Additionally, the Administrator recognizes that the available
epidemiologic studies enable the examination of the entire population
and include, and even focus on, those that may be at comparatively
higher risk of experiencing a PM2.5-related health effects.
The Administrator notes that the 2019 ISA found that factors that may
contribute to increased risk of PM2.5-related health effects
include lifestage (children and older adults), pre-existing diseases
(cardiovascular disease and respiratory disease), and SES, and that the
ISA Supplement noted new evidence that further supported racial and
ethnic differences in PM2.5 exposures and PM2.5-
related health risks. The Administrator also observes that at-risk
populations make up a substantial portion of the U.S. population
(section II.B.2 above), including children (22%) and older adults
(16%), as well as non-Hispanic Black (12%) and Hispanic populations
(18%) and that the prevalence of pre-existing diseases varies by
lifestage and

race/ethnicity. The Administrator notes that the cohorts examined in
the epidemiologic studies available in this reconsideration include
diverse populations that are broadly representative of the U.S.
population as a whole, and include those populations identified as at-
risk (i.e., children and older adults), as well as individuals in the
general population with pre-existing disease, such as cardiovascular
disease and respiratory disease.
    Recent epidemiologic studies also strengthen support for health
effect associations at lower ambient PM2.5 concentrations
than previous reviews and studies that examine the shapes of C-R
functions over the full distribution of ambient PM2.5
concentrations have not identified a threshold concentration, below
which associations no longer exist (U.S. EPA, 2019a, section 1.5.3;
U.S. EPA, 2022a, sections <IP_ADDRESS> and <IP_ADDRESS>). Though these analyses
are complicated by the relatively sparse data available at the lower
end of the air quality distribution (U.S. EPA, 2019a, section 1.5.3),
the evidence remains consistent in supporting a no-threshold
relationship, and in supporting a linear relationship for
PM2.5 concentrations > 8 [mu]g/m\3\, though uncertainties
remain about the shape of the C-R curve at PM2.5
concentrations < 8 [mu]g/m\3\.
    With respect to uncertainties in epidemiologic studies, a broad
range of approaches have been adopted across studies to examine
confounding and the results of those examinations support the
robustness of reported associations. Additionally, there is a
considerable amount of new epidemiologic evidence in this
reconsideration, including a large number of new epidemiologic studies
that use varying study designs that reduce uncertainties, including
studies that employ alternative methods for confounder control and
support associations between exposure and adverse health effects at
lower PM2.5 concentrations. Consistent findings from the
broad body of epidemiologic studies are supported by studies employing
alternative methods for confounder control, which used a variety of
statistical methods to control for confounding bias and consistently
report positive associations. The results of these studies support the
positive and significant effects seen in cohort studies associated with
short- and long-term exposure to PM2.5 and mortality.
Moreover, epidemiologic studies continue to evaluate the uncertainty
related to exposure measurement error, and while none of these
approaches eliminates the potential for exposure error in epidemiologic
studies, the consistent reporting of PM2.5 health effect
associations across exposure estimation approaches, even in the face of
exposure error, together with the larger effect estimates reported in
some studies that have attempted to reduce exposure error, provides
further support for the robustness of associations between
PM2.5 exposures and mortality and morbidity. Therefore,
given the strength of the available epidemiologic evidence, including
the ability of these studies to provide information about impacts on
the most at-risk populations, the Administrator concludes that the
strongest available evidence for evaluating alternative levels of the
annual standard continues to be the epidemiologic studies.
    The evidence base available in this reconsideration also consists
of experimental studies that include controlled human exposure studies
and animal toxicological studies. These studies demonstrate health
outcomes following long-term and short-term exposure to
PM2.5 at exposures that are well-above those typically found
in ambient air. This body of evidence provides support for the
biological mechanisms and the plausibility of the serious health
effects associated with ambient PM2.5 exposures in
epidemiologic studies. Thus, the Administrator recognizes that while
experimental studies may not be as useful in a decision-making
framework alone, results from these studies lend further support to the
use of the epidemiologic evidence base in informing the level of the
annual standard.
    In considering the level of the annual standard, the Administrator
recognizes that the annual standard, with its form based on the
arithmetic mean concentration, is most appropriately meant to limit the
``typical'' daily and annual exposures that are most strongly
associated with the health effects observed in epidemiologic studies.
However, the Administrator also recognizes that while epidemiologic
studies examine associations between distributions of PM2.5
air quality and health outcomes, they do not identify particular
PM2.5 exposures that cause effects. Thus, any approach that
uses epidemiologic information in reaching decisions on what standards
are appropriate necessarily requires judgments of the Administrator
about how to consider the information available from the epidemiologic
studies as a basis for appropriate standards. This includes
consideration of how to weigh the uncertainties in the reported
associations between daily or annual average PM2.5 exposures
and mortality or morbidity in the epidemiologic studies. Such an
approach is consistent with setting standards that are neither more nor
less stringent than necessary, recognizing that a zero-risk standard is
not required by the CAA.
    Thus, in recognizing the need to weigh these uncertainties in
reaching decisions on alternative standard levels to propose, the
Administrator judges that it is most appropriate to examine where the
evidence of associations observed in the epidemiologic studies is
strongest and, conversely, where he has appreciably less confidence in
the associations observed in the epidemiologic studies. Based on
information evaluated in the 2019 ISA and ISA Supplement, the
Administrator recognizes that health effects may occur over the full
range of concentrations observed in the long- and short-term
epidemiologic studies and that no discernible threshold for any effects
can be identified based on the currently available evidence (U.S. EPA,
2019a, section 1.5.3, U.S. EPA, 2022a, section <IP_ADDRESS> and <IP_ADDRESS>). He
also recognizes, in taking note of CASAC advice and the distributional
statistics analysis discussed in section II.B.3.b above and in the PA,
that there is significantly greater confidence in observed associations
over certain parts of the air quality distributions in the studies, and
conversely, that there is significantly diminished confidence in
ascribing effects to concentrations toward the lower part of the
distributions.
    The Administrator notes that in previous reviews, evidence-based
approaches noted that the evidence of an association in any
epidemiologic study is ``strongest at and around the long-term average
where the data in the study are most concentrated'' (78 FR 3140,
January 15, 2013). Given this, these approaches focused on identifying
standard levels near or somewhat below long-term mean concentrations
reported in key epidemiologic studies. These approaches were supported
by previous CASAC advice. The current CASAC also supported assessing
the mean (or median) concentrations, but also suggested additional
approaches that could be explored.\100\ In utilizing this evidence-
based approach, the Administrator looks to study-reported

means from the key epidemiologic studies (as shown in Figure 1 and
Figure 2) available in this reconsideration. He notes that there have
been new approaches to estimating exposure concentrations since the
2012 review, such that many of the available key epidemiologic studies
include new approaches that apply hybrid modeling techniques to
estimate exposures. In looking at the epidemiologic studies, he
considers these studies in two groups: (1) monitor-based studies
(epidemiologic studies that used ground-based monitors to estimate
exposure, similar to approaches used in past reviews), and (2) hybrid
modeling-based studies (epidemiologic studies that used hybrid modeling
approaches to estimate exposures). As such, he recognizes that reported
mean PM2.5 concentrations in monitor-based studies are
averaged across monitors in each study area with multiple monitors,
referred to as a composite monitor concentration, in contrast to the
highest concentration monitored in the study area, referred to as a
maximum monitor concentration (i.e., the ``design value''
concentration), which is used to determine whether an area meets a
given standard. Further, he recognizes that studies that use hybrid
modeling approaches employ methods to estimate ambient PM2.5
concentrations across large geographical areas, including those without
monitors, and thus, when compared to monitor-based studies, require
additional information to inform the relationship between the estimated
PM2.5 concentrations across an area to the maximum monitor
design values used to assess compliance. For the key U.S. monitor-based
epidemiologic studies, the study reported mean concentrations range
from 9.9-16.5 [mu]g/m\3\ and for the U.S. hybrid modeling based key
epidemiologic studies, the mean concentrations range from 9.3-12.2
[mu]g/m\3\.
---------------------------------------------------------------------------

    \100\ The Administrator notes that some members of the CASAC
advised that ``use of the mean to define where the data provide the
most evidence is conservative. . .'' (Sheppard, 2022a, p. 3 of
consensus letter) and advised that ``for the purpose of informing
the adequacy of the standards'' (Sheppard, 2022a, p. 8 of consensus
responses) that the EPA in future reviews include evaluation of
other metrics, including the distribution of concentrations reported
in epidemiologic studies and in analyses restricting concentrations
to below the current standard level.
---------------------------------------------------------------------------

    In thinking further about the relationship between mean
PM2.5 concentrations in key epidemiologic studies and annual
design values, the Administrator specifically notes that in a given
area, the area design value is determined by the monitor in an area
with the highest PM2.5 concentrations and is used to
determine compliance with the standard. He observes, as detailed above
in the air quality analyses in section I.D.5, that the highest
PM2.5 concentrations spatially distributed in the area would
generally occur at or near the area design value monitor and that
PM2.5 concentrations will be equal to or lower at other
monitors in the area. Furthermore, since monitoring strategies aim to
site monitors in areas with higher concentrations, monitored areas will
generally have higher concentrations than areas without monitors. Thus,
when a study reports a mean that reflects the average of annual average
measured concentrations for an area, the area design value will
generally be higher. Similarly, when a study reports a mean that
reflects the average of annual average concentrations estimated at
various points across an area using a hybrid modeling approach, the
area design value will generally be higher. More specifically, the
Administrator observes that the additional air quality analyses
(described in section I.D.5) suggest that the area annual design value
is greater than the study-reported mean values by 10-20% for monitor-
based studies and 15-18% for hybrid modeling with population weighting
applied.\101\ As such, the Administrator observes that a policy
approach for setting a standard level that requires the design value
monitor to meet study-reported means will generally result in lower
concentrations of PM2.5 across the entire area, such that
even those people living near an area design value monitor (where
PM2.5 concentrations are generally highest) will be exposed
to PM2.5 concentrations below the air quality conditions
reported in the epidemiologic studies where there is the highest
confidence of an association.\102\ In addition, he specifically notes
that an annual standard level that is no more than 10-20% higher than
the study-reported means in the U.S. monitor-based studies (i.e., for
the lowest study reported mean value of 9.9 [mu]g/m\3\, this means an
annual standard level of approximately 10.9-11.9 [mu]g/m\3\) and no
more than 15-18% higher for the U.S. hybrid modeling with population
weighting applied (i.e., for the lowest study reported mean value of
9.3 [mu]g/m\3\, this means an annual standard level of approximately
10.7-11.0 [mu]g/m\3\), would generally maintain air quality exposures
at or below those associated with the study-reported mean
PM2.5 concentrations, exposures for which we have the
strongest support for adverse health effects occurring. Based on this,
the Administrator concludes that a revised standard level of 9.0 to
10.0 [mu]g/m\3\ would generally limit air quality exposures to levels
well below those associated with the study-reported mean
PM2.5 concentrations in the key epidemiologic studies. A
revised standard level of 11.0 [mu]g/m\3\ would maintain air quality
exposures to below those associated with most of these study-reported
means, and a revised standard level of 8.0 [mu]g/m\3\ would maintain
air quality exposures to far below all of these study-reported means.
The Administrator notes that every member of the CASAC found that the
information on study-reported means supported revising the annual
standard level to 10.0 [mu]g/m\3\, with the minority of the CASAC
advising that these data also supported a revised annual standard level
of 10.0-11.0 [mu]g/m\3\ and the majority of the CASAC advising that
these study-reported means, in conjunction with additional bodies of
evidence, supported a revised annual standard level of 8.0-10.0 [mu]g/
m\3\.
---------------------------------------------------------------------------

    \101\ The Administrator also notes that there are a limited
number of studies that report a study mean that does not reflect the
exposure concentrations used in the epidemiologic study to assess
the reported association. These studies do not report population-
weighted study means and are not considered here given the
substantial difference in concentrations used to assess the
association versus those used to calculate the study-reported means.
    \102\ Based on the available air quality information, it would
be expected that an area with a study reported mean of 10 [mu]g/m\3\
would have a gradient of concentrations across the area, with higher
concentrations near the design value monitor and lower
concentrations away from it. If the level of the standard were
revised to 10.0 [mu]g/m\3\, then it would be expected that there
would still be a gradient of concentrations, but the
PM2.5 concentrations across the area would be reduced in
order to meet the revised standard at the design value monitor, and
therefore areas away from the design value monitor would be expected
to have a gradient of PM2.5 concentrations at or below
10.0 [mu]g/m\3\ as well.
---------------------------------------------------------------------------

