socioeconomic impacts expressed by these commenters have been rejected
by the courts, as summarized in section I.A above, including in Murray
Energy, with the reasoning that consideration of such impacts was
precluded by Whitman's holding that the ``plain text of the Act
`unambiguously bars cost considerations from the NAAQS-setting process'
'' (Murray Energy Corp. v. EPA, 936 F.3d at 621, quoting Whitman, 531
U.S. at 471).
---------------------------------------------------------------------------

    \90\ Comments related to implementation programs are not
addressed here because, as described in section I.A above, this
action is being taken pursuant to CAA section 109(d)(1) and relevant
case law. Accordingly, concerns related to implementation of the
existing or an alternate standard are outside the scope of this
action.
---------------------------------------------------------------------------

    We also note that some commenters that stated their support for
retaining the current standard without revision additionally claimed
that, based on the results of the exposure and risk analyses in this
review, the current standard provides somewhat more public health
protection than the EPA recognized in the 2015 decision establishing
it. As support for this view, these commenters cite conclusions
(including those in the PA) that the exposure and risk estimates are
equivalent or slightly lower than those from the 2014 HREA. In
generally agreeing with the commenters' observation with regard to the
differences in exposure/risk estimates from analyses in this review
compared to those from 2014, we note that the current exposure/risk
estimates, while based on conceptually similar approaches to those used
in the 2014 HREA, reflect a number of improvements to input data and
modeling approaches, summarized in section II.A.3 above, which have
reduced uncertainties. These updated analyses inform the
Administrator's judgments in this review.
b. Comments in Disagreement With Proposed Decision
    Of the commenters that disagreed with the proposal to retain the
current standard, some recommend tightening the standard, while one
submission recommends a less stringent standard. The commenters
supporting a less stringent standard generally assert that the current
standard is overprotective, stating that information they provide
supports returning to the pre-2015 standard of 75 ppb and/or revising
the form from the 4th highest daily maximum to the seventh highest
daily maximum. The commenters that recommended a more stringent
standard describe a need for revision to provide greater public health
protection, generally claiming that the current standard is inadequate
and does not provide an adequate margin of safety for potentially
vulnerable groups. We address these sets of comments in turn below.
(i) Comments in Disagreement With Proposed Decisions--Calling for Less
Stringent Standard
    The commenters recommending revision to a less stringent standard
generally expressed the view that the current standard is more
stringent than necessary to protect public health. In support of this
view the commenters argue (1) that in this review the EPA
``discredited'' a cardiovascular mortality study on which commenters
assert the 2015 decision had placed especially heavy weight; (2) that
in light of limitations they assert for the exposure and risk estimate
analyses conducted in this review, a 75 ppb standard would meet 2015
objectives; and, (3) that additional factors they identify indicate
that the current standard of 70 ppb is too close to background levels
while a standard of 75 ppb or one with a form that uses the seventh
(versus fourth) highest daily maximum 8-hour O3
concentration would not be.
    With regard to the first argument, the EPA knows of no
cardiovascular mortality study, much less any health study, that was
relied on in the 2015 review that has been discredited, and the
commenters provide no citation for such a study. To the extent that the
commenter may be intending to refer to the difference of the current
review from the 2015 review with regard to the Agency's causality
determinations for cardiovascular effects and all-cause mortality, we
note that these changes did not involve ``discrediting'' of any studies
in the 2013 ISA. Rather, as summarized in section II.A.2.a above, since
the time of the last review the controlled human exposure study
evidence base has been appreciably expanded from one study to several,
none of which report O3-induced cardiovascular endpoints.
This update to the evidence base for cardiovascular effects, which also
includes epidemiologic studies, has contributed to a change in the
weight of evidence that supports the Agency's causality determinations
for both cardiovascular effects and mortality. To the extent that the
commenters intend to suggest that these changes in causality
determinations indicate that the current standard is more stringent
than necessary to protect public health, the Agency disagrees. The
Administrator's reasons for concluding that the current standard
provides the requisite public

health protection are explained in section II.B.3 below.
    With regard to the risk and exposure analyses, the comment argues
that 2019 O3 ambient air monitoring data for locations
meeting a design value of 75 ppb indicate that a 75 ppb standard could
achieve comparable exposure estimates to those derived for air quality
just meeting the current standard by the EPA's exposure/risk analyses.
The comment also asserts that uncertainty in the controlled human
exposure evidence base with regard to children with asthma suggests
``some latitude'' is needed in the risk calculations. The analysis
provided in the comment appears to focus on counties in designated
nonattainment areas with 2019 design values ranging from 71 to 75. For
these counties, the commenters' analysis appears to sum the population
of the subset of these counties with at least one daily maximum 8-hour
average concentration in 2019 falling in the range from 73 to 79 ppb
(and, separately, the population of counties with at least one such
value above 80 ppb). From these population counts, the analysis derives
estimates of the subpopulations of children with asthma spending
afternoons outdoors (using national estimates for representation of
children in the total population, of children with asthma in the total
child population, and of children in asthma spending afternoons
outdoors using analysis of CHAD diaries for children). The analysis
divides the two values by the commenters' estimate of children with
asthma in the U.S. (304 million [total population of the U.S.] x 10.5%
[percentage representing children] x 9.7% [percentage representing
children with asthma]).
    There are many aspects of the analysis submitted with the comment
that are not focused on the objective of estimating exposures of
concern that might be expected to be experienced by at-risk populations
in U.S. areas that just meet a standard with an alternative level of 75
ppb. As just one example of these aspects, the denominator in the final
step of the commenters' calculation is inflated by population counts
for areas of the U.S. excluded from the commenters' analysis (with this
larger population multiplied by a national estimates of percent that
are children, 10.5%, and a national estimate of percent of children
that have asthma, 9.7%), yielding a percentage of unclear relevance to
consideration of exposures occurring in areas just meeting an
alternative standards of 75 ppb. If the population of the nonattainment
areas on which the commenters' focus is substituted in the calculation
for the total population of the U.S. as the denominator (29.5 million x
10.5% x 9.7% = 146,664), with the commenters' estimates of children in
those areas that may experience an exposure at or above 80 ppb (4,788)
or below 80 ppb and at or above 73 ppb (12,641), the percentages are
3.3% and 8.6%, respectively (and the percentage for at or above 73 ppb
would be 5.8%).\91\ Thus, contrary to the commenters' assertion, their
analytical approach, with use of a denominator that reflects the
commenters' focus areas, results in higher estimates of the percentage
of at-risk children that may experience particular exposures of concern
in areas meeting a 75 ppb standard than does the EPA's analysis, which
takes into account a number of factors in much greater detail (e.g.,
through the use of exposure modeling and human activity data to
estimate time series contributing to 7-hour exposure periods with
average O3 concentrations at or above benchmarks), and
focuses on temporal and spatial patterns of air quality in areas just
meeting a standard of 75 ppb. The commenters analysis is not focused on
the factors that are key determinants of population exposures of
concern, leading to results that are inconsistent with and less
informative than the findings of EPA's more detailed, extensive and
technically sound exposure and risk analyses (summarized in section
II.A.3 above and Appendices 3C and 3D of the PA). Based on
consideration of these analyses, among other factors, as described in
section II.B.3 below, the EPA disagrees that the available evidence and
quantitative analyses supports the conclusion that the current standard
is overprotective and that a standard of 75 ppb would protect public
health with an adequate margin of safety.
---------------------------------------------------------------------------

    \91\ The EPA's exposure and risk analyses estimate <.1 to 0.3%
of children with asthma might be expected to experience at least one
exposure, while at increased exertion, at or above 80 ppb, on
average across a 3-year period in areas just meeting a potential
alternative standard of 75 ppb (85 FR 49865,Table 4, August 14,
2020). For the 70 ppb benchmark, these percentages are 1.1 to 2.0%.
---------------------------------------------------------------------------

    In support of the commenters' additional argument that the current
standard is too close to background and that a 75 ppb standard (or a
standard using the seventh highest form) would not be, the commenters
(1) state that just because a D.C. Circuit decision has stated that EPA
is not required to take U.S. background O3 (USB) into
consideration in NAAQS decisions does not mean that such considerations
are precluded; (2) cite the lower number of counties (and associated
population) that would be in nonattainment for a 75 ppb standard as
compared to the current standard (while also suggesting that revision
of the form to a seventh highest would appropriately allow for
additional high O3 days due to wildfires); and (3) suggest
that the EPA is underestimating USB by a factor of three.
    With regard to the legal point, the EPA agrees that while it is not
required to take USB into account in NAAQS decisions, it may do so when
such consideration is consistent with the Clean Air Act and prior court
decisions. The EPA is not relying on consideration of background
O3 levels to support its decision in this review. Moreover,
given the differences in public health protection, as noted in the
Administrator's proposed conclusions and described in his conclusions
in section II.B.3 below, we do not believe that we could use proximity
to background concentrations as a basis for revising the current 70 ppb
standard to a potential 75 ppb standard.\92\ On the commenters' second
point, the EPA notes that the number of counties that would or would
not be in nonattainment, the size of population living in them, and the
increasing number of days for high O3 due to wildfires are
not relevant factors in judging whether a particular standard is
requisite under the Clean Air Act. Regardless of such implications of a
decision to retain or revise a NAAQS, the key consideration for the
review of a primary standard is whether the standard is judged to
provide the requisite protection of public health with an adequate
margin of safety.\93\ The commenters have provided no evidence
suggesting that the current standard provides more than the requisite
public health protection under the CAA or indicating that an alternate
standard

with a level of 75 ppb or with a seventh highest form would provide
requisite protection. For these reasons, we do not find these comments
persuasive in supporting consideration of revising the current standard
to an alternate standard with a level of 75 ppb or with a seventh
highest form.
---------------------------------------------------------------------------

    \92\ Taken together, the EPA generally understands prior court
decisions addressing consideration of background O3 in
NAAQS reviews to hold that while the Agency may not establish a
NAAQS that is outside the range of reasonable values supported by
the air quality criteria and the judgments of the Administrator
because of proximity to background concentrations, it is not
precluded from considering relative proximity to background
O3 as one factor in selecting among standards that are
within that range (American Trucking Ass'ns v. EPA, 283 F.3d 355,
379 [D.C. Cir. 2002]; Murray Energy v. EPA, 936 F.3d at 622-624;
American Petroleum Institute v. Costle, 665 F.2d 1176, 1185 [D.C.
Cir. 1982]).
    \93\ Comments related to implementation programs are not
addressed here because, as described in section I.A above, this
action is being taken pursuant to CAA section 109(d)(1) and relevant
case law. Furthermore, leaving the NAAQS unaltered will not require
the EPA to make new air quality designations, nor require States or
authorized tribes to undertake new planning or control efforts.
Accordingly, concerns related to implementation of the existing or
an alternate standard are outside the scope of this action.
---------------------------------------------------------------------------

