establishing standards to protect against adverse health effects
related to long-term NO2 exposures, the evidence supports
the consideration of both 1-hour and annual averaging times. In its
review of the draft PA, CASAC supported this approach to considering
the protection provided against long-term NO2 exposures by
considering the combination of the annual and 1-hour NO2
standards. With reference to the current annual standard, CASAC
specifically noted that ``it is the suite of the current 1-hour and
annual standards, together, that provide protection against adverse
effects'' (Diez Roux and Sheppard, 2017, p. 9).
c. Level and Form
    In evaluating the extent to which evidence supports or calls into
question the levels or forms of the current NO2 standards,
the EPA considers the following question: To what extent does the
evidence indicate adverse respiratory effects attributable to short- or
long-term NO2 exposures lower than previously identified or
below the existing standards? In addressing this question, it is useful
to consider the range of NO2 exposure concentrations that
have been evaluated in experimental studies (controlled human exposure
and animal toxicology) and the ambient NO2 concentrations in
locations where epidemiologic studies have reported associations with
adverse outcomes. The PA's consideration of these issues is discussed
below for short-term (II.F.1.c.i) and long-term (II.F.1.c.ii)
NO2 exposures.
i. Short-Term
    Controlled human exposure studies demonstrate the potential for
increased AR in some people with asthma following 30-minute to 1-hour
exposures to NO2 concentrations near those in the ambient
air (U.S. EPA, 2017a, Section 3.2.2).\97\ In evaluating the
NO2 exposure concentrations at which increased AR has been
observed, both the group mean results reported in individual studies
and the results from a recent meta-analysis evaluating individual-level
data are considered (Brown, 2015; U.S. EPA, 2016a, Section <IP_ADDRESS>).
Group mean responses in individual studies, and the variability in
those responses, can provide insight into the extent to which observed
changes in AR are due to NO2 exposures, rather than to
chance alone, and have the advantage of being based on the same
exposure conditions. The meta-analysis can aid in identifying trends in
individual-level responses across studies and can have the advantage of
increased power to detect effects, even in the absence of statistically
significant effects in individual studies.
---------------------------------------------------------------------------

    \97\ As discussed in Section II.C, experimental studies have not
reported other respiratory effects following short-term exposures to
NO2 concentrations at or near those found in the ambient
air.
---------------------------------------------------------------------------

    When individual-level data were combined in a meta-analysis, Brown
(2015) reported that statistically significant majorities of study
participants experienced increased AR following resting exposures to
NO2 concentrations from 100 to 530 ppb. In some affected
individuals, the magnitudes of these increases were large enough to
have potential clinical relevance. Following exposures to 100 ppb
NO2 specifically, the lowest exposure concentration
evaluated, a marginally statistically significant majority of study
participants experienced increased AR.\98\ As discussed in more detail
in Section II.C.1, individual studies consistently report statistically
significant NO2-induced increases in AR following resting
exposures to NO2 concentrations at or above 250 ppb, but
have generally not reported statistically significant increases in AR
following resting exposures to NO2 concentrations from 100
to 200 ppb. Limitations in this evidence include the lack of an
apparent dose-response relationship between NO2 and AR and
remaining uncertainty in the adversity of the reported increases in AR.
These uncertainties become increasingly important at the lower
NO2

exposure concentrations (i.e., at or near 100 ppb), as the evidence for
NO2-induced increases in AR becomes less consistent across
studies at these lower concentrations.
---------------------------------------------------------------------------

    \98\ Brown (2015) reported a p-value of 0.08 when data were
combined from studies of specific and non-specific AR. When the
analysis was restricted only to non-specific AR following exposures
to 100 ppb NO2, the percentage who experienced increased
AR was larger and statistically significant. In contrast, when the
analysis was restricted only to specific AR following exposures to
100 ppb NO2, the majority of study participants did not
experience increased AR (U.S. EPA, 2016a; Brown 2015).
---------------------------------------------------------------------------

    The epidemiologic evidence from U.S. and Canadian studies, as
considered in the PA, provides information about the ambient
NO2 concentrations in locations where such studies have
examined associations with asthma-related hospital admissions or
emergency department visits (short-term) or with asthma incidence
(long-term). In particular, these studies inform consideration of the
extent to which NO2-health effect associations are
consistent, precise, statistically significant, and present for
distributions of ambient NO2 concentrations that likely
would have met the current standards. To the extent NO2-
health effect associations are reported in study areas that would
likely have met the current standards, the evidence would support the
potential for the current standards to allow the NO2-
associated effects indicated by those studies. In the absence of
studies reporting associations in locations meeting the current
NO2 standards, there would be greater uncertainty regarding
the potential for reported effects to be caused by NO2
exposures that occur with air quality meeting those standards. There
are also important uncertainties in the evidence which warrant
consideration, including the potential for copollutant confounding and
exposure measurement error, and the extent to which near-road
NO2 concentrations are reflected in the available air
quality data.
    With regard to epidemiologic studies of short-term NO2
exposures conducted in the U.S. or Canada, the PA notes the following.
First, the only recent multicity study evaluated (Stieb et al., 2009),
which had maximum 1-hour DVs ranging from 67 to 242 ppb, did not report
a positive association between NO2 and ED visits. In
addition, of the single-city studies (U.S. EPA, 2017a, Figure 3-1) that
reported positive and relatively precise associations between
NO2 and asthma hospital admissions and ED visits, most
locations had NO2 concentrations likely to have violated the
current 1-hour NO2 standard over at least part of the study
period. Specifically, most of these locations had maximum estimated DVs
at or above 100 ppb and, had near-road NO2 monitors been in
place during study periods, DVs would likely have been higher. Thus, it
is likely that even the one study location with a maximum DV of 100 ppb
(Atlanta) would have violated the existing 1-hour standard during study
periods.\99\ For the study locations with maximum DVs below 100 ppb,
mixed results have been reported, with associations that are generally
statistically non-significant and imprecise. As with the studies
reporting more precise associations, near-road monitors were not in
place during these study periods. If they had been, 1-hour DVs could
have been above 100 ppb. In drawing conclusions based on this
epidemiologic evidence, the PA also considers the potential for
copollutant confounding as ambient NO2 concentrations are
often highly correlated with other pollutants. This can complicate
attempts to distinguish between independent effects of NO2
and effects of the broader pollutant mixture. While this has been
addressed to some extent in available studies, uncertainty remains for
the most relevant copollutants (i.e., those related to traffic such as
PM2.5, EC/BC, and CO). Taken together, while available U.S.
and Canadian epidemiologic studies report NO2-associated
hospital admissions and emergency department visits in locations likely
to have violated the current 1-hour NO2 standard, the PA
concludes that these studies do not indicate the occurrence of such
NO2-associated effects in locations and time periods with
NO2 concentrations that would clearly have met the current
1-hour NO2 standard (i.e., with its level of 100 ppb and
98th percentile form).
---------------------------------------------------------------------------

