 

at least four days with a daily maximum 8- 

hour average concentration. Under sections 

3(a) and 3(b), there will be a daily maximum 

8-hour average concentration on any day 

with at least one hourly concentration. One 

or more of these four days may be outside the 

required ozone monitoring season. 

(ii) A design value less than or equal to the 

standard is valid if for at least 75% of the 

days in the required ozone monitoring season 

in each of the three years there are at least 

18 8-hour averages in the day that are based 

on at least 6 measured hourly average 

concentrations. 

(iii) When computing whether the 

minimum data completeness requirement in 

section 3(d)(ii) has been met for the purpose 

of showing that a design value equal to or 

less than the standard is valid, 

meteorological or ambient data may be 

sufficient to demonstrate that ozone levels on 

days with missing data would not have 

affected the design value. At the request of 

the state, the Regional Administrator may 

consider demonstrations that meteorological 

conditions on one or more days in the 

required ozone monitoring season which do 

not have at least 18 8-hour averages in the 

day that are based on at least 6 measured 

hourly average concentrations could not have 

caused a daily maximum 8-hour 

concentration high enough to have been one 

of the four highest daily maximum 8-hour 

concentrations for the year. At the request of 

the state, days so demonstrated may be 

counted towards the 75% requirement for the 

purpose of validating the design value, 

subject to the approval of the Regional 

Administrator. 

(vi) Years that do not meet the 

completeness criteria stated in 3(d)(ii) may 

nevertheless be used to calculate a design 

value that will be deemed valid with the 

approval of, or at the initiative of, the 

Administrator, who may consider factors 

such as monitoring site closures/moves, 

monitoring diligence, the consistency and 

levels of the valid concentration 

measurements that are available, and nearby 

concentrations in determining whether to use 

such data. 

(e) Comparison With the Primary Ozone 

Standard 

(i) The primary ozone ambient air quality 

standard is met at an ambient air quality 

monitoring site when the design value is less 

than or equal to [0.075] ppm. 

(ii) Comparison with the primary ozone 

standard is demonstrated by examples 1 and 

2 as follows: 

Example 1. Ambient monitoring site 

attaining the primary ozone standard. 

Year 

Percent valid 

days (within 

the required 

monitoring 

season) 

1st Highest 

daily max 

8-hour conc. 

(ppm) 

2nd Highest 

daily max 

8-hour conc. 

(ppm) 

3rd Highest 

daily max 

8-hour conc. 

(ppm) 

4th Highest 

daily max 

8-hour conc. 

(ppm) 

5th Highest 

daily max 

8-hour conc. 

(ppm) 

2006 ....................................................... 80 0.092500 0.090375 0.085125 0 .078375 0.078125 

2007 ....................................................... 96 0.084750 0.083500 0.075375 0 .071875 0.070625 

2008 ....................................................... 98 0.080875 0.079750 0.077625 0 .075500 0.060375 

Average ........................................... ........................ ........................ ........................ ........................ 0 .075250 ........................

Rounded ......................................... ........................ ........................ ........................ ........................ 0 .075 ........................

As shown in Example 1, this monitoring 

site meets the primary ozone standard 

because the 3-year average of the annual 

fourth-highest daily maximum 8-hour 

average ozone concentrations (i.e., 0.075256 

ppm, rounded to 0.075 ppm) is less than or 

equal to [0.075] ppm. The data completeness 

requirement is also met because no single 

year has less than 75% data completeness. In 

Example 1, the individual 8-hour averages 

and the 3-year average are shown with six 

decimal digits. In actual calculations, all 

digits supported by the calculator or 

calculation software must be retained. 

Example 2. Ambient monitoring site failing 

to meet the primary ozone standard. 

Year 

Percent valid 

days (within 

the required 

monitoring 

season) 

(percent) 

1st 

Highest daily 

max 

8-hour conc. 

(ppm) 

2nd 

Highest daily 

max 

8-hour conc. 

(ppm) 

3rd 

Highest daily 

max 

8-hour conc. 

(ppm) 

4th 

Highest daily 

max 

8-hour conc. 

(ppm) 

5th 

Highest daily 

max 

8-hour conc. 

(ppm) 

2006 ....................................................... 96 0.105125 0.103500 0.101125 0 .078625 0.072375 

2007 ....................................................... 74 0.104250 0.103625 0.093000 0 .080250 0.069500 

2008 ....................................................... 98 0.103125 0.101875 0.101750 0 .075375 0.074625 

Average ........................................... ........................ ........................ ........................ ........................ 0 .078083 ........................

Rounded ......................................... ........................ ........................ ........................ ........................ 0 .078 ........................

