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Comments for Consideration by the CASAC Ozone Review Panel on the Reconsideration of the 

2008 NAAQS for its teleconference deliberations on February 18, 2011

Milan Hazucha, M.D., Ph.D.

Department of Medicine, School of Medicine and

Center for Environmental Medicine, Asthma, and Lung Biology

University of North Carolina

Chapel Hill, NC 27599-7310

and

Allen S. Lefohn, Ph.D.

A.S.L. & Associates, 302 North Last Chance Gulch, Suite 410

Helena, Montana 59601

asl-associates.com/

February 7, 2011

Last March 19, 2010 we submitted Comments for Consideration by the US EPA for its 

deliberations on the re-evaluation of the ozone (O3) standard entitled “Clarification to Some of 

the Scientific Issues Raised by the EPA Concerning Human Laboratory Studies”, Docket ID 

No.EPA-HQ-OAR-2005-0172.

In assessing the health effects, the proposed primary standard is based on the strength of 

evidence derived from human laboratory studies that, and as asserted by EPA, “provide data with 

the highest level of confidence” (75 FR, 2010, p.2945) because they provide human health 

effects data acquired under closely monitored conditions and can provide exposure-response 

relationships. As asserted by EPA, we fully agree that the informed judgment and conclusions 

about the health effects should be based on the nature and weight of the evidence, on biological 

plausibility, consistency, strength, and coherence of evidence. As indicated in the Federal 

Register (75 FR, 2010, p.2940), the reconsideration of the O3 standards is based on the scientific 

and technical information and analyses on which the March 2008 O3 NAAQS rulemaking was 

based. In the pages that follow, we have expressed concerns about some of the scientific issues 

summarized in the Federal Register (2010). We would also like to expand on our March 19, 2010 

comments with focus on the Charge Questions (Wegman, 2011) to be discussed at the February 

18 and March 3, 2011 CASAC teleconferences in the hope that our comments will provide more 
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accurate input into the decision making process associated with setting the level of the human 

health standard for O3.

1. Comments to Charge Question 1. 

1.1 Controlled human exposure studies.

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?

The first Charge Question on the overall strengths and limitations of the evidence from 

controlled human studies briefly summarizes the results of two Adams multi-exposure studies 

(2002, 2006) considered new for 2008 rulemaking. A point is made that these are “newly 

available in the 2008 rulemaking.... down to an exposure level of 0.060 ppm.” Actually, these 

studies discuss exposure levels down to 0.040 ppm.

A more recent study that was not available in 2008 provides some guidance on the O3 effects 

at 0.060 ppm level. It is a multi-exposure study of Schelegle et al. (2009) which reports lung 

function data effects following 6.6-hr exposure to 0.087, 0.080, 0.070, and 0.060 ppm. The 

authors used several parametric and nonparametric tests to analyze the data and found the effects 

of 0.060 exposure to be not significant from filtered air by any of the tests. All other O3 exposure 

effects were significant from filtered air. Our reanalyzes of Schelegle and colleagues (2009) data 

agreed with the authors' findings (Lefohn et al., 2010).

As reiterated in the Memorandum (Wegman, 2011), the current EPA (75 FR, 2010, p. 2950) 

approach in evaluating the “health effects” is placing the emphasis in interpretation of effects on 

the number of individuals whose FEV1 decrement at the end of exposure is greater than 10% 

(more specifically FEV1 decrements ≥ 10 % but <20%). The Memorandum (Wegman, 2011) 

states that “7 to 20% of the subjects in the Adams studies experienced lung function decrements 

(≥ 10%) at the 0.060 ppm exposure level” (75 FR, 2010, p. 2986). The 7% of the subjects 

represents 2 of 30 subjects in the Adams (2006) study population that experienced FEV1

decrements with ≥ 10% with the square-wave exposure pattern at the 0.060 ppm exposure level 
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(comparing pre- and post-exposures) when the results were adjusted for the effects of exercise 

alone in filtered air (FA). This number disagrees with data presented in Fig. 8-1B (US EPA, 

2006) showing that only 3%, i.e., 1/30 subjects in Adams (2006) study experienced ≥ 10%

decrement. Moreover, the upper range value of 20% (6/30) perpetuated throughout the EPA 

documents may apparently come from the 0.080 pm face-mask Adams (2002) study and, 

therefore, in this context is not relevant. However, it may also be possible that the 20% value (6 

of 30 subjects), although cited as Adams (2002) by the EPA, originated from his earlier study in 