    \99\ Based on recent air quality information for Atlanta, 98th
percentiles of daily maximum 1-hour NO2 concentrations
are higher at near-road monitors than non-near-road monitors (U.S.
EPA, 2017a, Figures 2-9 and 2-10). These differences could have been
even more pronounced during study periods, when NOX
emissions from traffic sources were higher (U.S. EPA, 2017a, Section
2.1.2).
---------------------------------------------------------------------------

    In giving further consideration specifically to the form of 1-hour
standard, the PA notes that the available evidence and information in
this review is consistent with that informing consideration of form in
the last review. The last review focused on the upper percentiles of
the distribution of NO2 concentrations based, in part, on
evidence for health effects associated with short-term NO2
exposures from experimental studies which provided information on
specific exposure concentrations that were linked to respiratory
effects (75 FR 6475, February 9, 2010). In that review, the EPA
specified a 98th percentile form, rather than a 99th percentile, for
the new 1-hour standard. In combination with the 1-hour averaging time
and 100 ppb level, a 98th percentile form was judged to provide
appropriate public health protection. In addition, compared to the 99th
percentile, a 98th percentile form was expected to provide greater
regulatory stability.\100\ In addition, a 98th percentile form is
consistent with the PA's consideration of uncertainties in the health
effects that have the potential to occur at 100 ppb. Specifically, when
combined with the 1-hour averaging time and the level of 100 ppb, the
98th percentile form limits, but does not eliminate, the potential for
exposures to 100 ppb NO2.\101\
---------------------------------------------------------------------------

    \100\ As noted in the last review, a less stable form could
result in more frequent year-to-year shifts between meeting and
violating the standard, potentially disrupting ongoing air quality
planning without achieving public health goals (75 FR 6493, February
9, 2010).
    \101\ The 98th percentile corresponds to about the 7th or 8th
highest daily maximum 1-hour NO2 concentration in a year.
---------------------------------------------------------------------------

ii. Long-Term
    With regard to health effects related to long-term NO2
exposures, the PA first considers the basis for the current annual
standard. It was originally set to protect against NO2-
associated respiratory disease in children reported in some
epidemiologic studies (36 FR 8186, April 30, 1973). In subsequent
reviews, the EPA has retained the annual standard, judging that it
provides protection with an adequate margin of safety against the
effects that have been reported in animal studies following long-term
exposures to NO2 concentrations well-above those found in
the ambient air (e.g., above 8,000 ppb for the development of lesions
similar to those found in humans with emphysema) (60 FR 52879, October
11, 1995). In the 2010 review, the EPA noted that, though some evidence
supported the need to limit long-term exposures to NO2, the
evidence for adverse health effects attributable to long-term
NO2 exposures did not support changing the level of the
annual standard.
    In the current review, the strengthened ``likely to be causal''
relationship between long-term NO2 exposures and respiratory
effects is supported by epidemiologic studies of asthma development and
related effects demonstrated in animal toxicological studies. While
these studies strengthen the evidence for effects of long-term
exposures, compared to the last review, they are subject to important
uncertainties, including the potential for confounding by traffic-
related copollutants. The potential for such confounding is
particularly important to consider when interpreting epidemiologic
studies of long-term NO2 exposures given (1) the relatively
high correlations observed between measured

and modeled long-term ambient concentrations of NO2 and
long-term concentrations of other roadway-associated pollutants; (2)
the general lack of information from copollutant models on the
potential for NO2 associations that are independent of other
traffic-related pollutants or mixtures; and (3) the general lack of
supporting information from experimental studies that evaluate long-
term exposures to NO2 concentrations near those in the
ambient air. Thus, it is unclear the degree to which the observed
effects in these studies are independently related to exposure to
ambient concentrations of NO2. The epidemiologic evidence
from some U.S. and Canadian studies is also subject to uncertainty with
regard to the extent to which the studies accurately characterized
exposures of the study populations, further limiting what these studies
can tell us regarding the adequacy of the current primary
NO2 standards.
    While the PA recognizes the above uncertainties, it considers what
studies of long-term NO2 and asthma development indicate
with regard to the adequacy of the current primary NO2
standards. As discussed above for short-term exposures, the PA
considers the degree to which the evidence indicates adverse
respiratory effects associated with long-term NO2 exposures
in locations that would have met the NAAQS. As summarized in Section
II.C.2, the causal determination for long-term exposures is supported
both by studies of long-term NO2 exposures and studies
indicating a potential role in asthma development for repeated short-
term exposures to high NO2 concentrations.
    As such, when considering the ambient NO2 concentrations
present during study periods, the PA considers these concentrations
within the context of both the 1-hour and annual NO2
standards. Analyses of historical data indicate that 1-hour DVs at or
below 100 ppb generally correspond to annual DVs below 35 ppb.\102\
CASAC noted this relationship, stating that ``attainment of the 1-hour
standard corresponds with annual design value averages of 30 ppb
NO2'' (Diez Roux and Sheppard, 2017). Thus, meeting the 1-
hour standard with its level of 100 ppb would be expected to maintain
annual average NO2 concentrations below the 53 ppb level of
the current annual standard.
---------------------------------------------------------------------------

    \102\ As noted in the PA, near-road monitors were not included
in this analysis due to the limited amount of data available.
---------------------------------------------------------------------------