    With regard to USB, the commenters present an argument focused on
an urban/``rural'' comparison and one focused on a 1-month analysis of
O3 concentrations in response to population mobility changes
attributed to restrictions placed to manage infections of Corona virus
19 disease (COVID-19). We find there to be limitations in both
arguments that undercut the conclusions reached by the commenter. As a
result, we disagree that the observations made by the commenters
support their statements regarding USB and with the implication that
they contradict the EPA's findings from the detailed and extensive
analyses presented in the PA (PA, section 2.5 and Appendix 2B).
    With regard to the urban/``rural'' comparison, the commenters'
first cite EPA's analysis in the PA which indicated, based on daily
maximum 8-hour (MDA8) concentrations for the nation as a whole, that
from one quarter (10 out of 42 ppb) to one third (14 out of 45 ppb) of
average MDA8 concentrations in spring and summer, respectively, are
derived from anthropogenic sources. They then state that differences in
monthly mean MDA8 concentration between two sets of monitoring sites in
the Philadelphia metropolitan area that they identify as the three
highest and the three most rural was 3.3 ppb in April 2020. The
commenters suggest that this amount is much smaller than the 10 to 14
ppb that EPA estimated to be from anthropogenic sources. Based on these
two statements, they contend that USB is being underestimated by a
factor of three.
    We find the commenters' analysis to have several flaws that
undercut their conclusion. First, the difference between the two sets
of sites, all of which fall in the Philadelphia metropolitan area, are
not indicative of either USA (i.e., U.S. anthropogenic) or USB
contributions. There is no evidence that this difference is indicative
of either USB or USA, and it is especially anomalous given that the
commenters' analysis is based on 2020 data (affected by reduced
emissions during the reduced travel during the initial months of the
COVID-19 epidemic in the U.S.) while EPA's is based on 2016 data.
Second, the authors cite a country-wide seasonal average despite the
fact that the U.S. anthropogenic contributions are clearly higher in
the nonattainment area (than a U.S. average) being referenced. Further,
the conclusions about USB underestimation appear quantitatively
incorrect and to perhaps confuse USA and USB in the calculations. Even
if all USA anthropogenic contributions cited (10 USA and 30 USB of
total 40 ppb) in spring of 2016 were actually USB, the underestimation
of USB would be 25% at most (0 USA and 40 USB of total 40 ppb; (40-30)/
40 = 25%), thus it is unclear how the commenter concluded a factor of
three (300%) under-estimation of USB. In addition, the commenter's
dataset is for the Philadelphia-Wilmington-Atlantic City CSA, where
O3 more frequently exceeds the level of the standard in May
through September (e.g., PA, Appendix 3C, Figure 3C-79), months that
have lower USB and higher US anthropogenic than month of April, which
the commenters analyzed. Finally, the commenter has focused on low
concentration days (averaging ~40-45ppb) that the PA shows tend to be
different than high days (PA, section 2.5 and Appendix 2B).
    The second argument is based on data on Apple Mobility data \94\
and O3 and NO2 concentrations for the period from
3/22/2020 to 4/20/2020 (when transportation activity was affected by
the behavioral changes in response to COVID-19) and differences from
the same period in prior years. Based on the differences, the
commenters conclude that O3 concentrations were less
responsive to the 40 to 60% reduction in mobility than were
NO2 concentrations (7% vs 22% difference), indicating to the
commenters that society is reaching a period of diminishing returns of
actions to control O3 concentrations. We note, however, that
the period of the commenters' analysis is April, while the majority of
days with MDA8 greater than 70 ppb in the Philadelphia nonattainment
area occur in May to September. In the mid to late summer period, local
production of O3 is increased (see PA section <IP_ADDRESS>) and
MDA8 concentrations in the Philadelphia nonattainment area more
frequently are above the level of the standard. Thus, the analysis does
not support the commenters' argument for a less stringent standard.\95\
---------------------------------------------------------------------------

    \94\ https://covid19.apple.com/mobility.
    \95\ We also note, contrary to the commenters' premise,
NO2 and/or NOX are not conserved over a day.
Rather, the overall lifetime of NOX is on the order of
six hours. Further, while the commenter describes the ``local''
nature of O3, it is well established that O3
has a large transport component. The diurnal pattern of
O3 concentrations highlighted on this point is likely
illustrating O3 concentrations subject to local
NOX-titration rather than purely local formation as
suggested by the commenters.
---------------------------------------------------------------------------

(ii) Comments in Disagreement With Proposed Decision and Calling for
More Stringent Standard
    Among the commenters that disagree with the proposed decision and
call for a more stringent standard, most express concerns regarding the
process for reviewing the criteria and standards in this review and
assert that the proposal must be withdrawn, and a new review conducted.
The commenters expressing the view that a more stringent standard is
needed variously cite a number of concerns. Some state that EPA cannot,
as some commenters imply it does, simply base its decision on a
judgment that the available evidence is similar to that when the
standard was established in a prior review, and some argue that the
available health effects evidence indicates that adverse health effects
occur from exposures allowed by the current standard. Further some
commenters express their views that the combined consideration of the
complete evidence base indicates that sensitive or vulnerable
populations are not protected by the current standard; and/or that the
standard does not provide an adequate margin of safety. Additionally,
in support of their view that the standard should be made more
stringent, some commenters disagree with the conclusions of the
exposure and risk analyses, characterizing the analyses as deficient,
and contending that other quantitative analyses they cite indicate
health impacts that would be avoided by a lower standard level. Most of
the commenters advocating a more stringent standard recommend revision
of the level to a value at or below 60 ppb and others support a level
at or below 65 ppb. Some of these commenters additionally note they had
raised similar concerns during the 2015 review.\96\ Some commenters
also express the view that the EPA should establish a separate long-
term standard.
---------------------------------------------------------------------------

    \96\ We note that comments raised in the prior review were fully
considered in reaching the decision in that review. Such comments
are addressed in the decision and associated Response to Comments
(80 FR 65292, October 26, 2020; U.S. EPA, 2015). To the extent that
commenters are raising similar issues in support of their comments
on the proposed decision in this review, we have addressed them in
the current decision, based on the information now available.
---------------------------------------------------------------------------

    With regard to the process by which this review has been conducted,
we disagree with the commenters that it is arbitrary and capricious or
that it does not comport with legislative requirements. The review
process, summarized in section I.D, implemented a number of features,
some of which have been employed in past reviews and others which have
not,

and several which represent efficiencies in consideration of the
statutorily required time frame for completion of the review. The
comments that raise concerns regarding specific aspects of the process
are addressed in the separate Response to Comments document. As
indicated there, the EPA disagrees with these comments. The EPA finds
the review to have been lawfully conducted, the process reasonably
explained, and thus finds no reason to withdraw the proposal.
    We disagree with some commenters' contention that the EPA based its
proposed decision simply on the similarity of the health effects
evidence to that available in the last review. While the health effects
information is generally similar to that available in the last review,
particularly with regard to respiratory effects (the effects causally
related to O3 exposure), the current health effects evidence
base includes hundreds of new health studies. Based on consideration of
the full evidence base, including that the newly available in the
current review, the EPA has reached different conclusions regarding
some categories of effects (as summarized in II.A.2.a above). The EPA's
observation that the nature of the evidence has not substantially
changed with regard to effects causally related to O3
exposure, was not, as implied by the comment, the primary consideration
in the Administrator's proposed decision. The Administrator considered
a number of factors in reaching his proposed decision, including the
full extent of the currently available health effects evidence, and the
details in which it is, and is not, similar to the last review, which
has led to conclusions similar to prior conclusions for some categories
of O3 effects and resulted in changes to others (85 FR
49868-49874, August 14, 2020).\97\ Further, in reaching his final
decision in this review, as described in section II.B.3 below, he has
again considered the currently available information, now in light of
the public comments received on the proposal, among other factors.\98\
In sum, while we have noted the similarities in the health effects
information between this review and the last review (particularly for
respiratory effects), we have engaged in independent analysis and
assessment of the health effects information in this review, and the
Administrator has exercised his independent judgment based on the
current health effects assessment, in combination with current
exposure/risk information, advice from the CASAC and public comment.
Thus, contrary to the suggestion by these commenters, the decision on
the primary standard has been made in consideration of the current
health effects evidence, current analyses of air quality, exposure and
risk, advice from the CASAC, and public comments, consistent with
requirements under the CAA.
---------------------------------------------------------------------------

    \97\ As just one example, the causal determinations for
cardiovascular effects and total mortality in this review differ
from those made in the last review, as described in section
II.A.2.a.
    \98\ In so doing, to the extent the current evidence before the
Administrator continues to support or reinforce conclusions reached
in prior reviews, he may reasonably reach those same conclusions.
---------------------------------------------------------------------------

    In support of their position that the available health effects
evidence indicates that O3 exposures occurring in areas that
meet the current standard are causing adverse effects, some commenters
cite studies that investigate associations of O3
concentrations and effects, such as respiratory effects, mortality, and
preterm birth.\99\ These studies include some already evaluated in the
air quality criteria,100 101 some published subsequent to
the literature cutoff date for the ISA, and some which some commenters
claim the EPA arbitrarily dismissed or inconsistently weighed in
reaching the proposed decision.\102\ As discussed in I.D above, we have
provisionally considered these ``new'' studies that have not already
been evaluated in the air quality criteria and that were cited by
commenters in support of their comments on the proposed decision (Luben
et al., 2020). Based on this consideration, we conclude that these
studies do not materially change the broad conclusions of the ISA with
regard to these health effects, including the conclusions that there is
a causal relationship of short-term respiratory effects with
O3 exposures; a relationship of long-term respiratory
effects with O3 exposure that is likely to be causal;
evidence that is suggestive of, but not sufficient to infer, causal
relationships of cardiovascular effects and total mortality with short-
or long-term O3 exposure; evidence that is suggestive of,
but not sufficient to infer, causal relationships of central nervous
system effects with short- or long-term O3 exposure; and,
evidence that is suggestive of, but not sufficient to infer, causal
relationships of reproductive and developmental effects with long-term
O3 exposure (ISA, section IS.1.3.1). Nor do we find that
these studies warrant reopening the air quality criteria for further
review (Luben et al., 2020). Thus, we do not find these publications to
be contrary to the discussions and associated conclusions in the PA and
proposal or to indicate the current standard to be inadequate. We
disagree that studies cited by commenters show these categories of
effects to be caused by O3 exposures associated with
O3 air quality that meets the current standard. We continue
to focus on the studies of respiratory effects as most important to the
Administrator's judgments concerning the public health protection
provided by the current standard.
---------------------------------------------------------------------------

    \99\ With regard to effects other than respiratory effects,
studies cited by these commenters include studies of cardiovascular
effects (Day et al., 2017; Shin et al., 2019; Wang et al., 2019b),
all-cause mortality (Bell et al., 2014; Cohen et al., 2017; Di et
al., 2017a, b), neurological effects (Cleary et al., 2018), and
reproductive and developmental effects (Wallace et al., 2016;
Lavigne et al., 2016; Salam et al., 2005; Steib et al, 2019;
Morello-Frosch et al., 2010).
    \100\ In updating the air quality criteria in the current
review, the current ISA evaluates relevant scientific literature
published since the 2013 ISA, integrating with key information and
judgments contained in the 2013 Ozone ISA and previous assessments
(ISA, p. lxix; 2013 ISA; U.S. EPA, 2006; U.S. EPA, 1996a; U.S. EPA,
1982; U.S. EPA, 1986; U.S. EPA 1978; NAPCA, 1969).
    \101\ This commenter cited a epidemiologic study (Day et al.,
2017) that had been among studies of short term O3 and
cardiovascular effects excluded from the draft ISA due to location,
however this study was considered by the EPA in response to advice
from the CASAC on the draft ISA (Luben, 2020). This consideration of
these studies did not change EPA's analysis of the weight of
evidence from that described in the draft ISA, thus supporting the
causality determination for cardiovascular effects described in the
final ISA (ISA, section IS.4.3).
    \102\ We note that one study identified by a commenter to
support their view that O3 concentrations allowed by the
current standard is causing health effects does not include
O3 among the pollutants it examines (Gan et al., 2014).
Accordingly, we do not find the study to provide support to the
commenter's point.
---------------------------------------------------------------------------

    The epidemiologic studies of respiratory effects identified by the
commenters include some investigating associations of O3
exposure with hospital admissions or emergency department visits for
respiratory outcomes, or with various respiratory effects for selected
population groups. Studies of O3 and respiratory effects
cited by these commenters in support of their comment include studies
that have already been evaluated in the air quality criteria (Goodman
et al., 2017; O'Lenick et al., 2017; Jerrett et al., 2009; Lin et al.,
2008; Islam et al., 2009; Galizia et al., 1999; Peters et al., 1999;
Wendt et al., 2014), and also several ``new'' studies, including four
that investigate a relationship between O3 and COVID-19
(Ware et al., 2016; Strosnider et al., 2019; Wang et al., 2019a;
Adhikari and Yin, 2020; Zhu et al., 2020; Zoran et al., 2020; Petroni
et al., 2020).\103\ We do not

find these studies to contradict any of the scientific conclusions on
respiratory effects described in the ISA.
---------------------------------------------------------------------------

    \103\ As discussed in section I.D above, the ``new'' studies
identified by commenters have not been through the comprehensive
CASAC and public review process that the air quality criteria went
through. To address these comments, we have provisionally considered
these studies, as discussed in I.D above, and found they do not
materially change the broad scientific conclusions of the ISA with
regard to respiratory effects, or warrant re-opening the air quality
criteria for further review (Luben et al., 2020).
---------------------------------------------------------------------------

