March 16, 2015 Environmental Protection Agency EPA Docket Center (EPA/DC) Mail code 28221T 1200 Pennsylvania Ave., NW Washington, D.C. 20460 via www.regulations.gov Re: Comments on the National Ambient Air Quality Standards for Ozone Proposed Rule; 79 Fed.

Reg. 75,234; Docket ID No. EPA–HQ–OAR–2008–0699 Attached please find comments regarding the National Ambient Air Quality Standards (NAAQS) for Ozone Proposed Rule. We discuss how new health effects evidence cited in the proposal does not differ substantially from evidence cited in previous NAAQS reviews, and that the totality of available evidence does not support lowering the primary NAAQS. Also, while we agree with EPA that a secondary standard expressed in the same form as the primary standard is equally effective at providing welfare protection as a secondary standard expressed in terms of a cumulative seasonal 3-year form (i.e., W126), the welfare analyses presented in the Proposed Rule do not support lowering the secondary standard. My colleagues at Gradient and I wrote these comments during the normal course of employment. We have the sole responsibility for the writing, content, and conclusions of these comments. We received financial support from the organizations listed below. American Forest & Paper Association American Chemistry Council American Petroleum Institute American Iron and Steel Institute American Wood Council Corn Refiners Association Council of Industrial Boiler Owners Industrial Minerals Association – North America National Industrial Sand Association National Oilseed Processors Association Rubber Manufacturers Association Utility Air Regulatory Group U.S. Chamber of Commerce Thank you for your consideration. Sincerely, /s/ Julie E. Goodman, Ph.D., DABT, ACE, ATS Principal cc: Gina McCarthy, Administrator

Susan Lyon Stone, EPA Health and Environmental Impacts Division, OAQPS Janet McCabe, EPA Acting Assistant Administrator for the Office of Air and Radiation Joseph Goffman, EPA Associate Assistant Administrator & Senior Counsel, OAQPS Steve Page, EPA Director, OAQPS

Comments on the National Ambient Air Quality Standards for Ozone Proposed Rule 79 Fed. Reg. 75,234 Docket ID No. EPA–HQ–OAR–2008–0699

March 16, 2015

Table of Contents

Page

Introduction .................................................................................................................................... 1

1 Primary Standard ................................................................................................................ 2 1.1 New Evidence .......................................................................................................... 2 1.2 Evidence-based Analysis ......................................................................................... 5

1.2.1 EPA's Causal Framework ............................................................................. 5 1.2.2 Controlled Human Exposure Studies of Lung Function .............................. 5 1.2.3 Epidemiology Studies .................................................................................. 8 1.2.4 Sensitive Populations ................................................................................ 11 1.2.5 Mode of Action ......................................................................................... 11

1.3 Exposure and Risk Assessment ............................................................................. 12 1.3.1 APEX .......................................................................................................... 12 1.3.2 BenMAP .................................................................................................... 14

1.4 Conclusions ........................................................................................................... 15

2 Secondary Standard .......................................................................................................... 16 2.1 A Distinct and Separate Secondary Standard Is Not Needed to Protect

Welfare.................................................................................................................. 16 2.2 The Current Level of the Secondary Standard Is Protective ................................. 16

2.2.1 There Are Substantial Uncertainties in the Welfare Exposure Assessment ............................................................................................... 17

2.2.2 There Are Substantial Uncertainties in the Welfare Risk Assessment ..... 18 2.3 Lowering the Secondary Standard Will Not Provide Meaningful Additional

Welfare Protection Beyond What Is Provided by Meeting The Current Standard ................................................................................................................ 20

2.4 Conclusions ........................................................................................................... 22

References .................................................................................................................................... 23

1

Introduction

The United States Environmental Protection Agency (EPA) Administrator concludes in the National Ambient Air Quality Standards for Ozone Proposed Rule (PR) that new evidence supports lowering the primary and secondary ozone National Ambient Air Quality Standards (NAAQS) to a level between 0.065 and 0.070 parts per million (ppm), calculated as the three-year average of the annual fourth highest daily maximum 8-hour concentrations (US EPA, 2014a). As described below, new health effects evidence cited in the PR does not differ substantially from evidence cited in previous NAAQS reviews, and the totality of available evidence does not support lowering the primary NAAQS. While we agree with EPA that a secondary standard expressed in the same form as the primary standard is equally effective at providing welfare protection as a secondary standard expressed in terms of a cumulative seasonal three-year form (i.e., W126), the welfare analyses presented in the PR do not support lowering the secondary standard.

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1 Primary Standard

The EPA Administrator concludes in the PR that new health effects evidence supports lowering the ozone NAAQS to a level between 0.065 and 0.070 ppm (US EPA, 2014a). This conclusion is based on EPA's evidence-, exposure-, and risk-based analyses. In its evidence-based analysis, EPA did not systematically review and integrate the health effects evidence, in that it did not use objective and standardized methods to evaluate the quality of individual studies and integrate evidence streams to develop scientifically supportable conclusions. A systematic, objective review of controlled human exposure, epidemiology, and mode-of-action (MoA) studies does not indicate increased public health benefits from a lower ozone standard. EPA's exposure and risk assessments were based on many conservative assumptions and also did not demonstrate that a lower NAAQS will be more health protective than the current one. Overall, new health effects evidence cited in the PR does not differ substantially from evidence cited in previous ozone NAAQS reviews, and the totality of available evidence does not support lowering the primary NAAQS. The Administrator should retain the current level of the ozone NAAQS at 0.075 ppm.

1.1 New Evidence

The PR indicates that the studies described in Table 1 are "highlights of the new evidence" that support lowering the NAAQS. As discussed in the table and the text that follows, each of these lines of evidence is subject to many of the same uncertainties and limitations that were present in studies evaluated in the previous ozone review. As such, they do not provide adequate evidence to support a revision to the ozone standard. Table 1 "New Evidence" Highlighted by EPA and Associated Limitations

EPA's New Evidence Since Last Review Limitations Kim et al. (2011), which showed lung function decrements and airway inflammation at 0.06 ppm. Schelegle et al. (2009), which showed lung function decrements and respiratory symptoms at 0.072 ppm.

Kim et al. (2011) inconsistent with other studies. Inappropriate to extrapolate a few people from Schelegle et al. (2009) study to entire US population.

Controlled exposure studies that showed systemic inflammation and cardiac changes.

Almost no findings were statistically or clinically significant. Many high-exposure studies.

Multi- and single-city epidemiology studies of respiratory hospital admissions (HA) and emergency department (ED) visits.

Results are inconsistent and may be confounded by co-pollutants. Exposure measurement error and model selection bias are major uncertainties

Multi-city and multi-continent studies of cardiovascular (CV), respiratory, and total mortality (e.g., Katsouyanni et al., 2009).

Many epidemiology studies are re-analyses of previous studies. Studies have same limitations as previous ones.

Long-term epidemiology studies reporting respiratory effects and interactions between exercise or genetics and new-onset asthma and symptoms in asthmatics.

Limited number of studies. Studies have same limitations as previous ones. Many results may be confounded by socioeconomic status (SES), smoking, and other factors.

New evidence of risk factors that modify ozone risks (e.g., genetics, nutrition).

Limited number of studies for each factor. Results are inconsistent.