    As discussed in Section II.C.1, while annual estimated DVs in study
locations were often below 53 ppb, maximum 1-hour estimated DVs in most
locations were near or above 100 ppb. Because these study-specific
estimated DVs are based on the area-wide NO2 monitors in
place during study periods, they do not reflect the NO2
concentrations near the largest roadways, which are expected to be
higher in most urban areas. Had near-road monitors been in place during
study periods, estimated NO2 DVs based on near-road
concentrations likely would have been higher in many locations, and
would have been more likely to exceed the level of the annual and/or 1-
hour standard(s).
    Given the paucity of epidemiologic studies conducted in areas that
were close to or below the current standards, and considering that no
near road monitors were in place during the study periods, the PA
concludes that the epidemiologic evidence does not provide support for
NO2-attributable asthma development in children in locations
with NO2 concentrations that would have clearly met the
current annual and 1-hour NO2 standards. The strongest
epidemiologic evidence informing the level at which effects may occur
comes from U.S. and Canadian epidemiologic studies that are subject to
critical uncertainties related to copollutant confounding and exposure
assessment. Furthermore, the PA's evaluation indicates that most of the
locations included in epidemiologic studies of long-term NO2
exposure and asthma incidence would likely have violated either one or
both of the current NO2 standards, over at least parts of
the study periods.
iii. PA Conclusions
    Taking note of the conclusions in the PA, and based on the
information discussed above, the EPA revisits the question posed above:
To what extent does the evidence indicate adverse respiratory effects
attributable to short- or long-term NO2 exposures lower than
previously identified or below the existing standards?
    In addressing this question, the PA notes that (1) experimental
studies do not indicate adverse respiratory effects attributable to
either short- or long-term NO2 exposures lower than
previously identified and that (2) epidemiologic studies do not provide
support for associations between adverse effects and ambient
NO2 concentrations that would have clearly met the current
standards. Taken together, the PA concludes that the available evidence
does not support the need for increased protection against short- or
long-term NO2 exposures, beyond that provided by the
existing standards. In its review of the draft PA, the CASAC agreed
with this conclusion, stating that ``[t]he CASAC concurs with the EPA
that the current scientific literature does not support a revision to
the primary NAAQS for nitrogen dioxide'' (Diez Roux and Sheppard, 2017,
p. 9). Therefore, the PA did not identify potential alternative
standard levels or forms for consideration.
2. Exposure- and Risk-Based Considerations
    As described in greater detail in Section II.D above, and in the
REA Planning document (U.S. EPA, 2015, Section 2.1.1) and the PA (U.S.
EPA, 2017a, Chapter 4), the EPA conducted updated analyses comparing
ambient NO2 concentrations (i.e., as surrogates of potential
exposures) to health-based benchmarks, with a particular focus on study
areas where near-road monitors have been deployed. In the PA, staff
concluded that updated quantitative risk assessments were not supported
in the current review, based on uncertainties in the available evidence
and the likelihood that such analyses would be subject to the same
uncertainties identified in the risk estimates in the prior review
(U.S. EPA, 2017a, Chapter 4). The CASAC stated that it was ``satisfied
with the short-term exposure health-based benchmark analysis presented
in the draft PA'' and that it ``support[ed] the decision not to conduct
any new or updated quantitative risk analyses related to long-term
exposure to NO2'' (Diez Roux and Sheppard, 2017).
    When considering analyses comparing NO2 air quality with
health-based benchmarks, the PA focuses on the following specific
questions: (1) To what extent are ambient NO2 concentrations
that may be of public health concern estimated to occur in locations
meeting the current NO2 standards? (2) What are the
important uncertainties associated with those estimates?
    As discussed in Section II.D, benchmarks are based on information
from controlled human exposure studies of NO2 exposures and
AR. In identifying specific NO2 benchmarks, and considering
the weight to place on each, the PA considers both the group mean
results reported in individual studies and the results of a meta-
analysis that combined data from multiple studies (Brown, 2015; U.S.
EPA, 2016a, Section <IP_ADDRESS>), as described above.
    When taken together, the results of individual controlled human
exposure studies and of the meta-analysis by Brown (2015) support
consideration of NO2 benchmarks between 100 and 300 ppb,
based largely on studies of non-

specific AR in people with asthma exposed at rest. As discussed in more
detail in II.D, benchmarks from the upper end of this range are
supported by the results of individual studies, the majority of which
reported statistically significant increases in AR following
NO2 exposures at or above 250 ppb, and by the results of the
meta-analysis by Brown (2015). Benchmarks from the lower end of this
range, including 100 ppb, are supported by the results of the meta-
analysis, even though individual studies do not consistently report
statistically significant NO2-induced increases in AR at
these lower concentrations. In particular, while the meta-analysis
indicates that the majority of study participants with asthma
experienced an increase in AR following exposures to 100 ppb
NO2 (Brown, 2015), individual studies have not generally
reported statistically significant increases in AR following resting
exposures to 100 ppb NO2.\103\
---------------------------------------------------------------------------

    \103\ Meta-analysis results for exposures to 100 ppb
NO2 were statistically significant when analyses were
restricted to non-specific AR, but not when analyses were restricted
to specific AR (Brown, 2015).
---------------------------------------------------------------------------

    In further considering the potential public health implications of
exposures to NO2 concentrations at or above benchmarks,
there are multiple uncertainties, as discussed in Section II.C.I. As
discussed in more detail in that section, there is no indication of a
dose-response relationship between NO2 and AR in people with
asthma, and there is uncertainty in the clinical relevance and
potential adversity of the reported NO2-induced increases in
AR.
    As discussed in Section II.D, analyses of unadjusted air quality,
which meets the current standards in all locations, indicate almost no
potential for 1-hour exposures to NO2 concentrations at or
above any of the benchmarks examined, including 100 ppb. Analyses of
air quality adjusted upwards to just meet the current 1-hour standard
\104\ indicate virtually no potential for 1-hour exposures to
NO2 concentrations at or above 200 ppb (or 300 ppb), and
almost none for exposures at or above 150 ppb. This is the case for
both estimates averaged over multiple years and estimates in worst-case
years, including at near-road monitoring sites within a few meters of
heavily trafficked roads. With respect to the lowest benchmark
evaluated, analyses estimate that there is potential for exposures to
1-hour NO2 concentrations at or above 100 ppb on some days
(e.g., about one to 10 days per year, on average, at near-road
monitoring sites). As described above, this result is consistent with
expectations, given that the current 1-hour standard, with its 98th
percentile form, is expected to limit, but not eliminate, the
occurrence of 1-hour NO2 concentrations of 100 ppb.
---------------------------------------------------------------------------

    \104\ In all study areas, ambient NO2 concentrations
required smaller upward adjustments to just meet the 1-hour standard
than to just meet the annual standard. Therefore, as noted above and
in the PA (U.S. EPA, 2017a, Section 4.2.1), when adjusting air
quality to just meet the current NO2 NAAQS, the
adjustment needed to just meet the 1-hour standard was applied.
---------------------------------------------------------------------------