As shown in Example 2, the data capture 

in 2007 is less than 75%. The primary ozone 

standard is not met for this monitoring site 

because the 3-year average of the fourthhighest daily maximum 8-hour average ozone 

concentrations (i.e., 0.078083 ppm, rounded 

to 0.078 ppm) is greater than [0.075] ppm and 

is therefore valid despite this 

incompleteness. In Example 2, the individual 

8-hour averages and the 3-year average are 

shown with six decimal digits. In actual 

calculations, all digits supported by the 


srobinson on DSKHWCL6B1PROD with PROPOSALS2
Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 3051 

calculator or calculation software must be 

retained. 

4. Secondary Ambient Air Quality Standard 

for Ozone 

(a) Computing the daily W126 index value. 

The secondary ozone ambient air quality 

standard is a seasonal standard expressed as 

a sum of weighted hourly concentrations, 

cumulated over the 12 hour daylight period 

from 8 a.m. to 8 p.m. local standard time, 

during the consecutive 3-month period 

within the ozone monitoring season with the 

maximum index value. The first step in 

determining whether the standard is met at 

a monitoring site is to compute the daily 

W126 index value for each day by applying 

the sigmoidal weighting function in Equation 

1 to each reported measurement of hourly 

average concentration. 

Equation 1

daily W w Cc i

i= am

i pm

i 126

8

8

=

<

∑

Where: 

Ci = hourly O3 at hour i, and 

w =

e c C

1

1 4403 126 + ⋅ −

The computed value of the sigmoidally 

weighted hourly concentration is not 

rounded or truncated. The daily W126 index 

is formed by summing the twelve computed 

hourly values, retaining all decimal places. 

An illustration of computing a daily W126 

index value is below: 

Example 3. Daily W126 index value 

calculation for an ambient ozone monitoring 

site. 

Start of hour Concentration 

(ppm) 

Weighted 

concentration 

(ppm) 

8:00 a.m. ...................................................................................................................................................... 0.045 0.002781 

9:00 a.m. ...................................................................................................................................................... 0.060 0.018218 

10:00 a.m. .................................................................................................................................................... 0.075 0.055701 

11:00 a.m. .................................................................................................................................................... 0.080 0.067537 

12:00 p.m. .................................................................................................................................................... 0.079 0.065327 

1:00 p.m. ...................................................................................................................................................... 0.082 0.071715 

2:00 p.m. ...................................................................................................................................................... 0.085 0.077394 

3:00 p.m. ...................................................................................................................................................... 0.088 0.082448 

4:00 p.m. ...................................................................................................................................................... 0.083 0.073683 

5:00 p.m. ...................................................................................................................................................... 0.081 0.069667 

6:00 p.m. ...................................................................................................................................................... 0.065 0.029260 

7:00 p.m. ...................................................................................................................................................... 0.056 0.011676 

Sum=Daily W126 index value .............................................................................................................. .............................. * 0.625406 

* ppm-hours. 

In Example 3, the individual weighted 

concentrations and their sum are shown with 

six decimal digits. In actual calculations, all 

digits supported by the calculator or 

calculation software must be retained. There 

are no data completeness requirements for 

the daily index. If fewer than 12 hourly 

values are available, only the available hours 

are weighted and summed. However, there 

are data completeness requirements for the 

monthly W126 index values and a required 

adjustment for incomplete data, as describe 

in the next section. 

(b) Computing the Monthly W126 Index 

As described in section 4(a), the daily 

index value is computed at each monitoring 

site for each calendar day in each month 

during the required ozone monitoring season 

with no rounding or truncation. The monthly 

W126 index is the sum of the daily index 

values over one calendar month. At an 

individual monitoring site, a monthly W126 

index is valid if hourly average ozone 

concentrations are available for at least 75% 

of the possible daylight hours in the month. 

For months with more than 75% but less 

than 100% data completeness, the monthly 

W126 value shall be adjusted for incomplete 

data by multiplying the unadjusted monthly 

W126 index value by the ratio of the number 

of possible reporting hours to the number of 

hours with reported ambient hourly 

concentrations using Equation 2 in this 

appendix: 

Equation 2

M.I. (D.I.) (n 12)/v

j=1

n

=

⎡

⎣

⎢

⎢

⎤

⎦

⎥

⎥ ∑ ∗ ∗

where 

M.I. = the adjusted monthly W126 index, 

D.I. = daily W126 index (i.e., the daily sum 

of the sigmoidally weighted daylight 

hourly concentrations), 

n = the number of days in the calendar 

month, 

v = the number of daylight reporting hours 

(8 a.m.–7:59 p.m. LST) in the month 

with reported valid hourly ozone 

concentrations. 

The resulting adjusted value of the 

monthly W126 index shall not be rounded or 

truncated. 