1998, which was not published in the peer-reviewed literature and is neither referenced in the 

Criteria Document (US EPA, 2006) nor Federal Register (75 FR, 2010). In this face mask 

study, which according to Adams presented an “artificial burden” with minute ventilation 15% 

greater than used in his 2002 and 2006 studies and 0.060 ppm O3 concentration, FEV1 changes 

were not statistically significant. We believe that it is inappropriate for EPA to use the non-peer 

reviewed Adams’ results from his 1998 report in its rulemaking considerations.

EPA subsequently states (Wegman, 2011; 75 FR, 2010, p. 2951) that such magnitude of lung 

function decrements is of 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 a relatively few responsive individuals. 

Furthermore, CASAC indicated (75 FR, 2010, p.2973) that focus should be on the lower end of 

the range of moderate levels of functional responses for estimating potentially adverse lung 

function decrements in people with lung disease. The EPA then uses the concentration at which a 

small percentage of volunteers who responded with ≥ 10% decrement in FEV1 to extrapolate to 

an entire population (US EPA, 2007). In the opinion of Prof. Smith1,2

EPA’s approach overlooks numerous modulating/confounding factors that will impact health 

effects assessment. The use of FA is not an appropriate control exposure because the 0 ppb O3

with which we concur the 

2 out of 30 subjects “is an extremely small number of individuals from which to conclude that 

the response is significant” (Smith, 2007). Moreover, to quote: “Given the large uncertainty in 

the probability of response at 0.06 ppm ozone, I do not believe that staff paper’s conclusions on 

this point are justified” (Smith, 2007).

 1 Prof. Richard L. Smith is Director of Statistical and Applied Mathematical Sciences Institute, 

University of North Carolina–Chapel Hill, NC.

2 Member of Health Effects Institute , Health Research Committee
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“air” that is generated in the laboratory does not exist under ambient or indoor air conditions. For 

example, the FA FEV1 responses associated with the controlled human exposure experiments 

show an improvement of FEV1 (Adams, 2006). Comparing changes across corresponding time 

intervals and expressing them as "corrected values" that take into consideration the absolute 

difference between the O3 and FA responses may perhaps “artificially” enhance the magnitude of 

the O3 response. Such enhanced responses may not be necessarily observed at relevant 

background levels of hourly average O3 concentrations with the result that statistically significant 

differences using FA may not be realized using actual ambient background levels. A comparison 

to a control that represents background O3 concentrations is more appropriate.

The selection of the background O3 level to be used as a control exposure is important. The 

EPA (75 FR, 2010, p.2980) has estimated, using a model that policy-relevant background (PRB) 

O3 concentrations are in the range of 15-35 ppb. Empirical O3 data collected at an O3 monitoring 

site where PRB conditions predominate show that the O3 concentration levels are frequently ≥ 50 

ppb (Oltmans and Lefohn, 2005; Oltmans et al., 2008). The range of maximum hourly average 

concentrations for April for the period 2003 to 2010 is 54 – 65 ppb and the range of hourly 

average concentrations ≥ 50 ppb is 30 – 188 occurrences. Eurasian emissions associated with 

biomass burning and their easterly transport enhance O3 concentrations at west coast O3

monitoring sites under PRB conditions, as well as inland O3 monitoring sites in Montana, 

Wyoming, and North Dakota (Oltmans et al., 2010). Thus, the EPA's modeled estimates of 

policy-relevant background O3 concentrations in the range of 15 to 35 ppb is much lower than 

actual measured ambient values when PRB conditions predominate.

In assessing the relevance of the small number of individuals that experience moderate lung 

function decrements, important considerations that must be taken into account are: (1) lack of 

relevant background O3 control profile in laboratory studies; (2) substantial intra-individual 

variability; (3) lack of coherence between responses of some individuals to a range of O3

concentrations; (4) post hoc statistical analyses; and (5) inadequate standard-setting assessment 

when applying square-wave exposure patterns.