    The Administrator also considers additional information from
epidemiologic studies, consistent with CASAC advice, to take into
account the broader distribution of PM2.5 concentrations,
including the 25th percentiles of the distributions, and the degree of
confidence in the observed associations over the broader air quality
distribution. In considering this additional information, he
understands that the PA presented information on the distributions of
PM2.5 concentrations, when available, from key epidemiologic
studies to provide a general frame of reference as to the part of the
distribution within which the data become appreciably more sparse and,
thus, where his confidence in the associations observed in
epidemiologic studies would become appreciably less. As discussed in
section II.B.3.b above and presented in Figure 1 and Figure 2 above, he
observes that most studies do not report such data and the conclusions
that can be drawn from such information across the full body of
evidence are quite limited. However, the Administrator takes note of
additional population-level data that are available and in considering
the long-term PM2.5 concentrations associated with the 25th

percentile values of the population-level data for the studies for
which such data are available, he observes that for the three key U.S.
epidemiologic studies that use hybrid modeling approaches that apply
population weighting and report these data, the values reported were
6.7 [mu]g/m\3\, 9.1 [mu]g/m\3\ and 9.1 [mu]g/m\3\. For the U.S.-based
studies that use ground-based monitors, the 25th percentiles ranged
from 11.5 [mu]g/m\3\ to just below 13.0 [mu]g/m\3\.
    The Administrator notes that there are substantial uncertainties
associated with using 25th percentile data for purposes of setting this
standard and these uncertainties are heightened by the relatively few
studies which report such data and the fact that, by definition, this
data is relatively less common even within a study for which it is
reported. At the same time, the Administrator is conscious of his
obligation to set primary standards with an adequate margin of safety
and recognizes that some members of the CASAC advised that these data
indicate that effects are occurring below the reported means of
studies. Balancing these concerns about the need to provide some
protection against uncertain risks with the obligation to not set
standards that are more stringent than necessary, the Administrator
preliminarily concludes that a revised standard should limit exposures
to ambient concentrations near the 25th percentile of reported studies.
Given this consideration, the Administrator recognizes that a standard
level of 8.0-10.0 [mu]g/m\3\ is generally within the range of these
values, while a standard level of 11.0 [mu]g/m\3\ is above the 25th
percentile values reported in the hybrid model-based studies but below
the 25th percentile values in studies that use ground-based monitors.
Based on this, the Administrator recognizes that a standard within the
range of 8.0-11.0 [mu]g/m\3\ would limit exposures to ambient
concentrations near the 25th percentile reported in the available
studies, with the lower end of this range further limiting those
exposures.
    The Administrator also takes into consideration the long-term mean
PM2.5 concentrations reported in Canadian epidemiologic
studies that, in the context of the larger body of available evidence,
provided support for causal or likely to be causal determinations
between PM2.5 exposure and health effects, as summarized in
the 2019 ISA and ISA Supplement. He notes that the study-reported means
from these Canadian studies tend to be somewhat lower than those
reported from the key epidemiologic studies in the U.S. ranging from
6.9-13.3 [mu]g/m\3\ for the monitor-based studies and 5.9-9.8 [mu]g/
m\3\ for the hybrid model-based studies. However, the Administrator is
also mindful that there are important differences between the exposure
environments in the U.S. and Canada and that interpreting the data
(e.g., mean concentrations) from the Canadian studies in the context of
a U.S.-based standard may present challenges in directly and
quantitatively informing decisions regarding potential alternative
levels of the annual standard, as detailed above. He additionally notes
that the majority of the CASAC pointed to the Canadian studies as
supporting their recommendation to revise the annual standard level to
within the range of 8.0-10.0 [mu]g/m\3\. Based on this, the
Administrator is not excluding Canadian studies from his consideration
in this reconsideration, but he is considering them in light of the
limitations and challenges presented.
    The Administrator also notes that the CASAC recommended looking at
the studies that included analyses that restrict annual average
PM2.5 concentrations to concentrations below the level of
the current annual standard in evaluating an appropriate range of
levels for a revised annual standard. In this reconsideration, there
are two key studies available (Di et al., 2017b and Dominici et al.,
2019) that restrict annual average PM2.5 concentrations to
less than 12 [mu]g/m\3\. These restricted analyses report positive and
statistically significant associations with all-cause mortality, and
both report mean PM2.5 concentrations of 9.6 [mu]g/m\3\. The
Administrator does note that uncertainties exist in these analyses
(described in more detail in sections II.B.3.b and II.D.2.a above),
including uncertainty in how the studies exclude concentrations (e.g.,
at what spatial resolution are concentrations being excluded), which
would make it difficult to compare concentrations in restricted
analyses directly to design values. However, he does note that an
annual standard level of 9.0-10.0 [mu]g/m\3\ would be close to these
reported mean values, while a standard level of 11.0 [mu]g/m\3\ would
be above and a standard level of 8.0 [mu]g/m\3\ would be much further
below.
    The Administrator additionally considers recent U.S. accountability
studies, which assess the health effects associated with actions that
improve air quality (e.g., air quality policies or implementation of an
intervention). The Administrator notes that there are three studies
available in this reconsideration (Henneman et al. (2019b), Corrigan et
al. (2018), and Sanders et al. (2020a)) that account for changes in
PM2.5 concentrations due to implementation of policies and
assess whether there was evidence of changes in associations with
mortality or cardiovascular morbidity due to changes in annual
PM2.5 concentrations. The Administrator notes that in each
of these studies, prior to implementation of the policies, mean
PM2.5 concentrations were below the level of the current
annual standard level (12.0 [mu]g/m\3\) and ranged from 10.0 [mu]g/m\3\
to 11.1 [mu]g/m\3\. The Administrator notes that these
studies report positive and significant associations between mortality
and cardiovascular morbidity and reductions in ambient PM2.5
(described above in section II.B.3.b and in Table 3-12 of the PA) and
notes that these studies suggest public health improvements may occur
following the implementation of a policy that reduces annual average
PM2.5 concentrations below the level of the current standard
of 12.0 [mu]g/m\3\. The Administrator notes that a revised annual
standard level of 9.0-10.0 [mu]g/m\3\ would be at or below the lowest
starting concentration of these accountability studies (i.e., 10.0
[mu]g/m\3\).
    In addition to the evidence, the Administrator also considers the
results of the risk assessment. The PA includes a risk assessment that
estimates PM2.5-attributable mortality risk associated with
PM2.5 air quality that has been adjusted to simulate ``just
meeting'' the current standards, as well as potential alternative
standards. These analyses of PM2.5-attributable mortality
use input data that include C-R functions from epidemiologic studies
that have no-threshold and a linear C-R relationship down to zero, as
well an air quality adjustment approach that incorporates proportional
decreases in PM2.5 concentrations to meet lower standard
levels. Such an approach does not incorporate any elements of
uncertainty in associations of health effects at lower concentrations
and simulated air quality improvements will always lead to proportional
decreases in risk (i.e., each additional [mu]g/m\3\ reduction produces
additional benefits with no clear stopping point). Therefore, the
Administrator recognizes that the risk estimates can help to place the
evidence for specific health effects into a broader public health
context, but should be considered along with the inherent uncertainties
and limitations of such analyses when informing judgments about the
potential for additional public health protection associated with
PM2.5 exposure and related health effects.
    The risk assessment estimates that the current primary
PM2.5 standards could allow a substantial number of
PM2.5-associated deaths in the U.S. Additionally, compared
to the current

annual standard, meeting a revised annual standard with a lower level
is estimated to reduce PM2.5-associated health risks in the
30 study areas controlled by the annual standard by about 7-9% for a
level of 11.0 [mu]g/m\3\, 15-19% for a level of 10.0 [mu]g/m\3\, 22-28%
for a level of 9.0 [mu]g/m\3\, and 30-37% for a level of 8.0 [mu]g/
m\3\) (U.S. EPA, 2022a, Table 3-17). The CASAC concurred with the PA's
assessment that meaningful risk reductions will result from lowering
the annual PM2.5 standard (Sheppard, 2022a, p. 16 of
consensus responses).
    The PA also provides information on the distribution of
concentrations associated with the estimated mortality risk at each
alternative standard level assessed (U.S. EPA, 2022a, sections <IP_ADDRESS>
and <IP_ADDRESS>, Figure 3-18 and 3-19). Further evaluating these results
can help clarify the percentage of the exposure reductions that fall
within the range of concentrations in which there is the most
confidence in the associations and thus, confidence that estimated risk
reductions will actually occur. When meeting a standard level of 11.0
[mu]g/m\3\, the risk is estimated to be associated with exposure
concentrations that are generally greater than 10.0 [mu]g/m\3\, while
for a standard level of 10.0 [mu]g/m\3\, the majority of the days
contributing to the risk estimates are estimated to be below 10.0
[mu]g/m\3\. When meeting an annual standard or 9.0 [mu]g/m\3\, the
majority of the exposure concentrations are estimated to be 8.0-9.0
[mu]g/m\3\, while for a standard level of 8.0 [mu]g/m\3\, most of the
days are below 8.0 [mu]g/m\3\. The Administrator notes that the
evidence suggests that majority of the study-reported means are above
10.0 [mu]g/m\3\ (concentrations at which the evidence is the strongest
in supporting an association between exposure to PM2.5 and
adverse health effects observed in the key epidemiologic studies
available in this reconsideration) and that at PM2.5
concentrations less than 8.0 [mu]g/m\3\, the 2019 ISA notes that
uncertainties remain in the shape of the C-R curve. He thus recognizes
that there is increasing uncertainty in quantitative estimates of
PM2.5-associated mortality risk for alternative standard
levels at the lower end of the range of 8.0-11.0 [mu]g/m\3\.
    As discussed more above, the Administrator also recognizes that the
risk assessment was able to include an at-risk analysis that estimated
the potential long-term PM2.5-attributable exposure and
mortality risk in older adults, stratified by racial/ethnic
demographics, when meeting a revised annual standard with a lower
level. While the Administrator recognizes that this analysis is subject
to the multiple uncertainties and limitations (sections II.C.2 and
II.D.2.b), he does note that the analysis suggests that a revised
annual standard level within the range of 8.0 to 11.0 [mu]g/m\3\ is
estimated to reduce PM2.5 exposure and may also help to
mitigate risks. Based on the case study areas included in the analysis,
The Administrator notes that what urban areas are included in the risk
assessment analysis will greatly influence the results but notes that
based on the areas included in the analyses, the results show the
largest impact is on reducing exposure and risk in Black populations,
who were estimated in the risk assessment case study areas to have the
highest levels of exposures and the greatest rates of premature
mortality risk. The Administrator also notes that, similar to the main
risk estimates discussed above, there is increasing uncertainty in
quantitative estimates of stratified risk estimates at the lower end of
the range of standard levels assessed.
    The Administrator recognizes that judgments about the appropriate
weight to place on any of the factors discussed above should reflect
consideration not only of the relative strength of the evidence but
also of the important uncertainties that remain in the evidence and the
quantitative information being considered in this reconsideration. The
Administrator also recognizes that the CAA requires him to set
standards that in his judgment are neither more stringent nor less
stringent than necessary to protect public health with an adequate
margin of safety. Based on the above considerations, the Administrator
concludes that it is appropriate to propose to set a level for the
primary annual PM2.5 standard within the range of 9.0 to
10.0 [mu]g/m\3\, while also taking comment on a level for the primary
annual PM2.5 standard as low as 8.0 [mu]g/m\3\ and as high
as 11.0 [mu]g/m\3\. The Administrator provisionally concludes that a
standard level within the range of 9.0 to 10.0 [mu]g/m\3\ would reflect
appropriate approaches to placing the most weight on the strongest
available evidence, while placing less weight on much more limited
evidence and on more uncertain analyses of information available from a
relatively small number of studies. He notes that a standard set at 9.0
to 10.0 [mu]g/m\3\ would be at or below the study-reported mean
PM2.5 concentrations in the key U.S. epidemiologic studies,
exposures for which we have the strongest support for adverse health
effects occurring. Further, in considering margin of safety, he notes
that an annual standard level that is no more than 10-20% higher than
the study-reported means in the U.S. monitor-based studies (i.e., for
the lowest study reported mean value of 9.9 [mu]g/m\3\, this means an
annual standard level of approximately 10.9-11.9 [mu]g/m\3\) and no
more than 15-18% higher for the U.S. hybrid modeling with population
weighting (i.e., for the lowest study reported mean value of 9.3 [mu]g/
m\3\, this means an annual standard level of approximately 10.7-11.0
[mu]g/m\3\), would generally maintain air quality exposures at or below
those associated with the study-reported mean PM2.5
concentrations. Additionally, the Administrator also notes that these
key U.S. epidemiologic studies utilize cohorts that include populations
identified as at-risk, including children and older adults, as well as
individuals in the general population with pre-existing disease, like
cardiovascular disease and respiratory disease. Based on this
information, he concludes that a revised standard level of 9.0-10.0
[mu]g/m\3\ would limit air quality exposures to concentrations well
below those associated with the study reported mean, studies which
include and assess impacts on the most at-risk populations. Thus, the
Administrator provisionally concludes that a standard level within this
range would appropriately provide an adequate margin of safety for the
populations most at risk for adverse health effects associated with
exposure to PM2.5.
    The Administrator also considers other lines of evidence, including
the study reported means from epidemiologic studies that restrict
concentrations to levels below 12 [mu]g/m\3\, the 25th percentiles
values reported by a subset of epidemiologic studies, and the
information from the accountability studies. He notes that a standard
in the range of 9.0 to 10.0 [mu]g/m\3\ would limit exposures to ambient
concentrations near the 25th percentile reported in the available
studies, with a standard level of 9.0 [mu]g/m\3\ limiting those
exposures somewhat more than a standard level of 10.0 [mu]g/m\3\. He
also notes that a standard in the range of 9.0 to 10.0 [mu]g/m\3\ would
be near the value of the study reported means from the two available
long-term restricted analyses studies (i.e., 9.6 [mu]g/m\3\). The
Administrator notes a standard level of 9.0-10.0 [mu]g/m\3\, would also
be at or below the lowest starting concentration of the newest
available accountability studies (i.e., 10.0-11.1 [mu]g/m\3\). The
Administrator also considers the results from the risk assessment. He
recognizes that the risk estimates should be considered along with the
inherent uncertainties and