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The limitations and uncertainties associated with the findings from the Kim et al. (2011) and Schelegle et al. (2009) studies are discussed in more detail below. Briefly, the results of these controlled exposure studies cannot be directly extrapolated to the US population. They each only evaluated a small number of people (fewer than 60) and few subjects were ozone responders (i.e., had a decrement in forced expiratory volume in 1 second [FEV1] greater than 10%) at exposures below 0.080 ppm. Kim et al. (2011) reported ozone responses in three subjects at 0.060 ppm and Schelegle et al. (2009) reported effects in six subjects at 0.072 ppm. These studies involved people performing quasi-continuous exercise for an extended period of time at an intensity that likely represents a worst-case scenario that most people, including children and other sensitive subgroups, will not reach in their daily lives. A systematic review of studies evaluating biomarkers of systemic inflammation indicates that, in controlled human exposure studies with ozone, almost no findings were statistically or clinically significant, even with high exposures (Goodman et al., 2015). Also, a recent systematic weight-of-evidence (WoE) analysis indicated that studies evaluating short-term ozone exposure and CV effects did not provide evidence of a causal relationship (Goodman et al., 2014a). It is unclear whether the few reported effects would be observed at current ambient ozone exposures, which are up to an order of magnitude lower than the concentrations used in these controlled exposure studies (e.g., Devlin et al., 2012). Further, as noted in the PR, these studies are not coherent with CV morbidity studies, which show no associations with ozone (US EPA, 2014a). The key epidemiology studies presented in the PR have limitations that are similar to those in studies that EPA reviewed in past ozone evaluations, including exposure measurement error, model specification issues, and confounders. Also, many of the studies were re-analyses of studies that were considered in previous EPA reviews, and thus do not actually constitute new evidence. The Administrator concludes that study limitations hinder the use of epidemiology data in the risk assessment, and it is inappropriate for her to conclude that these same studies are adequate for causal determinations. The Administrator specifically highlights new evidence from multi-city and multi-continent mortality and morbidity studies as supportive of a revision to the NAAQS. Recently, several researchers pursued multi-city analyses to address the disadvantages of singe-city studies, as well as to leverage increased statistical power conveyed by combining study populations into nationwide estimates. However, in multi-city studies, substantial between-city heterogeneity in effect estimates can make the results difficult to interpret. In the study by Katsouyanni et al. (2009), for example, which is cited repeatedly by the Administrator as being supportive of mortality associated with short-term ozone exposure, the percent increase in standardized all-cause mortality ranged from 1.66 to 5.87 per 0.040 ppm increase in ozone, with the lowest estimates found in Europe and the highest in Canada. Figure 1 below, which is modified from Smith et al. (2009), illustrates the striking degree of between-city heterogeneity observed across several US cities. In some cities, the relationship between ozone and mortality is quite strong, while in others it appears that ozone exposure protects against dying. This variability does not appear to be explained by differences in city characteristics, such as climate or underlying health of the population. It is unlikely that ozone would cause deaths in one city and be protective in other cities; it is more plausible that the differences in results between locations reflect aberrations caused by incorrect model specifications, residual confounding, or some other artifact of statistical analyses.

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Figure 1 8-Hour Ozone-Mortality Coefficients in the Multi-City Study by Smith et al. (2009).

Regarding risk factors that modify ozone risks, the PR suggests that the new evidence presented in the 2013 Integrated Science Assessment (ISA) (US EPA, 2013) expanded on what was available at the time of the last ozone review in 2006. EPA concluded in the ISA that there was adequate evidence for an increased risk of ozone-related health effects among individuals with asthma, younger and older age groups, individuals with reduced intake of certain nutrients (i.e., vitamins C and E), individuals with specific genetic variants, and outdoor workers (US EPA, 2013). However, the body of literature that addresses these subpopulations (including new and previously considered studies) does not meet the criteria for adequate evidence outlined in the ISA; specifically, it is neither "substantial" nor "consistent" and should not be used as the basis for revising the standard for ozone.

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1.2 Evidence-based Analysis

1.2.1 EPA's Causal Framework

Assessing causation requires a transparent, detailed framework that allows for a systematic and objective assessment of all of the available evidence. According to EPA, the NAAQS causal framework is largely based on the Institute of Medicine's (IOM, 2008) WoE framework and relies heavily on the postulates put forth by Sir Austin Bradford Hill in 1965 (Hill, 1965). However, the NAAQS framework deviates from the frameworks upon which it was based. For example, the NAAQS framework stated that only one positive study is sufficient to establish a suggestive causal relationship when other results are inconsistent, whereas the IOM framework has much stricter requirements for establishing such a classification. The NAAQS framework also lacks specific guidance in some instances, and this led to an inconsistent evaluation of the health effects evidence in the ozone ISA (Goodman et al., 2013, 2014b). For example, there is no guidance detailing the specific ways in which EPA should evaluate the strengths and weakness of the studies it reviews and how study quality characteristics should be considered when integrating evidence. In addition, the NAAQS framework states that an association is likely to be causal if "chance and bias can be ruled out with reasonable confidence but potential issues remain" (US EPA, 2013). According to EPA, "potential issues" include possible co-pollutant effects and limited or inconsistent findings from other lines of evidence. However, it is challenging to rule out bias and confounding with "reasonable confidence" for most epidemiology studies because of the inherent limitations with observational study designs and authors' methodological choices (Dominici et al., 2014). For example, potential confounding by co-pollutants is very difficult to assess even when data on multiple pollutants are available because multi-pollutant models, the standard method of controlling for co-pollutants, often produce unreliable results (Vedal and Kaufman, 2011). In addition to issues with the framework itself, EPA has not implemented the framework consistently. In the ozone ISA (US EPA, 2013), all available evidence was not presented in a clear, consistent manner; positive associations were often given more weight than null associations; confounders were not always adequately considered; the lack of coherence among epidemiology, toxicology, and mechanistic data was not acknowledged; effects that are not adverse were often interpreted as such; and alternative explanations for observed effects were not always considered. Overall, the lack of a systematic, objective, and transparent framework for evaluating the health effects of ozone, in addition to an inconsistent application of the available framework, means that the Administrator did not have a balanced assessment on which to base her conclusions. As a result, the Administrator should not conclude that there is sufficient evidence for any causal relationships at ozone exposures below the current standard of 0.075 ppm. 1.2.2 Controlled Human Exposure Studies of Lung Function

Four controlled exposure studies evaluated ozone at exposure concentrations below the current level of the NAAQS (Figure 2). These studies involved small numbers of people (fewer than 60) performing quasi-continuous exercise for a long duration at an intensity not common in the general population or sensitive individuals, and under worst-case exposure profiles. Adams (2002, 2006) found no effects of ozone at exposures below the current standard. The PR concludes, however, that two new controlled exposure studies, by Kim et al. (2011) and Schelegle et al. (2009), support lowering the standard.