    With regard to the four studies on COVID-19, we disagree with the
commenters that they provide evidence that O3 exposure
contributes to COVID-19 incidence, much less that they indicate that
O3 concentrations occurring when the current standard is met
would do so. These studies investigate an association between
O3 and COVID-19 cases or deaths. We note, however, that the
time-series study design used in three of these studies (Zhu et al.,
2020 [incorrectly cited by some commenters as Yongiian et al, 2020];
Adhikari and Yin, 2020; Zoran et al., 2020) is not appropriate for
infectious disease cases, which do not follow a Poisson distribution,
as they increase exponentially with community spread. The fourth study,
an ecological study (Petroni et al. 2020), is also limited by its study
design, which is susceptible to confounding or other biases related to
ecologic fallacy,\104\ as well as its manner of assigning exposure to
the population.\105\ Further, the time periods in none of the four
studies is long enough to rule out a coincidental increase in the
community spread of COVID-19 with the increased O3
concentrations expected with the beginning of O3 season in
these areas (e.g., March-April). Lastly, the biological basis by which
a gaseous pollutant such as O3 would be expected to
contribute to incidence of this disease is unclear.\106\ Thus, we do
not find these studies to support a conclusion that O3
exposure causes COVID-19 morbidity or mortality.\107\
---------------------------------------------------------------------------

    \104\ Ecologic fallacy is a specific type of bias that results
when group- or population-level data are used to estimate
individual-level risks in an epidemiologic study
    \105\ This study uses 2016 summertime average O3 as a
surrogate for O3 from 3/1/2020 to 7/11/2020 (Petroni et
al., 2020). Yet COVID-19 cases did not surge in many parts of the
U.S. until late summer or fall 2020. To the extent these areas
(e.g., rural upper midwest) have lower O3 concentrations
than areas of the country where COVID-19 cases surged earlier (e.g.,
New York City), a correlation between O3 concentrations
and COVID-19 deaths would be overestimated.
    \106\ While there may be correlations between O3
concentrations and COVID-19 cases and deaths, they could be
explained by coincidental timing of the COVID-19 community
transmission period in New York City and Milan with the early part
of the O3 seasons in those areas, and neither the
investigators or commenters provide evidence supporting an
alternative plausible basis (Adhikari and Yin, 2020; Zoran et al.,
2020).
    \107\ While the full evidence base indicates the potential for
O3 to increase susceptibility to some respiratory infections, the
studies cited by commenters do not provide evidence that short-term
or long-term O3 exposure increases susceptibility to
COVID-19.
---------------------------------------------------------------------------

    With regard to the commenters' claims that effects other than
respiratory effects (see above) are occurring as a result of
O3 concentrations allowed by the current standard, we note
that the standard is exceeded in nearly all of the locations and time
periods analyzed in these studies.\108\ Although some studies analyzed
multiple cities or locations in which the current standard was met
during some time periods, air quality during other time periods or
locations in the dataset does not meet the current standard. As noted
in past reviews, compared to single-city studies, there is additional
uncertainty in interpreting relationships between O3 air
quality in individual study cities and reported O3 multicity
effect estimates. Specifically, as recognized in section II.A.2.c
above, the available multicity effect estimates in studies of short-
term O3 do not provide a basis for considering the extent to
which O3 health effect associations are influenced by
individual locations with ambient O3 concentrations low
enough to meet the current O3 standards versus locations
with O3 concentrations that violate this standard (85 FR
49853, August 14, 2020; 80 FR 65344, October 26, 2015).\109\ Thus,
based on this information and the full health effects evidence base for
O3, we disagree with commenters about the implications of
the cited epidemiologic studies regarding health risks of O3
exposures resulting from the O3 concentrations in ambient
air allowed by the current standard.
---------------------------------------------------------------------------

    \108\ Locations and time periods analyzed in these studies
include three large metropolitan areas in Texas before 2012 (Goodman
et al., 2017); Atlanta, Dallas and St. Louis from 2002 to 2008
(O'Lenick et al., 2017); large cities across the U.S. from late
1970s through 2000 (Jerrett et al., 2009); New York State, primarily
during the 1990s (Lin et al., 2008); U.S. location chosen for O3
concentrations not meeting the standard (Galizia and Kinney, 1999);
a set of southern California communities during period (1990s)
recognized to be exceeding the NAAQS (Peters et al., 1999; Islam et
al., 2009); Houston metropolitan area during 2005 to 2007 (Wendt et
al., 2014); multiple locations including St. Louis, Memphis and
Atlanta 2003 through 2012 (Ware et al., 2016); six U.S. metropolitan
areas, including Los Angeles, Baltimore and New York City, from 1999
thru 2018 (Wang et al., 2019a); and 894 U.S. counties, including
those for New York City and Los Angeles, 2001 to 2014 (Strosnider et
al., 2019). Air quality data and design values derived by the U.S.
indicate that the current 70 ppb standard was not met throughout the
study period, or, for multicity studies for which single-city
analyses not performed, was not met in all cities throughout the
study (PA, Appendix 3B and Excell files available at: https://www.epa.gov/air-trends/air-quality-design-values).
    \109\ This uncertainty applies specifically to interpreting air
quality analyses within the context of multicity effect estimates
for short-term O3 concentrations, where effect estimates
for individual study cities are not presented, as is the case for
some of the multicity studies identified by commenters (85 FR 49870,
August 14, 2020).
---------------------------------------------------------------------------

    Protection of Sensitive Groups: Commenters expressing the view that
the current standard does not protect sensitive or at-risk populations,
variously state that the EPA does not consider risks to a number of
population groups the commenters identify as at higher risk for
O3-related health effects, and that retaining the current
standard ``creates additional and unacceptable risks'' for Black and
low-income communities. Further, some commenters express the views that
together the evidence from controlled human exposure studies and from
epidemiologic studies indicates adverse effects associated with
exposures allowed by the current standard; and that the EPA has not
appropriately considered a number of aspects of the evidence related to
risks to people with asthma.
    Some commenters, in addition to contending that the current
standard will not protect populations for which the EPA has concluded
there is adequate evidence for identification of increased risk (e.g.,
people with asthma, children, and outdoor workers), additionally assert
that the current standard will not protect populations of color,
American Indian/American Native groups, low SES communities, people of
any age with respiratory issues other than asthma, diabetes or atrial
fibrillation and pregnant women. As described in section I.A. above,
primary NAAQS are intended to protect the public health, including at-
risk populations, with an adequate margin of safety. Accordingly, in
reviewing the air quality criteria, the EPA evaluates the evidence with
regard to factors that place some populations at increased risk of harm
from the subject pollutant. In this review, the populations for which
the evidence indicates increased risk include people with asthma,
children and outdoor workers, among other groups, as summarized in
section II.A.2.b above (ISA, section IS.4.4).
    In support of their argument that individuals with atrial
fibrillation are at increased risk of O3-related health
effects, the commenter cited a study of O3 exposure and
total mortality that has been evaluated in the ISA (Medina-Ramon and
Schwartz, 2008). It was initially evaluated in the last review and
explicitly discussed again as part of the evidence base available in
the current review (ISA, section <IP_ADDRESS> and Table IS-10; 2013 ISA,
sections <IP_ADDRESS> and 8.2.4). Based on consideration of that study and
others investigating a potential for increased risk among populations
with cardiovascular disease

(CVD), the 2013 ISA concluded that the evidence was ``inadequate to
classify pre-existing CVD as a potential at-risk factor for
O3-related health effects'' (2013 ISA, sections 8.2.4). In
the current review, while a limited number of recent studies add to the
evidence available in the 2013 ISA,\110\ collectively the evidence
remains inadequate to conclude whether individuals with pre-existing
CVD are at greater risk of O3-related health effects (ISA,
Table IS-10, section IS.<IP_ADDRESS>). Thus, the evidence does not support
the commenters assertion that populations with atrial fibrillation are
at increased risk of O3-related effects and that the current
standard does not protect these groups.
---------------------------------------------------------------------------

    \110\ Further, we note that a more recent study than that cited
by the commenters investigated the potential for an association of
O3-related mortality risk with individuals with atrial
fibrillation and observed no evidence of an association (ISA,
Appendix 6, p. 6-11).
---------------------------------------------------------------------------

    The commenters who contend pregnant women are at increased risk do
not provide supporting evidence, and the ISA does not reach such a
conclusion based on the currently available evidence. Further, the ISA
determined the evidence to be suggestive of, but not sufficient to
infer, a causal relationship between O3 exposure and
reproductive effects (ISA, section IS.<IP_ADDRESS>). Thus, we disagree with
the commenters that pregnant women may be at increased risk of
O3-related effects and disagree that the current standard
does not protect these groups.
    With regard to a potential for increased risk of O3-
related health effects based upon race or ethnicity, including American
Indians or Native Americans), the available evidence is inadequate to
make such a determination (ISA, section IS.4.4, Tables IS-9 and IS-
10).\111\ Additionally, the evidence of increased O3 risk
based on SES has been evaluated in the ISA and concluded to be
``suggestive,'' but the evidence is limited by inconsistencies (ISA,
section IS.4.4). Thus, contrary to the view expressed by some
commenters, the EPA has considered this factor in this review and the
evidence was not adequate to identify SES as a risk factor for
O3 related health effects. As noted by the commenters, the
evidence for low SES populations is ``suggestive'' of increased risk
(ISA, section IS.4.4), in part because it includes several
inconsistencies (as summarized in section II.A.2.b above), including
studies that did not find O3-related risk to be higher in
lower SES communities.\112\ While we agree with the commenters that
populations of some particular races or ethnic backgrounds or with low
SES have higher rates of some health conditions, including asthma,\113\
the available evidence is not adequate to conclude an increased risk
status based solely on racial, ethnic or income variables alone (ISA,
section IS.4.4). Thus, we disagree with commenters that EPA has
arbitrarily not considered such factors in reaching the decision on the
primary standard.
---------------------------------------------------------------------------

    \111\ In support of their view that O3-related risk
is increased in Black populations, some commenters cite a study
published after the ISA (Gharibi et al., 2019). We have
provisionally considered this study, as described in section I.D.
above, and found that it does not materially affect the broad
conclusions in the ISA, including those regarding the adequacy of
evidence for finding an influence on O3-related risk of
different categories of population status, or warrant reopening the
air quality criteria for further review (Luben et al., 2020).
    \112\ We note that two studies described by one commenter as
indicating that those with low SES or who live in low SES
communities face higher risk of hospital admissions and emergency
department visits related to O3 pollution have been
evaluated by the EPA and found not to report such findings (2013
ISA, section 8.3.3; ISA, Table IS-10). In the first, a study of
O3 exposure and respiratory hospital admissions in 10
Canadian cities (Cakmak et al., 2006) ``no consistent trend in the
effect was seen across quartiles of income,'' and the second, a
study of O3 exposure and asthma hospital admissions and
emergency visits (Burra et al., 2009), ``reported inverse effects
for all levels of SES'' (2013 ISA, p. 8-27; ISA, Table IS-10).
    \113\ This is noted in the PA and proposal with regard to Black
non-Hispanic and several Hispanic population groups (PA, Table 3-1).
As some commenters note, this is also the case for American Indian
and Native American population groups. Based on the recently
available, 2016-2018 National Health Interview Survey, while just
under 8% of the U.S. population is estimated to have asthma, the
estimate is more than 10% for American Indian or Native American
populations in the U.S. (https://www.cdc.gov/asthma/most_recent_national_asthma_data.htm; document identifier EPA-HQ-
OAR-2018-0279-0086).
---------------------------------------------------------------------------

    Some commenters further claim that tribal populations and
communities of color are at increased risk of O3-related
health effects due to increased impacts of COVID-19. We disagree with
commenters that the studies they cite provide support for the role of
O3 exposure in the observed increase in prevalence. The
studies cited simply describe greater prevalence of COVID-19 among such
communities and do not investigate and therefore do not provide
evidence for a role for O3 exposure.\114\ An additional
study cited by one commenter in support of their statement that people
with COVID-19 are more susceptible to effects of O3, does
not include any analyses with O3 among its analyses (Wu et
al, 2020). With regard to diabetes, we note that the evidence related
to a potential for this to affect risk of O3-related effects
has been explicitly evaluated and found to be inadequate, thus
indicating a lack of basis in the evidence for the statement by some
commenters that diabetes prevalence in a community increases the risk
of O3-related effects (ISA, Table IS-10).
---------------------------------------------------------------------------

    \114\ The commenter cites Price-Haywood et al. (2020), Stokes et
al. (2020), Millett et al. (2020), Killerby et al. (2020), and Gold
et al. (2020). These studies present information regarding COVID-19
cases, hospitalizations and/or deaths among various population
groups, but they do not investigate association of those occurrences
with O3.
---------------------------------------------------------------------------