limitations of such analyses when informing judgments about the
potential for additional public health protection associated with
PM2.5 exposure and related health effects. When looking at
the risk assessment results, he notes that an annual standard level of
9.0-10.0 [mu]g/m\3\ is estimated to reduce exposure concentrations such
that those remaining risks are associated with exposure concentrations
that are below most of the study-reported means in the key U.S.
epidemiologic studies, where we have the strongest support for adverse
health effects occurring, and below PM2.5 concentrations
(i.e., 8 [mu]g/m\3\) where the 2019 ISA notes that uncertainties remain
in the shape of the C-R curve, particularly for a standard level as low
as 9.0 [mu]g/m\3\. Lastly, the Administrator also notes that every
member of the CASAC found that the available scientific evidence and
information supported revising the annual standard level to a level of
10.0 [mu]g/m\3\. Additionally, the majority of the CASAC also
recommended that the available evidence and information supported
revision to a level of 9.0 [mu]g/m\3\. Thus, recognizing the
uncertainties in the evidence and the necessity of providing requisite
protection, with an adequate margin of safety, the Administrator is
proposing to set the level of the annual standard in the range of 9.0-
10.0 [mu]g/m\3\, and solicits comments on the appropriate standard
level within that range.
    While the Administrator recognizes that some members of the CASAC
advised, and the PA concluded, that the available scientific
information provides support for considering a range that extends up to
11.0 [mu]g/m\3\ and down to 8.0 [mu]g/m\3\, he provisionally concludes
that proposing such an extended range would not be appropriate at this
time. More specifically, the Administrator provisionally concludes that
proposing to revise the annual standard level to above 10.0 [mu]g/m\3\
and as high as 11.0 [mu]g/m\3\ would reflect a public health policy
approach that would place less weight on setting a standard level at or
below the study-reported means from a number of key U.S. epidemiologic
studies and less weight on the risk assessment results. Such an
approach would also place little or no weight on the study reported
means from epidemiologic studies that restrict concentrations to below
12 [mu]g/m\3\ and the 25th percentile concentrations reported by a
subset of epidemiologic studies. The Administrator notes that such an
approach may fail to provide an adequate margin of safety in light of
the evidence available in this reconsideration. In considering revision
to the annual standard level to below 9.0 [mu]g/m\3\ and as low as 8.0
[mu]g/m\3\, the Administrator notes that such a level would be
substantially below the study-reported means and would not recognize
the controlling nature of the design value monitor with respect to the
concentration gradients consistently occurring across urban areas. The
Administrator also recognizes that the evidence and uncertainties for
public health benefits of lower standards exists on a continuum across
the range of possible standard levels. He preliminarily judges that the
evidence is sufficient to support standards in the range of 9.0-10.0
[mu]g/m\3\, recognizing that the selection of a final standard level
will depend on judgments about the relative weight to place on various
aspects of the evidence and how to provide for an adequate margin of
safety. However, the Administrator preliminarily judges that the
available information and evidence are not sufficient to warrant
revising the level of the annual standard below 9.0 [mu]g/m\3\. He
finds the uncertainties as to the public health risks and benefits
associated with such a standard to be too great at this time.
Nonetheless, while the Administrator notes these considerations above,
he solicits comment on revising the annual standard down to a level
below 9.0 [mu]g/m\3\ and as low as 8.0 [mu]g/m\3\, as well as to above
10.0 [mu]g/m\3\ and as high as 11.0 [mu]g/m\3\, and on approaches for
interpreting the scientific evidence and rationales that would support
such a level.

E. Proposed Decisions on the Primary PM2.5 Standards

    Taking the above considerations into account, upon reconsidering
the current primary PM2.5 standards in light of the
currently available scientific evidence and quantitative information,
the Administrator proposes to revise the level of the primary annual
PM2.5 standard from 12.0 [mu]g/m\3\ to within the range of
9.0 to 10.0 [mu]g/m\3\ and to retain the 24-hour standard level at 35
[mu]g/m\3\. In the Administrator's judgment, such a suite of primary
PM2.5 standards and the rationale supporting such levels
could reasonably be judged to reflect the appropriate consideration of
the strength of the available evidence and other information and their
associated uncertainties and the advice of the CASAC.
    The Administrator recognizes that the final suite of standards will
reflect the Administrator's ultimate judgments in the final rulemaking
as to the suite of primary PM2.5 standards that are
requisite to protect the public health with an adequate margin of
safety from effects associated with PM2.5 exposures. The
final judgments to be made by the Administrator will appropriately
consider the requirement for standards that are neither more nor less
stringent than necessary and will recognize that the CAA does not
require that primary standards be set at a zero-risk level, but rather
at a level that reduces risk sufficiently so as to protect public
health with an adequate margin of safety.
    Having reached his provisional judgment to propose revising the
annual standard level from 12.0 to within a range of 9.0 to 10.0 [mu]g/
m\3\ and to propose retaining the 24-hour standard level at 35 [mu]g/
m\3\, the Administrator solicits public comment on this range of levels
and on approaches to considering the available evidence and information
that would support the choice of levels within this range. The
Administrator also solicits public comment on alternative annual
standard levels down to 8.0 [mu]g/m\3\ and up to 11.0 [mu]g/m\3\, on an
alternative 24-hour standard level as low as 25 [mu]g/m\3\ and on the
combination of annual and 24-hour standards that commenters may believe
is appropriate, along with the approaches and rationales used to
support such levels. For example, the EPA solicits comments on the
uncertainties in the reported associations between daily or annual
average PM2.5 exposures and mortality or morbidity in the
epidemiologic studies, the significance of the 25th percentile of
ambient concentrations reported in studies, the relevance and
limitations of international studies, and other topics discussed in
section II.D.3.b.

III. Rationale for Proposed Decisions on the Primary PM10 Standard

    This section presents the rationale for the Administrator's
proposed decision to retain the existing primary PM10
standard. This decision is based on a thorough review of the latest
scientific information, published through January 2018,\103\ and
evaluated in the 2019 ISA, on human health effects associated with
PM10-2.5 in ambient air. As described in section 1.2 of the
ISA Supplement, the

scope of the updated scientific evaluation of the health effects
evidence is based on those PM size fractions, exposure durations, and
health effects category combinations where the 2019 ISA concluded a
causal relationship exists (U.S. EPA, 2019a, U.S. EPA, 2022a).
Therefore, because the 2019 ISA did not conclude a causal relationship
for PM10-2.5 for any exposure durations or health effect
categories, the ISA Supplement does not include an evaluation of
additional studies for PM10-2.5. As a result, the 2019 ISA
continues to serve as the scientific foundation for assessing the
adequacy of the primary PM10 standard in this
reconsideration of the 2020 final decision (U.S. EPA, 2019a, section
1.7; U.S. EPA, 2022a). The Administrator's rationale also takes into
account: (1) the PA evaluation of the policy-relevant information in
the 2019 ISA; (2) CASAC advice and recommendations, as reflected in
discussions of the draft of the PA at public meetings and in the
CASAC's letter dated March 18, 2022, to the Administrator; and (3)
public comments received during the development of the PA.
---------------------------------------------------------------------------

    \103\ In addition to the review's opening ``call for
information'' (79 FR 71764, December 3, 2014), the current ISA
identified and evaluated studies and reports that have undergone
scientific peer review and were published or accepted for
publication between January 1, 2009 through approximately January
2018 (U.S. EPA, 2019a, p. ES-2). References that are cited in the
2019 ISA, the references that were considered for inclusion but not
cited, and electronic links to bibliographic information and
abstracts can be found at: https://hero.epa.gov/hero/particulate-matter.
---------------------------------------------------------------------------

    In presenting the rationale for the Administrator's proposed
decision and its foundations, section III.A provides background and
introductory information for this reconsideration of the primary
PM10 standard. It includes background on the 2020 final
decision to retain the primary PM10 standard (section
III.A.1) and also describes the general approach for this
reconsideration (section III.A.2) Section III.B summarizes the key
aspects of the currently available scientific evidence for
PM10-2.5-related health effects. Section III.C presents the
Administrator's proposed conclusions regarding the adequacy of the
primary PM10 standard (section III.C.3), drawing on
evidence-based considerations (section III.C.2) and advice from the
CASAC (section III.C.1).

A. General Approach

    The current primary PM10 standard was affirmed in 2020
based on the scientific information available at that time, as well as
the Administrator's judgments regarding the available public health
effects evidence, and the appropriate degree of public health
protection for the existing standards (85 FR 82725, December 18, 2020).
With the 2020 decision, the Administrator retained the existing 24-hour
primary PM10 standard, with its level of 150 [mu]g/m\3\ and
its one-expected-exceedance form on average over three years, to
continue to provide public health protection against short-term
exposures to PM10-2.5 (85 FR 82725, December 18, 2020). The
subsection below focuses on the key considerations, and the prior
Administrator's conclusions, for PM10-2.5-related health
effects and the adequacy of the primary PM10 standard in the
2020 review.
1. Background on the Current Standard
    In the 2019 ISA, the strongest evidence for PM10-2.5-
related health effects was for cardiovascular effects, respiratory
effects, and premature mortality following short-term exposures. For
each of these categories of effects, the 2019 ISA concludes that the
evidence was ``suggestive of, but not sufficient to infer, a causal
relationship''. Specifically, the health effects evidence evaluated in
the 2019 ISA included an expanded body of scientific evidence that has
become available since the completion of the 2009 ISA linking short-
term PM10-2.5 to health outcomes such as premature death and
hospital visits (U.S. EPA, 2009a; U.S. EPA, 2019a). This evidence base
evaluated the causal relationships between short-term exposure to
PM10-2.5 and a broad range of health effects (U.S. EPA,
2019a, section 1.4.2). These effects associated with short-term
exposure ranged from hospital admissions and emergency department
visits for cardiovascular effects (documented in epidemiologic studies
that reported PM10-2.5 associations with cardiovascular
hospital admissions and emergency department visits in study locations
with mean 24-hour average PM10-2.5 concentrations ranging
from 7.4 to 13 [mu]g/m\3\) and respiratory effects (documented in
epidemiologic studies that reported PM10-2.5 associations
with respiratory hospital admissions and emergency department visits in
study locations with mean 24-hour average concentrations ranging from
5.6 to 16.2 [mu]g/m\3\) to mortality (documented in epidemiologic
studies that reported PM10-2.5 associations with mortality
in study areas with mean 24-hour average concentrations ranging from
6.1 to 16.4 [mu]g/m\3\). In addition to the epidemiologic studies, the
evidence base included a small number of controlled human exposure
studies and animal toxicological studies that provided insight into the
biological plausibility of these effects. Collectively, the
epidemiologic studies, controlled human exposure, and animal
toxicological studies, with their inherent uncertainties, contributed
to the causality determinations of ``suggestive of, but not sufficient
to infer, a causal relationship'' between short-term exposures to
PM10-2.5 and cardiovascular effects, respiratory effects,
cancer, and mortality (U.S. EPA, 2019a, section 1.4.2). The 2019 ISA
includes expanded evidence for the relationships between long-term
exposures and cardiovascular effects, metabolic effects, nervous system
effects, cancer, and mortality. While the evidence available in the
2019 ISA included additional health outcomes, including those
associated with long-term PM10-2.5 exposure, key limitations
in the evidence that were identified in the 2009 ISA persist in studies
evaluated in the 2019 ISA.
    In considering the available body of evidence, it was noted in the
2020 review there were considerable uncertainties and limitations
associated with the experimental evidence for PM2.5
exposures and health effects, and as such more weight was placed on the
available epidemiologic evidence. Therefore, the primary focus in the
2020 review was on multi-city and single-city epidemiologic studies
that evaluated associations between short-term PM10-2.5 and
mortality, cardiovascular effects (hospital admissions and emergency
department visits, as well as blood pressure and hypertension), and
respiratory effects. Despite differences in the approaches \104\ used
to estimate ambient PM10-2.5 concentrations, the majority of
the studies reported positive, though often not statistically
significant, associations with short-term PM10-2.5
exposures. Most PM10-2.5 effect estimates remained positive
in copollutant models that included either gaseous pollutants or other
particulate matter size fractions (e.g., PM2.5). In U.S.
study locations likely to have met the PM10 standard during
the study period, a few studies reported positive associations between
PM10-2.5 and mortality that were statistically significant
and remained so in copollutant models (U.S. EPA, 2019a). In addition to
the epidemiologic studies, there were a small number of controlled
human exposure studies evaluated in the 2019 ISA that reported
alterations in heart rate variability or increased pulmonary
inflammation following short-term exposure to PM10-2.5,
providing some support for the associations in the epidemiologic
studies. Animal toxicological studies examined the effect of short-term

PM10-2.5 exposures using non-inhalation (e.g., intratracheal
instillation) route.\105\ Therefore, these studies provided limited
evidence for the biological plausibility of PM10-2.5-induced
effects (U.S. EPA, 2019a). Although the scientific evidence available
in the 2019 ISA expanded the understanding of health effects associated
with PM10-2.5 exposures, a number of important uncertainties
remained. These uncertainties, and their implications for interpreting
the scientific evidence, include the following:
---------------------------------------------------------------------------