1.2 Questionable post-hoc statistical analyses of data.

In considering the weight of the evidence gained from the two Adams studies EPA has 

commented that although the two studies are by one investigator the studies are well designed 
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(Wegman, 2011). The 0.040 ppm exposure showed non-significant improvement of lung 

function (FEV1) in both studies. The 0.060 ppm effects in 2006 study were also found to be nonsignificant by the author. The EPA, however, has considered statistical analyses of this study to 

be “inconclusive” and did its own reanalysis finding the not significant 0.060 ppm square-wave 

exposure effects as statistically significant (Brown, 2007; Brown et al., 2008). This re-analyses 

was done “because of potential regulatory implications of the presence or absence of effects” 

(Brown et al., 2008), implicitly referring to statistical significance or non-significance of effects. 

Commenting on the EPA’s criticism of Adams (2006), Smith (2007) states that in considering 

the statistical aspect of Adams’ analysis “the evidence for a response at 0.06 ppm ozone level is 

still very uncertain”. Subsequently, Smith (2007) commented that “In my judgment, when all the 

comparisons are taken into account, there is insufficient evidence to conclude that there is any 

well-defined response to ozone exposure below the 0.08 ppm level”. Surprisingly, the effects of 

average 0.060 ppm step-wise exposures reported in the same study, which were also found not to 

be significant by the author, were not reanalyzed by EPA. 

The approach of Brown et al. (2008) is problematic. The selection of statistical method to 

analyze data is closely tied to and dependent upon study hypotheses. In all of the relevant 

Adams studies, the key interest was in hourly changes and not solely the end-exposure effects. 

Thus, Brown et al. (2008) reanalyzes of only end of exposure changes ignoring intermediate 

hourly changes is questionable. Our reanalyzes of Adams (2006) data using a statistical method 

different from both Adams (2006) and Brown (2008) found the effects of 0.040 and 0.060 ppm 

to be in agreement with Adams analyses, i.e., not significant from filtered air (Lefohn et al, 

2010). It is apparent that several statistical approaches are claimed to be appropriate for analyses 

of the same data by different investigators, even though they result in conflicting statistical 

significance of reported changes. The appropriate statistical test is the one that is in conformity 

with the study hypotheses and that would be Adams’ analyses as well as that of Lefohn et al 

(2010). To re-analyze data because the original statistical outcome did not produce desired 

results and expected “implications” of such outcome is inappropriate.
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1.3 The risk assessment based on infrequent square-wave-like exposure profile and not on 

a typical diurnal concentration pattern is troubling. 

The NAAQS (US EPA, 2006) document states that “the controlled exposure (or “clinical”) 

studies provide the clearest and most 

compelling evidence for human health 

effects directly attributable to acute 

exposures to O3 per se” (page E-9). 

Implicitly, such acute O3 exposures

mean exposures to diurnal (i.e., variable) 

concentration encountered by general 

public in ambient air.

One of the key topics discussed 

in Chapter 3 of the same document 

entitled “Environmental Concentrations, 

Patterns, and Exposure Estimates” is 

characterization of ambient O3

concentrations, particularly section 3.4 entitled “Diurnal and Seasonal variability of ozone”. 

More than 25 pages including 13 figures each with 4-6 panels show plots of a typical diurnal 

concentration pattern recorded across various US cities (US EPA, 2006). In our perusal of 

Chapter 3 we have not found any reference to a square-wave concentration profile occurring in 

the ambient atmosphere in the US. The figures and related discussion in this Chapter leave no 

doubt that the diurnal O3 profile across the US has a variable form with bell-like concentration 

pattern reaching peak in the early afternoon (see the Figure 3-12a-d). Therefore, one would 

expect that the health risk estimate would be based on real diurnal ambient atmosphere 

concentration profiles and not on an occasional occurrence of a near steady-state concentration.