    Additionally, commenters that contend that retaining the current
standard ``creates additional and unacceptable risks'' for minority and
low-income populations variously cite higher rates of asthma and other
preexisting conditions in these populations and higher levels of
pollution.\115\ In making this claim, these commenters state that non-
Hispanic Blacks have been found to be more likely to live in counties
with higher O3 pollution. To the extent that such patterns
in the distribution of certain population groups and O3
concentrations result in these populations residing in areas that do
not currently meet the current standard, we note that they are at
greater risk than populations residing in areas that meet the current
standard, and implementing the standard will reduce their risks. But we
disagree with the commenters' conclusion that retaining the current
standard, without any change, creates additional risks for these
populations.
---------------------------------------------------------------------------

    \115\ In making their argument, these commenters do not provide
any explanation for why retaining the existing standard (i.e.,
making no regulatory change) would create additional risk for these
populations. Rather, these commenters seem to be describing
differences in predicted risk or mortality of air quality associated
with a lower standard level and that of the current standard. In
that way, they are claiming that retaining the current standard
``creates'' additional risk. We address comments advocating a lower
standard based on commenter-cited risk estimates (e.g., mortality)
further below.
---------------------------------------------------------------------------

    Thus, contrary to statements by some commenters, the EPA's proposed
decision to retain the current standard did consider evidence regarding
risk to and thus protection of specific populations, such as those of
particular races or ethnicities or low-income populations. The proposed
decision, and the Administrator's decision described in section II.B.3
below, are based on consideration of the currently available evidence,
particularly that with regard to populations that may be at greater
risk of O3-related health effects than the general
population. As described in section II.B.3 below, the Administrator
judges that by basing his decision on consideration of these
populations, including adults and children with asthma, the at-risk
population groups for which the

evidence is strongest and most extensive, will also provide protection
for other at-risk populations for which the evidence is less certain
and less complete.
    The commenters who express the view that the current standard does
not provide sufficient protection of people with asthma raise concerns
with the EPA's consideration of this group and O3-related
effects. Further, some commenters state that the EPA has not adequately
explained how its approach for decision-making in this review protects
at-risk populations, such as people with asthma. Such commenters state
that the EPA does not explain how the proposed decision accounts for
the greater vulnerability of people with asthma, given the attention to
evidence from controlled human exposure studies of largely healthy
subjects. Some commenters contend that the EPA arbitrarily focuses on
lung function decrements and respiratory symptoms ahead of lung
inflammation, and/or that the EPA has not rationally considered the
most recent ATS statement with regard to consideration of effects in
people with respiratory disease, such as asthma (which the commenters
describe as a difference from past reviews).
    We disagree with these commenters. In this review, as in past
reviews, the EPA has fully considered the health effects evidence in
this review, including for sensitive populations, such as people with
asthma, and explained its conclusions regarding the adequacy of public
health protection offered by the current standard, including for such
populations. Thus, the decision in this review, as described in section
II.B.3 below, is based on the current scientific information. Further,
our approach in this review does not differ appreciably from our
approach in the last review. This approach is consistent with the
applicable legal requirements for this review, including with
provisions of the CAA related to the review of the NAAQS, and with how
the EPA and the courts have historically interpreted the CAA. The
approach is based fundamentally on the current health effects evidence
in the ISA and quantitative analyses of exposure and risk in the PA.
The policy implications of this information, along with guidance,
criteria or interpretive statements developed within the public health
community, including, also, statements from the ATS, in addition to
advice from the CASAC are evaluated in the PA for consideration by the
Administrator. The PA evaluations inform the Administrator's public
health policy judgments and conclusions. Thus, as in past reviews, the
Administrator's decision on the adequacy of the current primary
standard draws upon the scientific evidence for health effects,
quantitative analyses of population exposures and health risks, CASAC
advice, and judgments about how to consider the uncertainties and
limitations that are inherent in the scientific evidence and
quantitative analyses, as well as public comments on the proposed
decision.
    As described in section II.B.3 below, key aspects of the evidence
informing the Administrator's decision-making in this review include:
(1) The causal relationship of O3 with respiratory effects,
based on the full health effects evidence base, including both the
controlled human exposure studies conducted primarily in largely
healthy adult subjects, and the epidemiologic studies of health
outcomes for people with asthma, and particularly children with asthma;
(2) the increased risk to children and people with asthma, among other
groups (3) the respiratory effects reported at the lowest exposures in
the controlled human exposure studies; and (4) features of asthma that
contribute to the susceptibility of people with asthma to
O3-related effects. As a whole, the evidence base in this
NAAQS review generally reflects a continuum, consisting of exposure
levels at which scientists generally agree that health effects are
likely to occur, through lower levels at which the likelihood and
magnitude of the response become increasingly uncertain. As summarized
in section I.A above, the CAA does not require the Administrator to
establish a primary NAAQS at a zero-risk level or at background
concentration levels (see Lead Industries Ass'n v. EPA, 647 F.2d at
1156 n.51, Mississippi v. EPA, 744 F.3d at 1351), but rather at a level
that reduces risk sufficiently so as to protect public health with an
adequate margin of safety. The Administrator's consideration of the
scientific evidence is informed by the quantitative estimates of
exposure and risk for air quality allowed by the current standard, and
associated judgments on the adequacy of public health protection
provided by the current standard are informed by advice from the CASAC
and statements from ATS on adversity.
    With regard to the most recent ATS statement, the commenters' claim
that the EPA does not adequately consider the implications of the
sentence that ``small lung function changes should be considered
adverse in individuals with extant compromised function, such as that
resulting from asthma, even without accompanying respiratory symptoms''
and to consider the importance of examining effects in susceptible
subsets of broader populations (Thurston et al., 2017). We disagree.
The ATS statements (from the initial statement in 1985 to the recent
2017 statement) and their role in primary O3 standard
reviews, summarized in section II.A.2.b above, occupy a prominent role
in consideration of public health implications in the PA and the
proposal (PA, section 3.3.2; 85 FR 49848, 49866, 49871, August 14,
2020), and the Administrator considers them in his decision, as
described in section II.B.3 below. The PA presentation includes
summaries of the purpose and intentions articulated by the ATS, and of
the evolution and areas of consistency across the statements. The PA
gave particular attention to the ATS emphasis on consideration of the
significance or adversity of effects, particularly for more susceptible
individuals. It recognized both the 2000 ATS statement concluding that
``small transient changes in forced expiratory volume in 1 s[econd]
(FEV1) alone were not necessarily adverse in healthy
individuals, but should be considered adverse when accompanied by
symptoms'' (ATS, 2000), and also the more recent statement that also
gives weight to findings of such lung function changes in the absence
of respiratory symptoms in individuals with pre-existing compromised
function, such as that resulting from asthma (Thurston et al., 2017).
With regard to population risk (another aspect of the ATS statement
cited by commenters), the PA and proposal summarized the 2000 and 2017
ATS statements, recognizing that the 2017 statement references and
further describes concepts described in the 2000 statement, such as its
discussion of considering effects on the portion of the population that
may have a diminished reserve that puts its members at potentially
increased risk if affected by another agent (ATS, 2000).\116\ As
described in section II.B.3 below, the Administrator considers the ATS
statements in reaching his conclusions in this review.
---------------------------------------------------------------------------

    \116\ The sentence in the 2017 statement of which one commenter
quoted only a part, ``As discussed in the previous ATS statement, a
small but statistically significant mean reduction in
FEV1 in a population means that some people had larger
reductions, with the likelihood that reductions in a subset of
susceptible subjects can have passed a threshold for clinical
importance'' This paragraph goes on to note that a study in which
the mean decrement is about 3%, included two subjects with
decrements greater than 10% (Thurston et al., 2017).
---------------------------------------------------------------------------

    In support of their claim that the EPA has not appropriately
considered the ATS statements, some commenters

additionally take issue with the EPA's use of the number of subjects
experiencing at least a 15% FEV1 decrement in its
description in the proposal of the increased response evident by
comparing from the lowest exposure levels studied (40 ppb) up to 70 ppb
(85 FR 49851, August 14, 2020). These comments also state that EPA did
not discuss the clinical significance of FEV1 decrements of
10% or higher for people with existing lung disease, while stating that
the ATS statement mentions this magnitude of decrement. The ATS
statement references decrements at or above 10% in illustrating a point
about variation of subject responses beyond a group mean, noting that
while the mean of an exposed group of study subjects may be small, some
group members have larger reductions and can have passed a threshold
for clinical importance. It does not provide a discussion of thresholds
of clinical importance.\117\ In claiming that EPA's discussion on this
represents a difference from the last review, the commenters cite the
2014 HREA and state that we have not considered FEV1
decrements at or above 10% in the current review, however this is not
the case.\118\ Furthermore, the PA states that the mid- to upper-end of
the range of moderate levels of functional responses and higher (i.e.,
FEV1 decrements >=15% and >=20%) are included to generally
represent potentially adverse lung function decrements in active
healthy adults, while for people with asthma or lung disease, a focus
on moderate functional responses (FEV1 decrements down to
10%) may be appropriate (PA, Appendix 3D, p. 3D-76).
---------------------------------------------------------------------------

    \117\ With regard to 10% as a magnitude decrement, the prior ATS
statement noted that the EPA had graded this ``mild'' in a prior
review, while noting that such a grading has not been evaluated
against other measures (ATS, 2000). In this review, as in past
reviews, the EPA has summarized study results with regard to
multiple magnitudes of lung function decrement, including 10%,
recognizing that 10% has been used in clinical settings to detect a
FEV1 change likely indicative of a response rather than
intrasubject variability, e.g., for purposes of identifying subjects
with responses to increased ventilation (Dryden, 2010). For example,
the PA in the current review provides such a summary (PA, Appendix
3D, p. 3D-77).
    \118\ Contrary to this claim, the lung function risk analysis in
the current review (which is an update of the very same analysis in
the 2014 HREA to which the commenters cite) presents the results for
exactly the same categories of lung function decrement (at/above
10%, at/above 15% and at/above 20%) as in the 2014 HREA (e.g., PA,
Table 3-4).
---------------------------------------------------------------------------

    In objecting to the EPA's approach to considering the ATS
statement, these commenters cite a reference to the ATS statement in
CASAC's advice as additional evidence that the EPA approach to
considering the ATS statement is arbitrary.\119\ This comment was made
within the context of the CASAC comments on the draft PA that
emphasized the need to improve discussion of the susceptibility of
people with asthma, including giving attention to the occurrence of
lung function decrements in susceptible groups, specifically children
with asthma. This section of the CASAC letter also cautions against too
great a focus on lung function decrements and emphasizes the need for
fuller consideration of respiratory effects that are likely to be
important in people with asthma due to features of that disease. In
consideration of these comments, the final PA includes an improved
discussion on the unique vulnerability of people with asthma (PA,
sections <IP_ADDRESS>, 3.3.2, 3.3.4, and 3.5.1) that contributes to due
consideration of this population group in decision-making on the
primary O3 standard. Further, in considering the exposure
and risk analysis results, we recognize the comparison-to-benchmarks
analysis as providing a more robust consideration of risk to sensitive
groups as it provides the ability to consider O3 effects
more broadly, with each benchmark representing the array of effects, at
different severities, associated with that exposure level. This is one
of the reasons (consistent with the CASAC advice) that this analysis
(rather than the lung function risk analysis) receives greater emphasis
in the PA, consistent with the CASAC advice in this area.
---------------------------------------------------------------------------

    \119\ The citation provided by the commenters is the CASAC
letter on the draft PA; in this letter the CASAC cites the ATS
statement in making a comment on the draft PA indicating that the
concept that lung function decrements in the absence of symptoms do
not represent an adverse health effect should not apply to the
susceptible group of children with asthma (Cox, 2020a, Consensus
Responses to Charge Questions, pp. 8-9).
---------------------------------------------------------------------------