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Figure 2 Ozone Exposure and Lung Function Decrements in Controlled Exposure Studies with Exposures below the Current Standard (0.075 ppm). The PR indicates that a 10% FEV1 decrement is a moderate functional response in people with asthma and that a 15% decrement is a moderate functional response in healthy adults (US EPA, 2014a). Bars represent 95% confidence intervals (CIs). To adjust for multiple comparisons, Schelegle et al. (2009) used the Tukey post hoc test and Adams (2002, 2006) used the Scheffe post hoc test; we calculated corresponding 95% Tukey CIs and 95% Scheffe CIs accordingly. Kim et al. (2011) used linear mixed-effects models to predict the expected change in FEV1 and reported corresponding 95% CIs. CH = Chamber Exposure; FEV1 = Forced Expiratory Volume in One Second; FM = Face Mask Exposure; SQR = Square Exposure Profile; TRI = Triangle Exposure Profile. Adapted from Goodman et al. (2013). Kim et al. (2011) observed statistically significant lung function decrements and airway inflammation at 0.06 ppm. The PR indicates that a 10% FEV1 decrement is a moderate functional response in people with asthma and that a 15% decrement is a moderate functional response in healthy adults (US EPA, 2014a), and the mean decrements Kim et al. (2011) reported across the study population were so small (1.71% and 1.19% for FEV1 and forced vital capacity [FVC], respectively) that they most likely indicate normal variability in the population. Further, only 3 out of 31 participants had mean FEV1 decrements greater than 10%, and these responders are unlikely to represent a group of sensitive individuals in the US population. Also, the severity of symptoms for ozone-exposed subjects was similar to control subjects, indicating that ozone exposure did not cause noticeable effects (reviewed by Goodman et al., 2014b). These clinically insignificant data do not provide a basis for lowering the standard. Schelegle et al. (2009) reported small group mean lung function decrements (5.34% for FEV1 after a 6.6-hour exposure) and respiratory symptoms, including throat tickle, cough, shortness of breath, and pain on deep inspiration (measured as total symptom score), at 0.072 ppm, with lung function restored to baseline conditions between one and four hours after ozone exposure ended. This indicates that effects were mild and transient and not likely to be associated with long-term adverse effects. As shown in Figure 3 below, an independent analysis of the Schelegle et al. (2009) individual data showed no correlation between symptoms (expressed as total symptom score, or TSS) and the magnitude of lung function decrements (FEV1) in these individuals (p-value = 0.2764). In addition, because ozone has an acrid odor and an odor threshold (Alarie, 1973; NIOSH, 1978; Ruth, 1986) below the exposure levels used in this study, as well

-25-20-15-10-505

Group Mean Change in FEV1 (%)

BelowCurrent NAAQS

ExposureCH-TRI

FM-SQRCH-SQRCH-TRICH-SQRCH-TRICH-TRICH-SQRFM-SQRCH-TRICH-TRICH-TRI

FM-SQRCH-SQR

Ozone (ppm)0.040.040.060.060.06

0.0630.0720.080.080.08

0.0810.0880.120.12

Sample Size3030593030313130303031313030

StudyAdams (2006)Adams (2002)Kim et al. (2011)Adams (2006)Adams (2006)Schelegle et al. (2009)Schelegle et al. (2009)Adams (2006)Adams (2002)Adams (2006)Schelegle et al. (2009)Schelegle et al. (2009)Adams (2002)Adams (2002)

BelowCurrent NAAQS

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as in Adams (2002, 2006) and Kim et al. (2011), the participants in each of these studies most likely knew when they were being exposed to ozone vs. filtered air, and therefore may have been more likely to report symptoms after ozone exposure.

Figure 3 Correlation between Total Symptom Score (TSS) and FEV1 Decrements following Exposure to 0.072 ppm Ozone. Calculated from individual data from Schelegle et al. (2009).

With regard to the adversity of reported lung function decrements (i.e., whether the decrements are associated with noticeable symptoms or permanent lung damage), Schelegle et al. (2009) focused on group mean decrements greater than 10%. While EPA considers a 10% cutoff reasonable for moderate lung function decrements in asthmatics, in healthy populations, a 10% decrement (and possibly even a 15% decrement) would not be noticeable to the individual experiencing it (Alliance of Automobile Manufactures et al., 2007). Moreover, studies have shown that acute lung function decrements even after higher ozone exposures (~0.2 ppm) are not predictive of, or causally associated with, ozone-induced inflammation or subsequent lung injury (e.g., Blomberg et al., 1999). It is notable that in the Schelegle et al. (2009) study, the time period between the 0.072 ppm exposure and the filtered air exposure was 55 days on average (ranging from 13 to 302 days). Co-exposures, seasonal changes in lung function, and the physical conditioning of subjects could have changed over this time, making it difficult to interpret results (OSHA, 2013; Pellegrino et al., 2005). In addition, Schelegle et al. (2009) used a triangular exposure profile, where exposure is increased step-wise and then decreased step-wise to achieve a target average exposure concentration. While a triangular exposure profile is likely more reflective of ambient ozone fluctuations compared to constant exposure to the same ozone level, the specific patterns used by Schelegle et al. (2009) do not reflect average diurnal patterns in most cities (Lefohn and Hazucha, 2005). This means that although the Schelegle et al. (2009) exposure patterns may be useful for evaluating what could happen in worst-case exposure scenarios, since they are not reflective of conditions in most cities, they are not informative with regard to the NAAQS. Taken together, all of these issues associated with the Schelegle et al. (2009) study indicate that it does not provide a reliable basis for lowering the standard.

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The PR suggests that susceptible populations, such as asthmatics, would be more responsive to acute ozone exposure than healthy adults, but there is no evidence to support this (e.g., Kehrl et al., 1985; Linn et al., 1983; Mudway et al., 2001). Moreover, the exercise level maintained in these and other controlled ozone exposure studies is likely more strenuous and of a longer duration (i.e., up to 6.6 hours) than most of the general US population, including sensitive subpopulations, experiences, with the exception of some outdoor workers and athletes. The most sensitive populations have conditions that prevent them from exercising for the duration and at the intensity reached in these studies, even in the absence of ozone. Thus, it is inappropriate to conclude that these studies indicate that sensitive individuals, who are unlikely to be in these extreme exposure scenarios, would be more sensitive to the effects of ozone. The ultimate goal of the NAAQS is to protect the health of the general population, including groups that may be more sensitive to ozone-related health effects, and not necessarily people who are able to perform quasi-continuous strenuous exercise for six hours or more while exposed to outdoor ozone levels. Therefore, it is important that study designs reflect exposure conditions that all individuals, including sensitive ones, are likely to experience. It is unclear how the controlled exposure studies cited by the Administrator relate to exposure conditions that are more typical among the general population, particularly for the sensitive individuals whom the NAAQS is intended to protect. EPA should conclude that the atypical duration of exposure and near-continuous exercise levels limit the extrapolation of these results to the averaging time and numerical levels of the NAAQS. This is critical when considering that most studies do not show effects at exposure levels below the current NAAQS. Also, compliance with the NAAQS is conservatively based on the highest concentration measured at a single monitor in each area. If an area is in attainment with the standard, then the highest monitor is in attainment and ozone concentrations at all other monitors are below this level, indicating that most ozone concentrations in an area in compliance are below the level of the NAAQS. This is another reason why levels in controlled exposure studies do not directly correspond to the level of the NAAQS. Overall, the evidence from controlled exposure studies indicates that the current 0.075 ppm standard is public health protective, and that the Administrator should retain it. 1.2.3 Epidemiology Studies

The Administrator acknowledges critical uncertainties in epidemiology evidence when concluding that epidemiology results are not suitable for use in quantitative risk assessments; however, she does not seem to apply the same level of scrutiny when applying epidemiology research to causal determinations. She should acknowledge these limitations in epidemiology methodology when evaluating causal relationships, as well. The Administrator indicates that short-term ozone exposure causes respiratory effects and is likely associated with CV effects and all-cause mortality, while long-term ozone exposure is likely to be associated with respiratory morbidity and mortality (US EPA, 2014a). These conclusions appear to have been influenced by an imbalanced approach to reviewing the epidemiology literature, as EPA generally gives a disproportionate amount of attention to studies presenting positive findings and often selectively presents only the positive results from individual studies, even though exploration of multiple associations reveals mixed findings within an individual study. For example, in the PR, the Administrator asserts that epidemiology studies have "consistently" linked short-term increases in ozone to lung function decrements in a variety of populations, including children with asthma. However, inspection of results presented in the ISA reveal that the changes in FEV1 observed in studies of asthmatic children are inconsistent (Figure 4). EPA does not discuss studies that report increased lung function following ozone

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exposure, as found by Rabinovitch et al. (2004), who reported a nearly significant increase in morning FEV1 (55 mL, 95% CI: -2.4, 108) in a high quality study of children with severe asthma. (While Rabinovitch et al. (2004) observed evidence of elevated daytime asthma symptoms in association with ozone, this was only one positive finding among several null associations measured.) Similarly, when discussing findings of Gent et al. (2003), a study that calculated a very large number of associations between assorted asthma symptoms and varying metrics of ozone, EPA (2013) selectively highlighted the positive findings and did not mention that a high number of null associations were also found.