    These analyses indicate that the current 1-hour NO2
standard is expected to allow virtually no potential for exposures to
the NO2 concentrations that have been shown most
consistently to increase AR in people with asthma, even under worst-
case conditions across a variety of study areas with among the highest
NOX emissions in the U.S. Such NO2 concentrations
are not estimated to occur, even at monitoring sites adjacent to some
of the most heavily trafficked roadways. In addition, the current 1-
hour standard provides protection against NO2 exposures that
have the potential to exacerbate asthma symptoms, but for which the
evidence indicates greater uncertainty in both the occurrence of such
exacerbations and in their severity, should they occur (i.e., at or
near 100 ppb). Given the results of these analyses, and the
uncertainties inherent in their interpretation, the PA concludes that
there is little potential for exposures to ambient NO2
concentrations that would be of public health concern in locations
meeting the current 1-hour standard.
3. CASAC Advice
    As discussed above (Section II.E), in the current review of the
primary standards for NO2, the CASAC has provided advice and
recommendations based on its review of drafts of the ISA, of the REA
Planning document, and of the draft PA. The CASAC's advice on the
adequacy of the current primary NO2 standards was provided
as part of its review of the draft PA (Diez Roux and Sheppard, 2017).
Overall, the CASAC concurred with the draft PA's preliminary conclusion
that it is appropriate to consider retaining the current primary
NO2 standards without revision, stating that, ``the CASAC
recommends retaining, and not changing the existing suite of
standards'' (Diez Roux and Sheppard, 2017). The CASAC provided the
following advice with respect to the individual elements of the
standards:
     Indicator and averaging time: The CASAC stated ``there is
strong evidence for the selection of NO2 as the indicator of
oxides of nitrogen'' and ``for the selection of 1-hour and annual
averaging times'' (Diez Roux and Sheppard, 2017 p. 9). With regard with
to averaging time in particular, the CASAC stated that ``[c]ontrolled
human and animal studies provide scientific support for a 1-hour
averaging time as being representative of an exposure duration that can
lead to adverse effects'' (Diez Roux and Sheppard, 2017, p. 7). The
CASAC further concluded that ``[e]pidemiologic studies provide support
for the annual averaging time, representative of likely to be causal
associations between long-term exposures, or repeated short-term
exposures, and asthma development'' (Diez Roux and Sheppard, 2017, p.
7).
     Level of the 1-hour standard: The CASAC stated ``there are
notable adverse effects at levels that exceed the current standard, but
not at the level of the current standard. Thus, the CASAC advises that
the current 1-hour standard is protective of adverse effects and that
there is not a scientific basis for a standard lower than the current
1-hour standard'' (Diez Roux, and Sheppard 2017, p. 9).
     Form of the 1-hour standard: The CASAC also ``recommends
retaining the current form'' for the 1-hour standard (Diez Roux and
Sheppard 2017). Recognizing that the form allowed for some 1-hour
concentrations that exceeded 100 ppb, the CASAC explained that the
``scientific rationale for this form is there is uncertainty regarding
the severity of adverse effects at a level of 100 ppb NO2,
and thus some potential for maximum daily levels to exceed this
benchmark with limited frequency may nonetheless be protective of
public health'' (Diez Roux and Sheppard, 2017, p. 10). It further noted
that the choice of form reflected the Administrator's policy judgment.
(Diez Roux and Sheppard, 2017, p. 10).
     Level of the annual standard: In providing advice on the
level of the annual standard, the CASAC commented that the long-term
epidemiologic studies ``imply the possibility of adverse effects at
levels below that of the current annual standard'' (Diez Roux and
Sheppard, p. 8). However, CASAC recognized that these studies ``are
also subject to uncertainty, including possible confounding with other
traffic-related pollutants'' (Diez Roux and Sheppard, p. 8). CASAC also
commented that these epidemiologic studies may have uncertainty related
to exposure error and pointed out that estimated DVs in study areas do
not account for near-road monitoring. Furthermore, CASAC recognized the
causal associations between long-term exposures, or repeated short-term
exposures, and asthma development (Diez Roux and