    In light of the above discussion, we note that the PA, the
proposal, and the decision described in section II.B.3 below, focus
specifically on consideration of people with asthma, and particularly
children with asthma. While the evidence regarding the susceptibility
of people with asthma to the effects of O3 is robust, our
understanding of the exposures at which various effects (of varying
severity) would be elicited is less defined. For example, the inherent
characteristics of asthma contribute to a risk of asthma-related
responses, such as asthma exacerbation in response to asthma triggers,
which may increase the risk of more severe health outcomes (ISA,
section 3.1.5). This is supported by the strong and consistent
epidemiologic evidence that demonstrates associations between ambient
O3 concentrations and hospital admissions and emergency
department visits for asthma (ISA, section IS.<IP_ADDRESS>). In moving to
consideration of the potential specific exposure scenarios (e.g.,
multiple-hour exposures to 60 to 80 ppb O3 during quasi-
continuous exercise), we note that the evidence is for largely healthy
adult subjects. With regard to lung function decrements, the limited
evidence from controlled human exposure studies (primarily at higher
exposures and in adult subjects) indicates similar magnitude of
O3-related FEV1 decrements for people with as for
people without asthma (ISA, Appendix 3, section <IP_ADDRESS>.1). Further,
across other respiratory effects of O3 (e.g., increased
respiratory symptoms, increased airway responsiveness and increased
lung inflammation), the evidence has also found the observed responses
to generally not differ due to the presence of asthma, although the
evidence base is more limited with regard to study subjects with asthma
(ISA, Appendix 3, section <IP_ADDRESS>). Thus, in light of the uncertainties
in the evidence base with respect to people with asthma and exposures
eliciting effects and the severity of those effects, other aspects of
the evidence are informative to the necessary judgments. Accordingly,
the advice from the CASAC and the statements from the ATS are important
to the judgments made by the Administrator in basing his decision on
the current evidence and ensuring a primary standard that protects at-
risk populations, such as people with asthma.
    Contrary to the claim from some commenters, our consideration of
effects in people with asthma did not focus solely on lung function
responses. As noted above, we recognize that the inherent
characteristics of asthma as a disease provide the potential for
O3 exposures to trigger asthmatic responses, such as through
causing an increase in airway responsiveness. Based on the available
evidence, we consider the potential for such a response to be greater,
in general, at relatively higher, versus lower, exposure
concentrations, noting 80 ppb to be the lowest exposure concentration
at which increased airway responsiveness has been reported in generally
healthy adults. We recognize that this evidence and the evidence
represented by the three benchmark concentrations used in the exposure/
risk analyses (60, 70 and 80 ppb) is for largely healthy adults and
does not include data for people with

asthma. In reaching his decision in this review, the Administrator
gives additional consideration to the effects of particular concern for
people with asthma, such as asthma exacerbation, in light of the
limitations of the evidence represented by the benchmarks in this
regard, as discussed in section II.B.3 below.
    In support of their view that the EPA gives too little weight to
effects reported in studies of 60 ppb, some commenters assert that the
EPA arbitrarily focused on the evidence for lung function decrements
and respiratory symptoms, and does not explain how the proposed
decision protects against the harm posed by inflammatory responses to
O3. In making this statement they cite the study by Kim et
al. (2011) and discussions in the ISA regarding studies documenting the
role of O3 in eliciting inflammatory responses and regarding
possible conceptual mechanisms by which inflammatory responses can
contribute to other effects (including cardiovascular effects). In so
doing, they contend that exposures lower than those for which the
current standard is intended can cause inflammation resulting in
permanent lung damage and the development of severe lung disease. They
additionally state that airway inflammation of O3 is of
particular concern for people with asthma as airway inflammation is a
feature in the definition of asthma.
    Contrary to the view of some commenters, the Administrator has
given significant consideration (in the proposal and in section II.B.3
below) to the exposure estimates for the 60 ppb benchmark. In
considering the O3 inflammatory response, we note that
inflammation induced by a single exposure (or several exposures over
the course of a summer) can resolve entirely (2013 ISA, p. 6-76). Thus,
the inflammatory response observed following the single exposure to 60
ppb in the study by Kim et al. (2011) of largely healthy subjects is
not necessarily an adverse response.\120\ We further consider the
comments from the CASAC regarding airway inflammation as an important
aspect of asthma, including the CASAC's description of increased airway
inflammation in people with asthma as having the potential to increase
the risk of an asthma exacerbation. As described in section II.B.3
below, the Administrator also considers this, while noting also the
lack of evidence from studies of people with asthma at 60 ppb. In so
doing, he recognizes that, due to interindividual variability in
responsiveness, both in regard to O3 and in regard to asthma
exacerbation triggering events, not every occurrence of an exposure
considered to have the potential to increase airway inflammation will
result in such an adverse effect. We find it important to note,
however, that continued acute inflammation can contribute to a chronic
inflammatory state, with the potential to affect the structure and
function of the lung (2013 ISA, p. 6-76; ISA, sections <IP_ADDRESS>.2 and
<IP_ADDRESS>.2).\121\ In light of this evidence, the Administrator, in his
consideration of the exposure/risk estimates of exposures at or above
the 60 ppb benchmark (described in section II.B.3 below), is less
concerned about such estimates representing a single occurrence, and
gives weight to estimates of multiple occurrences and their associated
greater risk. Thus, rather than a sole focus on a single exposure level
or type of effect (such as lung function decrements), the Administrator
considers the quantitative estimates for all three benchmarks (with
regard to single and multiple occurrences), recognizing that they
represent differing levels of significance and severity of
O3-related effects, both with regard to the array of effects
and severity of each type of effects, as well as the implications for
the at-risk populations, including people with asthma. The comparison-
to-benchmarks analysis provides for this full characterization of risk
for the broad array of respiratory effects, including inflammation and
airway responsiveness, thus avoiding an inadequate and narrower focus,
e.g., limited to lung function decrements (85 FR 49872, August 14,
2020).
---------------------------------------------------------------------------

    \120\ One commenter contends that inflammation is apparent from
short-term O3 exposures ranging from 12 to 35 ppb, based
on air quality metrics reported in some epidemiologic studies, such
as mean 24-hour averages or monthly averages of 8-hour
concentrations (ISA, Table 4-28). The commenter implies that such
values for these metrics are lower than the level of the standard
(70 ppb) means that exposures allowed by the standard are causing
outcomes analyzed in the study. However, none of the metrics for
which values are cited by the commenter are in terms of design
values for the current standard, such that a direct comparison of
the values is not meaningful.
    \121\ The currently available evidence does not support the
implication of the commenters that the inflammatory response
reported in some individuals after a 6.6-hour exposure to 60 ppb,
during quasi-continuous exercise (as in Kim et al., 2011), causes
permanent lung damage or development of severe lung disease. While
the experimental animal evidence indicates the potential for
repeated exposures to elevated concentrations (e.g., at or above 500
ppb over multiple days) can contribute to other effects in animal
models or to other asthmatic responses in animal models of asthma,
the full evidence base for single exposures to lower concentrations
does not provide such a finding (ISA, sections <IP_ADDRESS>, <IP_ADDRESS>.2
and <IP_ADDRESS>.2; 2013 ISA, section 6.2.3). Thus, the potential for
effects reported from 6.6-hour exposures to 60 ppb O3,
during quasi-continuous exercise, including the inflammation
reported by Kim et al. (2011) to contribute to adverse health
effects is uncertain. Newly available evidence in this review does
not reduce this uncertainty or provide a contradiction to conclusion
regarding the implications of inflammation induced by single or
isolated exposures (ISA, Appendix 3).
---------------------------------------------------------------------------

    Contrary to the commenters' claims, the Administrator, in reaching
his proposed decision, and in his final decision, as described in
section II.B.3 below, placed primary focus on what the evidence
indicates with regard to health effects in the at-risk population of
people with asthma, particularly children with asthma, and on results
of the exposure and risk analysis for this population. In so doing, he
recognizes key aspects of the evidence, as summarized in section
II.A.2.a above, that indicate the array of O3-associated
respiratory effects to be of increased significance to people with
asthma given aspects of the disease that may put such peoples at
increased risk for prolonged bronchoconstriction in response to asthma
triggers. The increased significance of effects in people with asthma
and risk of increased exposure for children (from greater frequency of
outdoor exercise) is illustrated by the epidemiologic findings of
positive associations between O3 exposure and asthma-related
emergency department visits and hospital admissions for children with
asthma. In this context, the Administrator focuses on the breadth of
O3 respiratory effects evidence at the lowest exposures
tested in the controlled human exposure studies which provide the most
certain evidence, considering this in light of the fuller evidence base
which provides a foundation for necessary judgments in light of
uncertainties.
    Thus, we disagree with commenters that we have not considered the
full body of evidence and quantitative information available in this
review with regard to exposures that might be expected to elicit
effects in at-risk populations. In so doing, as summarized in section
II.A.2.a above, section II.B.1.a of the proposal, and the PA, we
recognize that the currently available evidence supports the conclusion
of a causal relationship between short-term O3 exposure and
respiratory effects, with the strongest evidence coming from controlled
human exposure studies that document subtle reversible effects in 6.6-
hour exposures of largely healthy adult subjects, engaged in quasi-
continuous exercise, to average concentrations as low as 60 ppb. The
epidemiologic evidence of associations of O3 concentrations
in ambient air with

increased incidence of hospital admissions and emergency department
visits for an array of respiratory health outcomes further indicates
the potential for O3 exposures to elicit health outcomes
more serious than those assessed in the experimental studies,
particularly for children with asthma, and the evidence base of such
epidemiologic studies as a whole provides strong support for the
conclusion of causality for respiratory effects.\122\ Further as
described in the PA and the proposal and summarized in section II.A.2.a
above, very few of these studies were conducted in locations during
periods when the current standard was met. While some commenters cite
the low values of some of the air quality metrics analyzed in such
studies, those metrics are not in the form of the design value for the
current standard and so, contrary to commenters' assertion, cannot show
that serious health effects are occurring under air quality conditions
allowed by the current 70 ppb standard.
---------------------------------------------------------------------------

    \122\ As described in section II.A.2.c above and in the PA,
these studies generally do not detail the specific exposure
circumstances eliciting such effects.
---------------------------------------------------------------------------

    Protection With an Adequate Margin of Safety: Some commenters
expressed the view that the current standard does not provide an
adequate margin of safety variously argue that the EPA is ignoring
precedent and CAA requirements for considering scientific uncertainty
in its judgments regarding an adequate margin of safety, and that
statements from the prior CASAC and new evidence suggests that the
current 70 ppb standard provides little margin of safety for protection
of sensitive subpopulations from harm. These commenters generally
advocate revision to a 60 ppb standard to address this concern. In
support of their views, some state that the EPA is ignoring findings of
a statistically significant lung function response to 6.6-hour exposure
to 60 ppb during quasi-continuous exercise while others cite the EPA
consideration of epidemiologic evidence, claiming that the EPA is
inappropriately using identified uncertainties as a basis for not
revising the standard. We disagree with these characterizations.
    As an initial matter, we note that, contrary to the statements made
by these commenters, the Administrator, in reaching his proposed
decision, as in reaching his final decision, has considered legal
precedent and CAA requirements for a primary standard that protects
public health, including the health of sensitive groups, with an
adequate margin of safety. With regard to scientific uncertainty, as
summarized in section I.A above, the CAA requirement that primary
standards provide an adequate margin of safety was intended to address
uncertainties associated with inconclusive scientific and technical
information available at the time of standard setting. It was also
intended to provide a reasonable degree of protection against hazards
that research has not yet identified. See Lead Industries Ass'n v. EPA,
647 F.2d 1130, 1154 (D.C. Cir. 1980); American Petroleum Institute v.
Costle, 665 F.2d at 1186; Coalition of Battery Recyclers Ass'n v. EPA,
604 F.3d 613, 617-18 (D.C. Cir. 2010); Mississippi v. EPA, 744 F.3d
1334, 1353 (D.C. Cir. 2013). Thus, in considering whether the primary
standard includes an adequate margin of safety, the Administrator is
seeking to ensure that the standard not only prevents pollution levels
that have been demonstrated to be harmful but also prevents lower
pollutant levels that may pose an unacceptable risk of harm, even if
the risk is not precisely identified as to nature or degree. In so
doing, however, the CAA does not require the Administrator to establish
a primary NAAQS at a zero-risk level or at background concentration
levels (see Lead Industries Ass'n v. EPA, 647 F.2d at 1156 n.51,
Mississippi v. EPA, 744 F.3d at 1351), but rather at a level that
reduces risk sufficiently so as to protect public health with an
adequate margin of safety.
    In the proposed decision, as in the decision described in section
II.B.3 below, the Administrator's consideration of the kind and degree
of uncertainties associated with the current information (as some of
the factors the EPA considers in addressing the requirement for an
adequate margin of safety) involved a number of judgments. With regard
to his consideration of the epidemiologic evidence, for example, the
Administrator recognizes that, as a whole, investigations of
associations between O3 and respiratory effects and health
outcomes (e.g., asthma-related hospital admission and emergency
department visits) provide strong support for the overarching
conclusion of that O3 causes respiratory effects, and its
risks to people with asthma. In his consideration of O3
exposures of concern, the Administrator, agrees with staff evaluations
in the PA, that such studies available in this review are less
informative to his judgments related to air quality conditions allowed
by the current standard (85 FR 49870, August 14, 2020). For example, as
summarized in section II.A.2.c above, none of the U.S. studies that
show associations between O3 and the clearly adverse health
outcomes of hospital admissions or emergency department visits for
respiratory causes were based in locations during time periods when the
current standard was always met (PA, section 3.3.3). While there were
two such studies based in single cities in Canada, as discussed above,
the interpretation of individual single-city results is complicated by
the presence of co-occurring pollutants or pollutant mixtures (PA,
section 3.3.3).\123\ Thus, as in reaching his decision in this review,
the Administrator has fully considered conclusions reached in the ISA
regarding the epidemiologic evidence and the policy evaluations in the
PA, and does not find the currently available epidemiologic studies to
provide insights regarding exposure concentrations associated with
health outcomes that might be expected under air quality conditions
that meet the current standard (85 FR 49870, August 14, 2020). Thus,
the EPA's decision on the standard in this review fully and
appropriately considers the full evidence base, including the
epidemiologic evidence, and associated uncertainties and limitations.
---------------------------------------------------------------------------