Figure 4 Association between Ambient Ozone Concentrations and Percent Change in FEV1 in Children with Asthma. Note that FEV1 decrements are shown to the left of the y-axis, in contrast to Figure 2. Source: US EPA (2013, Figure 6-7).

This practice of selectively presenting supporting results led to an unbalanced view of a nuanced and complicated body of research – a problem that is compounded by selection bias, the tendency of researchers to report positive findings in individual papers (Lumley and Sheppard, 2000), and publication bias, which is the pervasive practice of journals to selectively publish positive results (Anderson et al., 2005). Similarly, EPA downplays uncertainties and limitations inherent in air pollution epidemiology that can influence results. EPA selectively presents examples of errors that may mask true associations, without mentioning sources of errors that could inflate measured associations and exaggerate potential risks. For example, in several places in the ISA and the PR, EPA mentions exposure measurement error as a limitation of one specific study or a group of studies, and asserts that the error is nondifferential in nature and therefore biased results towards the null or increased the uncertainty of results, masking true associations. EPA does not, however, acknowledge that nondifferential exposure measurement errors can

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bias results in the opposite direction (Rhomberg et al., 2011), nor does it discuss key biases that favor false positive results, such as model selection bias and publication bias. Other important factors that remain largely unaddressed by EPA include residual confounding, uncertainties in modeling temporal and weather effects, model selection bias, and unexplained inconsistencies in results observed in different cities. For example, in the sensitivity analysis that was conducted as part of the Strickland et al. (2010) study discussed below, the authors included daily counts of ED visits for upper respiratory infections and found it to be an "extremely strong" predictor of ED visit rates. Adjustment for this factor attenuated many associations between air pollutants and ED visits, indicating that there was residual confounding by respiratory infections that likely biased associations away from the null. EPA should have taken a more objective and rigorous approach to evaluating epidemiology evidence that considered methodological issues and resultant biases and uncertainties, especially in light of associations between ozone and health measured in epidemiology analyses being small in magnitude and possibly arising from random chance or methodological shortcomings. The PR presents three key studies as evidence that respiratory effects occur following short-term exposures to ozone in areas meeting the current standard: Silverman and Ito (2010), Strickland et al. (2010), and Mar and Koenig (2009). However, the results of these studies should be interpreted in light of methodological limitations and uncertainties that are not fully acknowledged by EPA. Silverman and Ito (2010) analyzed New York City HAs for childhood asthma and found that school-age children had about a 20% increase in HAs, but after adjustment for particulate matter less than 2.5 µm in diameter (PM2.5), associations between HAs and ozone were attenuated, but still significant, across all age groups. Also, Silverman and Ito (2010) did not consider specific measurements of confounders such as aeroallergens and respiratory infections, which exhibit extremely strong associations with adverse respiratory outcomes, so it is unclear whether the associations observed were due to ozone exposure. Similarly, Strickland et al. (2010) investigated ED visits for pediatric asthma in Atlanta and found elevated risks, but they were inconsistent across the year and lost statistical significance when co-pollutants were added to the model. Strickland et al. (2010) also found that relationships with ozone and other pollutants were generally attenuated when upper respiratory infection rates were considered, and they concluded that associations between air pollution and respiratory morbidity may be confounded by upper respiratory infections. Mar and Koenig (2009) conducted a much smaller study of ED visits for asthma in Seattle and explored a large number of associations between ozone and ED visits by varying the ozone metric and monitors used to derive exposure estimates as well as subgroups of study subjects. Potential confounders such as aeroallergens, respiratory infections, and co-pollutants were not considered. Out of the 72 associations reported in the study, 30 were statistically significant, and many of the events occurred on the same day as elevated ozone. However, associations between ED visits and same-day ozone must be interpreted cautiously. Ozone concentrations typically peak in the early afternoon (US EPA, 2013), so the maximum ozone concentration measured on the day of an ED visit may have occurred after the ED event. Because it is impossible for ozone exposure to cause a health outcome when the exposure follows the outcome, these associations with same-day ozone exposure are unlikely to reflect a true relationship. EPA should consider that other factors, such as incorrect model specification and residual confounding, might have caused false positive results. In addition, the large number of comparisons explored in this analysis raise concerns about a potential "multiple comparison problem," in which false positive associations occur due to chance alone. EPA should have conducted a more rigorous and systematic review of the epidemiology literature, with a careful consideration of study quality and a balanced perspective on errors that may bias results in either direction. Key limitations in methodologies as well as overall inconsistency in results do not support the

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Administrator's conclusions about causality regarding ozone exposure and various health endpoints. The Administrator should retain the ozone standard, and acknowledge that epidemiology evidence does not support lowering it. 1.2.4 Sensitive Populations

EPA concluded in the ISA that there is adequate evidence supporting an increased risk of ozone-related health effects among people with asthma, individuals with specific genetic variants, children, older adults, individuals with reduced intake of certain nutrients (i.e., vitamins C and E), and outdoor workers (US EPA, 2013). In the PR, the Administrator places emphasis on adverse effects in children and asthmatics, despite weak and inconsistent evidence for increased risk in these populations versus the general population (US EPA, 2014a). Although there is evidence of increased exposures in outdoor workers and a larger body of literature that indicates the potential for increased sensitivity to some ozone-related health effects in older adults, the observed associations are weak and inconsistent across endpoints (e.g., Medina-Ramon and Schwartz, 2008; Cakmak et al., 2007, 2011; Kan et al., 2008; Stafoggia et al., 2010; US EPA, 2013; Tovalin et al., 2006); among the other subgroups discussed, studies are not consistent within and coherent across disciplines, and there are too few on which to base a revised ozone standard. For example, some studies reported respiratory health effects only in asthmatics (Escamilla-Nuñez et al., 2008) or greater effects in asthmatics (Alexeeff et al., 2007; Thaller et al., 2008), while others reported no differences in response between asthmatics and non-asthmatics (Barraza-Villarreal et al., 2008; Berhane et al., 2011; Khatri et al., 2009). Controlled human exposure studies the Administrator references also reported inconsistent results in asthmatics at ozone exposure concentrations well above the standard (0.16 to 0.40 ppm) (e.g., Alexis et al. 2000; Mudway et al., 2001; Kreit et al., 1989, as cited in US EPA, 2013). In controlled exposure studies that reported statistically significant outcomes, the effects were mild, transient, and reversible, indicating that these outcomes are unlikely to have clinical significance or result in adverse effects. The evidence for increased risks in children is also not consistently supported by the literature. For example, Middleton et al. (2008) reported that respiratory-related HAs were higher in children under 15 years of age compared to those older than 15, while Silverman and Ito (2010) found that children in the youngest age group (less than six years old) had lower risks for HAs compared to children 6 to 18 years old, and that these were approximately equal to those for adults. In addition, evidence from controlled human exposure studies suggesting that children are not as responsive to the respiratory effects of ozone as adults does not support EPA's conclusion that this is a sensitive subpopulation. The Administrator should acknowledge that among most of the populations discussed, the available evidence is too sparse and inconsistent to support an increased sensitivity to ozone relative to the general population and thus, this evidence does not support a revised ozone standard. 1.2.5 Mode of Action

The PR discusses MoA a great deal. To our knowledge, all identified ozone MoAs have thresholds below which the body's natural defenses can prevent adverse effects. For example, ozone reacts with components of the extracellular lining fluid of the respiratory tract and cellular membranes, producing secondary oxidation products that injure respiratory tract epithelium or cause airway remodeling, but only after the body's natural antioxidant defenses are overwhelmed (Schelegle et al., 2007; Avissar et al., 2000; Ballinger et al., 2005; Cross et al., 1994; Mudway et al., 1996; Samet et al., 2001). The Administrator should retain the standard, and acknowledge that this is supported by MoA evidence.

