are due solely to O3 exposures, and interpretation of study
results is not complicated by the presence of co-occurring pollutants
or pollutant mixtures.
    In considering the evidence from controlled human exposure studies,
the Administrator first noted that these studies have reported a
variety of respiratory effects in healthy adults following exposures to
O3 concentrations of 60, 72, or 80 ppb, and higher. The
largest respiratory effects, and the broadest range of effects, have
been studied and reported following exposures of healthy adults to 80
ppb O3 or higher, with most exposure studies conducted at
these higher concentrations. She further noted that recent evidence
includes controlled human exposure studies reporting the combination of
lung function decrements and respiratory symptoms in healthy adults
engaged in quasi-continuous, moderate exertion following 6.6 hour
exposures to concentrations as low as 72 ppb, and lung function
decrements and

pulmonary inflammation following exposures to O3
concentrations as low as 60 ppb. As discussed below, compared to the
evidence available in the last review, the Administrator viewed these
studies as having strengthened support for the occurrence of abnormal
and adverse respiratory effects attributable to short-term exposures to
O3 concentrations below the level of the current standard.
The Administrator stated that such exposures to O3
concentrations below the level of the current standard are potentially
important from a public health perspective, given the following:
    (1) The combination of lung function decrements and respiratory
symptoms reported to occur in healthy adults following exposures to 72
ppb O3 or higher, while at moderate exertion, meet ATS
criteria for an adverse response. In specifically considering the 72
ppb exposure concentration, CASAC noted that ``the combination of
decrements in FEV1 together with the statistically
significant alterations in symptoms in human subjects exposed to 72 ppb
ozone meets the American Thoracic Society's definition of an adverse
health effect'' (Frey, 2014c, p. 5).
    (2) With regard to 60 ppb O3, CASAC agreed that ``a
level of 60 ppb corresponds to the lowest exposure concentration
demonstrated to result in lung function decrements large enough to be
judged an abnormal response by ATS and that could be adverse in
individuals with lung disease'' (Frey, 2014c, p. 7). CASAC further
noted that ``a level of 60 ppb also corresponds to the lowest exposure
concentration at which pulmonary inflammation has been reported''
(Frey, 2014c, p. 7).
    (3) The controlled human exposure studies reporting these
respiratory effects were conducted in healthy adults, while at-risk
groups (e.g., children, people with asthma) could experience larger
and/or more serious effects. In their advice to the Administrator,
CASAC concurred with this reasoning (Frey, 2014a, p. 14; Frey, 2014c,
p. 5).
    (4) These respiratory effects are coherent with the serious health
outcomes that have been reported in epidemiologic studies evaluating
exposure to O3 (e.g., respiratory-related hospital
admissions, emergency department visits, and mortality).
    As noted above, the Administrator's proposed conclusions regarding
the adequacy of the current primary O3 standard placed a
large amount of weight on the results of controlled human exposure
studies. In particular, given the combination of lung function
decrements and respiratory symptoms following 6.6-hour exposures to
O3 concentrations as low as 72 ppb, and given CASAC advice
regarding effects at 72 ppb, along with ATS adversity criteria, she
concluded that the evidence in this review supports the occurrence of
adverse respiratory effects following exposures to O3
concentrations lower than the level of the current standard.\76\ As
discussed below, the Administrator further considered information from
the broader body of controlled human exposure studies within the
context of quantitative estimates of exposures of concern and
O3-induced FEV1 decrements.
---------------------------------------------------------------------------

    \76\ This CASAC advice and ATS recommendations are discussed in
more detail in section II.C.4 below (see also II.A.1.c, above).
---------------------------------------------------------------------------

    While putting less weight on information from epidemiologic studies
than on information from controlled human exposure studies, the
Administrator also considered what the available epidemiologic evidence
indicates with regard to the adequacy of the public health protection
provided by the current primary O3 standard. She noted that
recent epidemiologic studies provide support, beyond that available in
the last review, for associations between short-term O3
exposures and a wide range of adverse respiratory outcomes (including
respiratory-related hospital admissions, emergency department visits,
and mortality) and with total mortality. Associations with morbidity
and mortality are stronger during the warm or summer months, and remain
robust after adjustment for copollutants.
    In considering information from epidemiologic studies within the
context of her conclusions on the adequacy of the current standard, the
Administrator considered the extent to which available studies support
the occurrence of O3 health effect associations with air
quality likely to be allowed by the current standard. Most of the
epidemiologic studies considered by the Administrator were conducted in
locations likely to have violated the current standard over at least
part of the study period. However, she noted three U.S. single-city
studies that support the occurrence of O3-associated
hospital admissions or emergency department visits at ambient
O3 concentrations below the level of the current standard,
or when virtually all monitored concentrations were below the level of
the current standard (Mar and Koenig, 2009; Silverman and Ito, 2010;
Strickland et al., 2010) (section II.D.1 of the proposal). While the
Administrator acknowledged greater uncertainty in interpreting air
quality for multicity studies, she noted that O3
associations with respiratory morbidity or mortality have been reported
when the majority of study locations (though not all study locations)
would likely have met the current O3 standard. When taken
together, the Administrator reached the initial conclusion at proposal
that single-city epidemiologic studies and associated air quality
information support the occurrence of O3-associated hospital
admissions and emergency department visits for ambient O3
concentrations likely to have met the current standard, and that air
quality analyses in locations of multicity studies provide some support
for this conclusion for a broader range of effects, including
mortality.
    Beyond her consideration of the scientific evidence, the
Administrator also considered the results of the HREA exposure and risk
analyses in reaching initial conclusions regarding the adequacy of the
current primary O3 standard. In doing so, as noted above,
she focused primarily on exposure and risk estimates based on
information from controlled human exposure studies (i.e., exposures of
concern and O3-induced lung function decrements) and placed
relatively less weight on epidemiologic-based risk estimates.
    With regard to estimates of exposures of concern, the Administrator
considered the extent to which the current standard provides protection
against exposures to O3 concentrations at or above 60, 70,
and 80 ppb. Consistent with CASAC advice (Frey, 2014c), the
Administrator focused on children in these analyses of O3
exposures, noting that estimates for all children and asthmatic
children are virtually indistinguishable, in terms of the percent
estimated to experience exposures of concern.\77\ Though she focused on
children, she also recognized that exposures to O3
concentrations at or above 60 or 70 ppb could be of concern for adults.
As discussed in the HREA and PA (and II.C.2.a of the proposal), the
patterns of exposure estimates across urban study areas, across years,
and across air quality scenarios are similar in adults with asthma,
older adults, all children, and children with asthma, though smaller
percentages of adult populations are estimated to experience exposures
of concern than children and children with asthma. Thus, the
Administrator recognized that the exposure patterns for children across
years, urban study areas, and air

quality scenarios are indicative of the exposure patterns in a broader
group of at-risk populations that also includes asthmatic adults and
older adults.
---------------------------------------------------------------------------

    \77\ As noted above, HREA analyses indicate that activity data
for asthmatics is generally similar to non-asthmatics (U.S. EPA,
2014a, Appendix 5G, Tables 5G2-to 5G-5).
---------------------------------------------------------------------------

    She further noted that while single exposures of concern could be
adverse for some people, particularly for the higher benchmark
concentrations (70, 80 ppb) where there is stronger evidence for the
occurrence of adverse effects, she became increasingly concerned about
the potential for adverse responses as the number of occurrences
increases (61 FR 75122).\78\ In particular, she noted that repeated
occurrences of the types of effects shown to occur following exposures
of concern can have potentially adverse outcomes. For example, repeated
occurrences of airway inflammation could potentially result in the
induction of a chronic inflammatory state; altered pulmonary structure
and function, leading to diseases such as asthma; altered lung host
defense response to inhaled microorganisms; and altered lung response
to other agents such as allergens or toxins (U.S. EPA, 2013, section
6.2.3). Thus, the Administrator noted that the types of respiratory
effects shown to occur in some individuals following exposures to
O3 concentrations from 60 to 80 ppb, particularly if
experienced repeatedly, provide a mode of action by which O3
may cause other more serious effects (e.g., asthma exacerbations).
Therefore, the Administrator placed the most weight on estimates of two
or more exposures of concern (i.e., as a surrogate for the occurrence
of repeated exposures), though she also considered estimates of one or
more, particularly for the 70 and 80 ppb benchmarks.\79\
---------------------------------------------------------------------------

    \78\ The Administrator noted that not all people who experience
an exposure of concern will experience an adverse effect (even
members of at-risk populations). For most of the endpoints evaluated
in controlled human exposure studies (with the exception of
O3-induced FEV1 decrements, as discussed
below), the number of those experiencing exposures of concern who
will experience adverse effects cannot be reliably quantified.
    \79\ The Administrator's considerations related to estimated
O3 exposures of concern, including her views on estimates
of two or more and one or more such exposures, are discussed in more
detail within the context of her consideration of public comments on
the level of the revised standard and her final decision on level
(II.C.4.b and II.C.4.c, below).
---------------------------------------------------------------------------

    As illustrated in Table 1 (above), the Administrator noted that if
the 15 urban study areas evaluated in the HREA were to just meet the
current O3 standard, fewer than 1% of children in those
areas would be estimated to experience two or more exposures of concern
at or above 70 ppb, though approximately 3 to 8% of children, including
approximately 3 to 8% of asthmatic children, would be estimated to
experience two or more exposures of concern to O3
concentrations at or above 60 ppb \80\ (based on estimates averaged
over the years of analysis). To provide some perspective on these
percentages, the Administrator noted that they correspond to almost
900,000 children in urban study areas, including about 90,000 asthmatic
children, estimated to experience two or more exposures of concern at
or above 60 ppb. Nationally, if the current standard were to be just
met, the number of children experiencing such exposures would be
larger. In the worst-case year and location (i.e., year and location
with the largest exposure estimates), the Administrator noted that over
2% of children are estimated to experience two or more exposures of
concern at or above 70 ppb and over 14% are estimated to experience two
or more exposures of concern at or above 60 ppb.
---------------------------------------------------------------------------

    \80\ Almost no children in those areas would be estimated to
experience two or more exposures of concern at or above 80 ppb.
---------------------------------------------------------------------------

    Although, as discussed above and in section II.E.4.d of the
proposal, the Administrator was less concerned about single occurrences
of exposures of concern, she noted that even single occurrences can
cause adverse effects in some people, particularly for the 70 and 80
ppb benchmarks. Therefore, she also considered estimates of one or more
exposures of concern. As illustrated in Table 1 (above), if the 15
urban study areas evaluated in the HREA were to just meet the current
O3 standard, fewer than 1% of children in those areas would
be estimated to experience one or more exposures of concern at or above
80 ppb (based on estimates averaged over the years of analysis).
However, approximately 1 to 3% of children, including 1 to 3% of
asthmatic children, would be estimated to experience one or more
exposures of concern to O3 concentrations at or above 70 ppb
and approximately 10 to 17% would be estimated to experience one or
more exposures of concern to O3 concentrations at or above
60 ppb. In the worst-case year and location, the Administrator noted
that over 1% of children are estimated to experience one or more
exposures of concern at or above 80 ppb, over 8% are estimated to
experience one or more exposures of concern at or above 70 ppb, and
about 26% are estimated to experience one or more exposures of concern
at or above 60 ppb.
    In addition to estimated exposures of concern, the Administrator
also considered HREA estimates of the occurrence of O3-
induced lung function decrements. In doing so, she particularly noted
CASAC advice that ``estimation of FEV1 decrements of >=15%
is appropriate as a scientifically relevant surrogate for adverse
health outcomes in active healthy adults, whereas an FEV1
decrement of >=10% is a scientifically relevant surrogate for adverse
health outcomes for people with asthma and lung disease'' (Frey, 2014c,
p. 3). While these surrogates provide perspective on the potential for
the occurrence of adverse respiratory effects following O3
exposures, the Administrator agreed with the conclusion in past reviews
that a more general consensus view of the adversity of moderate
responses emerges as the frequency of occurrence increases (citing to
61 FR 65722-3) (Dec, 13, 1996). Therefore, in the proposal the
Administrator expressed increasing concern about the potential for
adversity as the frequency of occurrences increased and, as a result,
she focused primarily on estimates of two or more O3-induced
FEV1 decrements (i.e., as a surrogate for repeated
exposures).
    When averaged over the years evaluated in the HREA, the
Administrator noted that the current standard is estimated to allow
about 1 to 3% of children in the 15 urban study areas (corresponding to
almost 400,000 children) to experience two or more O3-
induced lung function decrements =15%, and to allow about 8
to 12% of children (corresponding to about 180,000 asthmatic children)
to experience two or more O3-induced lung function
decrements =10%. Nationally, larger numbers of children
would be expected to experience such O3-induced decrements
if the current standard were to be just met. The current standard is
also estimated to allow about 3 to 5% of children in the urban study
areas to experience one or more decrements =15% and about 14
to 19% of children to experience one or more decrements
=10%. In the worst-case year and location, the current
standard is estimated to allow 4% of children in the urban study areas
to experience two or more decrements =15% (and 7% to
experience one or more such decrements) and 14% of children to
experience two or more decrements =10% (and 22% to
experience one or more such decrements).\81\
---------------------------------------------------------------------------

    \81\ As discussed below (II.C.4), in her consideration of
potential alternative standard levels, the Administrator placed less
weight on estimates of the risk of O3-induced
FEV1 decrements. In doing so, she particularly noted
that, unlike exposures of concern, the variability in lung function
risk estimates across urban study areas is often greater than the
differences in risk estimates between various standard levels (Table
2, above). Given this, and the resulting considerable overlap
between the ranges of lung function risk estimates for different
standard levels, although the Administrator noted her confidence in
the lung function risk estimates themselves, she viewed them as
providing a more limited basis than exposures of concern for
distinguishing between the degree of public health protection
provided by alternative standard levels.