    \123\ Accordingly, uncertainties remain with regard to the
independent role of O3 exposures in eliciting the
reported health outcomes analyzed, and in the absence of analyses
that might reduce such uncertainties (e.g., analyses of the presence
and effects of co-occurring pollutants).
---------------------------------------------------------------------------

    With regard to the controlled human exposure studies, and the
nature and degree of effects that might be expected at exposures lower
than those studied or in unstudied population groups, the Administrator
has considered first what the evidence base indicates with regard to
the lowest exposures as well as differences and similarities between
the studied populations and the less well studied population groups
recognized to be at increased risk. In so doing, he considers the
findings of statistically significant respiratory responses in the
studies of 60 ppb exposures in largely healthy subjects, particularly
in his consideration of the exposure and risk estimates. For example,
in reaching his decision in section II.B.3 below, as for his proposed
decision, he finds it appropriate to consider the level of protection
provided by the current standard from single exposures, but to give
greater weight to multiple exposures, in judging adequacy of the margin
of safety provided by the current standard.\124\ Such considerations

contributed to the Administrator's proposed judgments with regard to
the requisite level of protection needed to protect at-risk populations
with an adequate margin of safety, as required by the Act and
consistent with the factors recognized in the relevant case law. Thus,
consistent with the CAA requirements and prior judicial decisions, the
Administrator based his proposed decision, and bases his final decision
(as summarized in II.B.4 below) on the scientific evidence, our current
understanding of it, and his judgments concerning associated
uncertainties, both those associated with inconclusive scientific and
technical information, and those associated with hazards that research
has not yet identified. These judgments, along with the factors
recognized above that the EPA generally considers in each NAAQS review,
contribute to his reasoned decision making in this review, as described
in section II.B.3 below.
---------------------------------------------------------------------------

    \124\ Contrary to implications of some commenters, this judgment
by the current Administrator is consistent with that made by the
prior Administrator in establishing the current standard, as seen
from the summary of the prior Administrator's judgment in that
regard that was summarized in the proposal and that these commenters
cite:
    Further, while the Administrator recognized the effects
documented in the controlled human exposure studies for exposures to
60 ppb to be less severe than those associated with exposures to
higher O3 concentrations, she also recognized there to be
limitations and uncertainties in the evidence base with regard to
unstudied population groups. As a result, she judged it appropriate
for the standard, in providing an adequate margin of safety, to
provide some control of exposures at or above the 60 ppb benchmark
(80 FR 65345-65346, October 26, 2015). [85 FR 49841, August 14,
2020]
---------------------------------------------------------------------------

    With regard to advice provide by CASAC in the last review as a
general matter, we disagree with the commenters' presumption that it is
necessary for EPA to address in this review each statement a prior
CASAC made in a prior review. The Clean Air Act does not impose such a
requirement. We further note that a prior CASAC's advice would be based
on review of the prior air quality criteria, exposure/risk analyses and
standard, as well as considerations pertinent in the prior review
(which may, depending on the issue, differ from the pertinent evidence,
information and considerations before a current CASAC). We note,
however, that this specific advice from the prior CASAC on the adequacy
of the margin of safety was cited by part of the CASAC in the current
review. As summarized in the proposal and in section II.B.1.b above,
while the prior CASAC advised that the size of the margin of safety
provided varied across different standard levels within the range from
70 to 60 ppb that the prior CASAC recommended, it found a level of 70
ppb could be supported by the scientific evidence. Further, the prior
CASAC recognized, as summarized in section II.B.1.b above, that with
regard to the ``size'' of the margin of safety, the selection of any
particular approach to providing an adequate margin of safety is a
policy choice left specifically to the Administrator's judgment (Lead
Industries Ass'n v. EPA, 647 F.2d at 1161-62; Mississippi v. EPA, 744
F.3d at 1353; section I.A above). Thus, in reaching his proposed
decision, the Administrator explicitly considered the advice provided
by the prior CASAC to the extent it was represented in advice from the
current CASAC as emphasized by part of the current CASAC (85 FR 49873,
August 14, 2020), and he has similarly again considered it reaching his
final decision, as described in section II.B.3 below, in light of
public comments raising it.
    Some commenters also express the view that EPA is using limited
data in sensitive population groups as an excuse for not establishing a
level at which there is ``an absence of adverse effect'' in sensitive
groups. In support of their view, some commenters claim that the EPA
has not addressed a statement of the prior CASAC regarding the
potential for lung function decrements and respiratory symptoms to
occur in people with asthma with exposure to 70 ppb (while at elevated
exertion). Contrary to this claim,\125\ the EPA considered in the last
review the point made by the prior CASAC in the statement highlighted
by the commenters. The statement from the prior CASAC that the
commenters reference was provided in the CASAC review of a draft PA in
the last review, fully considered in completing the final 2014 PA, and,
along with the totality of the prior CASAC advice, taken into account
in establishing the current primary standard (80 FR 65292, October 26,
2020). It is not necessary for the EPA to address in this review each
statement a prior CASAC made in a prior review.
---------------------------------------------------------------------------

    \125\ The context for this statement is in considering the
benchmark concentrations utilized in the exposure-to-benchmarks
analysis of the 2014 HREA and reflecting on responses reported in
controlled human exposure studies of healthy subjects exposed for
6.6 hours with quasi-continuous exercise. With regard to the
responses reported from exposure to 72 ppb, on average across the
exercise periods, the prior CASAC stated its view ``that these
effects almost certainly occur in some people, including asthmatics
and others with low lung function . . . at levels of 70 ppb and
below'' (Frey, 2014b, p. 6).
---------------------------------------------------------------------------

    We agree with commenters who express the view that to protect
sensitive populations from effects reported in some largely healthy
subjects from the 6.6 hour exposure to 73 ppb (with quasi-continuous
exercise), the standard should provide protection against somewhat
lower exposures. As summarized in section II.B.3 below, this is an
objective the Administrator identifies for the standard and, based on
the exposure/risk estimates, he finds the standard to provide strong
protection from such exposures (and associated risk of such effects).
In addition, in highlighting this isolated statement from the last
review, the commenters fail to distinguish CASAC advice on the primary
standard from consideration of the exposure benchmark for comparison to
a multi-hour exposure while engaged in quasi-continuous exercise.
    With regard to the prior CASAC's scientific and policy advice on
the primary standard,\126\ the prior CASAC concluded that the
scientific evidence supported a range of standard levels that included
70 ppb, and also recognized the choice of a level within that range to
be ``a policy judgment under the statutory mandate of the Clean Air
Act'' (85 FR 49873).\127\ We further note that the current CASAC
concludes in this review that newly available evidence relevant to
standard setting does not substantially differ from that available in
the last review (Cox, 2020a, Consensus Responses to Charge Questions p.
12; 85 FR 49873, August 14, 2020). As discussed further below, we note
that the CAA does not require the Administrator to establish a primary
NAAQS at a zero-risk level or at background concentration levels (see
Lead Industries Ass'n v. EPA, 647 F.2d at 1156 n.51, Mississippi v.
EPA, 744 F.3d at 1351), but rather at a level that reduces risk
sufficiently so as to protect public health with an adequate margin of
safety.
---------------------------------------------------------------------------

    \126\ In their 2014 advice, the prior CASAC concluded by
explicitly stating ``our policy advice is to set the level of the
standard lower than 70 ppb within a range down to 60 ppb, taking
into account your judgment regarding the desired margin of safety to
protect public health.''
    \127\ The legislative history of section 109 indicates that a
primary standard is to be set at ``the maximum permissible ambient
air level . . . which will protect the health of any [sensitive]
group of the population,'' and that for this purpose ``reference
should be made to a representative sample of persons comprising the
sensitive group rather than to a single person in such a group.''
---------------------------------------------------------------------------

    Some commenters also state that the primary NAAQS must be set at a
level at which there is an absence of adverse effects in sensitive
populations. While the EPA agrees that the NAAQS must be set to protect
sensitive populations with an adequate margin of safety, it is well
established that the NAAQS are not

meant to be zero risk standards. See Lead Industries v. EPA, 647 F.2d
at 1156 n.51; ATA III, 283 F. 3d at 360 (``[t]he lack of a threshold
concentration below which these pollutants are known to be harmless
makes the task of setting primary NAAQS difficult, as EPA must select
standard levels that reduce risks sufficiently to protect public health
even while recognizing that a zero-risk standard is not possible'');
Mississippi, 744 F. 3d at 1351 (same); see also id. at 1343
(``[d]etermining what is `requisite' to protect the `public health'
with an `adequate' margin of safety may indeed require a contextual
assessment of acceptable risk. See Whitman, 531 U.S. at 494-95 (Breyer
J. concurring)''). As the Court of Appeals for the D.C. Circuit said in
reviewing the 2015 O3 NAAQS, ``the primary standard for a
non-threshold pollutant like ozone is not required to produce zero
risk, and `[t]he task of determining what standard is `requisite' to
protect the qualitative value of public health or what margin of safety
is `adequate' to protect sensitive subpopulations necessarily requires
the exercise of policy judgment.' '' Murray Energy, 936 F.3d at 610
(quoting Mississippi v. EPA).\128\ The Administrator's judgments in
this review are rooted in his evaluation of the evidence, which
reflects the scientific uncertainty as to the O3
concentrations at which sensitive subpopulations would experience
adverse health effects, and his judgments weigh both the risks and the
uncertainties. This is a legitimate, and well recognized, exercise of
``reasoned decision-making.'' ATA III. 283 F. 3d at 370; see also id.
at 370 (``EPA's inability to guarantee the accuracy or increase the
precision of the . . . NAAQS in no way undermines the standards'
validity. Rather, these limitations indicate only that significant
scientific uncertainty remains about the health effects of fine
particulate matter at low atmospheric concentration. . . .'');
Mississippi, 744 F. 3d at 1352-53 (appropriate for EPA to balance
scientific uncertainties in determining level of revised O3
NAAQS).
---------------------------------------------------------------------------

    \128\ The legislative history of the Clean Air Act provides
further support for these holdings, as do the statutory deadlines
for attainment. See H. Rep. 95-294, 95th Cong. 1st sess. 127, 123
Cong. Rec. S9423 (daily ed. June 10, 1977) (statement of Senator
Muskie during the floor debates on the 1977 Amendments that ``there
is no such thing as a threshold for health effects. Even at the
national primary standard level, which is the health standard, there
are health effects that are not protected against.''
---------------------------------------------------------------------------