Sheppard, p. 7) and the appropriateness of considering the protection
provided by the current suite of standards together (Diez Roux and
Sheppard, p. 9). Therefore, the CASAC's advice on the annual standard
takes into account the degree of protection provided by this standard,
in combination with the current 1-hour standard. In particular, the
CASAC recognized that meeting the 1-hour NO2 standard can
limit long-term NO2 concentrations to below the level of the
annual standard, observing that ``an hourly DV of 100 ppb
NO2 is associated with DV values that average approximately
30 ppb NO2'' and that ``there is insufficient evidence to
make a scientific judgment that adverse effects occur at annual DVs
less than 30 ppb NO2'' (Diez Roux and Sheppard, 2017, p. 9).
Thus, in providing support for retaining the existing annual standard,
the CASAC specifically noted that ``the current suite of standards is
more protective of annual exposures compared to the annual standard by
itself'' and that ``it is the suite of the current 1-hour and annual
standards, together, that provide protection against adverse effects''
(Diez Roux and Sheppard, 2017, p. 9). Therefore, the CASAC ``recommends
retaining the existing suite of standards'' (Diez Roux and Sheppard,
2017, p. 9), including the current annual standard.
    In addition, CASAC also provided advice on areas for additional
research based on key areas of uncertainty that came up during the
review cycle (Diez Roux and Sheppard, 2017, p. 10-12). As part of this
advice, CASAC stated that ``[t]here is an ongoing need for research in
multipollutant exposure and epidemiology to attempt to distinguish the
contribution to NO2 exposure to human health risk'' (Diez
Roux and Sheppard, 2017, p. 10). More specifically, CASAC pointed to
the importance of further understanding the effects of co-pollutant
exposures and the variability in ambient NO2 concentrations,
particularly considering ``locations of peak exposure occurrences
(e.g., on road in vehicles, roadside for active commuters, in street
canyons, near other non-road facilities such as rail yards or
industrial facilities)'' (Diez Roux and Sheppard, 2017, p. 11). In
particular, CASAC recognized the importance of the new near-road
monitoring data in reducing those uncertainties, stating that ``[t]he
amount of data from near-road monitoring will increase between now and
the next review cycle and should be analyzed and evaluated'' (Diez Roux
and Sheppard, 2017, p. 11).
4. Administrator's Proposed Conclusions Regarding the Adequacy of the
Current Primary NO2 Standards
    Taking into consideration the large body of evidence concerning
NO2-related health effects and available estimates of the
potential for NO2 exposures, including the uncertainties and
limitations inherent in the evidence and those estimates, the
Administrator proposes to conclude that the current primary
NO2 standards provide the requisite protection of public
health, with an adequate margin of safety, and should be retained
without revision in this review. The Administrator's proposed
conclusions are informed by a careful consideration of the full body of
information available in this review, giving particular weight to the
assessment of the scientific evidence in the ISA; analyses in the PA
comparing NO2 air quality with health-based benchmarks; the
PA's consideration of the evidence and analyses; and the advice and
recommendations from the CASAC. The basis for the Administrator's
proposed conclusions on the current primary NO2 standards is
discussed below.
    As an initial matter, the Administrator takes note of the well-
established body of scientific evidence supporting the occurrence of
respiratory effects following NO2 exposures. As in the last
review, the clearest evidence indicates the occurrence of respiratory
effects following short-term NO2 exposures. The strongest
support for this relationship comes from controlled human exposure
studies demonstrating NO2-induced increases in AR in
individuals with asthma. As discussed above, the Administrator notes
that most of the controlled human exposure studies assessed in the ISA
were available in the last review, with the addition in this review of
an updated meta-analysis that synthesizes data from these studies. He
also notes that these studies provided an important part of the body of
evidence supporting the decision in the last review to establish the 1-
hour NO2 standard with its level of 100 ppb. Beyond the
controlled human exposure studies, additional supporting evidence comes
from epidemiologic studies reporting associations with a range of
asthma-related respiratory effects, including effects serious enough to
result in emergency room visits or hospital admissions. While there is
some new evidence in the current review from such epidemiologic studies
of short-term NO2 exposures, the results of these newer
studies are generally consistent with the epidemiologic studies that
were available in the last review.
    With regard to long-term NO2 exposures, the
Administrator notes that the evidence supporting associations with
asthma development in children has become stronger since the last
review, though uncertainties remain regarding the degree to which
estimates of long-term NO2 concentrations in these studies
are serving primarily as surrogates for exposures to the broader
mixture of traffic-related pollutants. Supporting evidence also
includes studies indicating a potential role for repeated short-term
NO2 exposures in the development of asthma (U.S. EPA, 2016a,
p. 6-64 and p. 6-65).
    In addition, the Administrator acknowledges that the evidence for
some non-respiratory effects has strengthened since the last review. In
particular, based on the assessment of the evidence in the ISA, he
notes the stronger evidence for NO2-associated
cardiovascular effects (short- and long-term exposures), premature
mortality (long-term exposures), and certain reproductive effects
(long-term exposures). As detailed in the ISA, while this evidence has
generally become stronger since the last review, it remains subject to
greater uncertainty than the evidence of asthma-related respiratory
effects (U.S. EPA, 2016a).
    The Administrator's evaluation of the public health protection
provided against ambient NO2 exposures also involves
consideration of populations and lifestages that may be at greater risk
of experiencing NO2-attributable health effects. In the
current review, the Administrator's consideration of potential at-risk
populations draws from the 2016 ISA's assessment of the evidence (U.S.
EPA, 2016a, Chapter 7). Based on the ISA's systematic approach to
evaluating factors that may increase risks in a particular population
or during a particular lifestage, the Administrator is most concerned
about the potential effects of NO2 exposures in people with
asthma, children, and older adults (U.S. EPA, 2016a, Table 7-27).
Support for potentially higher risks in these populations is based
primarily on evidence for asthma exacerbation or asthma development.
Evidence for other health effects is subject to greater uncertainty
(U.S. EPA, 2017a, Section 3.4).
    The Administrator further uses the scientific evidence outlined
above, and described in detail in the ISA (U.S. EPA, 2016a), to
directly inform his consideration of the adequacy of the public health
protection provided by the current primary NO2 standards.
Consistent with the approach in the PA

(U.S. EPA, 2017a), and with CASAC advice (Diez Roux and Sheppard,
2017), the Administrator specifically considers the evidence within the
context of the degree of public health protection provided by the
current 1-hour and annual standards together, including the combination
of all elements of these standards (i.e., indicator, averaging times,
forms, levels).
    In doing so, the Administrator focuses on the results of controlled
human exposure studies of AR in people with asthma and on the results
of U.S. and Canadian epidemiologic studies of asthma-related hospital
admissions, asthma-related emergency department visits, and asthma
development in children. He particularly emphasizes the results of
controlled human exposure studies, which were identified in the ISA as
providing ``[t]he key evidence that NO2 exposure can
independently exacerbate asthma'' (U.S. EPA, 2016a, p. 1-18). The
Administrator's decision to focus on these studies is in agreement with
the CASAC, which stated that, of the evidence for asthma exacerbation,
``[t]he strongest evidence is for an increase in AR based on controlled
human exposure studies, with supporting evidence from epidemiologic
studies'' (Diez Roux and Sheppard, 2017).
    In considering the controlled human exposure studies of AR, the
Administrator focuses both on the results of an updated meta-analysis
of data from these studies and on the consistency of findings across
individual studies. As discussed above, and consistent with the
evidence in the last review, the meta-analysis indicates that the
majority of study volunteers, generally with mild asthma, experienced
increased AR following 30-minute to 1-hour resting exposures to
NO2 concentrations from 100 to 530 ppb. Based on these
results, the Administrator notes the potential for people with asthma
to experience NO2-induced respiratory effects following
exposures in this range, and that people with more severe asthma could
experience more serious effects. The Administrator further notes that
individual studies consistently report statistically significant
increases in AR following exposures to NO2 concentrations at
or above 250 ppb, with less consistent results across studies conducted
at lower exposure concentrations, particularly 100 ppb (II.C.1).
Uncertainties in this evidence, discussed in sections II.C.1, II.D.3,
and II.F.2 above, include the lack of an apparent dose-response
relationship and uncertainty in the potential adversity of responses.
    When the information discussed above is taken together, the
Administrator judges it appropriate to consider the degree of
protection provided against exposures to NO2 concentrations
at and above 100 ppb, though his concern is greater for exposures to
higher concentrations. In particular, based on the results of the meta-
analysis and on the consistent results across individual studies, the
Administrator is most concerned about the potential for people with
asthma to experience adverse respiratory effects following
NO2 exposures at or above 250 ppb. Because results are less
consistent across individual studies that evaluated lower exposure
concentrations, the Administrator becomes increasingly concerned about
uncertainties in the evidence as he considers the potential
implications of such exposures. While taking these uncertainties into
consideration, the Administrator remains concerned about the potential
for respiratory effects following exposures to NO2
concentrations as low as 100 ppb, particularly in people with more
severe cases of asthma than have generally been evaluated in the
available NO2 controlled human exposure studies. Thus, when
the evidence and uncertainties are taken together, the Administrator
judges that it is appropriate to consider the degree of protection
provided against potential exposures to NO2 concentrations
at or above 100 ppb, with the most emphasis on the potential for
exposures at or above 250 ppb.
    In further considering the potential public health implications of
controlled human exposure studies, the Administrator looks to the
results of quantitative comparisons between NO2 air quality
and health-based benchmarks. As discussed in the PA, these comparisons
can help to place the results of the controlled human exposure studies,
which provide the basis for the benchmark concentrations, into a
broader public health context. In considering the results of the
analyses comparing NO2 air quality to specific health-based
benchmarks, the Administrator first recognizes that all areas of the
U.S. meet the current primary NO2 standards. When based on
recent unadjusted NO2 air quality, these analyses estimate
almost no days with the potential for 1-hour exposures to
NO2 concentrations at or above health-based benchmarks,
including the lowest benchmark examined (i.e., 100 ppb).
    The Administrator additionally recognizes that, even when ambient
NO2 concentrations are adjusted upward to just meet the
existing 1-hour standard, the analyses estimate no days with the
potential for exposures to the NO2 concentrations that have
been shown most consistently to increase AR in people with asthma
(i.e., above 250 ppb). Such NO2 concentrations were not
estimated to occur, even under worst-case conditions across a variety
of study areas with among the highest NOX emissions in the
U.S., and at monitoring sites adjacent to some of the most heavily
trafficked roadways in the U.S. In addition, analyses with adjusted air
quality indicate a limited number of days with the potential for
exposures to 1-hour NO2 concentrations at or above 100 ppb,
an exposure concentration with the potential to exacerbate asthma-
related respiratory effects, but for which uncertainties in the
evidence become increasingly important.
    Based on the information above, the Administrator reaches the
proposed conclusion that evidence from controlled human exposure
studies of AR, together with analyses comparing ambient NO2
concentrations to health-based benchmarks, supports the degree of the
public health protection provided by the current primary NO2
NAAQS. In particular, he is concerned about exposures to NO2
concentrations at and above 250 ppb, where the potential for
NO2-induced respiratory effects is supported by results of
the meta-analysis and by consistent results reported across individual
studies. With regard to this, the Administrator notes that meeting the
current standards is estimated to allow no potential for exposures to
1-hour NO2 concentrations at or above 250 ppb. The
Administrator is also concerned about exposures to lower NO2
concentrations, including concentrations as low as 100 ppb though, as
described above, he becomes increasingly concerned about the
uncertainties in the evidence at such low exposure concentrations. In
considering the degree of protection provided against exposures to 100
ppb NO2, in light of uncertainties, the Administrator judges
it appropriate to limit such exposures, but not necessarily to
eliminate them. With regard to this, he notes that the current standard
is estimated to allow limited potential for exposures to NO2
concentrations at or above 100 ppb. Thus, given the substantial
protection provided against exposures to NO2 concentrations
at and above 250 ppb, and the protection provided against exposures to
concentrations as low as 100 ppb, the Administrator reaches the
proposed conclusion that the evidence, when considered in light of its
uncertainties, supports the degree of