---------------------------------------------------------------------------

    In further considering the HREA results, the Administrator
considered the epidemiology-based risk estimates. Compared to the
weight given to HREA estimates of exposures of concern and lung
function risks, she placed relatively less weight on epidemiology-based
risk estimates. Consistent with the conclusions in the PA, her
determination to attach less weight to the epidemiologic-based risk
estimates reflected her consideration of key uncertainties, including
the heterogeneity in effect estimates between locations, the potential
for exposure measurement errors, and uncertainty in the interpretation
of the shape of concentration-response functions for O3
concentrations in the lower portions of ambient distributions (U.S.
EPA, 2014a, section 9.6) (section II.D.2 of the proposal).
    The Administrator focused on estimates of total mortality risk
associated with short-term O3 exposures.\82\ Given the
decreasing certainty in the shape of concentration-response functions
for area-wide O3 concentrations at the lower ends of warm
season distributions (U.S. EPA, 2013, section <IP_ADDRESS>), the
Administrator focused on estimates of risk associated with
O3 concentrations in the upper portions of ambient
distributions. Even when considering only area-wide O3
concentrations from these upper portions of seasonal distributions, the
Administrator noted that the current standard is estimated to allow
hundreds to thousands of O3-associated deaths per year in
urban study areas (79 FR 75291 citing to section II.C.3 of the
proposal).
---------------------------------------------------------------------------

    \82\ In doing so, she concluded that lower confidence should be
placed in the results of the assessment of respiratory mortality
risks associated with long-term O3 exposures, primarily
because that analysis is based on only one study (even though that
study is well-designed) and because of the uncertainty in that study
about the existence and identification of a potential threshold in
the concentration-response function (U.S. EPA, 2014a, section 9.6)
(section II.D.2 of the proposal). CASAC also called into question
the extent to which it is appropriate to place confidence in risk
estimates for respiratory mortality (Frey, 2014a, p. 11).
---------------------------------------------------------------------------

    In addition to the evidence and exposure/risk information discussed
above, the Administrator took note of the CASAC advice in the current
review and in the 2010 proposed reconsideration of the 2008 decision
establishing the current standard. As discussed in more detail above,
the current CASAC ``finds that the current NAAQS for ozone is not
protective of human health'' and ``unanimously recommends that the
Administrator revise the current primary ozone standard to protect
public health'' (Frey, 2014c, p. 5).
    In consideration of all of the above, the Administrator proposed
that the current primary O3 standard is not adequate to
protect public health, and that it should be revised to provide
increased public health protection. This proposed decision was based on
the Administrator's initial conclusions that the available evidence and
exposure and risk information clearly call into question the adequacy
of public health protection provided by the current primary standard
and, therefore, that the current standard is not requisite to protect
public health with an adequate margin of safety. With regard to the
evidence, she specifically noted that (1) controlled human exposure
studies provide support for the occurrence of adverse respiratory
effects following exposures to O3 concentrations below the
level of the current standard (i.e., as low as 72 ppb), and that (2)
single-city epidemiologic studies provide support for the occurrence of
adverse respiratory effects under air quality conditions that would
likely meet the current standard, with multicity studies providing
limited support for this conclusion for a broader range of effects
(i.e., including mortality). In addition, based on the analyses in the
HREA, the Administrator concluded that the exposures and risks
projected to remain upon meeting the current standard can reasonably be
judged to be important from a public health perspective. Thus, she
reached the proposed conclusion that the evidence and information,
together with CASAC advice based on their consideration of that
evidence and information, provide strong support for revising the
current primary standard in order to increase public health protection
against an array of adverse effects that range from decreased lung
function and respiratory symptoms to more serious indicators of
morbidity (e.g., including emergency department visits and hospital
admissions), and mortality.
2. Comments on the Need for Revision
    The EPA received a large number of comments, more than 430,000
comments, on the proposed decision to revise the current primary
O3 standard. These comments generally fell into one of two
broad groups that expressed sharply divergent views.
    Many commenters asserted that the current primary O3
standard is not sufficient to protect public health, especially the
health of sensitive groups, with an adequate margin of safety. These
commenters agreed with the EPA's proposed decision to revise the
current standard to increase public health protection. Among those
calling for revisions to the current primary standard were medical
groups (e.g., American Academy of Pediatrics (AAP), American Medical
Association, American Lung Association (ALA), American Thoracic
Society, American Heart Association, and the American College of
Occupational and Environmental Medicine); national, state, and local
public health and environmental organizations (e.g., the National
Association of County and City Health Officials, American Public Health
Association, Physicians for Social Responsibility, Sierra Club, Natural
Resources Defense Council, Environmental Defense Fund, Center for
Biological Diversity, and Earthjustice); the majority of state and
local air pollution control authorities that submitted comments (e.g.,
agencies from California Air Resources Board and Office of
Environmental Health Hazard Assessment, Connecticut, Delaware, Iowa,
Illinois, Maryland, Minnesota, New Hampshire, New York, North Dakota,
Oregon, Pennsylvania, Tennessee, and Wisconsin); the National Tribal
Air Association; State organizations (e.g., National Association of
Clean Air Agencies (NACAA), Northeast States for Coordinated Air Use
Management, Ozone Transport Commission). While all of these commenters
agreed with the EPA that the current O3 standard needs to be
revised, many supported a more protective standard than proposed by
EPA, as discussed in more detail below (II.C.4). Many individual
commenters also expressed similar views.
    A second group of commenters, representing industry associations,
businesses and some state agencies, opposed the proposed decision to
revise the current primary O3 standard, expressing the view
that the current standard is adequate to protect public health,
including the health of sensitive groups, and to do so with an adequate
margin of safety. Industry and business groups expressing this view
included the American Petroleum Institute (API), the Alliance of
Automobile Manufacturers (AAM), the American Forest and Paper
Association, the Dow Chemical Company, the National Association of
Manufacturers, the

National Mining Association, the U.S. Chamber of Commerce (in a joint
comment with other industry groups), and the Utility Air Regulatory
Group (UARG). State environmental agencies opposed to revising the
current primary O3 standard included agencies from Arkansas,
Georgia, Louisiana, Kansas, Michigan, Mississippi, Nebraska, North
Carolina, Ohio, Texas, Virginia, and West Virginia.
    The following sections discuss comments submitted by these and
other groups, and the EPA's responses to those comments. Comments
dealing with overarching issues that are fundamental to EPA's decision-
making methodology are addressed in section II.B.2.a. Comments on the
health effects evidence, including evidence from controlled human
exposure and epidemiologic studies, are addressed in section II.B.2.b.
Comments on human exposure and health risk assessments are addressed in
section II.B.2.c. Comments on the appropriate indicator, averaging
time, form, or level of a revised primary O3 standard are
addressed below in section II.C. In addition to the comments addressed
in this preamble, the EPA has prepared a Response to Comments document
that addresses other specific comments related to standard setting, as
well as comments on implementation- and/or cost-related factors that
the EPA may not consider as part of the basis for decisions on the
NAAQS. This document is available for review in the docket for this
rulemaking and through the EPA's OAQPS TTN Web site (http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_index.html).
a. Overarching Comments
    Some commenters maintained that the proposed rule (and by extension
the final rule) is fundamentally flawed because it does not quantify,
or otherwise define, what level of protection is ``requisite'' to
protect the public health. These commenters asserted that ``EPA has not
explained how far above zero-risk it believes is appropriate or how
close to background is acceptable. EPA has failed to explain how the
current standard is inadequate on this specific basis'' (e.g., UARG, p.
10). These commenters further maintained that the failure to quantify a
requisite level of protection ``drastically reduces the value of public
participation'' since ``the public does not understand what is driving
EPA's decision'' (e.g., UARG, p. 11).
    The EPA disagrees with these comments and notes that industry
petitioners made virtually the same argument before the D.C. Circuit in
ATA III, on remand from the Supreme Court, arguing that unless EPA
identifies and quantifies a degree of acceptable risk, it is impossible
to determine if a NAAQS is requisite (i.e., neither too stringent or
insufficiently stringent to protect the public health). The D.C.
Circuit rejected petitioners' argument, holding that ``[a]lthough we
recognize that the Clean Air Act and circuit precedent require EPA
qualitatively to describe the standard governing its selection of
particular NAAQS, we have expressly rejected the notion that the Agency
must `establish a measure of the risk to safety it considers adequate
to protect public health every time it establish a [NAAQS]''' ATA III,
283 F. 3d at 369 (quoting NRDC v. EPA, 902 F.2d 962, 973 (D.C. Cir.
1990)). The court went on to explain that the requirement is only for
EPA to engage in reasoned decision-making, ``not that it definitively
identify pollutant levels below which risks to public health are
negligible.'' ATA III, 283 F. 3d at 370.
    Thus, the Administrator is required to exercise her judgment in the
face of scientific uncertainty to establish the NAAQS to provide
appropriate protection against risks to public health, both known and
unknown. As discussed below, in the current review, the Administrator
judges that the existing primary O3 standard is not
requisite to protect public health with an adequate margin of safety, a
judgment that is consistent with CASAC's conclusion that ``there is
clear scientific support for the need to revise the standard'' (Frey,
2014c, p. ii). Further, in section II.C.4 below, the Administrator has
provided a thorough explanation of her rationale for concluding that a
standard with a level of 70 ppb is requisite to protect public health
with an adequate margin of safety, explaining the various scientific
uncertainties which circumscribe the range of potential alternative
standards, and how she exercised her ``judgment'' (per section 109
(b)(1) of the CAA) in selecting a standard from within that range of
scientifically reasonable choices. This ``reasoned decision making'' is
what the Act requires, 283 F. 3d at 370, not the quantification
advocated by these commenters.
    The EPA further disagrees with the comment that a failure to
quantify a requisite level of protection impaired or impeded public
notice and comment opportunities. In fact, the EPA clearly gave
adequate notice of the bases both for determining that the current
standard does not afford requisite protection,\83\ and for determining
how the standard should be revised. In particular, the EPA explained in
detail which evidence it considered critical, and the scientific
uncertainties that could cause the Administrator to weight that
evidence in various ways (79 FR 75308-75310). There were robust
comments submitted by commenters from a range of viewpoints on all of
these issues, an indication of the adequacy of notice. The public was
also afforded multiple opportunities to comment to the EPA and to CASAC
during the development of the ISA, REA, and PA. Thus, the EPA does not
agree that lack of quantification of a risk level that is ``requisite''
has deprived commenters of adequate notice and opportunity to comment
in this proceeding.
---------------------------------------------------------------------------

    \83\ See 79 FR 75287-91 (noting, among other things, that
exposure to ambient O3 concentrations below the level of
the current standard has been associated with diminished lung
function capacity, respiratory symptoms, and respiratory health
effects resulting in emergency room visits or hospital admissions,
and that a single-city epidemiologic study showed associations with
asthma emergency department visits in an area that would have met
the current standard over the entire study period). See also Frey
2014c, p. 5 (CASAC reiterated its conclusion, after multiple public
comment opportunities, that as a matter of science the current
standard ``is not protective of public health'' and provided the
bases for that conclusion).
---------------------------------------------------------------------------

    Various commenters maintained that it was inappropriate to revise
the current NAAQS based on their view that natural background
concentrations in several states are at or above O3
concentrations associated with meeting a NAAQS set at a level less than
75 ppb (presumably retaining the same indicator, form, and averaging
time), making the NAAQS impossible for those states to attain and
maintain, a result they claim is legally impermissible. In support for
their argument, the commenters cite monitoring and modelling results
from various areas in the intermountain west, state that EPA analyses
provide underestimates of background O3 and conclude that
high concentrations of background O3 \84\ exist

in many parts of the United States that will ``prevent attainment'' of
a revised standard (NMA, p. 5).
---------------------------------------------------------------------------