    Exposure/risk Analyses: In expressing the view that the standard
should be made more stringent, some commenters disagree with EPA
conclusions based on the exposure/risk analyses, and point to other
analyses that they state show that a lower standard level (e.g. 65 ppb
or lower) would avoid important health effects. These commenters'
claims of deficiencies with the exposure/risk analyses include claims
that the study area selection is not explained, that population size of
the study areas analyzed is too small to support conclusions and does
not include particular areas; that the analysis does not include
adults, and other groups of interest, and that selection of study areas
with air quality close to the current standard contributed to
underestimates of population exposures. We disagree with these
commenters' claims.
    With regard to study area selection and population size for the
analysis, we note that an exposure and risk analysis based on eight
study areas, all of which are major metropolitan areas provides a
robust foundation for population exposure estimates. The eight study
areas included reflect the full range of air quality and exposure
variation expected across major urban areas in the U.S and seven
different NOAA climate regions (PA, section 3.4.1).\129\ This number of
areas (8) and combined population size (more than 45 million in the
combined metropolitan areas [PA, Appendix 3D, Table 3D-1]) are much
larger than similar analyses in recent NAAQS reviews for other
pollutants (e.g., sulfur dioxide [U.S. 2018]), and not that dissimilar
to similar analyses in past O3 NAAQS reviews.\130\ Some
commenters claim that the exclusion of specific urban areas in which
O3 concentrations are much higher than those analyzed
resulted in underestimates of exposure. We disagree with this claim as
the air quality analyzed across all study areas was adjusted to just
meet the current standard (or alternative scenarios). Thus, an urban
area that currently has O3 concentrations well in exceedance
of the current standard would not necessarily have been found to have
higher exposure estimates if it were simulated to have air quality just
meeting the current standard. Such estimates would, however, have
greater uncertainty, which is the reason such study areas as those
identified by commenters (e.g., Los Angeles) were excluded. Areas
included were those for which only small adjustments were required for
the air quality to just meet the current standard (and alternative
scenarios), yielding reduced uncertainty (e.g., given the need for
larger air quality adjustments to achieve conditions that just meet the
current standard) in these estimates compared to those from the 2014
HREA (PA, sections 3.4.1 and 3.4.4, and Appendix 3D). In selecting such
areas, however, we considered a number of other characteristics in
order to achieve a varied set of study areas, including with regard to
air quality patterns.\131\ This variation contributed to variation in
exposure estimates, even for the same air quality scenario (PA,
Appendix 3D, Tables 3D-26, 3D-28 and 3D-30). Thus, in addition to
focusing on study areas with ambient air concentrations close to
conditions that reflect air quality that just meets the current
standard that would be more informative to evaluating the health
protection provided by the current standard than areas with much higher
(or much lower) concentrations, the approach employed recognizes that
capturing an appropriate diversity in study areas and air quality
conditions (that reflect the current standard scenario) is an important
aspect of the role of the exposure and risk analyses in informing the
Administrator's conclusions on the public health protection afforded by
the current standard.
---------------------------------------------------------------------------

    \129\ Contrary to the commenters' assertion of a lack of
explanation for the study areas included in the analyses, the PA
describes the study area selection criteria and process, including
steps taken to include adequate representation of diverse
conditions. As observed in the PA, seven of the eight study areas
were also included in the 2014 HREA, and the eighth study area
(Sacramento) was newly added in the current review to insure
representation of a large city in the southwest (PA, section 3.4.1
and Appendix 3D, section 3D.2.1). Clarification on this point in the
final PA was responsive to the only CASAC comment on completeness of
the description of study area selection (Cox, 2020a). We disagree
with the implication by some commenters that each review's analyses
must focus on the same areas. There is no such requirement under the
Act, and such a view ignores the need to consider the current
information in each review in planning appropriate analyses.
    \130\ For example, the exposure assessment for the 1997
O3 NAAQS review included nine urban study areas, for
which the combined population simulated was 41.7 million. The
exposure assessment for the current review included eight urban
study areas with a combined simulated population size of
approximately 39 million (PA, p. 3D-96; U.S. EPA, 1996b, p. 76). We
additionally note the focus on analysis results in terms of
population percentages rather than population counts.
    \131\ A broad variety of spatial and temporal patterns of O3
concentrations can exist when ambient air concentrations just meet
the current standard. These patterns will vary due to many factors
including the types, magnitude, and timing of emissions in a study
area, as well as local factors, such as meteorology and topography.
---------------------------------------------------------------------------

    Contrary to one commenter's assertion that adults were not included
in the exposure assessment, the populations assessed included two adult
populations groups: All adults and

adults with asthma.\132\ The results for these groups and all of the
populations assessed are presented in detail in the PA (PA, Appendix
3D). As described in the PA and proposal, the estimates for adults as a
percentage of the study populations were generally lower than those for
children. Thus, we focused discussion on the estimates for children,
including particularly children with asthma. As recognized by the
Administrator in section II.B.3 below, his judgments on the adequacy of
protection provided by the current standard takes into account
protection provided to the U.S. population, including those population
groups at increased risk, which includes children and people of all
ages with asthma, among other groups.
---------------------------------------------------------------------------

    \132\ Further, contrary to the implication of one comment, the
exposure/risk analyses did not exclude athletes, hikers and others
who exercise outdoors, using their full lung capacity, a group the
commenter characterizes as at increased risk. In fact, it is just
such individuals who are most likely, depending on their locations,
to experience exposures of concern due to their high exertion
levels. As described in the PA, the comparison to benchmarks
analysis identifies the portion of the exposed population whose 7-
hour average concentration, while at moderate or greater exertion,
is at or above the benchmarks (PA, section 3.4 and Appendix 3D).
---------------------------------------------------------------------------

    Some commenters claimed that the EPA should have separately
assessed exposure for certain additional population subgroups, such as
children at summer camps, adults with lung impairments other than
asthma or outdoor workers. As an initial matter, we recognize
appreciably increased uncertainty regarding key aspects of the
information necessary for such simulations for all of these groups. Of
the three groups, only outdoor workers are identified as an at-risk
population in this review (ISA, Table IS-10), and accordingly this
group was explicitly considered in designing the exposure
analyses.\133\ The information available, however, was considered to be
too uncertain to produce estimates for this population, as a separate
group, with confidence. As described in the PA, important uncertainties
exist in generating the simulated activity patterns for this group,
including the limited number of CHAD diary days available for outdoor
workers, assignment of diaries to proper occupation categories, and in
approximating number of days/week and hours/day outdoors, among other
pertinent aspects (PA, Appendix 3D, Table 3D-64). We note that these
appreciable data limitations and associated uncertainties were also
recognized in the 2014 HREA in which a limited sensitivity analyses was
conducted for this subgroup. Those limited analyses, conducted for a
single area with air quality just meeting the prior 75 ppb standard,
indicated that when diaries were selected to mimic exposures that could
be experienced by outdoor workers, the percentages of modeled
individuals estimated to experience exposures of concern were generally
similar to the percentages estimated for children (i.e., using the full
database of diary profiles) in the urban study areas and years with the
largest exposure estimates (2014 HREA, section <IP_ADDRESS>, Figure 5-
14).\134\ Accordingly, in this review, in recognition of the data
limitations that remain in the current review,\135\ outdoor workers
were not assessed as a separate population group, and in light of our
consideration of conclusions from the sensitivity analyses in the last
review, we have generally given primary focus to the estimates for the
populations of children.
---------------------------------------------------------------------------

    \133\ With regard to the other two groups, we note the ISA
explicitly evaluated evidence for people with the lung disease,
COPD, and concluded the evidence was inadequate to determine whether
this lung impairment confers increased risk of O3 related
effects (ISA, Table IS-10). With regard to children at summer camp,
we note that to the extent that the behaviors of such children
(e.g., exercising outdoors) are represented in the CHAD, they are
represented among the at-risk populations of children and children
with asthma that were simulated in the exposure/risk analyses.
    \134\ Similarly, the EPA also did not conduct an exposure
analysis for outdoor workers in the 2008 review and instead focused
on children since it was judged that school aged children presented
the greatest likelihood of being outdoors and exposed under moderate
exertion averaged over the critical time period based on prior
analysis findings. Thus, while as recognized in multiple reviews,
outdoor workers are also at risk, the EPA has focused, in past
reviews as in the current one, on children, the population group for
which the analysis estimates in terms of percentage of population
are greatest (PA, section 3.4.2). Accordingly, providing protection
for this population group will provide protection for other at-risk
populations as well.
    \135\ In support of their view that estimates should have been
derived for outdoor workers, one group of commenters cites a study
on research priorities for assessing climate change impacts on
outdoor workers (Moda et al., 2019). We note, that other than being
focused on outdoor workers and recognizing there to be significant
research needed for impacts assessment, this paper has little
relevance in this review. The paper is focused on climate change
impacts in tropical developing countries with a focus on sub-Saharan
Africa and does not discuss exposure modeling of outdoor workers or
O3.
---------------------------------------------------------------------------

    In summary, we disagree with comments stating that the exposure/
risk analyses were deficient and do not provide support for their
conclusions. As summarized above, in planning and conducting the
exposure/risk analyses, we have appropriately considered issues raised
by the commenters, such that the analyses reasonably reflect current
understanding, information, tools and methodologies. Further, in
presenting the analyses in the PA, we have recognized any associated
limitations and uncertainties in an uncertainty characterization that
utilized a largely qualitative approach adapted from the World Health
Organization approach (and commonly utilized in NAAQS exposure/risk
assessments, as discussed in the PA and proposal [85 FR 49857, August
14, 2020]), accompanied by a number of quantitative sensitivity
analyses. This characterization and accompanying analyses build on
previously conducted work in the 2014 HREA and provide a transparent
and explicit recognition of strengths, limitations and uncertainties of
the current exposure/risk analysis that were described the PA,
considered in the proposal and also in the Administrator's decision
described in section II.B.3 below. Thus, the exposure/risk analyses
conducted for this review appropriately and soundly reflect current
information and methodologies; and we have interpreted their results
appropriately in light of any associated limitations and uncertainties.
    With regard to other quantitative analyses identified by some
commenters and described as showing health impacts that would be
avoided by a more stringent standard (e.g. with a level of 65 ppb or
lower), we note that these analyses utilize epidemiologic study effect
estimates as concentration-response functions to generate predictions
of the occurrence of health outcomes, primarily mortality, under
different air quality conditions (characterized by the metric used in
the epidemiologic study).\136\ As an initial matter, we note that our
understanding of the relationship between O3 exposures and
total mortality is different in this review than it was in the last
review, based on the more extensive evidence base now available. As
summarized in section II.A.2.a above, and noted earlier in this
section, while our conclusion in the last review was that the
relationship of O3 exposure with mortality was likely to be
causal, the current evidence base does not support that conclusion
because of limited evidence for cardiovascular mortality, which is by
far the largest contributor to total mortality. Rather, the EPA has
concluded the evidence in