    \104\ As discussed further below, methods employed by the
epidemiologic studies to estimate ambient PM10-2.5
concentrations include: (1) calculating the difference between
PM10 and PM2.5 at co-located monitors, (2)
calculating the difference between county-wide averages of monitored
PM10 and PM2.5 based on monitors that are not
necessarily co-located, and (3) direct measurement of
PM10-2.5 using a dichotomous sampler (U.S. EPA, 2019a,
section 1.4.2).
    \105\ Non-inhalation exposure experiments (i.e., intratracheal
[IT] instillation) are informative for size fractions (e.g.,
PM10-2.5) that cannot penetrate the airway of a study
animal and may provide information relevant to biological
plausibility and dosimetry (U.S. EPA, 2019a, section A-12).
---------------------------------------------------------------------------

     The potential for confounding by copollutants, notably
PM2.5, was addressed with copollutant models in a relatively
small number of PM10-2.5 epidemiologic studies (U.S. EPA,
2019a). This was particularly important given the relatively small body
of experimental evidence (i.e., controlled human exposure and animal
toxicological studies) available to support the independent effect of
PM10-2.5 on human health. This increases the uncertainty
regarding the extent to which PM10-2.5 itself, rather than
one or more copollutants, is responsible for the mortality and
morbidity effects reported in epidemiologic studies.
     There was greater spatial variability in
PM10-2.5 concentrations than PM2.5
concentrations, resulting in the potential for increased exposure error
for PM10-2.5 (U.S. EPA, 2019a). Available measurements did
not provide sufficient information to adequately characterize the
spatial distribution of PM10-2.5 concentrations (U.S. EPA,
2019a). The limitations in estimates of ambient PM10-2.5
concentrations ``would tend to increase uncertainty and make it more
difficult to detect effects of PM10-2.5 in epidemiologic
studies'' (U.S. EPA, 2019a).
     Estimation of PM10-2.5 concentrations over
which reported health outcomes occur remain highly uncertain. When
compared with PM2.5, there is uncertainty spanning all
epidemiologic studies examining associations with PM10-2.5
including deficiencies in the existing monitoring networks, the lack of
a systematic evaluation of the various methods used to estimate
PM10-2.5 concentrations and the resulting uncertainty in the
spatial as well as the temporal variability in PM10-2.5
concentration (U.S. EPA, 2019a). Given these limitations in routine
monitoring, epidemiologic studies employed a number of different
approaches for estimating PM10-2.5 concentrations, including
(1) calculating the difference between PM10 and
PM2.5 at co-located monitors, (2) calculating the difference
between county-wide averages of monitored PM10 and
PM2.5 based on monitors that are not necessarily co-located,
and (3) direct measurement of PM10-2.5 using a dichotomous
sampler (U.S. EPA, 2019a, section 1.4.2). Given the relatively small
number of PM10-2.5 monitoring sites, the relatively large
spatial variability in ambient PM10-2.5 concentrations, the
use of different approaches to estimating ambient PM10-2.5
concentrations across epidemiologic studies, and the limitations
inherent in such estimates, the distributions of PM10-2.5
concentrations over which reported health outcomes occur remain highly
uncertain (U.S. EPA, 2019a).
     There was relatively little information available to
characterize the apparent variability in associations between short-
term PM10-2.5 exposures and health effects across study
locations (U.S. EPA, 2019a). Specifically, the relative lack of
information on the chemical and biological composition of
PM10-2.5 as well as potential spatial and temporal
variability in PM10-2.5 exposures complicates the
interpretation of results between study locations (U.S. EPA, 2009b;
U.S. EPA, 2019a).
    Consistent with the general approach routinely employed in NAAQS
reviews, the initial consideration in the 2020 review of the primary
PM10 standard was with regard to the adequacy of protection
provided by the then-existing standard. Key aspects of that
consideration are summarized below.
i. Considerations Regarding the Adequacy of the Existing Standard in
the 2020 Review
    In the 2020 final decision, the EPA retained the existing 24-hour
primary PM10 standard with its level of 150 [mu]g/m\3\ and
its one-expected-exceedance form on average over three years to
continue to provide public health protection against exposures to
PM10-2.5 (85 FR 82727, December 18, 2020). In reaching his
decision, the Administrator specifically noted that, while the health
effects evidence was somewhat expanded since the prior reviews, the
overall conclusions in the 2019 ISA, including uncertainties and
limitations, were generally consistent with what was considered in the
2012 review (85 FR 82725, December 18, 2020). In addition, the
Administrator recognized that there were still a number of
uncertainties and limitations associated with the available evidence.
With regard to the evidence on PM10-2.5-related health
effects, the Administrator noted that epidemiologic studies continued
to report positive associations with mortality and morbidity in cities
across North America, Europe, and Asia, where PM10-2.5
sources and composition were expected to vary widely. While significant
uncertainties remained in the 2020 review, the Administrator recognized
that this expanded body of evidence had broadened the range of effects
that have been linked with PM10-2.5 exposures. The studies
evaluated in the 2019 ISA expanded the scientific foundation presented
in the 2009 ISA and led to revised causality determinations (and new
determinations) for long-term PM10-2.5 exposures and
mortality, cardiovascular effects, metabolic effects, nervous system
effects, and cancer (85 FR 82726, December 18, 2020). Drawing from his
consideration of this evidence, the Administrator concluded that the
scientific information available since the time of the last review
supported a decision to maintain a primary PM10 standard to
provide public health protection against PM10-2.5 exposures,
regardless of location, source of origin, or particle composition (85
FR 82726, December 18, 2020). With regard to uncertainties in the
available evidence, the Administrator first noted that a number of
limitations were identified in the 2012 review related to: (1)
estimates of ambient PM10-2.5 concentrations used in
epidemiologic studies; (2) limited evaluation of copollutant models to
address the potential for confounding; and (3) limited experimental
studies supporting biological plausibility for PM10-2.5-
related effects. Despite the expanded body of evidence for
PM10-2.5 exposures and health effects, the Administrator
recognized that uncertainties in the 2020 review continued to include
those associated with the exposure estimates used in epidemiologic
studies, the independence of the PM10-2.5 health effect
associations, and the biologically plausible pathways for
PM10-2.5 health effects (85 FR 82726, December 18, 2020).
These uncertainties contributed to the 2019 ISA determinations that the
evidence is at most ``suggestive of, but not sufficient to infer''
causal relationships (85 FR 82726, December 18, 2020). In considering
the available evidence in his basis for the proposed decision, the
Administrator emphasized evidence supporting ``causal'' and ``likely to
be causal'' relationships, and therefore, judged that the
PM10-2.5-related health effects evidence provided

an uncertain scientific foundation for making standard-setting
decisions. He further judged limitations in the evidence raised
questions as to whether additional public health improvements would be
achieved by revising the existing PM10 standard (85 FR
24126, April 30, 2020). In the 2020 decision, for all of the reasons
discussed above and recognizing the CASAC conclusion that the evidence
provided support for retaining the current standard, the Administrator
concluded that it was appropriate to retain the existing primary
PM10 standard, without revision. His decision was consistent
with the CASAC advice related to the primary PM10 standard.
Specifically, the CASAC agreed with the 2020 PA conclusions that, while
these effects are important, the ``evidence does not call into question
the adequacy of the public health protection afforded by the current
primary PM10 standard'' and ``supports consideration of
retaining the current standard in this review'' (Cox, 2019b, p. 3 of
consensus letter). Thus, the Administrator concluded that the primary
PM10 standard (in all of its elements) was requisite to
protect public health with an adequate margin of safety against effects
that have been associated with PM10-2.5. In light of this
conclusion, the EPA retained the existing PM10 standard.
2. General Approach and Key Issues in This Reconsideration of the 2020
Final Decision
    To evaluate whether it is appropriate to consider retaining the
current primary PM10 standard, or whether consideration of
revision is appropriate, the EPA has adopted an approach in this
reconsideration that builds upon the general approach used in past
reviews and reflects the body of evidence and information now
available, as well as the assessments and evaluations performed in
those reviews. As summarized above, the Administrator's decision in the
2020 review was based on an integration of PM10-2.5-related
health effects information with the judgments on the public health
significance of key effects, policy judgments as to when the standard
is requisite, consideration of CASAC advice, and consideration of
public comments.
    Similarly, in this reconsideration, information is drawn from
recent studies of PM10-2.5-related health effects. In so
doing, the PA considers information critically analyzed and
characterized in the 2019 ISA, as well as consideration of the
associated uncertainties and limitations for the available evidence.

B. Overview of the Health Effects Evidence

    The information summarized here is based on the scientific
assessment of the health effects evidence available in this
reconsideration; this evaluation is documented in the 2019 ISA and its
policy implications are discussed further in the PA. As noted above,
the ISA Supplement does not include an evaluation of studies for
PM10-2.5 and the 2019 ISA continues to serve as the
scientific foundation for this reconsideration.
1. Nature of Effects
    For the health effect categories and exposure duration combinations
evaluated, the 2019 ISA concludes that the evidence supports causality
determinations for PM10-2.5 that are at most ``suggestive
of, but not sufficient to infer, a causal relationship. While the
evidence supporting the causal nature of relationships between exposure
to PM10-2.5 has been strengthened for some health effect
categories since the completion of the 2009 ISA, the 2019 ISA concludes
that overall ``the uncertainties in the evidence identified in the 2009
ISA have, to date, still not been addressed'' (U.S. EPA, 2019a, section
1.4.2, p. 1-41; U.S. EPA, 2022b, section 4.3.1). Specifically,
epidemiologic studies available in the 2012 review relied on various
methods to estimate PM10-2.5 concentrations, and these
methods had not been systematically compared to evaluate spatial and
temporal correlations in PM10-2.5 concentrations. Methods
included: (1) calculating the difference between PM10 and
PM2.5 concentrations at co-located monitors, (2) calculating
the difference between county-wide averages of monitored
PM10- and PM2.5-based on monitors that are not
necessarily co-located, and (3) direct measurement of
PM10-2.5 using a dichotomous sampler (U.S. EPA, 2019a,
section 1.4.2). As described in the 2019 ISA, there continues to be
variability across epidemiologic studies in the approaches used to
estimate PM10-2.5 concentrations. Additionally, some studies
estimate long-term PM10-2.5 exposures as the difference
between PM10 and PM2.5 concentrations based on
information from spatiotemporal or land use regression (LUR) models, in
addition to monitors. The various methods used to estimate
PM10-2.5 concentrations have not been systematically
evaluated (U.S. EPA, 2019a, section <IP_ADDRESS>), contributing to
uncertainty regarding the spatial and temporal correlations in
PM10-2.5 concentrations across methods and in the
PM10-2.5 exposure estimates used in epidemiologic studies
(U.S. EPA, 2019a, section <IP_ADDRESS>.3). Given the greater spatial and
temporal variability of PM10-2.5 and the lower number of
PM10-2.5 monitoring sites, compared to PM2.5,
this uncertainty is particularly important for the coarse size
fraction. Beyond the uncertainty associated with PM10-2.5
exposure estimates in epidemiologic studies, the limited information on
the potential for confounding by copollutants and the limited support
available for the biological plausibility of health effects following
PM10-2.5 exposures also continue to contribute to
uncertainty in the PM10-2.5 health evidence. Uncertainty
related to potential confounding stems from the relatively small number
of epidemiologic studies that have evaluated PM10-2.5 health
effect associations in copollutants models with both gaseous pollutants
and other PM size fractions. On the other hand, uncertainty related to
the biological plausibility of effects attributed to
PM10-2.5 exposures results from the small number of
controlled human exposure and animal toxicological studies that have
evaluated the health effects of experimental PM10-2.5
inhalation exposures. The evidence supporting the 2019 ISA's
``suggestive of, but not sufficient to infer, a causal relationship''
causality determinations for PM10-2.5, including
uncertainties in this evidence, is summarized below in sections
III.B.1.a through III.B.1.f.
a. Mortality
i. Long-Term Exposures
    Due to the dearth of studies examining the association between
long-term PM10-2.5 exposure and mortality, the 2009 ISA
concluded that the evidence was ``inadequate to determine if a causal
relationship exists'' (U.S. EPA, 2009a). As reported in the 2019 ISA,
some cohort studies conducted in the U.S. and Europe report positive
associations between long-term PM10-2.5 exposure and total
(nonaccidental) mortality, though results are inconsistent across
studies (U.S. EPA, 2019a, Table 11-11). The examination of copollutant
models in these studies remains limited and, when included,
PM10-2.5 effect estimates are often attenuated after
adjusting for PM2.5 (U.S. EPA, 2019a, Table 11-11). Across
studies, PM10-2.5 exposure concentrations are estimated
using a variety of approaches, including direct measurements from
dichotomous samplers, calculating the difference between
PM10 and PM2.5 concentrations