    \84\ Background O3 can be generically defined as the
portion of O3 in ambient air that comes from sources
outside the jurisdiction of an area and can include natural sources
as well as transported O3 of anthropogenic origin. EPA
has identified two specific definitions of background O3
relevant to this discussion: natural background (NB) and United
States background (USB). NB is defined as the O3 that
would exist in the absence of any manmade precursor emissions. USB
is defined as that O3 that would exist in the absence of
any manmade emissions inside the U.S. This includes anthropogenic
emissions outside the U.S. as well as naturally occurring ozone. In
many cases, the comments reference background O3 only in
the generic sense. Unless explicitly noted otherwise, we have
assumed all references to background in the comments are intended to
refer to USB.
---------------------------------------------------------------------------

    The courts have clearly established that ``[a]ttainability and
technological feasibility are not relevant considerations in the
promulgation of [NAAQS].'' API v. EPA, 665 F. 2d 1176, 1185 (D.C. Cir.
1981). Further, the courts have clarified that the EPA may consider
proximity to background concentrations as a factor in the decision
whether and how to revise the NAAQS only in the context of considering
standard levels within the range of reasonable values supported by the
air quality criteria and judgments of the Administrator. 79 FR 75242-43
(citing ATA III, 283 F. 3d at 379). In this review, the overall body of
scientific evidence and exposure/risk information, as discussed in
Section II.B of this notice, is clear and convincing: The existing
standard is not adequate to protect public health with an adequate
margin of safety and that the standard needs to be revised to reflect a
lower level to provide that protection. The EPA analyses indicate that
there may be infrequent instances in a limited number of rural areas
where background O3 would be appreciable but not the sole
contributor to an exceedance of the revised NAAQS, but do not indicate
U.S. background (USB) O3 concentrations will prevent
attainment of a revised O3 standard with a level of 70 ppb.
USB is defined as that O3 that would exist even in the
absence of any manmade emissions within the United States.
    The EPA's estimates of U.S. background ozone concentrations are
based on frequently-utilized, state-of-the-science air quality models
and are considered reasonable and reliable, not underestimates. In
support of their view, the commenters state that monitored (not
modelled) ozone concentrations in remote rural locations include
instances of 8-hour average concentrations very occasionally higher
than 70 ppb. Monitoring data from places like the Grand Canyon and
Yellowstone National Parks, are examples cited in comments. It is
inappropriate to assume that monitored O3 concentrations at
remote sites can be used as a proxy for background O3. Even
at the most remote locations, local O3 concentrations are
impacted by anthropogenic emissions from within the U.S. The EPA
modeling analyses (U.S. EPA, 2014c, Figure 2-18) estimate that, on a
seasonal basis, 10-20% of the O3 at even the most remote
locations in the intermountain western U.S. originates from manmade
emissions from the U.S., and thus is not part of USB. This conclusion
is supported by commenter-submitted recent data analyses of rural
O3 observations in Nevada and Utah (NMA, Appendices D and
H). These analyses conclude that natural sources, international
O3 transport, O3 transported from upwind states,
and O3 transported from urban areas within a state all
contributed to O3 concentrations at rural sites.\85\ Thus,
while O3 in high-altitude, rural portions of the
intermountain western U.S. can, at times, be substantially influenced
by background sources such as wildfires, international transport or the
stratosphere, measured O3 in rural locations are also
influenced by domestic emissions and so cannot, by themselves, be used
to estimate USB concentrations. Accordingly, the fact that 2011-2013
design values in locations like Yellowstone National Park (66 ppb) or
Grand Canyon National Park (72 ppb) approach or exceed 70 ppb, does not
support the conclusion that a standard with a level of 70 ppb is
impossible to attain.
---------------------------------------------------------------------------

    \85\ The analysis of observations in Utah notes the influence of
domestic emissions--either from Salt Lake City (for two of the
areas) or from Los Angeles and California (for the third of the
areas)--on O3 concentrations at each of the locations
included (NMA comments, Appendix E). Additionally, the analysis of
monitoring data for Nevada also describes the influence of the
monitoring sites by domestic emissions from other western states
(NMA, Appendix H).
---------------------------------------------------------------------------

    To accurately estimate USB concentrations, it is necessary to use
air quality models which can estimate how much of the O3 at
any given location originates from sources other than manmade emissions
within the U.S. As part of the rulemaking, the EPA has summarized a
variety of modeling-based analyses of background O3 (U.S.
EPA, 2013, Chapter 3) and conducted our own multi-model assessment of
USB concentrations across the U.S. (U.S. EPA, 2014c, Chapter 2). The
EPA analyses, which are consistent with the previously-summarized
studies highlighted by commenters, concluded that seasonal mean daily
maximum 8-hour average concentrations of USB O3 range from
25-50 ppb, with the highest estimates located across the intermountain
western U.S.
    Importantly, the modeling analyses also indicate that the highest
O3 days (i.e., the days most relevant to the form of the
NAAQS) generally have similar daily maximum 8-hour average USB
concentrations as the seasonal means of this metric, but have larger
contributions from U.S. anthropogenic sources. As summarized in the PA,
``the highest modeled O3 site-days tend to have background
O3 levels similar to mid-range O3 days . . .
[T]he days with highest O3 levels have similar distributions
(i.e. means, inter-quartile ranges) of background levels as days with
lower values, down to approximately 40 ppb. As a result, the proportion
of total O3 that has background origins is smaller on high O3 days
(e.g. greater than 60 ppb) than on the more common lower O3 days that
tend to drive seasonal means'' (U.S. EPA, 2014c, p. 2-21, emphasis
added). When averaged over the entire U.S., the models estimate that
the mean USB fractional contribution to daily maximum 8-hour average
O3 concentrations above 70 ppb is less than 35 percent. U.S.
anthropogenic emission sources are thus the dominant contributor to the
majority of modeled O3 exceedances across the U.S. (U.S.
EPA, 2014c, Figures 2-14 and 2-15).
    As noted in the PA, and as highlighted by the commenters based on
existing modeling, there can be infrequent events where daily maximum
8-hour O3 concentrations approach or exceed 70 ppb largely
due to the influence of USB sources like a wildfire or stratospheric
intrusion. As discussed below in Section V, the statute and EPA
implementing regulations allow for the exclusion of air quality
monitoring data from design value calculations when there are
exceedances caused by certain event-related U.S. background influences
(e.g., wildfires or stratospheric intrusions). As a result, these
``exceptional events'' will not factor into attainability concerns.
    In sum, the EPA believes that the commenters have failed to
establish the predicate for their argument. Uncontrollable background
concentrations of O3 are not expected to preclude attainment
of a revised O3 standard with a level of 70 ppb. The EPA
also disagrees with aspects of the specific statements made by the
commenters as support for their view that the EPA analyses have
underestimated background O3.\86\ Thus, even assuming the
commenters are correct that the EPA may use proximity to background as
a justification for not revising a standard that, in the judgment of
the Administrator, is inadequate to protect public health, the
commenters' arguments for the justification and need to do so for this
review are based on a flawed premise.
---------------------------------------------------------------------------

    \86\ Specific aspects of the comments on the EPA analyses are
addressed in more detail in the RTC.
---------------------------------------------------------------------------

b. Comments on the Health Effects Evidence
    As noted above, comments on the adequacy of the current standard
fell into two broad categories reflecting very

different views of the available scientific evidence. Commenters who
expressed support for the EPA's proposed decision to revise the current
primary O3 standard generally concluded that the body of
scientific evidence assessed in the ISA is much stronger and more
compelling than in the last review. These commenters also generally
emphasized CASAC's interpretation of the body of available evidence,
which formed an important part of the basis for CASAC's reiterated
recommendations to revise the O3 standard to provide
increased public health protection. In some cases, these commenters
supported their positions by citing studies published since the
completion of the ISA.
    The EPA generally agrees with these commenters regarding the need
to revise the current primary O3 standard in order to
increase public health protection though, in many cases, not with their
conclusions about the degree of protection that is appropriate
(II.C.4.b and II.C.4.c, below). The scientific evidence noted by these
commenters was generally the same as that assessed in the ISA (U.S.
EPA, 2013) and the proposal,\87\ and their interpretation of the
evidence was often, though not always, consistent with the conclusions
of the ISA and CASAC. The EPA agrees that the evidence available in
this review provides a strong basis for the conclusion that the current
O3 standard is not adequately protective of public health.
In reaching this conclusion, the EPA places a large amount of weight on
the scientific advice of CASAC, and on CASAC's endorsement of the
assessment of the evidence in the ISA (Frey and Samet, 2012).
---------------------------------------------------------------------------

    \87\ As discussed in section I.C above, the EPA has
provisionally considered studies that were highlighted by commenters
and that were published after the ISA. These studies are generally
consistent with the evidence assessed in the ISA, and they do not
materially alter our understanding of the scientific evidence or the
Agency's conclusions based on that evidence.
---------------------------------------------------------------------------

    In contrast, while commenters who opposed the proposed decision to
revise the primary O3 standard generally focused on many of
the same studies assessed in the ISA, these commenters highlighted
different aspects of these studies and reached substantially different
conclusions about their strength and the extent to which progress has
been made in reducing uncertainties in the evidence since the last
review. These commenters generally concluded that information about the
health effects of concern has not changed significantly since 2008 and
that the uncertainties in the underlying health science have not been
reduced since the 2008 review. In some cases, these commenters
specifically questioned the EPA's approach to assessing the scientific
evidence and to reaching conclusions on the strength of that evidence
in the ISA. For example, several commenters asserted that the EPA's
causal framework, discussed in detail in the ISA, is flawed and that it
has not been applied consistently across health endpoints. Commenters
also noted departures from other published causality frameworks (Samet
and Bodurow, 2008) and from the criteria for judging causality put
forward by Sir Austin Bradford Hill (Hill, 1965).
    The EPA disagrees with comments questioning the ISA's approach to
assessing the evidence, the causal framework established in the ISA, or
the consistent application of that framework across health endpoints.
While the EPA acknowledges the ISA's approach departs from assessment
and causality frameworks that have been developed for other purposes,
such departures reflect appropriate adaptations for the NAAQS. As with
other ISAs, the O3 ISA uses a five-level hierarchy that
classifies the weight of evidence for causation. In developing this
hierarchy, the EPA has drawn on the work of previous evaluations, most
prominently the IOM's Improving the Presumptive Disability Decision-
Making Process for Veterans (Samet and Bodurow, 2008), EPA's Guidelines
for Carcinogen Risk Assessment (U.S. EPA, 2005), and the U.S. Surgeon
General's smoking report (CDC, 2004). The ISA's weight of evidence
evaluation is based on the integration of findings from various lines
of evidence from across the health and environmental effects
disciplines. These separate judgments are integrated into a qualitative
statement about the overall weight of the evidence and causality. The
ISA's causal framework has been developed over multiple NAAQS reviews,
based on extensive interactions with CASAC and based on the public
input received as part of the CASAC review process. In the current
review, the causality framework, and the application of that framework
to causality determinations in the O3 ISA, have been
reviewed and endorsed by CASAC (Frey and Samet, 2012).
    Given these views on the assessment of the evidence in the ISA, it
is relevant to note that many of the issues and concerns raised by
commenters on the EPA's interpretation of the evidence, and on the
EPA's conclusions regarding the extent to which uncertainties have been
reduced since the 2008 review, are essentially restatements of issues
raised during the development of the ISA, HREA, and/or PA. The CASAC
O3 Panel reviewed the interpretation of the evidence, and
the EPA's use of information from specific studies, in drafts of these
documents. In CASAC's advice to the Administrator, which incorporates
its consideration of many of the issues raised by commenters, CASAC
approved of the scientific content, assessments, and accuracy of the
ISA, REA, and PA, and indicated that these documents provide an
appropriate basis for use in regulatory decision making for the
O3 NAAQS (Frey and Samet, 2012, Frey, 2014a, Frey, 2014c).
Therefore, the EPA's responses to many of the comments on the evidence
rely heavily on the process established in the ISA for assessing the
evidence, which is the product of extensive interactions with CASAC
over a number of different reviews, and on CASAC advice received as
part of this review of the O3 NAAQS.
    The remainder of this section discusses public comments and the
EPA's responses, on controlled human exposure studies (II.B.2.b.i);
epidemiologic studies (II.B.2.b.ii); and at-risk populations
(II.B.2.b.iii).
i. Evidence From Controlled Human Exposure Studies
    This section discusses major comments on the evidence from
controlled human exposure studies and provides the Agency's responses
to those comments. To support their views on the adequacy of the
current standard, commenters often highlighted specific aspects of the
scientific evidence from controlled human exposure studies. Key themes
discussed by these commenters included the following: (1) The adversity
of effects demonstrated in controlled human exposure studies,
especially studies conducted at exposure concentrations below 80 ppb;
(2) representativeness of different aspects of the controlled human
exposure studies for making inferences to the general population and
at-risk populations; (3) results of additional analyses of the data
from controlled human exposure studies; (4) evaluation of a threshold
for effects; and (5) importance of demonstration of inflammation at 60
ppb. This section discusses these key comment themes, and provides the
EPA's responses. More detailed discussion of individual comments, and
the EPA's responses, is provided in the Response to Comments document.
Adversity
    Some commenters who disagreed with the EPA's proposed decision to
revise the current primary O3 standard disputed the Agency's
characterization