this review to be suggestive of, but not sufficient to infer, causal
relationships of total mortality with short- or long-term O3
exposure, as summarized in section II.A.2.a above (ISA, Appendix 6).
Thus, we do not find the weight the commenter is suggesting we place on
predictions of total mortality from the epidemiologic study based risk
analyses cited by commenters to appropriately reflect the current
evidence base for O3 and mortality, or the evidence base for
O3 and cardiovascular effects (the primary contributor to
mortality in the U.S.).
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    \136\ The analyses cited by these commenters include Cromar et
al (2019) and OTC (2020). To address these comments, we have
provisionally considered the documents, as discussed in I.D above,
and found they do not materially change the broad scientific
conclusions of the ISA with regard to respiratory effects, or
warrant re-opening the air quality criteria for further review
(Luben et al., 2020). Further, some of these commenters reference
epidemiologic study based risk, analyses in the 2014 HREA.
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    With regard to estimates of avoided respiratory mortality from the
analyses cited by these commenters, we note that, while the
epidemiologic studies that are inputs to the quantitative analyses
cited by the commenters are part of the evidence base that supports our
conclusion of a causal relationship between short-term O3
exposure and respiratory effects, there are uncertainties inherent in
the derivation of estimates of mortality ascribed to O3
exposures using effect estimates from these studies. For example, in
planning for analyses in this review, the IRP recognized several
important uncertainties associated with aspects of the O3
epidemiologic study-based approach used in the 2014 HREA (one of the
analyses cited by commenters), and similar to the approach used in
other analyses cited by commenters, that the EPA concluded to have a
moderate or greater impact on risk estimates (IRP, Appendix 5A). Such
uncertainties include complications posed by the presence of co-
occurring pollutants or pollutant mixtures, as well as those involving
the correlation of population O3 exposures and ambient air
monitor concentrations (including the use of area wide average
O3 concentrations) and uncertainties in the derived
concentration-response functions (IRP, Appendix 5A; PA, Appendix 34D,
section 3D.1.4). Specifically with regard to the 2014 HREA estimates of
respiratory mortality, the EPA has recognized uncertainty about the
extent to which mortality estimates based on the long-term metric in
Jerrett et al. (2009) (i.e., seasonal average of 1-hour daily maximum
concentrations) reflect associations with long-term average
O3 versus repeated occurrences of elevated short-term
concentrations; and given potential nonlinearity of the C-R function to
reflect a threshold of the mortality response, these estimates should
be viewed with caution (IRP, Appendix 5A). Accordingly, the 2014 HREA
concluded that lower confidence should be placed in the results of the
assessment of respiratory mortality risks associated with long-term
O3, primarily because that analysis relies on just one study
(Jerrett et al., 2009), and because of the uncertainty in that study
about the existence and identification of a potential threshold in the
concentration-response function (2014 HREA, section 9.6; 80 FR 65316,
October 26, 2015). The other analysis cited by the commenters for
predictions of respiratory mortality is also based its estimates on
Jerrett et al. (2009). Thus, we find the conclusions regarding
uncertainty and low confidence recognized for the 2014 HREA estimates
to also apply to the other analysis by commenters and disagree with the
conclusions reached by these commenters on this analysis. Further, we
do not find that the 2014 HREA or other analyses cited by the
commenters, in combination with the full body of evidence currently
available, support a conclusion of significant health outcomes for
O3 air quality that meets the current standard.
    Long-term Standard Consideration: In support of their view that EPA
should establish an additional primary standard that targets long-term
exposure, some commenters stated that recent epidemiologic studies
indicate causal linkages between long-term exposures and adverse health
outcomes, while also suggesting there was support for such a standard
in a statement made by the CASAC in reviewing the draft PA. With regard
to the epidemiologic studies, these commenters cite several studies
published after the literature cut-off date for the ISA \137\ that they
describe as showing linkages of long-term O3 exposure to a
number of outcomes, including mortality, smokers progression to COPD,
hospital admissions for acute respiratory disease syndrome and
emergency department visits (Dominici et al., 2019; Seltzer et al.,
2020; Limaye and Knowlton, 2020; Dedoussi et al., 2020; Lim et al.,
2019; Paulin et al,. 2020; \138\ Rhee et al., 2019; Strosnider et al.,
2019).\139\ We have provisionally considered these ``new'' studies in
addressing these comments consistent with section I.D above (Luben et
al., 2020). Of the studies focused on mortality that these commenters
cite as providing new information in support of a long-term standard,
just three represent new evidence related to investigation of
associations of long-term O3 exposure with mortality (Lim et
al., 2019) or respiratory morbidity (Paulin et al., 2020 and Rhee et
al., 2019).\140\ The study by Lim et al. (2019) analyzes associations
between long-term O3 exposure and respiratory mortality in a
U.S. population of older adults in the U.S., reporting a positive
association with an effect estimate lower than a previously published
study included in the ISA. These results contribute to the evidence
base for respiratory effects, e.g., with an additional high-quality
study of a previously studied population group (Lim et al., 2019) or
with studies investigating additional populations and respiratory
outcomes (Paulin et al., 2020; Rhee et al., 2019), albeit with
limitations,\141\ without reducing uncertainties in the evidence base
as a whole. These studies are

generally consistent with the evidence assessed in the ISA, and they do
not materially change the broad conclusions in the ISA regarding the
scientific evidence.
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    \137\ These commenters also assert that some other studies
published after the ISA cut-off date were arbitrarily included in
the ISA, citing just a single study (Garcia et al., 2019). Contrary
to implication by the commenters, such an occurrence is clearly
described in the ISA, which states ``[s]tudies published after the
literature cutoff date for this review were also considered if they
were submitted in response to the Call for Information or identified
in subsequent phases of ISA development . . ., particularly to the
extent that they provide new information that affects key scientific
conclusions'' (ISA, Appendix 10, p. 10-1).
    \138\ Although the commenters submitted a document that appears
to be an unpublished draft of an earlier manuscript of this paper,
to which they assigned a 2019 publication date and a very slightly
different title (rather than the published paper, it is the
published study, Paulin et al., (2020) that we have provisionally
considered (Luben et al., 2020).
    \139\ Some commenters imply that projections of increasing
O3 concentrations in response to climate change in the
future will ``heighten'' long-term O3 concentrations and
chronic exposures and indicate a need for a long-term standard. In
making this claim, they cite an analysis of air quality projected in
2045 through 2055 (Nassikas et al., 2020) and an evaluation of the
effects of climate change on air quality including O3
concentrations. (Archer et al., 2019). The former ``new'' study has
been provisionally considered and found not to materially affect the
broad scientific conclusions regarding the air quality criteria
documented in the ISA or to warrant reopening the air quality
criteria (Luben et al., 2020) As neither is evaluating health
effects associated with air quality under the current standard, we
do not find these studies informative to consideration of a need for
a long-term standard to protect public health.
    \140\ Two others (Dedoussi et al 2020; Seltzer et al, 2020) are
quantitative assessments that estimate O3 impacts based
on use of effect estimates from previously published studies that
are included in the ISA, another (Dominici et al., 2019) is the full
technical report from the Health Effects Institute, the main results
of which were previously published in studies that are included in
the ISA, and a fourth (Limaye and Knowlton., 2020) is commentary on
a previously published study that is included in the ISA. One other
study cited by the commenters is focused on short-term O3
exposures, not long-term O3 exposure as indicated by the
commenters (Strosnider et al., 2019)
    \141\ While studies by Paulin et al. (2020) and Rhee et al.
(2019) provide evidence for a novel population sub-group (smokers)
or endpoint (e.g., acute respiratory distress syndrome, ARDS), each
study has limitations. For example, the cross-sectional design of
Paulin et al. (2020) is a major limitation, while limitations
associated with Rhee et al. (2019) relate to linking long-term
exposure with hospital admissions for ARDS based on exposure timing
and the mechanism for acute vs. chronic development of disease, and
to power in the study (e.g., very low hospital admission counts per
year per ZIP code [Rhee et al., 2019, Table 2]).
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    We additionally note that the O3 concentrations did not
meet the current standard in all locations and time periods analyzed in
these three multicity studies. Although two of these studies include
some locations across the U.S. in which the current standard was likely
met during some portions of the study period, air quality during other
time periods of locations in the dataset did not meet the current
standard.\142\ Further, the multicity effect estimates in these studies
do not provide a basis for considering the extent to which
O3 health effect associations are influenced by individual
locations with ambient O3 concentrations low enough to meet
the current O3 standards versus locations with O3
concentrations that violate this standard. Thus, while these more
recent studies may be consistent with the existing evidence base
evaluated in the ISA, they do not provide a basis for conclusions
regarding whether the O3 exposures occurring under air
quality conditions allowed by the current standard may be eliciting the
effects analyzed.
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    \142\ The studies by Lim et al (2019) and Rhee et al (2019)
include zip codes across the entire U.S., while Paulin et al (2020)
includes the cities of Baltimore, Maryland, New York City, New York,
Los Angeles and San Francisco, California, Ann Arbor, Michigan, Salt
Lake City, Utah and Winston-Salem, North Carolina. The study time
periods include ten or more years extending from the early 2000s to
the late 2010s; a period within which the design values for most of
those identified cities and many other U.S. metropolitan areas
exceeded the level of the current standard (as seen by the design
values presented for those areas during those time periods at
https://www.epa.gov/air-trends/air-quality-design-values).
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    We additionally note that while epidemiologic studies evaluate the
relationship between health effects and specific O3
concentrations during a defined study period and the generally
consistent and coherent associations observed in these epidemiologic
studies contribute to the causality determinations and conclusions
regarding the causal nature of the effect of O3 exposure on
health effects, ``they do not provide information about which averaging
times or exposure metrics may be eliciting the health effects under
study'' (ISA, section IS.6.1). As noted in the ISA, ``disentangling the
effects of short-term ozone exposure from those of long-term ozone
exposure (and vice-versa) is an inherent uncertainty in the evidence
base,'' as ``the populations included in epidemiologic studies have
long-term, variable, and uncharacterized exposures to ozone and other
ambient pollutants'' (ISA, section IS.6.1). As summarized in the
proposal, however, we have also considered the toxicological studies of
effects associated with long-term exposures and note that they involve
much higher exposures than those occurring at the current standard (85
FR, 49853, August 14, 2020).
    Lastly, we disagree with the commenters' implication that the EPA
has not addressed a CASAC recommendation. The commenters appear to be
asserting that the CASAC recommended that EPA consider a long-term
standard. However, the CASAC did not make such a recommendation (Cox,
2020a). In making this assertion, the commenter cites a comment the
CASAC makes with regard to a sentence in the draft PA that is drawn
from the Administrator's conclusions section of the 2015 decision.
Rather than ignoring this CASAC comment, as asserted by the commenters,
we made a revision to that section of the PA (moving the statement from
the draft PA to a footnote in the final PA with the objective of
retaining an accurate description of a consideration related to that
2015 decision, while lessening the potential for confusion of a 2015
consideration with considerations in the current review).\143\
Notwithstanding sentences pertaining to the last review, we note the PA
evaluates the information in the current review with regard to the
protection offered by the current standard (and that the Administrator
considered the PA evaluation, as well as the CASAC advice in his
proposed decision [summarized in section II.B.1.c above] as in his
final decision below). We further note that the description of the
Administrator's conclusion in the last review, which is also summarized
in the proposal (and in section II.A.1 above), does not describe health
effects associated with long-term average concentrations likely under
the current standard.
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    \143\ In its comments regarding the 2015 statement, the CASAC
and its consultants stated that controls that reduce peak
O3 concentrations will not consistently reduce mean
O3 concentrations. We don't disagree with this statement,
and we note that we did not make a statement to the contrary in
either the proposal or this final decision document.
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    Further, in considering an implication of the commenters' claim
that a ``long-term standard'' is needed in order to provide protection
from health effects that may be elicited by long-term exposures to
O3, we note that the impact of standards with short
averaging times, such as eight hours, is not limited to reducing short-
term exposures. This is because a reduction in magnitude of short-term
exposure concentrations (e.g., daily maximum 8-hour concentrations) is
also a reduction in exposure to such concentrations over the longer
term. For example, a standard, such as the current one, that limits
daily maximum 8-hour concentrations to not exceed 70 ppb as a 3-year
average of the annual fourth highest value, in addition to limiting the
magnitude of concentrations to which a population is exposed in eight
hour periods, also limits the frequency to which the population is
exposed to such concentrations over the long term. That is, the
reduction in frequency of the higher concentrations reduces exposures
to such concentrations over the short and long term. Thus, given that,
as indicated by the current and established evidence, the O3
concentrations most likely to contribute to health effects are the
higher concentrations, the current standard provides control of
exposures to such concentrations over both the short and long term. In
light of all of the considerations raised here, we disagree with the
commenters assertion of the need for a long-term O3
standard.
4. Administrator's Conclusions
    Having carefully considered the public comments, as discussed
above, the Administrator believes that the fundamental scientific
conclusions on effects of photochemical oxidants, including
O3, in ambient air that were reached in the ISA and
summarized in the PA, and estimates of potential O3
exposures and risks described in the PA, and summarized above and in
sections II.B and II.C of the proposal, remain valid. Additionally, the
Administrator believes the judgments he proposed to reach in the
proposal (section II.D.3) with regard to the evidence and the
quantitative exposure/risk information remain appropriate. Thus, as
described below, the Administrator concludes that the current primary
O3 standard provides the requisite protection of the public
health with an adequate margin of safety, including for at-risk
populations, and should be retained. In considering the adequacy of the
current primary O3 standard, the Administrator has carefully
considered the assessment of the available health effects evidence and
conclusions contained in the ISA; the evaluation of policy-relevant
aspects of the evidence and quantitative analyses in the PA (summarized
in sections II.A.2 and II.A.3 above); the advice and recommendations
from the CASAC (summarized in section II.B.1.b above); and public
comments (discussed in section II.B.2 above and in the separate RTC
document).

    In the discussion below, the Administrator considers the key
aspects of the evidence and exposure/risk estimates important to his
judgment regarding the adequacy of protection provided by the current
standard. First, the Administrator considers the evidence base on
health effects associated with exposure to photochemical oxidants,
including O3, in ambient air. He additionally considers the
quantitative exposure and risk estimates developed in this review,
including associated limitations and uncertainties, and what they
indicate regarding the magnitude of risk, as well as degree of
protection from adverse health effects, associated with the current
standard. He additionally considers uncertainties in the evidence and
the exposure/risk information, as a part of public health judgments