public health protection provided by the current primary NO2
NAAQS.
    Although the NO2 epidemiologic evidence is subject to
greater uncertainty than the controlled human exposure studies of
NO2-induced changes in AR, the Administrator also considers
what the available epidemiologic studies indicate with regard to the
adequacy of the public health protection provided by the current
standards. In particular, he considers analyses of NO2 air
quality in the locations, and during the time periods, of available
U.S. and Canadian epidemiologic studies. These analyses can provide
insights into the extent to which NO2-health effect
associations are present for distributions of ambient NO2
concentrations that would be allowed by the current standards. The
presence of such associations would support the potential for the
current standards to allow the NO2-associated effects
indicated by epidemiologic studies. To the degree studies have not
reported associations in locations meeting the current NO2
standards, there is greater uncertainty regarding the potential for
reported effects to occur following the NO2 exposures that
are associated with air quality meeting those standards.
    With regard to studies of short-term NO2 exposures, the
Administrator notes that epidemiologic studies provide consistent
evidence for asthma-related emergency department visits and hospital
admissions with exposure to NO2 in locations likely to have
violated the current standards over at least parts of study periods
(based on the presence of relatively precise and generally
statistically significant associations across several studies). These
studies have not consistently shown such NO2-associated
outcomes in areas that would have clearly met the current standards. In
this regard, the Administrator recognizes that the NO2
concentrations identified in these epidemiologic studies are based on
an NO2 monitoring network that, during study periods, did
not include monitors meeting the current near-road monitoring
requirements. This is particularly important given that NO2
concentrations near the most heavily-trafficked roadways were likely to
have been higher than those reflected by the NO2
concentrations measured at monitors in operation during study years. As
such, the estimated DVs associated with the areas at the times of the
studies could have been higher had a near-road monitoring network been
in place. Thus, while these epidemiologic studies provide consistent
evidence for associations with asthma-related effects, the
Administrator notes that studies conducted in the U.S. and Canada do
not provide support for associations with asthma-related hospital
admissions or emergency department visits in locations that would have
clearly met the current standards.
    With regard to studies of long-term NO2 exposures, the
Administrator notes that the preponderance of evidence for respiratory
health effects comes from epidemiologic studies evaluating asthma
development in children. As discussed above, these studies report
associations with long-term average NO2 concentrations,
while the broader body of evidence indicates the potential for repeated
short-term NO2 exposures to contribute to the development of
asthma. Because of this, and because air quality analyses indicate that
meeting the current 1-hour standard can also limit annual
NO2 concentrations, when considering these studies of asthma
development, the Administrator considers the protection provided by the
combination of both the annual and 1-hour standards. While available
epidemiologic studies conducted in the U.S. and Canada consistently
report associations between long-term NO2 exposures and
asthma development in children in locations likely to have violated the
current standards over at least parts of study periods, those studies
do not indicate such associations in locations that would have clearly
met the current annual and 1-hour standards. This is particularly the
case given that NO2 concentrations near the most heavily-
trafficked roadways are not likely reflected by monitors in operation
during study years. Thus, while recognizing the public health
significance of asthma development in children, and recognizing that
NO2 concentrations violating the current standards have been
associated with asthma development, the Administrator places weight on
the PA's conclusion that the evidence does not provide support for
NO2-attributable asthma development in children in locations
with NO2 concentrations that would have clearly met both the
annual and 1-hour standards.
    Taking all of these considerations into account, the Administrator
reaches the proposed conclusion that the current body of scientific
evidence, in combination with the results of quantitative analyses
comparing NO2 air quality with health-based benchmarks,
supports the degree of public health protection provided by the current
1-hour and annual primary NO2 standards and does not call
into question any of the elements of those standards. He further
reaches the proposed conclusion that the current 1-hour and annual
NO2 primary standards, together, are requisite to protect
public health with an adequate margin of safety.
    In particular, with regard to short-term exposures and the current
1-hour standard, the Administrator takes note of the well-established
body of scientific evidence supporting the occurrence of respiratory
effects following short-term NO2 exposures. In reaching the
proposed conclusion that the current standards provide requisite
protection against these effects, the Administrator notes:

     Meeting the current 1-hour NO2 standard
provides a substantial margin of safety against exposures to
NO2 concentrations that have been shown most consistently
to increase AR in people with asthma, even under worst-case
conditions across a variety of study areas with among the highest
NOX emissions in the U.S. Such NO2
concentrations were not estimated to occur, even at monitoring sites
adjacent to some of the most heavily trafficked roadways.
     Meeting the current 1-hour standard limits the
potential for exposures to 1-hour concentrations at or above 100
ppb. Thus, the current standard provides protection against
NO2 exposures with the potential to exacerbate symptoms
in some people with asthma, but for which uncertainties in the
evidence become increasingly important.
     Meeting the current 1-hour standard is expected to
maintain ambient NO2 concentrations below those present
in locations where key U.S. and Canadian epidemiologic studies
reported precise and statistically significant associations between
short-term NO2 and asthma-related hospitalizations.