of the adversity of the O3-induced health effects shown to
occur in controlled human exposure studies. Some of these commenters
contended that the proposal does not provide a clear definition of
adversity or that there is confusion concerning what responses the
Administrator considers adverse. The EPA disagrees with these comments,
and notes that section II.E.4.d of the proposal describes the
Administrator's proposed approach to considering the adversity of
effects observed in controlled human exposure studies. Her final
approach to considering the adversity of these effects, and her
conclusions on adversity, are described in detail below (II.C.4.b,
II.C.4.c).
    Other commenters disagreed with the EPA's judgments regarding
adversity and expressed the view that the effects observed in
controlled human exposure studies following 6.6-hour exposures to
O3 concentrations below the level of the current standard
(i.e., 75 ppb) are not adverse.\88\ This group of commenters cited
several reasons to support their views, including that: (1) The lung
function decrements and respiratory symptoms observed at 72 ppb in the
study by Schelegle et al. (2009) were not correlated with each other,
and therefore were not adverse; and (2) group mean FEV1
decrements observed following exposures below 75 ppb are small (e.g.,
<10%, as highlighted by some commenters), transient and reversible, do
not interfere with daily activities, and do not result in permanent
respiratory injury or progressive respiratory dysfunction.
---------------------------------------------------------------------------

    \88\ Commenters who supported revising the primary O3
standard often concluded that there is clear evidence for adverse
effects following exposures to O3 concentrations at least
as low as 60 ppb, and that such adverse effects support setting the
level of a revised primary O3 standard at 60 ppb. These
comments, and the EPA's responses, are discussed below within the
context of the Administrator's decision on a revised level
(II.C.4.b).
---------------------------------------------------------------------------

    While the EPA agrees that not all effects reported in controlled
human exposure studies following exposures below 75 ppb can reasonably
be considered to be adverse, the Agency strongly disagrees with
comments asserting that none of these effects can be adverse. As an
initial matter, the Administrator notes that, when considering the
extent to which the current or a revised standard could allow adverse
respiratory effects, based on information from controlled human
exposure studies, she considers not only the effects themselves, but
also quantitative estimates of the extent to which the current or a
revised standard could allow such effects. Quantitative exposure and
risk estimates provide perspective on the extent to which various
standards could allow populations, including at-risk populations such
as children and children with asthma, to experience the types of
O3 exposures that have been shown in controlled human
exposure studies to cause respiratory effects. As discussed further
below (II.B.3, II.C.4.b, II.C.4.c), to the extent at-risk populations
are estimated to experience such exposures repeatedly, the
Administrator becomes increasingly concerned about the potential for
adverse responses in the exposed population. Repeated exposures provide
a plausible mode of action by which O3 may cause other more
serious effects. Thus, even though the Administrator concludes there is
important uncertainty in the adversity of some of the effects observed
in controlled human exposure studies based on the single exposure
periods evaluated in these studies (e.g., FEV1 decrements
observed following exposures to 60 ppb O3, as discussed in
sections II.C.4.b and II.C.4.c below), she judges that the potential
for adverse effects increases as the number of exposures increases.
Contrary to the commenters' views noted above, the Administrator
considers the broader body of available information (i.e., including
quantitative exposure and risk estimates) when considering the extent
to which the current or a revised standard could allow adverse
respiratory effects (II.B.3, II.C.4.b, II.C.4.c, below).
    In further considering commenters' views on the potential adversity
of the respiratory effects themselves (i.e., without considering
quantitative estimates), the EPA notes that although the results of
controlled human exposure studies provide a high degree of confidence
regarding the occurrence of health effects following exposures to
O3 concentrations from 60 to 80 ppb, there are no
universally accepted criteria by which to judge the adversity of the
observed effects. Therefore, as in the proposal, the Administrator
relies upon recommendations from the ATS and advice from CASAC to
inform her judgments on adversity.
    In particular, the Administrator focuses on the ATS recommendation
that ``reversible loss of lung function in combination with the
presence of symptoms should be considered adverse'' (ATS, 2000a). The
study by Schelegle et al. (2009) reported a statistically significant
decrease in group mean FEV1 and a statistically significant
increase in respiratory symptoms in healthy adults following 6.6-hour
exposures to average O3 concentrations of 72 ppb. In
considering these effects, CASAC noted that ``the combination of
decrements in FEV1 together with the statistically
significant alterations in symptoms in human subjects exposed to 72 ppb
ozone meets the American Thoracic Society's definition of an adverse
health effect'' (Frey, 2014c, p. 5).
    As mentioned above, some commenters nonetheless maintained that the
effects observed in Schelegle et al. (2009) following exposure to 72
ppb O3 (average concentration) were not adverse because the
magnitudes of the FEV1 decrements and the increases in
respiratory symptoms (as measured by the total subjective symptoms
score, TSS) were not correlated across individual study subjects. A
commenter submitted an analysis of the individual-level data from the
study by Schelegle et al. (2009) to support their position. This
analysis indicated that, while the majority of study volunteers (66%)
did experience both lung function decrements and increased respiratory
symptoms following 6.6-hour exposures to 72 ppb O3, some
(33%) did not (e.g., Figure 3 in comments from Gradient).\89\ In
addition, the study subjects who experienced relatively large lung
function decrements did not always also experience relatively large
increases in respiratory symptoms. These commenters interpreted the
lack of a statistically significant correlation between the magnitudes
of decrements and symptoms as meaning that the effects reported by
Schelegle et al. (2009) at 72 ppb did not meet the ATS criteria for an
adverse response.
---------------------------------------------------------------------------

    \89\ The figure provided in comments by Gradient only clearly
illustrated the responses of 30 out of 31 subjects.
---------------------------------------------------------------------------

    However, the ATS recommendation that the combination of lung
function decrements and symptomatic responses be considered adverse is
not restricted to effects of a particular magnitude nor a requirement
that individual responses be correlated. Similarly, CASAC made no such
qualifications in its advice on the combination of respiratory symptoms
and lung function decrements (See e.g., Frey, 2014c, p. 5). Therefore,
as in the proposal and consistent with both CASAC advice and ATS
recommendations, the EPA continues to conclude that the finding of both
statistically significant decrements in lung function and significant
increases in respiratory symptoms following 6.6-hour exposures to an
average O3 concentration of 72 ppb provides a strong
indication of the

potential for exposed individuals to experience this combination of
effects.\90\
---------------------------------------------------------------------------

    \90\ Indeed, the finding of statistically significant decreases
in lung function and increases in respiratory symptoms in the same
study population indicates that, on average, study volunteers did
experience both effects.
---------------------------------------------------------------------------

    In particular, the Administrator notes that lung function provides
an objective measure of the respiratory response to O3
exposure while respiratory symptoms are subjective, and as evaluated by
Schelegle et al. (2009) were based on a TSS score. If an O3
exposure causes increases in both objectively measured lung function
decrements and subjective respiratory symptoms, which indicate that
people may modify their behavior in response to the exposure, then the
effect is properly viewed as adverse. As noted above, the commenter's
analysis shows that the majority of study volunteers exposed to 72 ppb
O3 in the study by Schelegle et al. (2009) did, in fact,
experience both a decrease in lung function and an increase in
respiratory symptoms.
    In further considering this comment, the EPA recognizes that,
consistent with commenter's analysis, some individuals may experience
large decrements in lung function with minimal to no respiratory
symptoms (McDonnell et al., 1999), and vice versa. As indicated above
and discussed in the proposal (79 FR 75289), the Administrator
acknowledges such interindividual variability in responsiveness in her
interpretation of estimated exposures of concern. Specifically, she
notes that not everyone who experiences an exposure of concern,
including for the 70 ppb benchmark, is expected to experience an
adverse response. However, she further judges that the likelihood of
adverse effects increases as the number of occurrences of O3
exposures of concern increases. In making this judgment, she notes that
the types of respiratory effects that can occur following exposures of
concern, particularly if experienced repeatedly, provide a plausible
mode of action by which O3 may cause other more serious
effects.\91\ Therefore, her decisions on the primary standard emphasize
the public health importance of limiting the occurrence of repeated
exposures to O3 concentrations at or above those shown to
cause adverse effects in controlled human exposure studies (II.B.3,
II.C.4.b, II.C.4.c). The Administrator views this approach to
considering the evidence from controlled human exposure studies as
being consistent with commenter's analysis indicating that, while the
majority did, not all study volunteers exposed to 72 ppb O3
experienced the adverse combination of lung function decrements and
respiratory symptoms following the single exposure period evaluated by
Schelegle et al. (2009).
---------------------------------------------------------------------------

    \91\ For example, as discussed in the proposal (79 FR 75252) and
the ISA (p. 6-76), inflammation induced by a single exposure (or
several exposures over the course of a summer) can resolve entirely.
However, repeated occurrences of airway inflammation could
potentially result in the induction of a chronic inflammatory state;
altered pulmonary structure and function, leading to diseases such
as asthma; altered lung host defense response to inhaled
microorganisms; and altered lung response to other agents such as
allergens or toxins (ISA, section 6.2.3).
---------------------------------------------------------------------------

Representativeness
    A number of commenters raised issues concerning the
representativeness of controlled human exposure studies considered by
the Administrator in this review, based on different aspects of these
studies. These commenters asserted that since the controlled human
exposure studies were not representative of real-world exposures, they
should not be relied upon as a basis for finding that the current
standard is not adequate to protect public health. Some issues
highlighted by commenters include: Small size of the study populations;
unrealistic activity levels used in the studies; unrealistic exposure
scenarios (i.e., triangular exposure protocol) used in some studies,
including Schelegle et al. (2009); and differences in study design that
limit comparability across studies.
    Some commenters noted that the controlled human exposure studies
were not designed to have individuals represent portions of any larger
group and that the impacts on a small number of people do not implicate
the health of an entire subpopulation, particularly when the
FEV1 decrements are small, temporary, and reversible. These
commenters also noted that the Administrator failed to provide an
explanation or justification for why the individuals in these studies
can be viewed as representatives of a subpopulation. Further, they
asserted that EPA's use of results from individuals, rather than the
group mean responses, contradicts the intent of CAA section 109 to
protect groups of people, not just the most sensitive individuals in
any group (79 FR 75237).
    Consistent with CASAC advice (Frey, 2014c, p. 5), the EPA concludes
that the body of controlled human exposure studies are sufficiently
representative to be relied upon as a basis for finding that the
current standard is not adequate to protect public health. These
studies generally recruit healthy young adult volunteers, and often
expose them to O3 concentrations found in the ambient air
under real-world exposure conditions. As described in more detail above
in section II.A.1.b, the evidence from controlled human exposure
studies to date makes it clear that there is considerable variability
in responses across individuals, even in young healthy adult
volunteers, and that group mean responses are not representative of
more responsive individuals. It is important to look beyond group mean
responses to the responses of these individuals to evaluate the
potential impact on more responsive members of the population.
Moreover, relying on group mean changes to evaluate lung function
responses to O3 exposures would mask the responses of the
most sensitive groups, particularly where, as here, the group mean
reflects responses solely among the healthy young adults who were the
study participants. Thus, the studies of exposures below 80 ppb
O3 show that 10% of young healthy adults experienced
FEV1 decrements >10% following exposures to 60 ppb
O3, and 19% experienced such decrements following exposures
to 72 ppb (under the controlled test conditions involving moderate
exertion for 6.6 hours). These percentages would likely have been
higher had people with asthma or other at-risk populations been exposed
(U.S. EPA, 2013, pp. 6-17 and 6-18; Frey 2014c, p. 7; Frey, 2014a, p.
14).\92\
---------------------------------------------------------------------------

    \92\ See also National Environmental Development Associations
Clean Action Project v. EPA, 686 F. 3d 803, 811 (D.C. Cir. 2012)
(EPA drew legitimate inference that serious asthmatics would
experience more serious health effects than clinical test subjects
who did not have this degree of lung function impairment).
---------------------------------------------------------------------------