measured at collocated monitors, and calculating difference of area-
wide concentrations of PM10 and PM2.5. As
discussed above, temporal and spatial correlations between these
approaches have not been evaluated, contributing to uncertainty
regarding the potential for exposure measurement error (U.S. EPA,
2019a, section <IP_ADDRESS> and Table 11-11). The 2019 ISA concludes that
this uncertainty ``reduces the confidence in the associations observed
across studies'' (U.S. EPA, 2019a, p. 11-125). The 2019 ISA
additionally concludes that the evidence for long-term
PM10-2.5 exposures and cardiovascular effects, respiratory
morbidity, and metabolic disease provide limited biological
plausibility for PM10-2.5-related mortality (U.S. EPA,
2019a, sections 11.4.1 and 11.4). Taken together, the 2019 ISA
concludes that, ``this body of evidence is suggestive, but not
sufficient to infer, that a causal relationship exists between long-
term PM10-2.5 exposure and total mortality'' (U.S. EPA,
2019a, p. 11-125).
ii. Short-Term Exposures
    The 2009 ISA concluded that the evidence is ``suggestive of a
causal relationship between short-term exposure to PM10-2.5
and mortality'' (U.S. EPA, 2009a). The 2019 ISA included multicity
epidemiologic studies conducted primarily in Europe and Asia that
continue to provide consistent evidence of positive associations
between short-term PM10-2.5 exposure and total
(nonaccidental) mortality (U.S. EPA, 2019a, Table 11-9). Although these
studies contribute to increasing confidence in the PM10-2.5-
mortality relationship, the use of a variety of approaches to estimate
PM10-2.5 exposures continues to contribute uncertainty to
the associations observed. Recent studies expand the assessment of
potential copollutant confounding of the PM10-2.5-mortality
relationship and provide evidence that PM10-2.5 associations
generally remain positive in copollutant models, though associations
are attenuated in some instances (U.S. EPA, 2019a, section <IP_ADDRESS>,
Figure 11-28, Table 11-10). The 2019 ISA concludes that, overall, the
assessment of potential copollutant confounding is limited due to the
lack of information on the correlation between PM10-2.5 and
gaseous pollutants and the small number of locations in which
copollutant analyses have been conducted. Associations with cause-
specific mortality (i.e., cardiovascular and respiratory mortality)
provide some support for associations with total (nonaccidental)
mortality, though associations with respiratory mortality are more
uncertain (i.e., wider confidence intervals) and less consistent (U.S.
EPA, 2019a, section 11.3.7). The 2019 ISA concludes that the evidence
for PM10-2.5-related cardiovascular effects provides only
limited support for the biological plausibility of a relationship
between short-term PM10-2.5 exposure and cardiovascular
mortality (U.S. EPA, 2019a, section 11.3.7). Based on the overall
evidence, the 2019 ISA concludes that, ``this body of evidence is
suggestive, but not sufficient to infer, that a causal relationship
exists between short-term PM10-2.5 exposure and total
mortality'' (U.S. EPA, 2019a, p. 11-120).
b. Cardiovascular Effects
i. Long-Term Exposures
    In the 2009 ISA, the evidence describing the relationship between
long-term exposure to PM10-2.5 and cardiovascular effects
was characterized as ``inadequate to infer the presence or absence of a
causal relationship.'' The limited number of epidemiologic studies
reported contradictory results and experimental evidence demonstrating
an effect of PM10-2.5 on the cardiovascular system was
lacking (U.S. EPA, 2019a, section 6.4).
    The evidence relating long-term PM10-2.5 exposures to
cardiovascular mortality remains limited, with no consistent pattern of
associations across studies and, as discussed above, uncertainty
stemming from the use of various approaches to estimate
PM10-2.5 concentrations (U.S. EPA, 2019a, Table 6-70). The
evidence for associations with cardiovascular morbidity has grown and,
while results across studies are not entirely consistent, some
epidemiologic studies report positive associations with ischemic heart
disease (IHD) and MI (U.S. EPA, 2019a, Figure 6-34); stroke (U.S. EPA,
2019a, Figure 6-35); atherosclerosis (U.S. EPA, 2019a, section 6.4.5);
venous thromboembolism (VTE) (U.S. EPA, 2019a, section 6.4.7); and
blood pressure and hypertension (U.S. EPA, 2019a, Section 6.4.6).
PM10-2.5 cardiovascular mortality effect estimates are often
attenuated, but remain positive, in copollutants models that adjust for
PM2.5. For morbidity outcomes, associations are inconsistent
in copollutant models that adjust for PM2.5, NO2,
and chronic noise pollution (U.S. EPA, 2019a, p. 6-276). The lack of
toxicological evidence for long-term PM10-2.5 exposures
represents a data gap (U.S. EPA, 2019a, section 6.4.10), resulting in
the 2019 ISA conclusion that ``evidence from experimental animal
studies is of insufficient quantity to establish biological
plausibility'' (U.S. EPA, 2019a, p. 6-277). Based largely on the
observation of positive associations in some epidemiologic studies, the
2019 ISA concludes that ``evidence is suggestive of, but not sufficient
to infer, a causal relationship between long-term PM10-2.5
exposure and cardiovascular effects'' (U.S. EPA, 2019a, p. 6-277).
ii. Short-Term Exposures
    The 2009 ISA found that the available evidence for short-term
PM10-2.5 exposure and cardiovascular effects was
``suggestive of a causal relationship.'' This conclusion was based on
several epidemiologic studies reporting associations between short-term
PM10-2.5 exposure and cardiovascular effects, including IHD
hospitalizations, supraventricular ectopy, and changes in heart rate
variability (HRV). In addition, dust storm events resulting in high
concentrations of crustal material were linked to increases in total
cardiovascular disease emergency department visits and hospital
admissions. However, the 2009 ISA noted the potential for exposure
measurement error primarily due to the different methods used across
studies to estimate PM10-2.5 concentrations and copollutant
confounding in these epidemiologic studies. In addition, there was only
limited evidence of cardiovascular effects from a small number of
experimental studies (e.g. animal toxicological studies and controlled
human exposure studies) that examined short-term PM10-2.5
exposures (U.S. EPA, 2009a, section <IP_ADDRESS>). In the 2019 ISA, key
uncertainties included the potential for exposure measurement error,
copollutant confounding, and limited evidence of biological
plausibility for cardiovascular effects following inhalation exposure
(U.S. EPA, 2019a, section 6.3.13).
    The evidence for short-term PM10-2.5 exposure and
cardiovascular outcomes has expanded since the 2009 ISA, though
important uncertainties remain. The 2019 ISA notes that there are a
small number of epidemiologic studies reporting positive associations
between short-term exposure to PM10-2.5 and cardiovascular-
related morbidity outcomes. However, the 2019 ISA notes that there is
limited evidence to support that these associations are biologically
plausible, or independent of copollutant confounding. The 2019 ISA also
concludes that it remains unclear how the approaches used to estimate
PM10-2.5 concentrations in epidemiologic studies compare
amongst one another and subsequently how exposure measurement error
varies between each method. Specifically, it is unclear how

well-correlated PM10-2.5 concentrations are both temporally
and spatially across these methods and therefore whether exposure
measurement error varies across these methods. Taken together, the 2019
ISA concludes that ``the evidence is suggestive of, but not sufficient
to infer, a causal relationship between short-term PM10-2.5
exposures and cardiovascular effects'' (U.S. EPA, 2019a, p. 6-254).
c. Respiratory Effects--Short-Term Exposures
    Based on a small number of epidemiologic studies observing
associations with some respiratory effects and limited evidence from
experimental studies to support biological plausibility, the 2009 ISA
(U.S. EPA, 2009a) concluded that the relationship between short-term
exposure to PM10-2.5 and respiratory effects is ``suggestive
of a causal relationship.'' Epidemiologic findings were consistent for
respiratory infection and combined respiratory-related diseases, but
not for COPD. Studies were characterized by overall uncertainty in the
exposure assignment approach and limited information regarding
potential copollutant confounding. Controlled human exposure studies of
short-term PM10-2.5 exposures found no lung function
decrements and inconsistent evidence for pulmonary inflammation. Animal
toxicological studies were limited to those using non-inhalation (e.g.,
intra-tracheal instillation) routes of PM10-2.5 exposure.
    Recent epidemiologic findings consistently link PM10-2.5
exposure to asthma exacerbation and respiratory mortality, with some
evidence that associations remain positive (though attenuated in some
studies of mortality) in copollutant models that include
PM2.5 or gaseous pollutants. Epidemiologic studies provide
limited evidence for positive associations with other respiratory
outcomes, including COPD exacerbation, respiratory infection, and
combined respiratory-related diseases (U.S. EPA, 2019a, Table 5-36). As
noted above for other endpoints, an uncertainty in these epidemiologic
studies is the lack of a systematic evaluation of the various methods
used to estimate PM10-2.5 concentrations and the resulting
uncertainty in the spatial and temporal variability in
PM10-2.5 concentrations compared to PM2.5 (U.S.
EPA, 2019a, sections <IP_ADDRESS>.3 and <IP_ADDRESS>). Specifically, the existing
monitoring networks do not provide a great sense of how well correlated
concentrations are both spatially and temporally across the
PM10-2.5 estimation methods and overall spatial and temporal
patterns in PM10-2.5 concentrations. Taken together, the
2019 ISA concludes that ``the collective evidence is suggestive of, but
not sufficient to infer, a causal relationship between short-term
PM10-2.5 exposure and respiratory effects'' (U.S. EPA,
2019a, p. 5-270).
d. Cancer--Long-Term Exposures
    In the 2012 review, little information was available from studies
of cancer following inhalation exposures to PM10-2.5. Thus,
the 2009 ISA determined the evidence was ``inadequate to evaluate the
relationship between long-term PM10-2.5 exposures and
cancer'' (U.S. EPA, 2009a). The scientific information evaluated in the
2019 ISA of long-term PM10-2.5 exposure and cancer remains
limited, with a few recent epidemiologic studies reporting positive,
but imprecise, associations with lung cancer incidence (U.S. EPA,
2019a). Moreover, uncertainty remains in these studies with respect to
exposure measurement error due to the use of PM10-2.5
predictions that have not been validated by monitored
PM10-2.5 concentrations (U.S. EPA, 2019a, sections <IP_ADDRESS>
and 10.3.4). Relatively few experimental studies of PM10-2.5
have been conducted, though available studies indicate that
PM10-2.5 exhibits two key characteristics of carcinogens:
genotoxicity and oxidative stress. While limited, such experimental
studies provide some evidence of biological plausibility for the
findings in a small number of epidemiologic studies (U.S. EPA, 2019a,
section 10.3.4).
    Taken together, the small number of epidemiologic and experimental
studies, along with uncertainty with respect to exposure measurement
error, contribute to the determination in the 2019 ISA that, ``the
evidence is suggestive of, but not sufficient to infer, a causal
relationship between long-term PM10-2.5 exposure and
cancer'' (U.S. EPA, 2019a, p. 10-87).
e. Metabolic Effects--Long-Term Exposures
    The 2009 ISA did not make a causality determination for
PM10-2.5-related metabolic effects. One epidemiologic study
in the 2019 ISA reports an association between long-term
PM10-2.5 exposure and incident diabetes, while additional
cross-sectional studies report associations with effects on glucose or
insulin homeostasis (U.S. EPA, 2019a, section 7.4). As discussed above
for other outcomes, uncertainties with the epidemiologic evidence
include the potential for copollutant confounding and exposure
measurement error due to the different methods used across studies to
estimate PM10-2.5 concentrations (U.S. EPA, 2019a, Tables 7-
14 and 7-15). The evidence base to support the biological plausibility
of metabolic effects following PM10-2.5 exposures is
limited, but a cross-sectional study that investigated biomarkers of
insulin resistance and systemic and peripheral inflammation may support
a pathway leading to type 2 diabetes (U.S. EPA, 2019a, sections 7.4.1
and 7.4.3). Based on the expanded, though still limited evidence base,
the 2019 ISA concludes that, ``[o]verall, the evidence is suggestive
of, but not sufficient to infer, a causal relationship between [long]-
term PM10-2.5 exposure and metabolic effects'' (U.S. EPA,
2019a, p. 7-56).
f. Nervous System Effects--Long-Term Exposures
    The 2009 ISA did not make a causality determination for
PM10-2.5-related nervous system effects. In the 2019 ISA,
available epidemiologic studies report associations between
PM10-2.5 and impaired cognition and anxiety in adults in
longitudinal analyses (U.S. EPA, 2019a, Table 8-25, section 8.4.5).
Associations of long-term exposure with neurodevelopmental effects are
not consistently reported in children (U.S. EPA, 2019a, sections 8.4.4
and 8.4.5). Uncertainties in these studies include the potential for
copollutant confounding, as no studies examined copollutants models
(U.S. EPA, 2019a, section 8.4.5), and for exposure measurement error,
given the use of various methods to estimate PM10-2.5
concentrations (U.S. EPA, 2019a, Table 8-25). In addition, there is
limited animal toxicological evidence supporting the biological
plausibility of nervous system effects (U.S. EPA, 2019a, sections 8.4.1
and 8.4.5). Overall, the 2019 ISA concludes that, ``the evidence is
suggestive of, but not sufficient to infer, a causal relationship''
between long-term PM10-2.5 exposure and nervous system
effects (U.S. EPA, 2019a, p. 8-75).