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1.3 Exposure and Risk Assessment

EPA conducted several exposure and risk analyses in the Health Risk and Exposure Assessment (HREA) (US EPA, 2014b). EPA used the Air Pollutants Exposure (APEX) model, which is based on the results of controlled exposure studies, to estimate the percent of susceptible population groups (e.g., children) that would be exposed to concentrations of ozone above specified benchmarks. Specifically, EPA evaluated the percent and number of exposed individuals under current air quality conditions, as well as scenarios in which air quality meets the current (0.075 ppm) and alternative possible standards (0.070, 0.065, and 0.060 ppm). For these same five scenarios, EPA also used the APEX model to estimate the percent and number of individuals who would experience particular lung function decrements, focusing on FEV1 decrements greater than 10%. APEX is a sophisticated model that simulates individual people and the microenvironments through which they move on a given day. Here, we focus on the children modeled by APEX, whom we refer to as "simulated children." In addition to APEX analyses, EPA modeled mortality and morbidity (e.g., HAs) from ozone exposures under the same five scenarios using the Benefits Mapping and Analysis Program (BenMAP), which is based on epidemiology data. 1.3.1 APEX

The results of the APEX exposure and lung function risk assessments do not support lowering the ozone NAAQS. The APEX exposure assessment demonstrates that lowering the NAAQS will not lead to a significant decrease in the number of individuals experiencing multi-day, high-ozone exposures. In addition, the APEX risk assessment indicates that the largest benefits with regard to preventing lung function decrements result from just meeting the current standard of 0.075 ppm, and that there are generally smaller gains from lowering the standard below this level, although the results vary by city and year. For example, in the base case scenario for Atlanta in 2006, 12% fewer children had FEV1 decrements greater than 10% when moving from the current air quality scenario to the scenario meeting the 0.075 ppm standard, while only 3% fewer children had these decrements when moving from the current 0.075 ppm standard to the proposed 0.070 ppm standard (US EPA, 2014b, Table 6B-1). Further, the results presented in the PR likely overestimate ozone exposure and risk because they focus on children with "moderate or greater exertion level at the time of exposure" who do not exhibit averting behavior (i.e., staying indoors when there are high ozone concentrations) (US EPA, 2014b, p. 5-2). Because of their exertion level, these modeled children would naturally have high ventilation rates. Collectively, these assumptions likely led to overestimated ozone exposures and lung function decrements in the modeled children. In addition, a statistical analysis of the uncertainty in APEX-modeled FEV1 decrements greater than 10%, greater than 15%, and greater than 20% showed that there is a large degree of both statistical and model uncertainty in the lung function decrements calculated by the APEX model, which should be considered when interpreting the model results (NERA, 2015). Table 2 shows the percent of APEX-simulated children that experience at least two exposures at or above 0.060, 0.070, and 0.080 ppm when modeling air quality to meet the current standard (0.075 ppm) and possible alternative standards (0.070, 0.065, and 0.060 ppm). In this table, these four possible standards modeled are listed in the '8-hr Standard Level' column, and the percent of children with exposures above 0.060, 0.070, and 0.080 ppm are listed in the subsequent columns. Kim et al. (2011) and Schelegle et al. (2009) did not observe FEV1 decrements greater than 10% at exposures below 0.075 ppm in controlled exposure studies, except for in a few individuals, but Table 2 demonstrates that in all but one of the 15 APEX study areas, there are no simulated children with more than two exposures greater than 0.080 ppm, and that in all of the 15 areas, fewer than 1% of children have two or more exposures greater than 0.070 ppm. Therefore, most of the simulated children have exposures less than the 0.075 ppm, even under conditions that meet the current standard. Yet, the APEX model calculates that many of these children

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have FEV1 decrements greater than 10%. This inconsistency between the modeled results and observations in the controlled exposure studies provides further evidence that EPA likely overestimated the number of children with FEV1 decrements greater than 10% using the APEX model.

Table 2 Mean and Maximum Percent of APEX-simulated Children Experiencing at Least Two Daily Maximum 8-hour Average Ozone Exposures. Each row shows the mean and maximum percents for the five simulation years (2006-2010). Source: US EPA (2014b, Table 5-12).

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We assessed whether the simulated children with FEV1 decrements greater than 10% were modeled realistically through an independent analysis of the model output for the base-case air quality scenario for Los Angeles in 2006. We found that the simulated children generally experienced lung function decrements while outdoors and engaged in activities such as organized sports, playing, walking, biking, or jogging, which is consistent with our expectations for children who could be exposed to concentrations of ozone that might result in FEV1 decrements greater than 10%. However, many of the simulated children had ventilation rates above 21-25 L/min, and some had rates above 37-49 L/min, which are the ranges of ventilation rates given by the US EPA Exposure Factors Handbook (US EPA, 2011, Table 6-27) for children engaging in medium- and high-intensity activities, respectively. It is not realistic to assume that such a large number of children would approach or exceed these high ventilation rates while engaging in typical outdoor play and sports. In addition, some of the children with FEV1 decrements greater than 10% were simulated by APEX to spend a large percent of the day outdoors (e.g., up to 24 hours per day on the days when they experienced the lung function decrements). This can be contrasted with the National Human Activity Pattern survey data that show that 5- to 17-year-olds, on average, spend 7.88%, or 1.9 hours, of their day outside. These data demonstrate that not all of the children in the APEX model are realistically simulated, and that the number of simulated children with FEV1 decrements greater than 10% is likely overestimated. Finally, in the PR, the Administrator presents the total number of children in the urban case study areas that are estimated to have lung function decrements greater than 10% (US EPA, 2014a, Table 5). These population numbers are based on the results of the APEX simulations, which have conservative and sometimes unrealistic inputs (e.g., high number of hours spent outside or high ventilation rates) and therefore, like the APEX results, these numbers are likely overestimates of the actual number of children that would have lung function decrements. 1.3.2 BenMAP

The Administrator acknowledges in the PR that there are significant limitations of the BenMAP model risk estimates, and therefore places less emphasis on this risk assessment than on the APEX assessment (US EPA, 2014a). One major limitation of BenMAP that is not discussed by the Administrator is that thresholds for ozone effects are not adequately considered in the concentration-response functions (CRFs) used for the modeling, despite evidence (discussed above) supporting a threshold MoA. Although not discussed in the PR, EPA evaluated the impact of adding a threshold for long-term ozone exposures and found that this could reduce mortality risk estimates by 71-98%, highlighting the uncertainty in the BenMAP modeling. EPA did not evaluate a threshold for short-term ozone exposures on mortality, so we used the BenMAP model to evaluate this. As shown in the first column of Table 3, below, we first replicated the results of EPA's "base-case" analysis for the predicted number of deaths attributable to short-term ozone exposure in 12 cities using CRFs from Smith et al. (2009). We also calculated the number of deaths predicted when thresholds of 0.020, 0.030, 0.040, 0.050, and 0.060 ppm were included in the CRFs. We found that the results for mortality in all 12 cities are extremely sensitive to the inclusion of a threshold. The number of predicted deaths are dramatically reduced by including a threshold as low as 0.020 ppm and decrease accordingly with higher thresholds. For example, in Baltimore, the number of expected deaths decreased by 42% when a threshold of 0.020 ppm is included in the model, and by 96% when a threshold of 0.060 ppm is used.