Results from controlled laboratory exposures (e.g., variable concentration profile) of human 

volunteers indicate that higher O3 hourly average concentrations elicit a greater effect on hourby-hour physiologic response (i.e., FEV1) than lower hourly average values, which implies a 

nonlinear dose-response relationship (US EPA, 2006; Adams, 2006b; Hazucha and Lefohn, 

2007). Thus, identical 8-h average dose produces different responses, depending on the hour-byhour O3 concentration pattern. The current 8-h average human-health O3 standard is not adequate 
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for describing this nonlinear FEV1 hour-by-hour pattern of response. For developing a consistent 

standard to protect human health, it is important to identify those ambient-type concentration 

patterns that elicit adverse human health effects. The EPA appears to be focused on the squarewave regimes to establish the lower-level of response although it is clear that a variable pattern 

is typical of outdoor ambient conditions (US EPA, 2006, page AX6-19). Diurnal patterns 

predominate in urban, suburban, and low-elevation rural areas (US EPA, 2006). Using EPA AQS 

data for 2002, out of 28,148 8-h sequences, only 426 (1.51%) were classified as a square-wave 

ambient O3 concentration profile (Lefohn et al., 2010). Consequently, the prevalence of a 

variable O3 concentration profile in ambient air associated with greater spirometric effects should 

make the variable exposure studies “the highlights of evidence” and the key studies for standard 

setting. However, such is not the case; EPA has focused only on the 0.06 ppm square-wave 

results from Adams (2006) and possibly the 1998 non peer reviewed report by Adams that is 

cited in Adams (2002). We are concerned that by omitting data from the variable profile 

studies, the EPA has provided an inadequate assessment for the human health considerations.

2. Comments to Charge Question 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

Human O3 studies at concentration ≥ 0.08 ppm exploring changes in inflammatory variables 

show much greater intra- and inter-individual variance of measured endpoints than spirometric 

variables. At this time we do not have a sufficient number of human controlled studies exploring 

these endpoints to make a definitive statement concerning the importance of these observations 

in the standard-setting process. A recent study by Kim et al. (2011) reports on both spirometry 

and inflammatory cell changes to square-wave 0.060 ppm and perhaps may provide some 

general guidance as to the magnitude and individual variability of inflammatory endpoints 

following square-wave 0.060 exposures. However, for future rulemaking activities, we believe 

that variable/stepwise exposures and the application of realistic background O3 levels as a 

control would be required to provide specific guidance to the EPA. 

healthy adults at exposures levels from 0.060 to 0.070 ppm?
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3. Comments to Charge Question 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

EPA recognizes that the intra-individual variability of various endpoints may be substantial 

but believes that the variability tends to be reproducible (75 FR, 2010, p. 2949). Although there 

is a tendency by the investigators to interpret their findings of repeated exposures to the same 

concentration as “reproducible” since the group averages are similar and correlations between 

two separate exposures are high (i.e., for some spirometric endpoints), closer examination shows 

that for many individuals, the differences in FEV1 response may be substantial and, in some 

cases, different by as much as 40 percentage points. Hazucha et al. (2003) noted that many 

individuals, who were initially classified as weak responders, became strong responders on the 

second exposure and vice versa. Such a shift in an individual’s O3 responsiveness has a direct 

bearing on the current approach to data interpretation and usage by EPA in support of a lower O3

standard.

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

Furthermore, there is a considerable intra-individual inconsistency of response within an 

exposure period. Some individuals show no response during, for example, 6.6-h exposure, but a 

sudden decrease in FEV1 at the end of exposure. Others show an up and down response during 

exposure with a chance FEV1 decrement of ≥ 10% at the end of exposure. Other individuals may 

respond with ≥ 10 % or even 15% decrement at the first hour, but minimal or no response at the 

end. With such individual variability, the utility of using only individuals’ end exposure FEV1 

value for health assessment is questionable. These findings illustrate the large individual 

variability of response. Thus, because of the large intra-individual inconsistencies in response 

between and within exposures observed in the controlled health experiments, it is our opinion 

that the end of exposure value of an FEV1 ≥ 10% decrement may not be indicative of a 

detrimental health effect.

Adams (2006) reported no statistical significance at the 0.06 ppm level using both variable 

and square-wave profiles. Similarly, Schelegle et al. (2009) reported similar results using a

variable profile. Lefohn et al. (2010), using the data from Adams (2006) and Schelegle et al. 

(2009) and a different statistical approach, reported no statistical significance. Using almost 
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double the number of subjects as Adams (2006) and Schelegle et al. (2009), Kim et al. (2011) 

reported statistical significance using 0.06 ppm square-wave profiles. However, the resulting 

FEV1 effects were compared with FA instead of realistic ambient variable exposure pattern that 

represented background O3 concentrations. Actual PRB O3 concentrations have been reported to 

frequently occur at some monitoring sites ≥ 50 ppb (Oltmans et al., 2008; Oltmans et al., 2010). 