C. Proposed Conclusions on the Primary PM10 Standard

    In reaching proposed conclusions on the current primary
PM10 standard (presented in section III.C.3), the
Administrator has taken into account policy-relevant evidence-based
considerations discussed in the PA (summarized in section III.C.2), as
well as advice from the CASAC and public comments on the standard
received thus far in the reconsideration (section III.C.1). In general,
the role of the PA is

to help ``bridge the gap'' between the Agency's assessment of the
available evidence, and the judgments required of the Administrator in
determining whether it is appropriate to retain or revise the NAAQS.
Evidence-based considerations draw upon the EPA's integrated evaluation
of the scientific evidence of PM10-2.5-related health
effects presented in the 2019 ISA (summarized in section III.B above)
to address key policy-relevant questions in the reconsideration.
    The approach to reviewing the primary PM10 standard is
consistent with requirements of the provisions of the CAA related to
the review of the NAAQS and how the EPA and the courts have
historically interpreted the CAA. As discussed in section I.A above,
these provisions require the Administrator to establish primary
standards that, in the Administrator's judgment, are requisite (i.e.,
neither more nor less stringent than necessary) to protect public
health with an adequate margin of safety. Consistent with the Agency's
approach across all NAAQS reviews, the EPA's approach to informing
these judgments is based on a recognition that the available health
effects evidence generally reflects a continuum that includes ambient
air concentrations for which scientists generally agree that health
effects are likely to occur, through lower concentrations at which the
likelihood and magnitude of response becomes increasingly uncertain.
The CAA does not require the Administrator to establish a primary
standard at a zero-risk level or at background concentration levels,
but rather at a level that reduces risk sufficiently so as to protect
public health, including the health of sensitive groups, with an
adequate margin of safety.
    The proposed decision on the adequacy of the primary
PM10 standard described below is a public health policy
judgment by the Administrator that draws on the scientific evidence for
health effects and judgments about how to consider the uncertainties
and limitations that are inherent in the scientific evidence. The four
basic elements of the NAAQS (i.e., indicator, averaging time, form, and
level) have been considered collectively in evaluating the health
protection afforded by the current standard. The Administrator's final
decision will additionally consider public comments received on this
proposed decision.
1. CASAC Advice in This Reconsideration
    The CASAC has provided advice on the adequacy of the current
primary PM10 standard in the context of its review of the
draft PA (Sheppard, 2022a).\106\ In this context, the CASAC supported
the preliminary conclusion in the draft PA that the evidence reviewed
in the 2019 ISA does not call into question the public health
protection provided by the current primary PM10 standard
against PM10-2.5 exposures and concurs with the draft PA's
overall preliminary conclusion that it is appropriate to consider
retaining the current primary PM10 standard (Sheppard,
2022a, p. 4 of consensus letter). Additionally, the CASAC concurred
that ``. . . at this time, PM10 is an appropriate choice as
the indicator for PM10-2.5'' and ``that it is important to
retain the level of protection afforded by the current PM10
standard'' (Sheppard, 2022a, p. 4 of consensus letter). The CASAC also
recognized uncertainties associated with the scientific evidence,
including ``compared to PM2.5 studies, the more limited
number of epidemiology studies with positive statistically significant
findings, and the difficulty in extracting the sole contribution of
coarse PM to observed adverse health effects'' (Sheppard, 2022a, p. 19
of consensus responses).
---------------------------------------------------------------------------

    \106\ A limited number of public comments have also been
received in this reconsideration to date, including comments focused
on the draft PA. Of the public comments that addressed the adequacy
of the current primary PM10 standard, most commenters
supported the preliminary conclusion that it is appropriate to
consider retaining the current primary PM10 standard,
without revision. However, one nonprofit organization suggested that
the primary PM10 standard should be strengthened to a
level of 45 [mu]g/m\3\, consistent with the World Health
Organization Global Air Quality Guideline (WHO, 2021).
---------------------------------------------------------------------------

    The CASAC recommended several areas for additional research to
reduce uncertainties in the PM10-2.5 exposure estimates used
in the epidemiologic studies, to evaluate the independence of
PM10-2.5 health effect associations, to evaluate the
biological plausibility of PM10-2.5-related effects, and to
increase the number of studies examining PM10-2.5-related
health effects in at-risk populations (Sheppard, 2022a, p. 20 of
consensus responses). Furthermore, the CASAC ``recognizes a need for,
and supports investment in research and deployment of measurement
systems to better characterize PM10-2.5'' and to ``provide
information that can improve public health'' (Sheppard, 2022a, p. 20 of
consensus responses).
2. Evidence-Based Considerations in the Policy Assessment
    With regard to the current evidence on health effects associated
with long and short--term PM10-2.5 exposure health effects,
the PA notes that recent epidemiologic studies that continue to report
positive associations with mortality and morbidity in cities across
North America, Europe, and Asia, where PM10-2.5 sources and
composition are expected to vary widely (U.S. EPA, 2022b, section
4.3.1). While significant uncertainties remain, as described below and
summarized in the PA (U.S. EPA, 2022b, section 4.5), the PA recognizes
that this expanded body of evidence has broadened the range of effects
that have been linked with PM10-2.5 exposures. The
uncertainties in the available epidemiologic studies contribute to the
determinations in the 2019 ISA that the evidence for short- and long-
term exposures to PM10-2.5 and cardiovascular effects,
cancer, and mortality and long-term PM10-2.5 exposures and
metabolic effects and nervous system effects is ``suggestive of, but
not sufficient to infer'' causal relationships (U.S. EPA, 2019a; U.S.
EPA, 2022b, section 4.3.1). Drawing from this information, the PA
concludes that the evidence continues to provide support for
maintaining a standard that provides some measure of protection against
exposures to PM10-2.5, regardless of location, sources of
origin, or particle composition (U.S. EPA, 2022b, section 4.5).
    With regard to uncertainties, the PA recognizes that the 2019 ISA
notes that important uncertainties remain in the evidence base for
PM10-2.5-related health effects. As summarized in section
III.B above and in the PA (U.S. EPA, 2022b, sections 4.3.1 and 4.5).
These uncertainties include those related to variability in
PM10-2.5 exposure estimates used in epidemiologic studies,
in the independence of PM10-2.5 health effect associations,
and in the biological plausibility of the PM10-2.5-related
health effects. These uncertainties contribute to the determinations in
the 2019 ISA that the evidence for short- and long-term
PM10-2.5 exposure in key health effect categories is
``suggestive of, but not sufficient to infer'' causal relationships
(U.S. EPA, 2019a). Taking this information into consideration, the PA
concludes that, as in previous reviews, such uncertainties raised
questions regarding the degree to which additional public health
protection would be achieved by revising the existing PM10
standard (U.S. EPA, 2022b, section 4.5).
    With regard to the indicator for the primary PM10
standard, the PA notes that the evidence continues to support retaining
the PM10 indicator to provide public health protection
against PM10-2.5-related effects. Consistent with the
approaches in previous reviews, a standard with a PM10 mass-
based

indicator, in conjunction with a PM2.5 mass-based standard,
will result in controlling allowable concentrations of
PM10-2.5. Given that the use of the PM10
indicator does include consideration of both PM2.5 and
PM10-2.5 concentrations, the 2019 ISA provides a comparison
of the relative contribution of PM2.5 and
PM10-2.5 to PM10 concentrations, finding that the
relative contribution of PM2.5 and PM10-2.5 to
PM10 concentrations can vary across the U.S. by region and
season, with urban locations having a somewhat higher contribution of
PM2.5 contributing to PM10 concentrations than
PM10-2.5 (U.S. EPA, 2019a, section <IP_ADDRESS>.4, Table 2-7). In
these urban locations, where PM2.5 concentrations are
somewhat higher than in rural locations, the toxicity of the
PM10 may be higher due to contaminating PM2.5.
Further, although uncertainties with the evidence persist, the
strongest health effects evidence associated with PM10-2.5
comes from epidemiologic studies conducted in urban areas. In light of
this and consistent with the approaches in previous reviews, the PA
concludes that a PM10 standard, set at a single unvarying
level, will generally result in lower allowable concentrations of
PM10-2.5 in urban areas than in nonurban areas. In this way,
the PM10 indicator will target protection by allowing less
PM10-2.5 in areas that experience high concentrations of
potentially contaminating PM2.5. Thus, the evidence
continues to support retaining the PM10 indicator.
    When the above information is taken together, the PA concludes that
available evidence does not call into question the adequacy of the
public health protection provided by the current primary
PM10 standard in order to protect against
PM10-2.5 exposures. Specifically, the PA notes that while
the evidence supports maintaining a PM10 standard to provide
some measure of protection against PM10-2.5 exposures,
uncertainties in the evidence lead to questions regarding the potential
public health implications of revising the existing PM10
standard. Thus, the PA concludes that the evidence does not call into
question the adequacy of the public health protection afforded by the
current primary PM10 standard (U.S. EPA, 2022b, section
4.5).
3. Administrator's Proposed Decision on the Current Primary
PM10 Standard
    This section summarizes the Administrator's considerations and
proposed conclusions related to the current primary PM10
standard and presents his proposed decision to retain that standard,
without revision. In establishing primary standards under the Act that
are ``requisite'' to protect the public health with an adequate margin
of safety, the Administrator is seeking to establish standards that are
neither more nor less stringent than necessary for this purpose. He
recognizes that the Act does not require that primary standards be set
at a zero-risk level; rather, the NAAQS must be sufficiently
protective, but not more stringent than necessary.
    Given these requirements, and consistent with the primary
PM2.5 standards discussed above (section II.C.3), the
Administrator's final decision in this reconsideration of the current
primary PM10 standard will be a public health policy
judgment that draws upon the scientific information examining the
health effects of PM10-2.5 exposures, including how to
consider the range and magnitude of uncertainties inherent in that
information. The Administrator recognizes that his final decision will
be based on an interpretation of the scientific evidence that neither
overstates nor understates its strengths and limitations, nor the
appropriate inferences to be drawn.
    Consistent with previous reviews, the Administrator first considers
the available scientific evidence for PM10-2.5-related
exposures and health effects, as evaluated in the 2019 ISA. As an
initial matter, the Administrator recognizes that the scientific
evidence for PM10-2.5-related effects available in this
reconsideration is the same body of evidence that was available at the
time of the 2020 review, as evaluated in the 2019 ISA and summarized in
section III.B above. The 2019 ISA concludes that the evidence supports
``suggestive of, but not sufficient to infer'' causal relationships
between short- and long-term exposures to PM10-2.5 and
cardiovascular effects, cancer, and mortality and long-term
PM10-2.5 exposures and metabolic effects and nervous system
effects (U.S. EPA, 2019a). The Administrator notes that the evidence
for several PM10-2.5-related health effects has expanded
since the completion of the 2009 ISA, but important uncertainties
remain. Epidemiologic studies evaluated in the 2019 ISA continue to
report positive associations between short-term exposure to
PM10-2.5 and mortality and morbidity in cities across North
America, Europe, and Asia, where PM10-2.5 sources and
composition are expected to vary widely, but across studies
inconsistency remains in the approaches used to estimate
PM10-2.5 exposures. While the Administrator recognizes that
important uncertainties remain, he also recognizes that the expansion
in the number of studies evaluating PM10-2.5 exposures and
health effects since the completion of the 2009 ISA has broadened the
range of effects that may be linked with PM10-2.5 exposures.
The uncertainties in the epidemiologic studies contribute to the
determinations in the 2019 ISA that the evidence for short and long-
term PM10-2.5 exposures and mortality, cardiovascular
effects, metabolic effects, nervous system effects, and cancer is
``suggestive of, but not sufficient to infer'' causal relationships
(U.S. EPA, 2019a; U.S. EPA, 2022b, section 4.3.1). Although most of
these studies examined PM10-2.5 health effect associations
in urban areas, some studies have also linked mortality and morbidity
with relatively high ambient concentrations of particles of non-urban
crustal origin from dust storm events (U.S. EPA, 2019a).
    In considering the available evidence, the Administrator recognizes
that the evidence continues to provide support for maintaining a
standard that provides some measure of protection against exposures to
PM10-2.5, regardless of location, source of origin, or
particle composition, consistent with previous reviews (78 FR 3176,
January 15, 2013; 85 FR 82726, December 18, 2020). Drawing from the
evidence evaluated in the 2019 ISA and consideration of the scientific
evidence in the PA, the Administrator notes that, consistent with
previous reviews, the 2019 ISA and the PA highlight a number of
uncertainties associated with the evidence, including those related to
PM10-2.5 exposure estimates used in epidemiologic studies,
in the independence of PM10-2.5 health effect associations,
and in the biological plausibility of the PM10-2.5-related
effects. These uncertainties contribute to the determinations in the
2019 ISA that the evidence for short-term PM10-2.5 exposures
and key health effects is ``suggestive of, but not sufficient to
infer'' causal relationships. In considering the available scientific
evidence, consistent with approaches employed in past NAAQS reviews,
the Administrator places the most weight on evidence supporting
``causal'' and ``likely to be causal'' relationships. In so doing, he
notes that the available evidence for short-term PM10-2.5
exposures and health effects does not support causality determinations
of a ``causal relationship'' or ``likely to be causal relationship.''
Furthermore, the Administrator recognizes that, because of the
uncertainties and limitations in the evidence base, the PA does not
include a quantitative assessment of