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Table 3 Predicted Mortality Associated with Ozone in 12 US Cities Estimated Using EPA's "Core Analysis" for 2007 and with Threshold CRFs

Study Area Number of Deaths

(95% CI) Base Case 0.020 ppm 0.030 ppm 0.040 ppm 0.050 ppm 0.060 ppm

Atlanta 250 (-350-830)

160 (-220-520)

110 (-150-370)

69 (-95-230)

35 (-48-120)

13 (-18-43)

Baltimore 240 (-130-600)

140 (-79-360)

97 (-53240)

58 (-32-150)

29 (-16-73)

11 (-6-29)

Boston 200 (-290-680)

110 (-160-370)

68 (-95-230)

35 (-49-120)

17 (-23-56)

7 (-10-24)

Cleveland 270 (-19-550)

150 (-10-300)

90 (-6-180)

45 (-3-91)

18 (-1-37)

6 (0-12)

Denver 60 (-190-300)

38 (-120-190)

26 (-84-130)

16 (-51-81)

7 (-23-38)

2 (-6-10)

Detroit 520 (25-990)

300 (15-580)

200 (10-380)

110 (5-210)

55 (3-110)

27 (1-53)

Houston 540 (96-980)

250 (44-460)

140 (24-250)

65 (11-120)

27 (5-49)

9 (2-16)

Los Angeles 650 (-280-1560)

330 (-140-810)

200 (-86-480)

99 (-43-240)

37 (-16-89)

10 (-5-25)

New York 3,350 (1,990-4,690)

1,850 (1,090-2,590)

1,150 (680-1,620)

620 (370-870)

300 (180-425)

120 (72-170)

Philadelphia 960 (220-1,670)

570 (130-1,000)

380 (87-670)

230 (52-400

120 (27-210)

50 (11-89)

Sacramento 160 (-170-490)

86 (-90-260)

51 (-53-150)

25 (-26-76)

10 (-10-29)

3 (-3-8)

St. Louis 370 (-89-810)

220 (-53-490)

150 (-36-330)

88 (-21-190)

43 (-10-95)

17 (-4-38)

Notes: 95% CI = 95% Confidence Interval; CRF = Concentration-Response Function; ppm = parts per million. Other uncertainties in the BenMAP modeling (acknowledged by the Administrator) include the influence of regional heterogeneity in mortality effects, the use of area-wide averages of air monitoring data, and the influence of co-pollutants on model results (US EPA, 2014a). Given the limitations of the model and the results of the threshold sensitivity analyses, we agree with the Administrator that the BenMAP results should not inform the level of the ozone NAAQS.

1.4 Conclusions

Taken together, the WoE from controlled human exposure, epidemiology, and MoA studies indicates that the current ozone NAAQS is protective of public health, and that revising the standard to a level between 0.065 and 0.070 ppm is unwarranted. Thus, the Administrator should retain the standard at 0.075 ppm.

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2 Secondary Standard

In the PR, the EPA Administrator is proposing to revise the secondary ozone NAAQS to a level set within a range between 0.065 and 0.070 ppm, calculated as the three-year average of the annual fourth-highest daily maximum 8-hour concentrations (US EPA, 2014a). As such, the Administrator is proposing a secondary ozone standard in the same form as the primary ozone standard and concludes that this will provide air quality that would be comparable to a standard set at a level in terms of the alternative W1261 cumulative secondary standard at or below 13-17 ppm-hours. We agree with the Administrator that a secondary standard expressed in the same form as the primary standard is equally effective at providing welfare protection as a secondary standard expressed in terms of W126 index values. We disagree with the Administrator's proposal to revise the level of the current standard within the range of 0.065 to 0.070 ppm. As illustrated by EPA's analyses and discussed further in these comments, meeting the current standard of 0.075 ppm is predicted to result in a substantial reduction in ozone exposure and associated welfare risks, with further reductions in proposed standard levels predicted to result in only marginal and highly uncertain incremental air quality and welfare improvements. The Administrator should retain the current level of the ozone NAAQS at 0.075 ppm.

2.1 A Distinct and Separate Secondary Standard Is Not Needed to Protect Welfare

The W126 form is redundant with the current primary form, as illustrated by the significant correlation between the two metrics, as acknowledged by EPA. Using air quality data from 2011-2013, EPA examined the relationship between ozone concentrations expressed in the current standard form and the W126 form (Wells, 2014, Figure 5a). On the basis of this analysis, EPA concludes in the PR that, "the 4th high metric and a three-year average W126 metric are highly correlated, as are the relative changes in these two metrics over the past decade" [emphasis added] (US EPA, 2014a, p. 75346). We agree with EPA's assessment that the current standard is an effective surrogate for the alternative cumulative form. Therefore, there is no need for a secondary standard in a distinct and separate form. EPA also recognizes in the PR that a distinct secondary standard would result in unique implementation issues "related to, but not limited to, PSD [prevention of significant deterioration] implementation, nonattainment area classification thresholds, attainment planning, and conformity demonstrations" (US EPA, 2014a, p. 75375). These issues would need to be better understood before a distinct secondary standard is considered.

2.2 The Current Level of the Secondary Standard Is Protective

As illustrated below, just meeting the current standard is predicted to result in the greatest reduction in ozone exposure and associated welfare risks. Given substantial uncertainties in the welfare exposure (see Section 2.2.1) and welfare risk (see Section 2.2.2) assessment, further reductions in proposed standard levels are predicted to result in only marginal and highly uncertain incremental air quality and welfare

1 W126 is a cumulative seasonal three-year metric (three-year average of the annual maximum three-months' sum of the weighted daytime concentrations, in ppm-hours).

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improvements. Therefore, a further reduction in the level of the secondary standard is not warranted and the Administrator should retain the current level of the secondary ozone NAAQS at 0.075 ppm. 2.2.1 There Are Substantial Uncertainties in the Welfare Exposure Assessment

The Welfare Risk and Exposure Assessment for Ozone (WREA) (US EPA, 2014c) evaluated ozone exposure and risks for several national-scale air quality scenarios: recent conditions (2006 to 2008),2 the current standard, and W126 index values of 15, 11, and 7 ppm-hrs, using three-year averages. There are several important uncertainties related to EPA's air quality analyses and W126 estimates. Because the W126 estimates generated for the different air quality scenarios assessed are inputs to the welfare risk assessment (see Section 2.2.2), those uncertainties are propagated in the welfare risk assessment. Uncertainty associated with emissions reductions assumptions: To meet the existing

standard, W126 concentrations were adjusted based on model-predicted relationships between ozone and US-wide emissions reductions in oxides of nitrogen (NOx). EPA indicates in the PR that, "model-based adjustments…characterize only one potential distribution of air quality across a region when all monitor locations meet the standard" (US EPA, 2014a, p. 75323). Consequently, these model-based adjustments do not reflect the spatial and temporal heterogeneity that is expected to occur under real-world local and regional emissions reductions.

Uncertainty associated with ozone monitoring network: Air quality monitors are more densely positioned near urban centers, which require interpolations of ozone concentrations over large portions of the nation because of a limited monitoring network in rural areas (US EPA, 2014c, Figure 4-1). For example, spatial interpolation between stations in rural sites, especially where commercial forests are located, results in higher ozone levels over a larger area than would be the case if rural areas were well sampled.