    In addition, with regard to long-term NO2 exposures, the
Administrator notes that the evidence supporting associations with
asthma development in children has become stronger since the last
review, though important uncertainties remain. As discussed above,
meeting the current annual and 1-hour standards is expected to maintain
ambient NO2 concentrations below those present in locations
where key U.S. and Canadian epidemiologic studies reported such
associations between long-term NO2 and asthma development.
In considering the protection provided against exposures that could
contribute to asthma development, the Administrator recognizes the air
quality relationship between the current 1-hour standard and annual
standard, and that analyses of historical ambient NO2
concentrations suggest that meeting the 1-hour standard with its level
of 100 ppb would be expected to maintain annual average NO2
concentrations well-below the 53 ppb level of the annual standard, and
generally below 35

ppb.\105\ The Administrator judges that, as additional years of data
become available from the recently deployed near-road NO2
monitors, it will be important to evaluate the degree to which this
relationship is also observed in the near-road environment, and the
degree to which the annual standard provides additional protection,
beyond that provided by the 1-hour standard. Such an evaluation could
inform future reviews of the primary NO2 NAAQS, consistent
with the CASAC advice that ``in the next review cycle for oxides of
nitrogen . . . EPA should review the annual standard to determine if
there is need for revision or revocation'' (Diez Roux and Sheppard,
2017, p. 9).
---------------------------------------------------------------------------

    \105\ This air quality relationship was discussed in the PA
where it was noted that the analysis did not include data from near-
road monitors due to the limited amount of data available for the
years analyzed (1980-2015).
---------------------------------------------------------------------------

    Therefore, in this review, the Administrator proposes to retain the
current primary NO2 standards, without revision. As
described in section II.F.3 above, the Administrator notes that his
proposed decision to retain the current primary NO2
standards in this review is consistent with CASAC advice provided as
part of its review of the draft PA. In particular, the Administrator
notes that ``the CASAC recommends retaining, and not changing the
existing suite of standards'' (Diez Roux and Sheppard, 2017). CASAC
specifically focused its conclusions on the degree of protection
provided by the combination of the 1-hour and annual standards against
short- and long-term NO2 exposures. In particularly, the
CASAC stated that ``it is the suite of the current 1-hour and annual
standards, together, that provide protection against adverse effects''
(Diez Roux and Sheppard, 2017, p. 9).
    Inherent in the Administrator's proposed conclusions are public
health policy judgments on the public health implications of the
available scientific evidence and analyses, including how to weigh
associated uncertainties. These public health policy judgments include
judgments related to the appropriate degree of public health protection
that should be afforded against risk of respiratory morbidity in at-
risk populations, such as the potential for worsened respiratory
effects in people with asthma, as well judgments related to the
appropriate weight to be given to various aspects of the evidence and
quantitative analyses, including how to consider their associated
uncertainties. Based on these considerations and the judgments
identified here, the Administrator reaches the proposed conclusion that
the current standards provide the requisite protection of public health
with an adequate margin of safety, including protection of at-risk
populations, such as people with asthma.
    In reaching this proposed conclusion, the Administrator recognizes
that in establishing primary standards under the Act that are requisite
to protect public health with an adequate margin of safety, he is
seeking to establish standards that are neither more nor less stringent
than necessary for this purpose. The Act does not require that primary
standards be set at a zero-risk level, but rather at a level that
avoids unacceptable risks to public health. In this context, the
Administrator's proposed conclusion is that the current standards
provide the requisite protection and that more or less stringent
standards would not be requisite.
    More specifically, given the adverse effects reported to be
associated with NO2 concentrations above the current
standards, the Administrator does not believe standards less stringent
than the current standards would be sufficient to protect public health
with an adequate margin of safety. In this regard, he particularly
notes that, compared to the current standards, less stringent standards
would be more likely to allow (1) NO2 exposures that could
exacerbate respiratory effects in people with asthma, particularly
those with more severe asthma and (2) ambient NO2
concentrations that have been reported in epidemiologic studies to be
associated with asthma-related hospitalizations and with asthma
development in children. Consistent with these observations, the
Administrator further notes CASAC's conclusion, based on its
consideration of the evidence, that ``there are notable adverse effects
at levels that exceed the current standard, but not at the level of the
current standard'' (Diez Roux and Sheppard, 2017 pg. 9). Therefore, the
Administrator reaches the proposed conclusion that standards less
stringent than the current 1-hour and annual standards (e.g., with
levels higher than 100 ppb and 53 ppb, respectively) would not be
sufficient to protect public health with an adequate margin of safety.
    The Administrator additionally recognizes that the uncertainties
and limitations associated with the many aspects of the estimated
relationships between respiratory morbidity and NO2
exposures are amplified with consideration of progressively lower
ambient NO2 concentrations. In his view, and consistent with
the conclusions in the PA, there is appreciable uncertainty in the
extent to which reductions in asthma exacerbations or asthma
development would result from revising the primary NO2 NAAQS
to be more stringent than the current standards. Therefore, the
Administrator also does not believe standards more stringent than the
current standards would be appropriate. With regard to this, CASAC
advised that ``there is not a scientific basis for a standard lower
than the current 1-hour standard'' (Diez Roux and Sheppard, 2017 pg.
9). The CASAC also did not advise setting the level of the annual
standard lower than the current level of 53 ppb, noting that the 1-hour
standard can generally maintain long-term NO2 concentrations
below the level of the annual standard (Diez Roux and Sheppard, 2017).
    Based on all of the above considerations, and consistent with CASAC
advice, the Administrator reaches the proposed conclusion that it is
appropriate to retain the current standards, without revision, in this
review. He further proposes that the available evidence and information
do not warrant the identification of potential alternative standards
that provide a different degree of public health protection. In
reaching these proposed conclusions, the Administrator recognizes that
different public health policy judgments could lead to different
conclusions regarding the extent to which the current standards protect
the public health. Such judgments include those related to the
appropriate degree of public health protection that should be afforded
as well as the appropriate weight to be given to various aspects of the
evidence and information, including how to consider uncertainties.
Therefore, the Administrator solicits comment on his proposed
conclusions regarding the public health protection provided by the
current primary NO2 standards and on his proposal to retain
those standards, without revision, in this review. He invites comment
on all aspects of these proposed conclusions and their underlying
rationales, including on his proposal that the current standards are
requisite, i.e., neither more nor less stringent than necessary, to
protect the public health with an adequate margin of safety and on the
evidence-based and exposure-/risk-based considerations supporting that
proposal.