PM10-2.5 exposures and risk that might further inform
decisions regarding the adequacy of the current 24-hour primary
PM10 standard. Therefore, in light of the 2019 ISA
conclusions that the evidence supports ``suggestive of, but not
sufficient to infer'' causal relationships, specifically for
cardiovascular effects, respiratory effects, cancer, and mortality and
short-term exposures to PM10-2.5, and the lack of available
quantitative assessments, the Administrator judges that there are
substantial uncertainties that raise questions regarding the degree to
which additional public health improvements would be achieved by
revising the existing PM10 standard. Furthermore, the
Administrator recognizes that the 2019 ISA also concludes that the
evidence supports ``suggestive of, but not sufficient to infer'' causal
relationships for long-term PM10-2.5-exposures and
cardiovascular effects, metabolic effects, nervous system effects,
cancer, and mortality. However, in considering the available evidence
for long-term PM10-2.5 exposures, he notes that there is
limited evidence that would support consideration of an annual standard
to provide protection against such effects, in conjunction with the
current primary 24-hour PM10 standard. He preliminarily
concludes that the current primary 24-hour PM2.5 standard
that reduces 24-hour exposures also likely reduces long-term average
exposures, and therefore provides some margin of safety against the
health effects associated with long-term PM10-2.5 exposures.
    In reaching proposed conclusions on adequacy of the current primary
24-hour PM10 standard, the Administrator also considers
advice from the CASAC. As noted above, the CASAC recognizes
uncertainties associated with the scientific evidence, including
``compared to PM2.5 studies, the more limited number of
epidemiology studies with positive statistically significant findings,
and the difficulty in extracting the sole contribution of coarse PM to
observed adverse health effects'' (Sheppard, 2022a, p. 19 of consensus
responses). Given these uncertainties, the CASAC agrees with the PA
conclusion that the scientific evidence does not call into question the
adequacy of the primary PM10 standard and supports
consideration of retaining the current standard, noting that ``[t]he
CASAC supports this decision'' (Sheppard, 2022a, p. 4 of consensus
letter). Additionally, the CASAC concurred that ``. . . at this time,
PM10 is an appropriate choice as the indicator for
PM10-2.5'' and ``that it is important to retain the level of
protection afford by the current PM10 standard'' (Sheppard,
2022a, p. 4 of consensus letter).
    When the above information is taken together, the Administrator
proposes to conclude that the available scientific evidence continues
to support a PM10 standard to provide some measure of
protection against PM10-2.5 exposures. This proposed
conclusion reflects the available evidence for PM10-2.5-
related health effects, for both short and long-term exposure, as
evaluated in the 2019 ISA. However, he also recognizes that important
limitations in the evidence remain. Consistent with the decisions in
previous reviews, the Administrator proposes to conclude that these
limitations lead to considerable uncertainty regarding the potential
public health implications of revising the level of the current primary
24-hour PM10 standard. Thus, based on his consideration of
the evidence and associated uncertainties and limitations for
PM10-2.5-related health effects, as described above, and his
consideration of CASAC advice on the primary PM10 standard,
the Administrator proposes to retain the current standard, without
revision. The Administrator solicits comments on this proposed
decision.
    Having reached the proposed decision described here based on the
interpretation of the PM10-2.5-related health effects
evidence, as evaluated in the 2019 ISA; the evaluation of policy-
relevant aspects of the evidence in the PA; the advice and
recommendations from the CASAC; public comments received to date in
their reconsideration; and the public health policy judgments described
above, the Administrator recognizes that other interpretations,
assessments and judgments might be possible. Therefore, the
Administrator solicits comment on the array of issues associated with
reconsideration of the primary 24-hour PM10 standard,
including public health and science policy judgments inherent in his
proposed decision, as described above, and the rationales upon which
such views are based.

IV. Communication of Public Health

A. Air Quality Index Overview

    Information on the public health implications of ambient
concentrations of criteria pollutants is made available primarily by
Air Quality Index (AQI) reporting through the EPA's AirNow
website.\107\ The current AQI has been in use since its inception in
1999.\108\ It provides useful, timely, and easily understandable
information about the daily degree of pollution. The goal of the AQI is
to establish a nationally uniform system of indexing pollution
concentrations for ozone, carbon monoxide, nitrogen dioxide, PM, and
sulfur dioxide. The AQI is recognized internationally as a proven tool
to effectively communicate air quality information to the public. In
fact, many countries have created similar indices based on the AQI.
---------------------------------------------------------------------------

    \107\ See http://www.airnow.gov/.
    \108\ In 1976, the EPA established a nationally uniform air
quality index, then called the Pollutant Standard Index (PSI), for
use by State and local agencies on a voluntary basis (41 FR 37660,
September 7, 1976; 52 FR 24634, July 1, 1987). In August 1999, the
EPA adopted revisions to this air quality index (64 FR 42530, August
4, 1999) and renamed the index the AQI.
---------------------------------------------------------------------------

    The AQI converts an individual pollutant concentration in a
community's air to a number on a scale from 0 to 500. Reported AQI
values for specific pollutants enable the public to know whether air
pollution levels in a particular location are characterized as good (0-
50), moderate (51-100), unhealthy for sensitive groups (101-150),
unhealthy (151-200), very unhealthy (201-300), or hazardous (301+).
Across criteria pollutants, the AQI index value of 100 typically
corresponds to the level of the short-term (e.g., 24-hour, 8-hour, or
1-hour standard) NAAQS for each pollutant. Below an index value of 100,
an intermediate value of 50 is defined either as the level of the
annual standard if an annual standard has been established (e.g.,
PM2.5, nitrogen dioxide), a concentration equal to one-half
the value of the 24-hour standard used to define an index value of 100
(e.g., carbon monoxide), or a concentration based directly on health
effects evidence (e.g., ozone). An AQI value greater than 100 means
that a pollutant is in one of the unhealthy categories (i.e., unhealthy
for sensitive groups, unhealthy, very unhealthy, or hazardous). An AQI
value at or below 100 means that a pollutant concentration is in one of
the satisfactory categories (i.e., moderate or good). The scientific
evidence on pollutant-related health effects for each NAAQS review
evaluated in the ISA\109\ support decisions related to pollutant
concentrations at which to set the various AQI breakpoints, which
delineate the AQI categories for each individual pollutant (i.e., the
pollutant concentrations corresponding to index values of 150, 200,
300, and 500). The AQI is reported three ways, all of which

are useful and complementary. The daily AQI is reported for the
previous day and used to observe trends in community air quality, the
AQI forecast helps people plan their outdoor activities for the next
day, and the near-real-time AQI, or NowCast AQI, tells people whether
it is a good time for outdoor activity.
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    \109\ In some NAAQS reviews, there may also be an ISA Supplement
or a Provisional Assessment of scientific evidence that becomes
available during a review after an ISA is finalized. To the extent
that such evidence can inform decisions on the AQI, that information
is also considered.
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    Historically, State and local agencies have primarily used the AQI
to provide general information to the public about air quality and its
relationship to public health. For more than two decades, many states
and local agencies, as well as the EPA and other Federal agencies, have
been developing new and innovative programs and initiatives to provide
more information related to air quality and health messaging to the
public in a more timely way. These initiatives, including air quality
forecasting, near real-time data reporting through the AirNow website,
use of data from air quality sensors on the Fire and Smoke Map, and air
quality action day programs, provide useful, up-to-date, and timely
information to the public about air pollution and its health effects.
Such information can help the public learn when their well-being may be
compromised, so they can take actions to avoid or to reduce exposures
to ambient pollution at concentrations of concern. This information can
also encourage the public to take actions that will reduce air
pollution on days when concentrations are projected to be of concern to
local communities (e.g., air quality action day programs can encourage
individuals to drive less or carpool). The EPA and state, local and
Tribal agencies recognize that these programs are interrelated with AQI
reporting and with the information related to the effects of air
pollution on public health that is evaluated through the periodic
review, and revision when appropriate, of the NAAQS.

B. Air Quality Index Category Breakpoints for PM2.5

    One purpose of the AQI is to communicate to the public when air
quality is poor and thus when they should consider taking actions to
reduce their exposures. The higher the AQI value, the higher the level
of air pollution and the greater the health concern. In recognition of
the scientific information available that is informing the
reconsideration of the 2020 final decision on the primary
PM2.5 standards, including a number of new controlled human
exposure and epidemiologic studies published since the completion of
the 2009 ISA, as well as additional epidemiologic studies from other
peer reviewed documents that evaluate the health effects of wildfire
smoke exposure and that can inform the AQI at higher PM2.5
concentrations, the EPA proposes to make two sets of changes to the
PM2.5 sub-index of the AQI. First, the EPA proposes to
continue to use the approach used in the revisions to the AQI in 2012
(77 FR 38890, June 29, 2012) of setting the lower breakpoints (50, 100
and 150) to be consistent with the levels of the primary
PM2.5 annual and 24-hour standards and proposes to revise
the lower breakpoints to be consistent with any changes to the primary
PM2.5 standards that are part of this reconsideration.
Second, the EPA proposes to revise the upper AQI breakpoints (200 and
above) and to replace the linear-relationship approach used in 1999 to
set these breakpoints, with an approach that more fully considers the
PM2.5 health effects evidence from controlled human exposure
and epidemiologic studies that have become available in the last 20
years. Thus, the EPA considers it appropriate to consider scientific
evidence for these purposes beyond the scope of the ISA. More details
on these proposed revisions to the AQI are provided below.
    Although revisions of the air quality criteria and NAAQS for PM
generally prompt changes to the AQI, the AQI is not part of the NAAQS.
The AQI is aimed at communicating risks of ambient concentrations which
may far exceed the level of the NAAQS. While the AQI was not originally
developed to be used as a regulatory tool or for other purposes and EPA
does not provide guidance on the use of the AQI for such purposes, the
EPA acknowledges that some organizations and entities have identified
other uses for the AQI.\110\ As such, the EPA is requesting information
about how other organizations and entities are applying the AQI. The
EPA's goal is to update the PM2.5 AQI in conjunction with
the Agency's final decisions on the primary annual and 24-hour
PM2.5 standards, if proposed revisions to such standards are
promulgated.
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    \110\ For example, the Occupational Safety and Health divisions
in California, Oregon, and Washington have linked outdoor worker
regulations to the upper AQI breakpoints.
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1. Air Quality Index Values of 50, 100 and 150
    With respect to the lower AQI breakpoints, the EPA concludes that
it is still appropriate to continue to set these breakpoints to be
consistent with the primary annual and 24-hour PM2.5
standard levels. The lowest AQI value of 50 provides the breakpoint
between the ``good'' and ``moderate'' categories. At and below this
concentration, air quality is considered ``good'' for everyone. Above
this concentration, in the ``moderate'' category, the AQI contains
advisories for unusually sensitive individuals. The EPA has
historically set this breakpoint at the level of the primary annual
PM2.5 standard. In doing so, the EPA has recognized that:
(1) the annual standard is set to provide protection to the public,
including at-risk populations, from PM2.5 concentrations
which, when experienced on average for a year, have the potential to
result in adverse health effects; and that (2) the AQI exposure period
represents a shorter exposure period (e.g., 24-hour (or less)) while
focusing on the most sensitive individuals. The EPA sees no basis for
deviating from this approach in this reconsideration. Thus, the EPA
proposes to set the AQI value of 50 at a daily (i.e., 24-hour) average
concentration equal to the level of the primary annual PM2.5
standard that is promulgated. In this document, the EPA is proposing to
revise the primary annual PM2.5 standard level to 9 to 10
[mu]g/m\3\ and soliciting comments on levels down to 8 [mu]g/m\3\ and
up to 11 [mu]g/m\3\ (section II.D.3.a).
    The historical approach to setting an AQI value of 100, which is
the breakpoint between the ``moderate'' and ``unhealthy for sensitive
groups'' categories, and above which advisories are generated for
sensitive groups, is to set it at the same level as the primary 24-hour
PM2.5 standard. In so doing, the EPA has recognized that the
primary 24-hour PM2.5 standard is set to provide protection
to the public, including at-risk populations, from short-term exposures
to PM2.5 concentrations which have the potential to result
in adverse health effects. Given this, it is appropriate to generate
advisories for sensitive groups at concentrations above this level. In
the past, state, local, and Tribal air quality agencies have expressed
strong support for this approach (78 FR 3086, January 15, 2013). The
EPA sees no basis to deviate from this approach in this
reconsideration. In this proposal, the EPA is proposing to retain the
current primary 24-hour PM2.5 standard with its level of 35
[mu]g/m\3\ but is taking comment on revising the level of that standard
to 25 [mu]g/m\3\ (section II.D.3.b). Thus, the EPA proposes to retain
the AQI value of 100 set at the level of the current primary 24-hour
PM2.5 standard concentration of 35 [mu]g/m\3\ (i.e., 24-hour
average), but if the level of the 24-hour