    Moreover, the EPA may legitimately view the individuals in these
studies as representatives of the larger subpopulation of at-risk or
sensitive groups. As stated in the Senate Report to the 1970
legislation establishing the NAAQS statutory provisions, ``the
Committee emphasizes that included among these persons whose health
should be protected by the ambient standard are particularly sensitive
citizens such as bronchial asthmatics and emphysematics who in the
normal course of daily activity are exposed to the ambient environment.
In establishing an ambient standard necessary to protect the health of
these persons, reference should be made to a representative sample of
persons comprising the sensitive group rather than to a single person
in such a group. . . . For purposes of this description, a
statistically related sample is the number of persons necessary to test
in order to detect a deviation in the health of any person within such
sensitive group which is attributable to the condition of the ambient
air.'' S. Rep. No. 11-1196, 91st

Cong. 2d sess. at 10. As just noted above, 10% of healthy young adults
in these studies experienced >10% FEV1 decrements following
exposure to 60 ppb O3, and the proportion of individuals
experiencing such decrements increases with increasing O3
exposure concentrations. This substantial percentage certainly can be
viewed as ``a representative sample of persons'' and as a sufficient
number to ``detect a deviation in the health of any person within such
sensitive group,'' especially given that it reflects the percentage of
healthy adults who experienced decrements >10%.
    These results are consistent with estimates from the MSS model,
which makes reliable quantitative predictions of the lung function
response to O3 exposures, and reasonably predicts the
magnitude of individual lung function responses following such
exposures. As described in section II.A.2.c above, and documented in
the HREA, when the MSS model was used to quantify the risk of
O3-induced FEV1 decrements in 15 urban study
areas, the current standard was estimated to allow about 8 to 12% of
children to experience two or more O3-induced
FEV1 decrements >=10%, and about 2 to 3% to experience two
or more decrements >=15% (Table 2, above). These percentages correspond
to hundreds of thousands of children in urban study areas, and tens of
thousands of asthmatic children. While the Administrator judges that
there is uncertainty with regard to the adversity of these
O3-induced lung function decrements (see II.C.4.b, II.C.4.c,
below), such risk estimates clearly indicate that they are a matter of
public health importance on a broad scale, not isolated effects on
idiosyncratically responding individuals.
    Other commenters considered the ventilation rates used in
controlled human exposure studies to be unreasonably high and at the
extreme of prolonged daily activity. Some of these commenters noted
that these scenarios are unrealistic for sensitive populations, such as
asthmatics and people with COPD, whose conditions would likely prevent
them from performing the intensity of exercise, and therefore
experiencing the ventilation rates, required to produce decrements in
lung function observed in experimental settings.
    The EPA disagrees with these commenters. The activity levels used
in controlled human exposure studies were summarized in Table 6-1 of
the ISA (U.S. EPA, 2013). The exercise level in the 6.6-hour exposure
studies by Adams (2006), Schelegle et al. (2009), and Kim et al. (2011)
of young healthy adults was moderate and ventilation rates are
typically targeted for 20 L/min-m\2\ BSA.\93\ Following the exposures
to 60 ppb at this activity level, 10% of the individuals had greater
than a 10% decrement in FEV1 (U.S. EPA, 2013, p. 6-18).
Similar 6.6-hour exposure studies of individuals with asthma are not
available to assess either the effects of O3 on their lung
function or their ability to perform the required level of moderate
exercise.
---------------------------------------------------------------------------

    \93\ Exercise consisted of alternating periods walking on a
treadmill at a pace of 17-18 minutes per mile inclined to a grade of
4-5% or cycling at a load of about 72 watts. Typical heart rates
during the exercise periods were between 115-130 beats per minute.
This activity level is considered moderate (Table 6-1, U.S. EPA,
2013, p. 6-18).
---------------------------------------------------------------------------

    However, referring to Tables 6-9 and 6-10 of the HREA (U.S. EPA,
2014a), between 42% and 45% of FEV1 decrements >= 10% were
estimated to occur at exercise levels of <13 L/min-m\2\ BSA. This
corresponds to light exercise, and this level of exercise has been used
in a 7.6-hour study of healthy people and people with asthma exposed to
160 ppb O3 (Horstman et al., 1995). In that study, people
with asthma exercised with an average minute ventilation of 14.2 L/min-
m\2\ BSA. Adjusted for filtered air responses, an average 19%
FEV1 decrement was seen in the people with asthma versus an
average 10% FEV1 decrement in the healthy people. In
addition, the EPA noted in the HREA that the data underlying the
exposure assessment indicate that ``activity data for asthmatics [is]
generally similar to [that for] non-asthmatics'' (U.S. EPA, 2014a, p.
5-75, Tables 5G-2 and 5G-3). Thus, contrary to the commenters'
assertion, based on both the HREA and the Horstman et al. (1995) study,
people with respiratory disease such as asthma can exercise for a
prolonged period under conditions where they would experience >10%
FEV1 decrements in response to O3 exposure.
    Additionally, a number of commenters asserted that the exposure
scenarios in Schelegle et al. (2009), which are based on a so-called
triangular study protocol, where O3 concentrations ramp up
and down as the study is conducted, are not directly generalizable to
most healthy or sensitive populations because of large changes in the
O3 concentrations from one hour to the next. Commenters
stated that although large fluctuations in O3 are possible
in certain locations due to meteorological conditions (e.g., in valleys
on very hot, summer days), they believe that, in general,
concentrations of O3 do not fluctuate by more than 20-30 ppb
from one hour to the next. Thus, commenters suggested the Schelegle et
al. (2009) study design could happen in a ``worst-case'' exposure
scenario, but that the exposure protocol was not reflective of
conditions in most cities and thus not informative with regard to the
adequacy of the current standard.
    The EPA disagrees with the comment that these triangular exposure
scenarios are not generalizable because of hour-to-hour fluctuations.
Adams (2002, 2006) showed that FEV1 responses following 6.6
hours of exposure to 60 and 80 ppb average O3 exposures do
not differ between triangular (i.e. ramping concentration up and down)
and square-wave (i.e. constant concentration). Schelegle et al. (2009)
used the 80 ppb triangular protocol and a slightly modified 60 ppb
triangular protocol (concentrations during the third and fourth hours
were reversed) from Adams (2006). Therefore, in considering pre- to
post-exposure changes in lung function, concerns about the hour-by-hour
changes in O3 concentrations at 60 and 80 ppb in the
Schelegle et al. (2009) study are unfounded.
    Finally, some commenters also stated that the Kim et al. (2011)
study is missing critical information and its study design makes
comparison to the other studies difficult. That is, the commenter
suggests that data at times other than pre- and post-exposure should
have been provided.
    The EPA disagrees with this comment. With regard to providing data
at other time points besides pre- and post-exposure, there is no
standard that suggests an appropriate frequency at which lung function
should be measured in prolonged 6.6-hour exposure studies. The Adams
(2006) study showed that lung function decrements during O3
exposures with moderate exercise become most apparent following the
third hour of exposure. As such, it makes little sense to measure lung
function during the first couple hours of exposure. However, having
data at multiple time points toward the end of an exposure can provide
evidence that the mean post-exposure FEV1 response is not a
single anomalous data point. The FEV1 response data for the
3-, 4.6-, 5.6-, and 6.6-hour time points of the Kim et al. (2011) study
are available in Figure 6 of the McDonnell et al. (2012) paper where
they are plotted with the Adams (2006) data for 60 ppb. Similar to the
Adams (2006) study, the responses at 5.6 hours are only marginally
smaller than the response at 6.6 hours in the Kim et al. (2011) study.
This indicates that the post-exposure FEV1 responses in both
studies are consistent with responses at an earlier time point and thus
not likely to be anomalous data.

Additional Studies
    Several commenters analyzed the data from controlled human exposure
studies, or they commented on the EPA's analysis of the data from some
of these studies (Brown et al., 2008), to come to a different
conclusion than the EPA's interpretation of these studies thereby
questioning the proposed decision that the current standard is not
adequate to protect public health. One commenter submitted an
independent assessment of the scientific evidence and risk, and used
this analysis to assert that there are multiple flaws in the underlying
studies and their interpretation by the EPA. This commenter stated that
the EPA's discussion of the spirometric responses of children and
adolescents and older adults to O3 was misleading. They
claimed that the EPA did not mention that ``the responses of children
and adolescents are equivalent to those of young adults (18-35 years
old; McDonnell et al., 1985) and that this response diminishes in
middle-aged and older adults (Hazucha 1985).'' The EPA notes that the
commenter misrepresented our characterization of the effect of age on
FEV1 responses to O3 and asserted mistakenly that
EPA did not mention diminished responses on older adults. In fact, the
proposal clearly states that, ``Respiratory symptom responses to
O3 exposure appears to increase with age until early
adulthood and then gradually decrease with increasing age (U.S. EPA,
1996b); lung function responses to O3 exposure also decline
from early adulthood (U.S. EPA, 1996b)'' (79 FR 75267) (see also U.S.
EPA, 2014c p. 3-82). With regard to differences between children and
adults, it was clearly stated in the ISA (U.S. EPA, 2013, p. 6-21) that
healthy children exposed to filtered air and 120 ppb O3
experienced similar spirometric responses, but lesser symptoms than
similarly exposed young healthy adults (McDonnell et al., 1985). In
addition, the EPA's approach to modeling the effect of age on responses
to O3 is clearly provided in the HREA (U.S. EPA, 2014a,
Table 6-2).
    The commenter also stated that the EPA's treatment of filtered air
responses in the dose-response curve was incorrect. They claimed that
when creating a dose-response curve, it is most appropriate to include
a zero-dose point and not to subtract the filtered air response from
responses to O3. Contrary to this assertion, EPA correctly
adjusted FEV1 responses to O3 by responses
following filtered air, as was also done in the McDonnell et al. (2012)
model. As indicated in the ISA (U.S. EPA, 2013, p. 6-4), the majority
of controlled human exposure studies investigating the effects
O3 are of a randomized, controlled, crossover design in
which subjects were exposed, without knowledge of the exposure
condition and in random order, to clean filtered air and, depending on
the study, to one or more O3 concentrations. The filtered
air control exposure provides an unbiased estimate of the effects of
the experimental procedures on the outcome(s) of interest. Comparison
of responses following this filtered air exposure to those following an
O3 exposure allows for estimation of the effects of
O3 itself on an outcome measurement while controlling for
independent effects of the experimental procedures, such as ventilation
rate. Thus, the commenter's approach does not provide an estimate of
the effects of O3 alone. Furthermore, as illustrated in
these comments, following ``long'' filtered air exposures, there is
about a 1% improvement in FEV1. By not accounting for this
increase in FEV1, the commenter underestimated the
FEV1 decrement due to O3 exposure. The
commenter's approach thus is fundamentally flawed.
    The commenter also asserted that the McDonnell et al. (2012) model
and exposure-response (E-R) models incorrectly used only the most
responsive people and that EPA's reliance on data from clinical trials
that use only the most responsive people irrationally ignores large
portions of relevant data. The EPA rejects this assertion that the
McDonnell et al. (2012) model and the E-R analysis ignored large
portions of relevant data. The McDonnell et al. (2012) model was fit to
the FEV1 responses of 741 individuals to O3 and
filtered air (i.e., reflecting all available data for O3-
induced changes in FEV1). The filtered air responses were
subtracted from responses measured during O3 exposures.
Subsequently, as illustrated by the figures in the McDonnell et al.
(2012) paper and described in the text of paper, the model was fit to
all available FEV1 data measured during the course of
O3 exposures, including exposures shorter than 6.6 hours.
Thus, the model predicts temporal dynamics of FEV1 response
to any set of O3 exposure conditions that might reasonably
be experienced in the ambient environment, predicting the mean
responses and the distribution of responses around the mean. For the
HREA (EPA, 2014a), the proportion of individuals, under variable
exposure conditions, predicted to have FEV1 decrements >=10,
15 and 20% was estimated.
    Finally, the commenter referenced the exposure-response model on p.
6-18 of the HREA. However, they neglected to note that this was in a
section describing the exposure-response function approach used in
prior reviews (U.S. EPA, 2014a, starting on p. 6-17). Thus, the
commenter confused the exposure-response model used in the last review
with the updated approach used in this review.
    The commenter also stated that EPA did not properly consider
O3 dose when interpreting the human clinical data. Ozone
total dose includes three factors: duration of exposure, concentration,
and ventilation rate. The commenter claimed the EPA emphasized only
concentration without properly considering and communicating duration
of exposure and ventilation rate. Further, they asserted that because
people are not exposed to the same dose, they cannot be judged to have
the same exposure and would therefore not be expected to respond
consistently. The EPA rejects the claim that we emphasized only
concentration without properly incorporating the other two factors. As
noted in the ISA, total O3 dose does not describe the
temporal dynamics of FEV1 responses as a function of
concentration, ventilation rate, time and age of the exposed
individuals (U.S. EPA, 2013, p. 6-5). Thus, the use of total
O3 dose is antiquated and the EPA therefore conducted a more
sophisticated analysis of FEV1 response to O3 in
the HREA. In this review, the HREA estimates risks of lung function
decrements in school-aged children (ages 5 to 18), asthmatic school-
aged children, and the general adult population for 15 urban study
areas. A probabilistic model designed to account for the numerous
sources of variability that affect people's exposures was used to
simulate the movement of individuals through time and space and to
estimate their exposure to O3 while occupying indoor,
outdoor, and in-vehicle locations. That information was linked with the
McDonnell et al. (2012) model to estimate FEV1 responses
over time as O3 exposure concentrations and ventilation
rates changed. As noted earlier, CASAC agreed that this approach is
both scientifically valid and a significant improvement over approaches
used in past O3 reviews (Frey, 2014a, p. 2).
    Several commenters criticized the EPA analysis published by Brown
et al. (2008). One commenter suggested that the EPA needed to state why
the Brown et al. (2008) analysis was relied on rather than Nicolich
(2007) or Lefohn et