(c) Secondary Standard Design Value 

The secondary standard design value is the 

3-year average of the annual maximum 

consecutive 3-month sum of adjusted 

monthly W126 index values expressed in 

ppm-hours. Specifically, the annual W126 

index value is computed on a calendar year 

basis using the three highest, consecutive 

adjusted monthly W126 index values. The 3- 

year average shall be computed using the 

most recent, consecutive three calendar years 

of monitoring data meeting the data 

completeness requirements described in 

section 4(c). The computed 3-year average of 

the annual maximum consecutive 3-month 

sum of adjusted monthly W126 index values 

in ppm-hours shall be rounded to a whole 

number with decimal values equal to or 

greater than 0.500 rounding up. 

(c) Data Completeness Requirement 

(i) The annual W126 index is valid for 

purposes of calculating a 3-year design value 

if each full calendar month in the required 

ozone monitoring season has at least 75% 

data completeness for daylight hours. 

(ii) If one or more months during the ozone 

monitoring seasons of three successive years 

has less than 75% data completeness, the 

three years shall nevertheless be used in the 

computation of a valid design value for the 

site if substituting the lowest hourly ozone 

concentration observed during daylight hours 

in the required ozone monitoring season of 

each year, or one-half of the method 

detection limit of the ozone instrument, 

whichever is higher, for enough of the 

missing hourly concentrations within each 

incomplete month to make the month 75% 

complete, and then adjusting for the 

remaining missing data using Equation 2, 

above results in a design value greater than 

the level of the standard. 

(d) Comparisons With the Secondary Ozone 

Standard 

(i) The secondary ambient ozone air quality 

standard is met at an ambient air quality 

monitoring site when the design value is less 

than or equal to [15] ppm-hours. 

(ii) Comparison with the secondary ozone 

standard is demonstrated by example 4 as 

follows: 

Example 4. Ambient Monitoring Site 

Failing to Meet the Secondary Ozone 

Standard 


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3052 Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules 

April May June July August September October Overall 

2006 

Adjusted monthly W126 index ..................... 4.442 9.124 12.983 16.153 13.555 4.364 1.302 ..................

3-Month sum ................................................ na na 26.549 38.260 42.691 34.072 19.221 ..................

2006 Maximum ............................................ ................ ................ ................ ................ 42.691 .................. ................ 42.691 

2007 

Adjusted monthly W126 index ..................... 3.114 7.214 8.214 8.111 7.455 7.331 5.115 ..................

3-Month sum ................................................ na na 18.542 23.539 23.780 22.897 19.901 ..................

2007 Maximum ............................................ ................ ................ ................ ................ 23.780 .................. ................ 23.780 

2008 

Adjusted monthly W126 index ..................... 4.574 5.978 6.786 8.214 5.579 4.331 2.115 ..................

3-Month sum ................................................ na na 17.338 20.978 20.579 18.124 12.025 ..................

2008 Maximum ............................................ ................ ................ ................ 20.978 ................ .................. ................ 20.978 

3-Year average W126 index ........................ ................ ................ ................ ................ ................ .................. ................ 29.149666 

Rounded ............................................... ................ ................ ................ ................ ................ .................. ................ 29 

As shown in example 4, the secondary 

ozone standard is not met for this monitoring 

site because the 3-year average of the annual 

W126 index value for this site is greater than 

[15] ppm-hours: 

3-year average W126 index = (42.691 + 

23.780 + 20.978)/3 = 29.149666, which 

rounds to 29 ppm-hours. 

In Example 4, the adjusted monthly W126 

index values and the 3-month sums of the 

adjusted monthly W126 index values are 

shown with three decimal digits. In actual 

calculations, all digits supported by the 

calculator or calculation software must be 

retained. 

PART 58—AMBIENT AIR QUALITY 

SURVEILLANCE 

5. The authority citation for part 58 

continues to read as follows: 

Authority: 42 U.S.C. 7410 7403, 7410, 

7601(a), 7611, and 7619. 

6. Section 58.50 is amended by 

revising paragraph (c) and adding 

paragraph (d) to read as follows: 

§ 58.50 Index reporting. 

* * * * * 

(c) The population of a metropolitan 

statistical area for purposes of index 

reporting is the latest available U.S. 

census population. 

(d) For O3, reporting is required in 

metropolitan and micropolitan 

statistical areas wherever monitoring is 

required under Appendix D to Part 58— 

SLAMS Minimum O3 Monitoring 

Requirements. 

7. Appendix G of Part 58 is amended 

by revising section 3. to read as follows: 

Appendix G to Part 58—Uniform Air 

Quality Index (AQI) and Daily 

Reporting 

* * * * * 

3. Must I Report the AQI? 

You must report the AQI daily if yours is 

a metropolitan statistical area (MSA) with a 

population over 350,000. For O3, reporting is 

required in metropolitan and micropolitan 

statistical areas wherever monitoring is 

required under Appendix D to Part 58— 

SLAMS Minimum O3 Monitoring 

Requirements. 

* * * * * 

[FR Doc. 2010–340 Filed 1–15–10; 8:45 am] 

BILLING CODE 6560–50–P 


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