An important issue to consider is whether Kim et al. (2011) would have observed a statistically 

significant difference between the square-wave 0.06 ppm exposure and a control that reflected 

observed PRB O3 concentrations (i.e., concentrations ≥ 50 ppb). No evidence is currently 

available to conclude that Kim et al. (2011) would have reported a statistically significant 

difference between the enhanced treatment of 0.06 ppm and a control that represented observed 

PRB concentrations.

4. Comments to Charge Question 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

To date EPA has used only selected data (square-wave) from a few controlled human 

exposure studies that have reported on the effects of O3 at 0.060. The available database could be 

substantially enhanced if (1) the variable/stepwise concentration profile studies were included, 

and (2) the hourly responses data were considered as well. However, addition of these data to the 

database may require a modified approach to risk estimation based on a cumulative approach as 

described in Lefohn et al. (2010).

question from both a public health and a clinical perspective.

As we already pointed out in comments to Charge Question 1, Adams (2006) and Fig. 8-1B 

(US EPA, 2006) reported only 1/30 subjects (3%) showing FEV1 decrement ≥ 10% following 

exposure to 0.060 ppm O3. This becomes 7% (2/30) when adjusted for filtered air response by 

EPA (Brown et al., 2008), which we do not necessarily consider appropriate because of 

enhancements at FA, which is not a relevant background O3 concentration.The upper limit of 

20% is misleading because it is either based on the 0.080 ppm results of face-mask exposure 

(Adams, 2002) or on a non-peer reviewed Adams (1998) report. Consequently, the use of such 

data is highly questionable. Thus, for 0.060 ppm exposure (square-wave), we do not have a range 

but 1 or possibly 2 subjects with ≥10% decrement. Considering “the large uncertainty in the 
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probability of response at 0.06 ppm ozone” (Smith, 2007) and considering that 2/30 subjects “ is

an extremely small number of individuals from which to conclude that the response is 

significant” (Smith, 2007), we find the available evidence of pulmonary function effects, based

on the Adams (2006) study, to be inadequate and believe that an extrapolation to a general 

population is inappropriate.

5. Conclusions

EPA in its current approach in evaluating the “health effects” is placing the emphasis in 

interpretation of effects on the number of individuals whose FEV1 decrement at the end of 

exposure is greater than 10%. The EPA states that this is of 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 a 

relatively few responsive individuals. However, in assessing the relevance of the small number 

of individuals that experience moderate lung function decrements, important considerations must 

be taken into account. Based on our analysis, we conclude:

1. The use of FA may not be an appropriate control exposure because the 0 ppb O3 “air’ that 

is generated in the laboratory does not exist under ambient or indoor air conditions. 

Actual PRB O3 concentrations are greater the 15-35 ppb levels modeled by the EPA and 

PRB hourly average concentrations frequently occur at some sites ≥ 50 ppb. Comparing 

changes across corresponding time intervals and expressing them as "corrected values" 

that take into consideration the absolute difference between the O3 and FA responses may 

perhaps “artificially” enhance the magnitude of the O3 response.

2. Intra-individual variability of various endpoints may be substantial. Although there is a 

tendency by the investigators to interpret their findings of repeated exposures as 

reproducible, closer examination shows that for many individuals the differences in FEV1

response may be substantial and, in some cases, different by as much as 40 percentage 

points. With such individuals, between and within exposure inconsistencies, the utility of 

using only individuals’ end exposure FEV1 value for health assessment is questionable.

3. The lack of coherence between responses of many individuals to a range of O3

concentrations further reflects on instability of these effects.

4. Post hoc statistical analyses are questionable because they may violate a priori statistical 

design. Approaches based on the behavior of extreme responses within specific 

experiments, treatments, and measurement times have not been presented in a way to 

have any confidence in attempts to reinterpret the analysis in a meaningful statistical 

sense.

5. Focusing on square-wave versus realistic variable exposures provides an inadequate 

assessment for the human health considerations.
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6. Inflammatory variables show much greater intra- and inter-individual variance of 

measured endpoints than spirometric variables. At this time we do not have a sufficient 

number of human controlled studies exploring these endpoints to make a definitive 

statement concerning the importance of these observations in the standard-setting 

process.