al. (2010). Further, commenters stated that the analysis of the Adams
(2006) data in Brown et al. (2008) was flawed. Among other reasons, one
commenter expressed the opinion that it was not appropriate for Brown
et al. (2008) to only examine a portion of the Adams (2006) data,
citing comments submitted by Gradient.
    The EPA disagrees with these commenters.\94\ As an initial matter,
Nicolich (2007) was a public comment and is not a peer-reviewed
publication that would be used to assess the scientific evidence for
effects of O3 on lung function in the ISA (U.S. EPA, 2013).
The Nicolich (2007) comments were specifically addressed by the EPA on
pp. 24-25 in the Response to Comments Document for the 2007 proposed
rule (U.S. EPA, 2008). On page A-3 of his comments, Dr. Nicolich stated
``that the residuals are not normally distributed and the observations
do not meet the assumptions required for the model'' and that ``the
subject-based errors are not independently, identically and normally
distributed and the subjects do not meet the assumptions required for
the model.'' The EPA reasonably chose not to rely on this analysis:
``Therefore, given that the underlying statistical assumptions required
for his analyses were not met and that significance levels are
questionable, in EPA's judgment the analyses presented by Dr. Nicolich
are ambiguous'' (U.S. EPA, 2008). It is likely that the Lefohn et al.
(2010) analysis of the Adams (2006) data would similarly not meet the
statistical assumptions of the model (e.g., homoscedasticity). In
contrast, recognizing the concerns related to the distribution of
responses, Brown et al. (2008) conservatively used a nonparametric sign
test to obtain a p-value of 0.002 for the comparison responses
following 60 ppb O3 versus filter air. Other common
statistical tests also showed significant effects on lung function. In
addition, the effects of 60 ppb O3 on FEV1
responses in Brown et al. (2008) remained statistically significant
even following the exclusion of three potential outliers.
---------------------------------------------------------------------------

    \94\ The DC Circuit has held that EPA reasonably used and
interpreted the Brown (2007) study in the last review. Mississippi,
744 F. 3d at 1347. In this review, there is now additional
corroborative evidence supporting the Brown (2007) analysis, in the
form of further controlled human clinical studies finding health
effects in young, healthy adults at moderate exercise at
O3 concentrations of 60 ppb over a 6.6 hour exposure
period.
---------------------------------------------------------------------------

    EPA disagrees with the comment stating that it was not appropriate
for Brown et al. (2008) to only examine a portion of the Adams (2006)
data. In fact, there is no established single manner or protocol
decreeing that data throughout the protocol must be analyzed and
included. Furthermore, Brown et al. (2008) was a peer-reviewed journal
publication. CASAC also expressed favorable comments in their March 30,
2011, letter to Administrator Jackson. With reference to a memorandum
(Brown, 2007) that preceded the Brown et al. (2008) publication, on p.
6 of the CASAC Consensus Responses to Charge Questions CASAC stated,
``The results of the Adams et al. study also have been carefully
reanalyzed by EPA investigators (Brown et. al., [2008]), and this
reanalysis showed a statistically significant group effect on
FEV1 after 60 ppb ozone exposure.'' On p. A-13, a CASAC
panelist and biostatistician stated, ``Thus, from my understanding of
the statistical analyses that have been conducted, I would argue that
the analysis by EPA should be preferred to that of Adams for the
specific comparison of the FEV1 effects of 0.06 ppm exposure
relative to filtered air exposure.'' (Samet 2011, p. a-13)
Threshold
    Several commenters used the new McDonnell et al. (2012) and
Schelegle et al. (2012) models to support their views about the
O3 concentrations associated with a threshold for adverse
lung function decrements. For example, one commenter who supported
retaining the current standard noted that McDonnell et al. (2012) found
that the threshold model fit the observed data better than the original
(no-threshold) model, especially at earlier time points and at the
lowest exposure concentrations. The commenter expressed the view that
the threshold model showed that the population mean FEV1
decrement did not reach 10% until exposures were at least 80 ppb,
indicating that O3 exposures of 80 ppb or higher may cause
lung function decrements and other respiratory effects.\95\
---------------------------------------------------------------------------

    \95\ Conversely, another group of commenters who supported
revising the standard to a level of 60 ppb noted that the results of
these models are consistent with the results of controlled human
exposure studies finding adverse health effects at 60 ppb. These
comments are discussed below (II.C.4.b), within the context of the
Administrator's decision on a revised standard level.
---------------------------------------------------------------------------

    As described above in section II.A.1.b, the McDonnell et al. (2012)
and Schelegle et al. (2012) models represent a significant
technological advance in the exposure-response modeling approach since
the last review, and these models indicate that a dose-threshold model
fits the data better than a non-threshold model. However, the EPA
disagrees that using the predicted group mean response from the
McDonnell model provides support for retaining the current standard. As
discussed above, the group mean responses do not convey information
about interindividual variability, or the proportion of the population
estimated to experience the larger lung function decrements (e.g., 10
or 15% FEV1 decrements) that could be adverse. In fact, it
masks this variability. These variable effects in individuals have been
found to be reproducible. In other words, a person who has a large lung
function response after exposure to O3 will likely have
about the same response if exposed again in a similar manner (raising
health concerns, as noted above). Group mean responses are not
representative of this segment of the population that has much larger
than average responses to O3.
Inflammation
    Some commenters asserted that the pulmonary inflammation observed
following exposure to 60 ppb in the controlled human exposure study by
Kim et al. (2011) was small and unlikely to result in airway damage. It
was also suggested that this inflammation is a normal physiological
response in all living organisms to stimuli to which people are
normally exposed.
    The EPA recognized in the proposal (79 FR 75252) and the ISA (U.S.
EPA, 2013, p. 6-76) that inflammation induced by a single exposure (or
several exposures over the course of a summer) can resolve entirely.
Thus, the inflammatory response observed following the single exposure
to 60 ppb in the study by Kim et al. (2011) is not necessarily a
concern. However, the EPA notes that it is also important to consider
the potential for continued acute inflammatory responses to evolve into
a chronic inflammatory state and to affect the structure and function
of the lung.\96\ The Administrator considers this possibility through
her consideration of estimated exposures of concern for the 60 ppb
benchmark (II.B.3, II.C.4). As discussed in detail below (II.C.4.b),
while she judges that there is uncertainty in the adversity of the
effects shown to occur following exposures to 60 ppb O3,
including the inflammation reported by Kim et al.

(2011), she gives some consideration to estimates of two or more
exposures of concern for the 60 ppb benchmark (i.e., as a health-
protective surrogate for repeated exposures of concern at or above 60
ppb), particularly when considering the extent to which the current and
revised standards incorporate a margin of safety.
---------------------------------------------------------------------------

    \96\ Inflammation induced by exposure of humans to O3
can have several potential outcomes, ranging from resolving entirely
following a single exposure to becoming a chronic inflammatory state
(U.S. EPA, 2013, section 6.2.3). Lung injury and the resulting
inflammation provide a mechanism by which O3 may cause
other more serious morbidity effects (e.g., asthma exacerbations)
(U.S. EPA, 2013, section 6.2.3). See generally section II.A.1.a
above.
---------------------------------------------------------------------------

ii. Evidence Fom epidemiologic studies
    This section discusses key comments on the EPA's assessment of the
epidemiologic evidence and provides the Agency's responses to those
comments. The focus in this section is on overarching comments related
to the EPA's approach to assessing and interpreting the epidemiologic
evidence as a whole. Detailed comments on specific studies, or specific
methodological or technical issues, are addressed in the Response to
Comments document. As discussed above, many of the issues and concerns
raised by commenters on the interpretation of the epidemiologic
evidence are essentially restatements of issues raised during the
development of the ISA, HREA, and/or PA, and in many instances were
considered by CASAC in the development of its advice on the current
standard. The EPA's responses to these comments rely heavily on the
process established in the ISA for assessing the evidence, and on CASAC
advice received as part of this review of the O3 NAAQS.
    As with evidence from controlled human exposure studies, commenters
expressed sharply divergent views on the evidence from epidemiologic
studies, and on the EPA's interpretation of that evidence. One group of
commenters, representing medical, public health and environmental
organizations, and some states, generally supported the EPA's
interpretation of the epidemiologic evidence with regard to the
consistency of associations, the coherence with other lines of
evidence, and the support provided by epidemiologic studies for the
causality determinations in the ISA. These commenters asserted that the
epidemiologic studies evaluated in the ISA provide valuable information
supporting the need to revise the level of the current primary
O3 standard in order to increase public health protection.
In reaching this conclusion, commenters often cited studies (including
a number from the past review) which they interpreted as showing health
effect associations in locations with O3 air quality
concentrations below the level of the current standard. A second group
of commenters, mostly representing industry associations, businesses,
and states opposed to revising the primary O3 standard,
expressed the general view that while many new epidemiologic studies
have been published since the last review of the O3 NAAQS,
inconsistencies and uncertainties inherent in these studies as a whole,
and in the EPA's assessment of study results, should preclude any
reliance on them as justification for a more stringent primary
O3 standard. To support their views, these commenters often
focused on specific technical or methodological issues that contribute
to uncertainty in epidemiologic studies, including the potential for
exposure error, confounding by copollutants and by other factors (e.g.,
weather, season, disease, day of week, etc.), and heterogeneity in
results across locations.
    The EPA agrees with certain aspects of each of these views.
Specifically, while the EPA agrees that epidemiologic studies are an
important part of the broader body of evidence that supports the ISA's
causality determinations, and that these studies provide support for
the decision to revise the current primary O3 standard, the
Agency also acknowledges that there are important uncertainties and
limitations associated with these epidemiologic studies that should be
considered when reaching decisions on the current standard. Thus,
although these studies show consistent associations between
O3 exposures and serious health effects, including morbidity
and mortality, and some of these studies reported such associations
with ambient O3 concentrations below the level of the
current standard, there are also uncertainties regarding the ambient
O3 concentrations in critical studies, such that they lend
only limited support to establishing a specific level for a revised
standard. (See generally, Mississippi, 744 F. 3d at 1351 (noting that
in prior review, EPA reasonably relied on epidemiologic information in
determining to revise the standard but appropriately gave the
information limited weight in determining a level of a revised
standard); see also ATA III, 283 F. 3d at 370 (EPA justified in
revising NAAQS when health effect associations are observed in
epidemiologic studies at levels allowed by the current NAAQS);
Mississippi, 744 F. 3d at 1345 (same)).
    Uncertainties in the evidence were considered by the Administrator
in the proposal, and contributed to her decision to place less weight
on information from epidemiologic studies than on information from
controlled human exposure studies when considering the adequacy of the
current primary O3 standard (see 79 FR 75281-83). Despite
receiving less weight in the proposal, the EPA does not agree with
commenters who asserted that uncertainties in the epidemiologic
evidence provide a basis for concluding that the current primary
standard does not need revision. The Administrator specifically
considered the extent to which available studies support the occurrence
of O3 health effect associations with air quality likely to
be allowed by the current standard, while also considering the
implications of important uncertainties, as assessed in the ISA and
discussed in the PA. This consideration is consistent with CASAC
comments on consideration of these studies in the draft PA (Frey,
2014c, p. 5).
    Based on analyses of study area air quality in the PA, the EPA
notes that most of the U.S. and Canadian epidemiologic studies
evaluated were conducted in locations likely to have violated the
current standard over at least part of the study period. Although these
studies support the ISA's causality determinations, they provide
limited insight into the adequacy of the public health protection
provided by the current primary O3 standard. However, as
discussed in the proposal, air quality analyses in the locations of
three U.S. single-city studies provide support for the occurrence of
O3-associated hospital admissions or emergency department
visits at ambient O3 concentrations below the level of the
current standard.\97\ Specifically, a U.S. single-city study reported
associations with respiratory emergency department visits in children
and adults in a location that would have met the current O3
standard over the entire study period (Mar and Koenig, 2009). In
addition, for two studies conducted in locations where the current
standard was likely not met (i.e., Silverman and Ito, 2010; Strickland
et al., 2010), PA analyses indicate that reported concentration-
response functions and available air quality data support the
occurrence of O3-health effect associations on subsets of
days with virtually all monitored ambient O3 concentrations
below the level of the current standard (U.S. EPA, 2014c,

section <IP_ADDRESS>, pp. 3-66 to 67).\98\ Thus, the EPA notes that a small
number of O3 epidemiologic studies provide support for the
conclusion that the current primary standard is not requisite, and that
it should be revised to increase public health protection.
---------------------------------------------------------------------------