standard is revised to a different concentration, the EPA is proposing
to set the final AQI value of 100 equal to any revised level of the
primary 24-hour PM2.5 standard.
    With respect to an AQI value of 150, which is the breakpoint
between the ``unhealthy for sensitive groups'' and ``unhealthy
categories,'' this breakpoint concentration in this reconsideration is
based upon the considering the same health effects information, as
assessed in the 2019 ISA and ISA Supplement and described in section II
above, that informs the proposed decisions on the level of the 24-hour
standard and the AQI value of 100. Previously, the Agency has used a
proportional adjustment in which the AQI value of 150 was set
proportionally to the AQI value of 100. This proportional adjustment
inherently recognizes that the available epidemiologic studies provide
no evidence of discernible thresholds, below which effects do not occur
in either sensitive groups or in the general population, that could
inform conclusions regarding concentrations at which to set this
breakpoint. Given that the epidemiologic evidence continues to be the
most relevant health effects evidence for informing this range of AQI
values, the EPA sees no basis to deviate from this approach in this
reconsideration. Therefore, the EPA proposes to set an AQI value of 150
proportionally, depending on the breakpoint concentration of the AQI
value of 100. This means that if the EPA retains the current primary
24-hour PM2.5 standard of 35 [mu]g/m\3\, we propose to also
retain the current AQI value of 150 at a daily (i.e., 24-hour average)
concentration of 55 [mu]g/m\3\. If, however, the EPA revises the level
of the primary 24-hour PM2.5 standard, we propose to adjust
the AQI value of 150 proportional to that revision (e.g., a 24-hour
standard of 30 [mu]g/m\3\ might result in an AQI value for 150 of 45
[mu]g/m\3\).
2. Air Quality Index Values of 200 and Above
    In 1999, the EPA established AQI breakpoints for the AQI values of
200 and above (64 FR 42530, August 4, 1999). For this approach the AQI
values between 100 and 500 were based on PM2.5
concentrations that generally reflected a linear relationship between
increasing index values and increasing PM2.5
concentrations.\111\ It was found that this linear relationship was
generally consistent with the health effect evidence, which suggested
that as PM2.5 concentrations increase, increasingly larger
numbers of people are likely to experience serious health effects in
this range of PM2.5 concentrations (64 FR 42536, August 4,
1999). For the AQI breakpoint of 500, the concentration was based on
the method used to establish a previously existing PM10
breakpoint that was informed by studies conducted in London using the
British Smoke method, which uses a different particle size
cutpoint.\112\ Due to limited ambient PM2.5 monitoring data
available at that time, the decision on the 500 breakpoint
concentration for PM2.5 was based on the stated assumption
that PM concentrations measured by the British Smoke method were
approximately equivalent to PM2.5 concentrations (64 FR
42530, August 4, 1999). However, the assumption of approximate
equivalence between the British Smoke method and the current
PM2.5 monitoring method is not consistent with the view
cited in the 1987 Federal Register document about the PM10
AQI value of 500, in which the British Smoke method was noted to have a
particle size cutpoint of 4.5 microns (52 FR 24688, July 1, 1987).
Given that the British Smoke method has a larger particle size cutpoint
than the current PM2.5 monitoring method which has a
cutpoint of 2.5 microns, a concentration of 500 [mu]g/m\3\ based on the
British Smoke method would be equivalent to a lower PM2.5
concentration.
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    \111\ The AQI breakpoint at 150 was originally set in 1999 to be
linearly related to the concentrations at the 100 and 500
breakpoints but then revised in 2012 to be proportional to the AQI
breakpoint concentration at 100 (78 FR 3181, January 15, 2013).
    \112\ The current AQI value of 500 for PM10 was set
in 1987 at the concentration of 600 [mu]g/m\3\ based on a 24-hour
average, on the basis of increased mortality associated with
historical wintertime pollution episodes in London (52 FR 24687 to
24688, July 1, 1987). Particle concentrations during these episodes,
measured by the British Smoke method, were in the range of 500 to
1000 [mu]g/m\3\. In the 1987 rulemaking that established the upper
bound index value for PM10, the EPA cited a generally
held opinion that the British Smoke method measures PM with a
cutpoint of approximately 4.5 microns (52 FR 24688, July 1, 1987).
In establishing this value for PM10, the EPA assumed that
concentrations of PM10, which includes both coarse
(PM10-2.5) and fine particles (PM2.5), during
episodes of concern, would be about 100 [mu]g/m\3\ higher than the
PM concentration measured in terms of British Smoke (52 FR 24688,
July 1, 1987). The PM10 upper bound index value of 600
[mu]g/m\3\ was developed by selecting the lower end of the range of
concentrations during the historical wintertime pollution episodes
in London (500 [mu]g/m\3\) and adding a margin of 100 [mu]g/m\3\ to
account for this measurement difference.
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    As part of this reconsideration, the EPA recognizes that the health
effects evidence associated with PM2.5 exposure has greatly
expanded in recent years. While many of the new studies evaluated in
the 2019 ISA focused on examining health effects associated with
exposure to lower PM2.5 concentrations, there are also
several new studies, specifically controlled human exposure studies,
that can provide information about health effects at concentrations
well above the standard levels. Additionally, there are also studies
now available and evaluated in other Agency documents that can inform
health effects at higher PM2.5 concentrations. Thus, the EPA
concludes that it is appropriate to reevaluate the upper AQI
breakpoints, taking into account the expanded body of scientific
evidence. In particular, because these breakpoints were established in
1999 (64 FR 42530, August 4, 1999), several new epidemiologic studies
have become available that provide information about exposures during
high pollution events, such as wildfires. Additionally, multiple
controlled human exposure studies have become available that provide
information about health effects across a range of concentrations.
While it remains unclear the exact PM2.5 concentrations at
which specific health effects occur, the more recent studies do provide
more refined information about the concentration range in which these
effects might occur. For example, while human exposure studies
generally report only subclinical effects, the consistent observation
of these effects in multiple studies can provide an indication of
subclinical effects that are on the pathway to more serious health
effects as PM2.5 concentrations increase above 55 [micro]g/
m\3\. These studies provide support for coherence of effects across
scientific disciplines and potentially biologically plausible pathways
for the overt population-level health effects observed in epidemiologic
studies. Therefore, taking into account the short exposure time period
in these studies (e.g., 1-6 hours) and that the studies generally do
not include at-risk (or sensitive) populations, but rather young,
healthy adults, these studies, in conjunction with information from
epidemiologic studies, the EPA preliminarily concludes it would be
appropriate to be more cautionary and offer advisories to the public
for reducing exposures at lower concentrations than recommended with
the current AQI breakpoints. Thus, the discussion below focuses on the
EPA's proposed revisions to the AQI breakpoints of 200 and above and
the EPA's interpretation of the available health effects evidence that
supports those proposed revisions.
    The AQI value of 200 is the breakpoint between the ``unhealthy''
and ``very unhealthy'' categories. At AQI values above 200, the AQI
would be providing a health warning that the risk of anyone
experiencing a health

effect following short-term exposures to these PM2.5
concentrations has increased. To inform proposed decisions on this
breakpoint, the EPA takes note of studies indicating the potential for
respiratory or cardiovascular effects that are associated with more
serious health outcomes (e.g., emergency department visits, hospital
admissions). The controlled human exposure studies evaluated in the
2009 and 2019 ISAs provide evidence of inflammation as well as
cardiovascular effects in healthy subjects at and above 120 [micro]g/
m\3\. For example, Ramanathan et al. (2016) observed a transient
reduction in antioxidant/anti-inflammatory function after exposing
healthy young subjects to a mean concentration of 150 [micro]g/m\3\ of
PM2.5 for 2 hours. Urch et al. (2010) also reported
increased markers of inflammation when exposing both asthmatic and non-
asthmatic subjects to a mean concentration of 140 [micro]g/m\3\ of
PM2.5 for 3 hours. In studies specifically examining
cardiovascular effects, Ghio et al. (2000) and Ghio et al. (2003)
exposed healthy subjects to a mean concentration of 120 [micro]g/m\3\
for 2 hours and reported significantly increased levels of fibrinogen,
a marker of coagulation that increases during inflammation.
Sivagangabalan et al. (2011) exposed healthy subjects to a mean
concentration of 150 [micro]g/m\3\ of PM2.5 for 2 hours and
noted an increased QT interval (3.4  1.4) indicating some
evidence for conduction abnormalities, an indicator of possible
arrhythmias. Lastly, Brook et al. (2009) reported a transient increase
of 2.9 mm Hg in diastolic blood pressure in healthy subjects during the
2-hour exposure to a mean concentration of 148 [micro]g/m\3\ of
PM2.5.
    In addition to epidemiologic studies evaluated in the 2019 ISA that
analyzed exposures at ambient PM2.5 concentrations, there
are a number of recent epidemiologic studies focusing on wildfire smoke
that have become available that were evaluated in the EPA's recently
released peer-reviewed assessment on wildland fire (U.S. EPA, 2021b).
One of these studies, Hutchinson et al. (2018), conducted a
bidirectional case-crossover analysis to examine associations between
wildfire-specific PM2.5 exposure and respiratory-related
healthcare encounters (i.e., ED visits, inpatient hospital admissions,
and outpatient visits) prior and during the 2007 San Diego wildfires.
This study found positive and significant associations to
PM2.5 exposures and respiratory-related healthcare
encounters. Further, during the initial 5-day period of the wildfire
event, the study observed that there was evidence of increases in a
number of respiratory-related outcomes particularly ED visits for
asthma, upper respiratory infection, respiratory symptoms, acute
bronchitis, and all respiratory-related visits (Hutchinson et al.,
2018), giving the EPA increased confidence in the association between
exposure to PM2.5 and respiratory-related outcomes at
concentrations experienced during this time period. When examining the
air quality during the wildfire event, PM2.5 concentrations
were highest during the initial five days of the wildfire, with 24-hour
average PM2.5 concentrations of 89.1 [micro]g/m\3\ across
all zip codes and with the highest 24-hour average of 160 [micro]g/m\3\
on the first day (Hutchinson et al., 2018).
    When considering this collective body of evidence from controlled
human exposure and epidemiologic studies, the Agency proposes to set an
AQI value of 200 at a daily (i.e., 24-hour average) concentration of
PM2.5 of 125 [mu]g/m\3\. This concentration is at the lower
end of the concentrations consistently shown to be associated with
effects in controlled human exposure studies following short-term
exposures (e.g., 2-3 hours) and in young, healthy adults (Ghio et al.,
2000; Ghio et al., 2003; Urch et al., 2010; Ramanathan et al., 2016;
Sivagangabalan et al., 2011; and Brook et al., 2009) and also within
the range of 5-day average and maximum concentrations observed to be
associated with respiratory-related outcomes following exposure to
wildfire smoke (Hutchinson et al., 2018).
    The AQI value of 300 denotes the breakpoint between the ``very
unhealthy'' and ``hazardous'' categories, and thus marks the beginning
of the ``hazardous'' AQI category. At AQI values above 300, the AQI
provides a health warning that everyone is likely to experience effects
following short-term exposures to these PM2.5
concentrations. To inform decisions on this AQI breakpoint, the EPA
takes note of controlled human exposure studies that consistently show
subclinical effects which are often associated with more severe
cardiovascular outcomes. As discussed above, Brook et al. (2009)
reported a transient increase of 2.9 mm Hg in diastolic blood pressure
in healthy subjects during the 2-hour exposure to a mean concentration
of 148 [micro]g/m\3\ of PM2.5. Bellavia et al. (2013)
exposed healthy subjects to an average PM2.5 concentration
of 242 [micro]g/m\3\ for 2 hours and reported increased systolic blood
pressure (2.53 mm Hg). Tong et al. (2015) exposed healthy subjects to
an average PM2.5 concentration of 253 [micro]g/m\3\ for 2
hours and observed a significant increase in diastolic blood pressure
(2.1 mm Hg) and a nonsignificant increase in systolic blood pressure
(2.5 mm Hg). Lucking et al. (2011) reported impaired vascular function
and increased potential for coagulation when exposing healthy subjects
to diesel exhaust (DE) with an average PM2.5 concentration
of 320 [micro]g/m\3\ for a duration of 1 hour.\113\ These studies all
provided evidence of impaired vascular function, including
vasodilatation impairment and increased thrombus formation, with Tong
et al. (2015), Bellavia et al. (2013), Brook et al. (2009) all
reporting increases in blood pressure. Additionally, Behbod et al.
(2013) reported increased inflammatory markers following a 2-hour
exposure to an average PM2.5 concentration of 250 [micro]g/
m\3\ in healthy subjects.
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    \113\ Although participants in Lucking et al. (2011) were
exposed to DE, the authors also conducted analyses using a particle
trap, and as noted in the 2019 ISA, this type of study design allows
for the assessment of the role of PM2.5 on the health
effects observed by removing PM from the DE mixture.
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    In addition to the controlled human exposure studies discussed
above, the epidemiologic study conducted by DeFlorio-Barker et al.
(2019) examined the relationship between wildfire smoke and
cardiopulmonary hospitalizations among adults 65 years of age and older
from 2008-2010 in 692 U.S. counties. The authors reported a 2.22%
increase in all-cause respiratory hospitalizations on wildfire smoke
days for a 10 [micro]g/m\3\ increase in 24-hour average
PM2.5 concentrations (DeFlorio-Barker et al., 2019). The
maximum 24-hour average concentration in this study on wildfire smoke
days was 212.5 [micro]g/m\3\ (DeFlorio-Barker et al., 2019). In
considering this study, the EPA notes the increased probability that
even healthy adults experience effects at this maximum exposure
concentration, particularly given that this maximum concentration is
near the exposure concentrations in controlled human exposure studies
that consistently reported evidence of impaired vascular function and
several that reported increases in blood pressure in healthy adults
following 2-hour exposures.
    Based on the information above, the EPA proposes to revise the 300
level of the AQI, which marks the beginning of the ``hazardous'' AQI
category, to a concentration that is consistent with the
PM2.5 concentrations associated with health effects as
reported in the controlled human exposure and epidemiologic studies
discussed above. Specifically, the Agency proposes to set an AQI value
of 300 at a daily (i.e., 24-hour average) PM2.5
concentration of

225 [mu]g/m\3\. This concentration falls between the 2-hour average
concentrations reported in controlled human exposure studies found to
be consistently associated, in healthy adults, with impaired vascular
function and/or increases in blood pressure, which can both be a
precursor to more severe cardiovascular effects following short-term
(1- to 2-hour) exposures, and the maximum 24-hour average
PM2.5 concentrations on wildfire smoke days reported in the