Uncertainty associated with background contributions: EPA notes in the PR (US EPA, 2014a) that ozone concentrations in certain high-elevation sites in the western US can be substantially impacted by ozone contributions from international transport, stratospheric ozone, and ozone originating from wildfires. Each of these may influence the concentration estimates in the West and Southwest regions.

Uncertainty associated with non-average climate conditions: The W126 metric may be overestimating ozone exposures in regions that are characterized by non-average climate conditions, such as drought or low soil moisture. The W126 sigmoidal weighting function gives greater weight to ozone concentrations from approximately 0.040 to 0.100 ppm. These higher ozone concentrations are likely to occur during high light and high temperature conditions that are usually associated with low ambient humidity. These same conditions cause some plants to progressively close their stomata, thereby limiting air movement into the foliage reducing ozone exposure (Panek et al., 2002). Thus, W126 levels likely overestimate ozone exposure in regions characterized by drought years or low soil moisture conditions (i.e., West and Southwest regions; these regions are additionally affected by other uncertainties as described above).

Taken together, the W126 estimates derived by EPA in the welfare exposure assessment are substantially uncertain, particularly in the West and Southwest regions. This is critical since the only regions of the US predicted to have monitors above 15 ppm-hrs (W126) at modeled conditions just meeting the current 0.075 ppm standard are in the West and Southwest (Wells, 2014, Figure 3a). These projected

2 Certain visible foliar injury analyses assessed recent conditions from 2006 to 2010 on an annual basis.

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exceedances should be considered in light of these uncertainties, which provide further support for retaining the secondary standard in its current form and at its current level. 2.2.2 There Are Substantial Uncertainties in the Welfare Risk Assessment

Several key uncertainties identified by EPA in the previous review (US EPA, 2007, p. 8-27–8-29) remain applicable to the current welfare risk assessment. Instead of addressing these uncertainties, EPA expanded the current welfare risk assessment by including analyses of ecosystem services, which carry even greater uncertainty. Key uncertainties with EPA's welfare risk assessment are discussed below. Relative Biomass Loss (RBL) There a several important uncertainties associated with the RBL analyses EPA conducted: Exposure (W126) estimates: The RBL analyses propagate the uncertainties associated with the

W126 estimates discussed in Section 2.2.1.

Outlier studies: EPA revised its RBL analyses from what was originally presented in the second draft WREA (US EPA, 2014d) by conducting the analyses both with and without Eastern Cottonwood and Black Cherry. We support removal of these two species from the RBL analyses, because their exposure-response (E-R) functions are outliers (US EPA, 2014c, Figure 6-2). As shown in Figure 5, the inclusion of these two species has a significant impact on the analysis in a manner that shows much greater estimated RBL for a given ozone exposure.

Figure 5 Median Relative Biomass Loss Exposure-Response Functions for 10 (Excluding Black Cherry and Cottonwood), 11 (Excluding Cottonwood), and 12 (All) Species. Figure created using data taken from Appendix 5C of the Policy Assessment (PA) (US EPA, 2014e) and Appendix 6F (Table 6F-1) of the WREA (US EPA, 2014f).

Arbitrary RBL threshold: EPA revised its discussion of RBL in the final PA and PR from what

was originally presented in the second draft PA (US EPA, 2014g) by considering a range from 2 to 6% tree RBL, rather than narrowly focusing on an arbitrary 2% tree RBL cutoff. While we

0.00%

1.00%

2.00%

3.00%

4.00%

5.00%

6.00%

7.00%

8.00%

9.00%

7 8 9 10 11 12 13 14 15 16 17 18 19 20 21

Rela

tive

Biom

ass L

oss

W126

Median (12 species)

Median (11 species)

Median (10 species)

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support EPA's revised discussion of the RBL analyses, the scientific basis for an appropriate RBL threshold range is unclear, as acknowledged by EPA (US EPA, 2008, p. 12), and a 2-6% range remains an arbitrary selection. Further, five species (i.e., Red Alder, Ponderosa Pine, Aspen, Tulip Poplar, and Eastern White Pine) evaluated in the WREA never meet the 2% RBL threshold for W126 levels ranging from 8 to 17 ppm-hrs. For these species, a 2% RBL threshold is simply not practicable, because it would require W126 levels consistent with background ozone concentrations. Yet, EPA continues to use these targets for estimating acceptable RBL and substantiating recommended levels for the secondary standard.

Seedling exposure-response functions: The seedling E-R functions form the basis of the RBL analyses, several ecosystem service analyses (e.g., timber production), as well as the proposed level of the secondary standard. Despite the important role of these functions in informing the welfare risk assessment, they remain uncertain and largely unchanged from the prior review:

• Most studies comprising the basis of the E-R functions included only two levels of exposure. In addition, very few studies have included measurements of exposure using the W126 metric or the hourly ozone concentration data that would allow computing exposure using the W126.

• EPA has not improved the E-R function database since the previous review. E-R functions are currently only available for 12 tree species (with the Cottonwood study no longer considered robust by EPA), and there remains significant intra- and inter-species variability in the current E-R functions (US EPA, 2014c, Figure 6-5).

• Some species have high seedling/adult comparability (e.g., Aspen), while other species do not (e.g., Black Cherry). As a result, the E-R functions both over- or underestimate biomass losses in mature trees (US EPA, 2014c, Table 6-5).

• While EPA cites two recent Free-Air Carbon Dioxide Enrichment studies as validation for using available E-R functions, these studies also carry significant uncertainties (discussed in US EPA, 2013, Section 9.6.3). For example, these studies were conducted using only two exposure levels – ambient (3-4 ppm-hrs) and elevated (28-46 ppm-hrs) – which are well outside the range of the W126 levels being considered by EPA (13-17 ppm-hrs).

• The E-R functions are forced through an intercept of 0% RBL at 0 ppm-hrs, thus extending the E-R function beyond the original concentration-response curve to non-existent ozone exposure conditions below natural background (US EPA, 2013). This adjustment results in the potential for overestimating RBL within the W126 range being considered by EPA.

Visible Foliar Injury A national dataset was used to develop benchmark criteria reflecting different prevalence levels of visible foliar injury at different W126 levels and soil moisture conditions. There are several limitations and uncertainties with the visible foliar injury analyses: While foliar injury can be an indicator of the presence of ozone, foliar injury is not a reliable

indicator of significant injury to the leaf or to the plant as a whole. Visible foliar injury varies from year to year and site to site, among co-members of a population exposed to similar ozone levels, and as a function of soil moisture conditions, due to the influence of co-occurring environmental and genetic factors.

Low soil moisture reduces the potential for foliar injury, and it is unclear if there is a threshold for drought below which visible foliar injury would not occur. If there is such a threshold, the foliar injury may be overestimated at lower levels of soil moisture.

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The E-R relationships between ozone and visible foliar injury have not been adequately evaluated across both field and laboratory using the W126 metric. Therefore, the significance of foliar injury relative to an individual plant or to an ecosystem has not been quantitatively evaluated.

High variability in ozone W126 estimates from year to year resulted in substantial variability in the results (i.e., between 22 and 44% difference between 2006-2008 and 2008-2010 timeframes, as shown in US EPA, 2014c, Table 7-11). This observed variation indicates that the foliar injury results are imprecise and inconsistent.

Certain species were included in the analysis as a result of observed ozone-induced visible foliar injury in the field. It is inappropriate to assume that species of unknown sensitivity are tolerant or intolerant to ozone; therefore, the foliar injury assessment may be biased by species selection (US EPA, 2014c, Section 7.5).