    \97\ As discussed in section II.E.4.d of the proposal, is the
Administrator noted the greater uncertainty in using analyses of
short-term O3 air quality in locations of the multicity
studies in this review to inform decisions on the primary
O3 standard. This is because the health information in
these studies cannot be disaggregated by individual city. Thus, the
multicity effect estimates reported in these studies do not provide
clear indication of the extent to which health effects are
associated with the ambient O3 concentrations in the
study locations that met the current O3 standard, versus
the ambient O3 concentrations in the study locations that
violated the standard.
    \98\ Air quality analyses in locations of the studies by
Silverman and Ito (2010) and Strickland et al. (2010) were used in
the PA to inform staff conclusions on the adequacy of the current
primary O3 standard. However, the appropriate
interpretation of these analyses became less clear for standard
levels below 75 ppb, as the number of days increased with monitored
concentrations exceeding the level being evaluated (U.S. EPA, 2014c,
Appendix 3B, Tables 3B-6 and 3B-7). Therefore, these analyses were
not used in the PA to inform conclusions on potential alternative
standard levels lower than 75 ppb (U.S. EPA, 2014c, Chapters 3 and
4).
---------------------------------------------------------------------------

    As part of a larger set of comments criticizing the EPA's
interpretation of the evidence from time series epidemiologic studies,
some commenters objected to the EPA's reliance on the studies by
Strickland et al. (2010), Silverman and Ito (2010), and Mar and Koenig
(2009). These commenters highlighted what they considered to be key
uncertainties in interpreting these studies, including uncertainties
due to the potential for confounding by co-pollutants, aeroallergens,
or the presence of upper respiratory infections; and uncertainties in
the interpretation of zero-day lag models (i.e., specifically for Mar
and Koenig, 2009).
    While the EPA agrees that there are uncertainties associated with
interpreting the O3 epidemiologic evidence, as discussed
above and elsewhere in this preamble, we disagree with commenters'
assertion that these uncertainties should preclude the use of the
O3 epidemiologic evidence in general, or the studies by
Silverman and Ito, Strickland, or Mar and Koenig in particular, as part
of the basis for the Administrator's decision to revise the current
primary standard. As a general point, when considering the potential
importance of uncertainties in epidemiologic studies, we rely on the
broader body of evidence, not restricted to these three studies, and
the ISA conclusions based on this evidence. The evidence, the ISA's
interpretation of specific studies, and the use of information from
these studies in the HREA and PA, was considered by CASAC in its review
of drafts of the ISA, HREA, and PA. Based on the assessment of the
evidence in the ISA, and CASAC's endorsement of the ISA conclusions, as
well as CASAC's endorsement of the approaches to using and considering
information from epidemiologic studies in the HREA and PA (Frey, 2014c,
p. 5), we do not agree with these commenters' conclusions regarding the
usefulness of the epidemiologic studies by Strickland et al. (2010),
Silverman and Ito (2010), and Mar and Koenig (2009).
    More specifically, with regard to confounding by co-pollutants, we
note the ISA conclusion that, in studies of O3-associated
hospital admissions and emergency department visits ``O3
effect estimates remained relatively robust upon the inclusion of PM .
. . and gaseous pollutants in two-pollutant models'' (U.S. EPA, 2013,
pp. 6-152 and 6-153). This conclusion was supported by several studies
that evaluated co-pollutant models including, but not limited to, two
of the studies specifically highlighted by commenters (i.e., Silverman
and Ito, 2010; Strickland et al., 2010) (U.S. EPA, 2013, section
<IP_ADDRESS>; Figure 6-20 and Table 6-29).
    Other potential uncertainties highlighted by commenters have been
evaluated less frequently (e.g., confounding by allergen exposure,
respiratory infections). However, we note that Strickland et al. (2010)
did consider the potential for pollen (a common airborne allergen) to
confound the association between ambient O3 and emergency
department visits. While quantitative results were not presented, the
authors reported that ``estimates for associations between ambient air
pollutant concentrations and pediatric asthma emergency department
visits were similar regardless of whether pollen concentrations were
included in the model as covariates'' (Strickland et al., 2010, p.
309). This suggests a limited impact of aeroallergens on O3
associations with asthma-related emergency department visits and
hospital admissions.
    With respect to the comment about epidemiologic studies not
controlling for respiratory infections in the model, the EPA disagrees
with the commenter's assertion. We recognize that asthma is a multi-
etiologic disease and that air pollutants, including O3,
represent only one potential avenue to trigger an asthma exacerbation.
Strickland et al. attempted to further clarify the relationship between
short-term O3 exposures and asthma emergency department
visits by controlling for the possibility that respiratory infections
may lead to an asthma exacerbation. By including the daily count of
upper respiratory visits as a covariate in the model, Strickland et al.
were able to account for the possibility that respiratory infections
contribute to the daily counts of asthma emergency department visits,
and to identify the O3 effect on asthma emergency department
visits. In models that controlled for upper respiratory infection
visits, associations between O3 and emergency department
visits remained statistically significant (Strickland et al., Table 4
in published study), demonstrating a relatively limited influence of
respiratory infections on the association observed between short-term
O3 exposures and asthma emergency department visits,
contrary to the commenter's claim.
    In addition, with regard to the criticism of the results reported
by Mar and Koenig, the EPA disagrees with commenters who questioned the
appropriateness of a zero-day lag. These commenters specifically noted
uncertainty in the relative timing of the O3 exposure and
the emergency department visit when they occurred on the same day.
However, based on the broader body of evidence the ISA concludes that
the strongest support is for a relatively immediate respiratory
response following O3 exposures. Specifically, the ISA
states that ``[t]he collective evidence indicates a rather immediate
response within the first few days of O3 exposure (i.e., for
lags days averaged at 0-1, 0-2, and 0-3 days) for hospital admissions
and [emergency department] visits for all respiratory outcomes, asthma,
and chronic obstructive pulmonary disease in all-year and seasonal
analyses'' (U.S. EPA, 2013, p. 2-32). Thus, the use of a zero-day lag
is consistent with the broader body of evidence supporting the
occurrence of O3-associated health effects. In addition,
while Mar and Koenig reported the strongest associations for zero-day
lags, they also reported positive associations for lags ranging from
zero to five days (Mar and Koenig, 2009, Table 5 in the published
study). In considering this study, the ISA stated that Mar and Koenig
(2009) ``found consistent positive associations across individual lag
days'' and that ``[f]or children, consistent positive associations were
observed across all lags . . . with the strongest associations observed
at lag 0 (33.1% [95% CI: 3.0, 68.5]) and lag 3 (36.8% [95% CI: 6.1,
77.2])'' (U.S. EPA, 2013, p. 6-150). Given support for a relatively
immediate response to O3 and given the generally consistent
results in analyses using various lags, we disagree with commenters who
asserted that the use of a zero-day lag represents an important
uncertainty in the interpretation of the study by Mar and Koenig
(2009).
    Given all of the above, we do not agree with commenters who
asserted that uncertainties in the epidemiologic evidence in general,
or in specific key studies, should preclude the

Administrator from relying on those studies to inform her decisions on
the primary O3 standard.
    Some commenters also objected to the characterization in the ISA
and the proposal that the results of epidemiologic studies are
consistent. These commenters contended that the purported consistency
of results across epidemiologic studies is the result of inappropriate
selectivity on the part of the EPA in focusing on specific studies and
specific results within those studies. In particular, commenters
contend that EPA favors studies that show positive associations and
selectively ignores certain studies that report null results. They also
cite a study published after the completion of the ISA (Goodman et al.,
2013) suggesting that, in papers where the results of more than one
statistical model are reported, the EPA tends to report the results
with the strongest associations.
    The EPA disagrees that it has inappropriately focused on specific
positive studies or specific positive results within individual
studies. The ISA appropriately builds upon the assessment of the
scientific evidence presented in previous AQCDs and ISAs.\99\ When
evaluating new literature, ``[s]election of studies for inclusion in
the ISA is based on the general scientific quality of the study, and
consideration of the extent to which the study is informative and
policy-relevant'' (U.S. EPA, 2013, p. liii). In addition, ``the intent
of the ISA is to provide a concise review, synthesis, and evaluation of
the most policy-relevant science to serve as a scientific foundation
for the review of the NAAQS, not extensive summaries of all health,
ecological and welfare effects studies for a pollutant'' (U.S. EPA,
2013, p. lv). Therefore, not all studies published since the previous
review would be appropriate for inclusion in the ISA.\100\ With regard
to the specific studies that are included in the ISA, and the analyses
focused upon within given studies, the EPA notes that the ISA undergoes
extensive peer review in a public setting by the CASAC. This process
provides ample opportunity for CASAC and the public to comment on
studies not included in the ISA, and on the specific analyses focused
upon within individual studies. In endorsing the final O3
ISA as adequate for rule-making purposes, CASAC agreed with the
selection and presentation of analyses on which to base the ISA's key
conclusions.
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    \99\ Cf. Coalition for Responsible Regulation v. EPA, 684 F. 3d
102, 119 (D.C. Cir. 2012) (aff'd in part and rev'd in part on other
grounds sub. nom UARG v. EPA, S Ct. (2014)) (``EPA simply did here
what it and other decision-makers often must do to make a science-
based judgment: it sought out and reviewed existing scientific
evidence to determine whether a particular finding was warranted. It
makes no difference that much of the scientific evidence in large
part consisted of `syntheses' of individual studies and research.
Even individual studies and research papers often synthesize past
work in an area and then build upon it. That is how science
works'').
    \100\ See also section II.C.4.b below responding to comments
from environmental interests that EPA inappropriately omitted many
studies which (in their view) support establishing a revised
standard at a level of 60 ppb or lower. Although, as explained
there, the EPA disagrees with these comments, the comments
illustrate that the EPA was even-handed in its consideration of the
epidemiologic evidence, and most certainly did not select merely
studies favorable to the point of view of revising the current
standard.
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iii. Evidence Pertaining to At-Risk Populations and Lifestages
    A number of groups submitted comments on the EPA's identification
of at-risk populations and lifestages. Some industry commenters who
opposed revising the current standard disagreed with the EPA's
identification of people with asthma or other respiratory diseases as
an at-risk population for O3-attributable effects, citing
controlled human exposure studies that did not report larger
O3-induced FEV1 decrements in people with asthma
than in people without asthma. In contrast, comments from medical,
environmental, and public health groups generally agreed with the at-
risk populations identified by EPA, and also identified other
populations that they stated should be considered at risk, including
people of lower socio-economic status, people with diabetes or who are
obese, pregnant women (due to reproductive and developmental effects,
and African American, Asian, Hispanic/Latino or tribal communities. As
support for the additional populations, these commenters cited various
studies, including some that were not included in the ISA (which we
have provisionally considered, as described in section I.C above).
    With regard to the former group of comments stating that the
evidence does not support the identification of asthmatics as an at-
risk population, we disagree. As summarized in the proposal, the EPA's
identification of populations at risk of O3 effects is based
on a systematic approach that assesses the current scientific evidence
across the relevant scientific disciplines (i.e., exposure sciences,
dosimetry, controlled human exposure, toxicology, and epidemiology),
with a focus on studies that conducted stratified analyses allowing for
an evaluation of different populations exposed to similar O3
concentrations within the same study design (U.S. EPA, 2013, pp. 8-1 to
8-3). Based on this established process and framework, the ISA
identifies individuals with asthma among the populations and lifestages
for which there is ``adequate'' evidence to support the conclusion of
increased risk of O3-related health effects. Other
populations for which the evidence is adequate are individuals with
certain genotypes, younger and older age groups, individuals with
reduced intake of certain nutrients, and outdoor workers. These
conclusions are based on consistency in findings across studies and
evidence of coherence in results from different scientific disciplines.
    For example, with regard to people with asthma, the ISA notes a
number of epidemiologic and controlled human exposure studies reporting
larger and/or more serious effects in people with asthma than in people
without asthma or other respiratory diseases. These include
epidemiologic studies of lung function, respiratory symptoms, and
medication use, as well as controlled human exposure studies showing
larger inflammatory responses and markers indicating altered immune
functioning in people with asthma, and also includes evidence from
animal models of asthma that informs the EPA's interpretation of the
other studies. We disagree with the industry commenters' focus solely
on the results of certain studies without an integrated consideration
of the broader body of evidence, and wider range of respiratory
endpoints. It is such an integrated approach that supports EPA's
conclusion that ``there is adequate evidence for asthmatics to be an
at-risk population'' (U.S. EPA, 2013, section 8.2.2).
    We also disagree with commenters' misleading reference to various
studies cited to support the claim that asthmatics are not at increased
risk of O3-related health effects. One of the controlled
human studies cited in those comments (Mudway et al. 2001) involved
asthmatic adults who were older than the healthy controls, and it is
well-recognized that responses to O3 decrease with age (U.S.
EPA, 2014c, p. 3-80). Another study (Alexis et al. 2000) used subjects
with mild asthma who are unlikely to be as responsive as people with
more severe disease (Horstman et al., 1995) (EPA 2014c, p. 3-80).
Controlled human exposure studies and epidemiologic studies of adults
and children amply confirm that ``there is adequate evidence for
asthmatics to be an at-risk population'' (U.S. EPA, 2014c, p. 3-81).