5. 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., 2006. Comparison of chamber 6.6-h exposures to 0.04-0.08 ppm ozone via squarewave and triangular profiles on pulmonary responses. Inhal. Toxicol. 18:127-136.

Adams W.C., 2006b. Human pulmonary responses with 30-minute time intervals of exercise and 

rest when exposed for 8 hours to 0.12 ppm ozone via square-wave and acute triangular 

profiles. Inhal. Toxicol. 18:413-422.

Brown, J.S. The effects of ozone on lung function at 0.06 ppm in healthy adults. June 14, 2007. 

Memo to the Ozone NAAQS Review Docket. EPA-HQ-OAR-2005-0172-0175. Available 

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

Brown, J.S., Bateson, T.F., McDonnell, W.F., 2008. Effects of exposure to 0.06 ppm ozone on 

FEV1 in humans: a secondary analysis of existing data. Environ. Health Perspect. 116:1023-

1026.

Federal Register, 2010. National Ambient Air Quality Standards for Ozone: Proposed rule. 40 

CFR Parts 50 and 58 (EPA-HQ-OAR-2005-0172; FRL-9102-1). RIN 2060-AP98. Vol. 75, 

No. 11, p. 2938-3052.

Hazucha, M., Lefohn, A.S., 2007. Nonlinearity in Human Health Response to Ozone: 

Experimental Laboratory Considerations Atmospheric Environment. 41:4559-4570.

Hazucha, M., Lefohn, A.S., 2010. An alternative form and level of the human health ozone 

standard. Inhal Toxicol 22:999-1011.

Kim, C.S., Neil E Alexis, Ana G Rappold, Howard Kehrl, Milan J Hazucha, John C Lay, Mike 

Schmitt, Martin Case, Robert B Devlin, David B Peden, and David Diaz-Sanchez. Lung 

Function and Inflammatory Responses in Healthy Young Adults Exposed to 0.06 ppm Ozone 

for 6.6 Hours. Am J Respir Crit Care Med, prepubl. Jan, 7, 2011.

Lefohn, A.S., Hazucha, M.J., Shadwick, D., Adams, W.C., 2010. An Alternative Form and Level 

of the Human Health Ozone Standard. Inhalation Toxicology. 22:999–1011.
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Oltmans, S.J., Lefohn, A.S., 2005. Using empirical data to estimate policy relevant background 

for ozone exposures. Submitted to the U.S. EPA as part of the comments on the second draft 

of the Ozone Criteria Document.

Oltmans, S.J., Lefohn, A.S., Harris, J.M., Shadwick, D., 2008. Background ozone levels of air 

entering the west coast of the U.S. and assessment of longer-term changes. Atmospheric 

Environment 42:6020-6038. 

Oltmans, S.J., Lefohn, A.S., Harris, J.M., Tarasick, D.W., Thompson, A.M., Wernli, H., 

Johnson, B.J., Novelli, P.C., Montzka, S.A., Ray, J.D., Patrick, L.C., Sweeney, C., Jefferson, 

A., Dann, T., Davies, J., Shapiro, M., Holben, B.N., 2010. Enhanced ozone over western 

North America from biomass burning in Eurasia during April 2008 as seen in surface and 

profile observations. Atmos Environ 44:4497-4509.

Smith, R.L. Public Comments to CASAC Ozone Review Panel, March 7, 2007.

U.S. Environmental Protection Agency, 2006. Air Quality Criteria for Ozone and Related 

Photochemical Oxidants. Environmental Protection Agency, Office of Research and 

Development, Research Triangle Park, NC. U.S. EPA report no. EPA/600/R-05/004bF. 

U.S. Environmental Protection Agency, 2007. Review of the National Ambient Air Quality

Standards for Ozone: Policy Assessment of Scientific and Technical Information. OAQPS 

Staff Paper, Report EPA-452/R-07-007. Research Triangle Park, NC:Office of Air Quality 

Planning and Standards, U.S. Environmental Protection Agency. Available online at:

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

Wegman L.N. Memorandum: Solicitation of CASAC Advice on EPA’s Reconsideration of the 

2008 Primary Ozone National Ambient Air Quality Standard, EPA, HEID, OAQPS, January 

26, 2011.