Since foliar injury can lead to growth suppression (i.e., increase in RBL), the use of both visible foliar injury and RBL may be duplicative or even redundant.

Given the significant uncertainties that remain with the foliar injury analyses, those analyses do not provide information capable of supporting decisions to revise the level of a secondary ozone standard. This is acknowledged by EPA in the PA: "We take note of the appreciable variability in this endpoint…which poses challenges to giving it primary emphasis in identifying potential alternative standard levels" (US EPA, 2014e, p. 6-56). Ecosystem Services The uncertainties associated with four ecosystem services analyses (i.e., consumer surplus for timber production, consumer surplus for agricultural production, carbon sequestration, and pollution removal) are substantial, as indicated in our previous comments on the WREA and PA (Gradient, 2014) and as acknowledged by EPA:

[I]n selecting a target level of protection for forest trees and their associated ecosystem services, the Administrator will need to exercise judgments regarding the appropriate weight to place on the potential for benefits to the public welfare with respect to ecosystem services of carbon storage and urban air pollution removal associated with tree growth, as well as the large uncertainties associated with this information. (US EPA, 2014g, p. 6-45).

As such, these analyses are of limited value in informing the appropriate level of the secondary standard.

2.3 Lowering the Secondary Standard Will Not Provide Meaningful Additional Welfare Protection Beyond What Is Provided by Meeting The Current Standard

EPA concluded that "reductions in W126 between recent air quality and air quality just meeting the existing standard (Figure 4-8) are much larger than the additional reductions in W126 between air quality just meeting the existing standard and air quality meeting the alternative standards..." (US EPA, 2014c, p. 4-17). In fact, EPA's own air quality analyses show that by just meeting the existing standard (0.075 ppm), W126 concentrations would already be within the range recommended by EPA in the PR (13-17 ppm-hrs), with the exception of a few monitors in the Southwest and West climate regions, where modeled predictions carry significant uncertainties, as discussed in Section 2.2.1. In addition, there are

21

four climate regions (East North Central, Northeast, Northwest, and South) where all monitors were predicted to be below 7 ppm-hrs when air quality was adjusted to meet the existing 0.075 ppm standard (US EPA 2014c, Table 4-3). As illustrated by EPA's own analyses, meeting the current level of the secondary standard is similarly predicted to result in substantial welfare benefits, with only marginal and increasingly uncertain benefits observed at levels below the current standard (shown by EPA to equate to a W126 level of around 15 ppm-hrs),3 as summarized below. Relative Biomass Loss (RBL) Median RBLs were below 1% when just meeting the current standard for 10 out the 11 tree

species for which E-R functions were included in the WREA (US EPA, 2014c, Table 6-6). Black Cherry had a median RBL of just below 5% when just meeting the current standard. However, Black Cherry was shown to be an exception, because adult trees of this species are much less sensitive than would be predicted on the basis of seedling studies and the Black Cherry E-R seedling function is considered an outlier (See Section 2.2.2).

RBL was estimated nationally (weighted Relative Biomass Loss [wRBL]) to provide an indication of ecosystem-level impacts. The percentage of total basal area that exceeds 2% wRBL is 7.6% (recent conditions), 0.2% (0.075 ppm), 0.2% (15 ppm-hrs), 0.1% (11 ppm-hrs), and <0.1% (7 ppm-hrs). In the wRBL analysis for Class I areas, the number of Class I areas exceeding a 2% wRBL is 13 (recent conditions), 2 (current standard), 2 (15 ppm-hrs), 2 (11 ppm-hrs), and 1 (7 ppm-hrs). These analyses show that a substantial predicted reduction in welfare risks is observed when just meeting the existing standard. Incremental benefits are small for lower W126 levels (11 and 7 ppm-hrs) and are likely insignificant given the above-discussed uncertainties associated with the RBL analysis.

EPA relies on an analysis of 22 Class I Areas to conclude in the PR that attainment of the current standard does not adequately protect against potential tree growth impacts in Class I areas (US EPA, 2014a, Table 7). However, due to the long-range transport of ozone and ozone precursors to Class I areas from upwind non-attainment areas, it is not appropriate for EPA to evaluate the level of protection offered by the current primary ozone standard under current conditions. When these upwind areas make emissions reductions to attain the current standard, downwind areas will see improvements in air quality and decreasing W126 levels. As a result, this analysis should not be considered justification for promulgating a more stringent standard.

The WREA discussed the relative annual yield loss in 10 crop species. At W126 values ranging from 7 to 15 ppm-hrs, all 10 species had median crop relative yield loss values below the arbitrary 5% threshold that EPA used.

Visible Foliar Injury Visible foliar damage has limited usefulness as a criterion on which to base the secondary standard, because it is not a good indicator of growth suppression and it is not quantitative. In fact, EPA noted that "ozone is not a good predictor of the presence or absence of foliar injury…" (US EPA, 2014c, p. 7-63). Despite such a statement, EPA assessed the relationship between ozone and foliar injury and discussed significant reductions in the presence of foliar injury below W126 index values of 10.46 ppm-hrs but marginal changes in foliar injury presence/absence for W126 values above 10.46 ppm-hrs. Based on a

3 US EPA's air quality analysis (see US EPA, 2014c, Figure 4-15) shows that just meeting the current standard (0.075 ppm) corresponds closely to a W126 level of 15 ppm-hrs.

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screening-level assessment of visible foliar injury in parks, when adjusted to just meet the existing standard at 0.075 ppm, none of the 214 parks evaluated would exceed the 10.46 ppm-hrs benchmark identified by EPA. In other words, the visible foliar injury analyses conducted by EPA provide no useful information for the purpose of setting a secondary standard, let alone for supporting a more stringent standard. Ecosystem Services Four ecosystem services were evaluated for just meeting the existing standard and for three air quality scenarios (15, 11, and 7 ppm-hrs): consumer/producer surplus for timber production, consumer/producer surplus for agricultural production, carbon sequestration, and pollution removal. The consumer/producer surplus services analyses predicted that increased yield from lower ozone levels would generally increase supply and produce lower prices, resulting in a loss for producers and a gain for consumers. The national-scale analysis of impacts from carbon sequestration and carbon storage (due to reduced biomass loss) indicates appreciably more storage by just meeting the existing standard, compared to recent ozone conditions, with somewhat smaller additional increases for lower W126 levels. Similarly, potential air pollution removal increases substantially by just meeting the current standard, compared to recent ozone conditions (US EPA, 2014e). Based on the significant uncertainties associated with these analyses, the small predicted differences between just meeting the existing standard and the three W126 scenarios analyzed (7, 11, and 15 ppm-hrs) are highly uncertain. This was further acknowledged by EPA, which stated, "...that staff places limited weight on the absolute magnitude of the risk results for these ecosystem service endpoints due to the identification of significant associated uncertainties" (US EPA, 2014a, p. 75332-75333). 2.4 Conclusions

The current secondary form can provide welfare protection equivalent to a seasonal standard in the form of the W126. It is therefore entirely appropriate for the Administrator to propose to retain the current form of the secondary standard, which shares the form of the primary standard. We disagree with the Administrator that the exposure and risk analyses presented in the current review justify lowering the level of the secondary standard. A more stringent standard will provide no meaningful additional welfare protection beyond what is already provided by just meeting the current standard. Our conclusions to retain the current standard in the same form and at the same level are further supported in comments provided by the National Council for Air and Stream Improvement (Loehle et al., 2015). The Administrator should retain the standard at 0.075 ppm

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