    We also do not agree with the latter group of commenters that there
is sufficient evidence to support the identification of additional
populations as at risk of O3-attributable health effects.
Specifically with regard to pregnant women, the ISA concluded that the
``evidence is suggestive of a causal relationship between exposures to
O3 and reproductive and developmental effects'' including
birth outcomes, noting that ``the collective evidence for many of the
birth outcomes examined is generally inconsistent'' (U.S. EPA, 2013,
pp. 7-74 and 7-75). At the time of the completion of the ISA, no
studies had been identified that examined the relationship between
exposure to O3 and the health of pregnant women (e.g.,
studies on pre-eclampsia, gestational hypertension). Due to the
generally inconsistent epidemiologic evidence for effects on birth
outcomes, the lack of studies on the health of pregnant women, and the
lack of studies from other disciplines to provide biological
plausibility for the effects examined in epidemiologic studies,
pregnant women were not considered an at-risk population. Based on the
EPA's provisional consideration of studies published since the
completion of the ISA (I.C, above), recent studies that examine
exposure to O3 and pre-eclampsia and other health effects
experienced by pregnant women are not sufficient to materially change
the ISA's conclusions on at-risk populations (I.C, above). In addition,
as summarized in the proposal, the ISA concluded that the evidence for
other populations was either suggestive of increased risk, with further
investigation needed (e.g., other genetic variants, obesity, sex, and
socioeconomic status), or was inadequate to determine if they were of
increased risk of O3-related health effects (influenza/
infection, COPD, CVD, diabetes, hyperthyroidism, smoking, race/
ethnicity, and air conditioning use) (U.S. EPA, 2013, section <IP_ADDRESS>).
The CASAC has concurred with the ISA conclusions (Frey, 2014c).
c. Comments on Exposure and Risk Assessments
    This section discusses major comments on the EPA's quantitative
assessments of O3 exposures and health risks, presented in
the HREA and considered in the PA, and the EPA's responses to those
comments. The focus in this section is on overarching comments related
to the EPA's approach to assessing exposures and risks, and to
interpreting the exposure/risk results within the context of the
adequacy of the current primary O3 standard. More detailed
discussion of comments and Agency responses is provided in the Response
to Comments document. Section II.B.2.c.i discusses comments on
estimates of O3 exposures of concern, section II.B.2.c.ii
discusses comments on estimates of the risk of O3-induced
lung function decrements, and section II.B.2.b.iii discusses comments
on estimates of the risk of O3-associated mortality and
morbidity.
i. O3 Exposures of Concern
    The EPA received a number of comments expressing divergent views on
the estimation of, and interpretation of, O3 exposures of
concern. In general, comments from industry, business, and some state
groups opposed to revising the current primary O3 standard
asserted that the approaches and assumptions that went into the HREA
assessment result in overestimates of O3 exposures. These
commenters highlighted several aspects of the assessment, asserting
that the HREA overestimates the proportion of the population expected
to achieve ventilation rates high enough to experience an exposure of
concern; that the use of out-of-date information on activity patterns
results in overestimates of the amount of time people spend being
active outdoors; and that exposure estimates do not account for the
fact that people spend more time indoors on days with bad air quality
(i.e., they engage in averting behavior). In contrast, comments from
medical, public health, and environmental groups that supported
revision of the current standard asserted that the HREA assessment of
exposures of concern, and the EPA's interpretation of exposure
estimates, understates the potential for O3 exposures that
could cause adverse health effects. These commenters claimed that the
EPA's focus on 8-hour exposures understates the O3 impacts
on public health since effects in controlled human exposure studies
were shown following 6.6-hour exposures; that the HREA exposure
estimates do not capture the most highly exposed populations, such as
highly active children and outdoor workers; and that the EPA's
interpretation of estimated exposures of concern impermissibly relies
on the assumption that people stay indoors to avoid dangerous air
pollution (i.e., that they engage in averting behavior).
    In considering these comments, the EPA first notes that as
discussed in the HREA, PA, and the proposal, there are aspects of the
exposure assessment that, considered by themselves, can result in
either overestimates or underestimates of the occurrence of
O3 exposures of concern. Commenters tended to highlight the
aspects of the assessment that supported their positions, including
aspects that were discussed in the HREA and/or the PA and that were
considered by CASAC. In contrast, commenters tended to ignore the
aspects of the assessment that did not support their positions. The EPA
has carefully described and assessed the significance of the various
uncertainties in the exposure analysis (U.S. EPA, 2014a, Table 5-10),
noting that, in most instances, the uncertainties could result in
either overestimates or underestimates of exposures and that the
magnitudes of the impacts on exposure results were either ``low,''
``low to moderate,'' or ``moderate'' (U.S. EPA, 2014a, Table 5-10).
    Consistent with the characterization of uncertainties in the HREA,
PA, and the proposal, the EPA agrees with some, though not all, aspects
of these commenters' views. For example, the EPA agrees with the
comment by groups opposed to revision that the equivalent ventilation
rate (EVR) used to characterize individuals as at moderate or greater
exertion in the HREA likely leads to overestimates of the number of
individuals experiencing exposures of concern (U.S. EPA, 2014a, Table
5-10, p. 5-79). In addition, we note that other physiological processes
that are incorporated into exposure estimates are also identified in
the HREA as likely leading to overestimates of O3 exposures,
based on comparisons with the available scientific literature (U.S.
EPA, 2014a, Table 5-10, p. 5-79). These aspects of the exposure
assessment are estimated to have either a ``moderate'' (i.e., EVR) or a
``low to moderate'' (i.e., physiological processes) impact on exposure
estimates (U.S. EPA, 2014a, Table 5-10, p. 5-79). Focusing on these
aspects of the assessment, by themselves, could lead to the conclusion
that the HREA overstates the occurrence of O3 exposures of
concern.
    However, the EPA notes that there are also aspects of the HREA
exposure assessment that, taken by themselves, could lead to the
conclusion that the HREA understates the occurrence of O3
exposures of concern. For example, as noted above, some medical, public
health, and environmental groups asserted that the exposure assessment
could underestimate O3 exposures for highly active
populations, including outdoor workers and children who spend a large
portion of time outdoors during summer. In support of these assertions,
commenters highlighted sensitivity analyses conducted in the HREA.
However, as noted in the HREA (U.S. EPA, 2014a, Table 5-10), this

aspect of the assessment is likely to have a ``low to moderate'' impact
on exposure estimates (i.e., a smaller impact than uncertainty
associated with the EVR, and similar in magnitude to uncertainties
related to physiological processes, as noted above). Therefore, when
considered in the context of all of the uncertainties in exposure
estimates, it is unlikely that the HREA's approach to using data on
activity patterns leads to overall underestimates of O3
exposures. The implications of this uncertainty are discussed in more
detail below (II.C.4.b), within the context of the Administrator's
decision on a revised standard level.
    In addition, medical, public health, and environmental groups also
pointed out that the controlled human exposures studies that provided
the basis for health effect benchmarks were conducted in healthy
adults, rather than at-risk populations, and these studies evaluated
6.6 hour exposures, rather than the 8-hour exposures evaluated in the
HREA exposure analyses. They concluded that adverse effects would occur
at lower exposure concentrations in at-risk populations, such as people
with asthma, and if people were exposed for 8 hours, rather than 6.6
hours. In its review of the PA, CASAC clearly recognized these
uncertainties, which provided part of the basis for CASAC's advice to
consider exposures of concern for the 60 ppb benchmark. For example,
when considering the results of the study by Schelegle et al. (2009)
for 6.6-hour exposures to an average O3 concentration of 72
ppb, CASAC judged that if subjects had been exposed for eight hours,
the adverse combination of lung function decrements and respiratory
symptoms ``could have occurred'' at lower O3 exposure
concentrations (Frey, 2014c, p. 5). With regard to at-risk populations,
CASAC concluded that ``based on results for clinical studies of healthy
adults, and scientific considerations of differences in responsiveness
of asthmatic children compared to healthy adults, there is scientific
support that 60 ppb is an appropriate exposure of concern for asthmatic
children'' (Frey, 2014c, p. 8). As discussed below (II.B.3, II.C.4.b,
II.C.4.c), based in large part on CASAC advice, the Administrator does
consider exposure results for the 60 ppb benchmark.
    Thus, rather than viewing the potential implications of various
aspects of the HREA exposure assessment in isolation, as was done by
many commenters, the EPA considers them together, along with other
issues and uncertainties related to the interpretation of exposure
estimates. As discussed above, CASAC recognized the key uncertainties
in exposure estimates, as well as in the interpretation of those
estimates in the HREA and PA (Frey, 2014a, c). In its review of the 2nd
draft REA, CASAC concluded that ``[t]he discussion of uncertainty and
variability is comprehensive, appropriately listing the major sources
of uncertainty and their potential impacts on the APEX exposure
estimates'' (Frey, 2014a, p. 6). Even considering these and other
uncertainties, CASAC emphasized estimates of O3 exposures of
concern as part of the basis for their recommendations on the primary
O3 NAAQS. In weighing these uncertainties, which can bias
exposure results in different directions but tend to have impacts that
are similar in magnitude (U.S. EPA, 2014a, Table 5-10), and in light of
CASAC's advice based on its review of the HREA and the PA, the EPA
continues to conclude that the approach to considering estimated
exposures of concern in the HREA, PA, and the proposal reflects an
appropriate balance, and provides an appropriate basis for considering
the public health protectiveness of the primary O3 standard.
    The EPA disagrees with other aspects of commenters' views on HREA
estimates of exposures of concern. For example, commenters on both
sides of the issue objected to the EPA's handling of averting behavior
in exposure estimates. Some commenters who supported retaining the
current standard claimed that the HREA overstates exposures of concern
because available time-location-activity data do not account for
averting behavior. These commenters noted sensitivity analyses in the
HREA that estimated fewer exposures of concern when averting behavior
was considered. In contrast, commenters supporting revision of the
standard criticized the EPA's estimates of exposures of concern,
claiming that the EPA ``emphasizes the role of averting behavior,
noting that it may result in an overestimation of exposures of concern,
and cites this behavior (essentially staying indoors or not exercising)
in order to reach what it deems an acceptable level of risk'' (e.g.,
ALA et al., p. 120).
    The EPA disagrees with both of these comments. In brief, the NAAQS
must ``be established at a level necessary to protect the health of
persons,'' not the health of persons refraining from normal activity or
resorting to medical interventions to ward off adverse effects of poor
air quality (S. Rep. No. 11-1196, 91st Cong. 2d Sess. at 10). On the
other hand, ignoring normal activity patterns for a pollutant like
O3, where adverse responses are critically dependent on
ventilation rates, will result in a standard which provides more
protection than is requisite. This issue is discussed in more detail
below (II.C.4.b), within the context of the Administrator's decision on
a revised standard level.
    These commenters also misconstrue the EPA's limited sensitivity
analyses on impacts of averting behavior in the HREA. The purpose of
the HREA sensitivity analyses was to provide perspective on the
potential role of averting behavior in modifying O3
exposures. These sensitivity analyses were limited to a single urban
study area, a 2-day period, and a single air quality adjustment
scenario (U.S. EPA, 2014a, section <IP_ADDRESS>). In addition, the approach
used in the HREA to simulate averting behavior was itself uncertain,
given the lack of actual activity pattern data that explicitly
incorporated this type of behavioral response. In light of these
important limitations, sensitivity analyses focused on averting