III. Statutory and Executive Order Reviews

    Additional information about these statutes and Executive Orders
can be found at http://www2.epa.gov/laws-regulations/laws-and-executive-orders.

A. Executive Order 12866: Regulatory Planning and Review and Executive
Order 13563: Improving Regulation and Regulatory Review

    The Office of Management and Budget (OMB) determined that this
action is a significant regulatory action. Accordingly, it was
submitted to OMB for review. Any changes made in response to OMB
recommendations have been documented in the docket. Because this rule
does not propose to change the existing NAAQS for NO2, it
does not impose costs or benefits relative to the baseline of
continuing with the current NAAQS in effect. EPA has thus not prepared
a Regulatory Impact Analysis for this rule.

B. Paperwork Reduction Act (PRA)

    This action does not impose an information collection burden under
the PRA. There are no information collection requirements directly
associated with a decision to retain a NAAQS without any revision under
section 109 of the CAA and this action proposes to retain the current
primary NO2 NAAQS without any revisions.

C. Regulatory Flexibility Act (RFA)

    I certify that this action will not have a significant economic
impact on a substantial number of small entities under the RFA. This
action will not impose any requirements on small entities. Rather, this
action proposes to retain, without revision, existing national
standards for allowable concentrations of NO2 in ambient air
as required by section 109 of the CAA. See also American Trucking
Associations v. EPA. 175 F.3d at 1044-45 (NAAQS do not have significant
impacts upon small entities because NAAQS themselves impose no
regulations upon small entities).

D. Unfunded Mandates Reform Act (UMRA)

    This action does not contain any unfunded mandate as described in
the UMRA, 2 U.S.C. 1531-1538 and does not significantly or uniquely
affect small governments. This action imposes no enforceable duty on
any state, local or tribal governments or the private sector.

E. Executive Order 13132: Federalism

    This action does not have federalism implications. It will not have
substantial direct effects on the states, on the relationship between
the national government and the states, or on the distribution of power
and responsibilities among the various levels of government.

F. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments

    This action does not have tribal implications, as specified in
Executive Order 13175. This action does not change existing
regulations. It does not have a substantial direct effect on one or
more Indian Tribes, since Tribes are not obligated to adopt or
implement any NAAQS. The Tribal Authority Rule gives Tribes the
opportunity to develop and implement CAA programs such as the primary
NO2 NAAQS, but it leaves to the discretion of the Tribe
whether to develop these programs and which programs, or appropriate
elements of a program, they will adopt. Thus, Executive Order 13175
does not apply to this action.

G. Executive Order 13045: Protection of Children From Environmental
Health and Safety Risks

    This action is not subject to Executive Order 13045 because it is
not economically significant as defined in Executive Order 12866. The
health effects evidence and risk assessment information for this
action, which focuses on children, people with asthma, and older
adults, in addressing the at-risk populations, is summarized in section
II.C.3 above and described in the ISA and PA, copies of which are in
the public docket for this action.

H. Executive Order 13211: Actions That Significantly Affect Energy
Supply, Distribution or Use

    This action is not a ``significant energy action'' because it is
not likely to have a significant adverse effect on the supply,
distribution, or use of energy. The purpose of this notice is to
propose to retain the current primary NO2 NAAQS. This
proposal does not change existing requirements. Thus, the EPA concludes
that this proposal does not constitute a significant energy action as
defined in Executive Order 13211.

I. National Technology Transfer and Advancement Act (NTTAA)

    This action does not involve technical standards.

J. Executive Order 12898: Federal Actions To Address Environmental
Justice in Minority Populations and Low-Income Populations

    The EPA believes that this action does not have disproportionately
high and adverse human health or environmental effects on minority,
low-income populations and/or indigenous peoples, as specified in
Executive Order 12898 (59 FR 7629, February 16, 1994). The
documentation for this decision is contained in Section II. The action
proposed in this notice is to retain without revision the existing
primary NAAQS for oxides of nitrogen based on the Administrator's
conclusion that the existing standards protect public health, including
the health of sensitive groups, with an adequate margin of safety. The
EPA expressly considered the available information regarding health
effects among at-risk populations in reaching the proposed decision
that the existing standards are requisite.

K. Determination Under Section 307(d)

    Section 307(d)(1)(V) of the CAA provides that the provisions of
section 307(d) apply to ``such other actions as the Administrator may
determine.'' Pursuant to section 307(d)(1)(V), the Administrator
determines that this action is subject to the provisions of section
307(d).

References

Ahmed, T; Dougherty, R; Sackner, MA. (1983a). Effect of 0.1 ppm
NO2 on pulmonary functions and non-specific bronchial
reactivity of normals and asthmatics [final report]. (CR-83/11/BI).
Warren, MI: General Motors Research Laboratories.
Ahmed, T; Dougherty, R; Sackner, MA. (1983b). Effect of
NO2 exposure on specific bronchial reactivity in subjects
with allergic bronchial asthma [final report]. (CR-83/07/BI).
Warren, MI: General Motors Research Laboratories.
Anderson, HR; Ponce de Leon, A; Bland, JM; Bower, JS; Emberlin, J;
Strachan, DP. (1998). Air pollution, pollens, and daily admissions
for asthma in London 1987-92. Thorax 53: 842-848. http://dx.doi.org/10.1136/thx.53.10.842.
Arbex, MA; de Souza Concei[ccedil][atilde]o, GM; Cendon, SP; Arbex,
FF; Lopes, AC; Moys[eacute]s, EP; Santiago, SL; Saldiva, PHN;
Pereira, LAA; Braga, ALF. (2009). Urban air pollution and chronic
obstructive pulmonary disease-related emergency department visits. J
Epidemiol Community Health 63: 777-783. http://dx.doi.org/10.1136/jech.2008.078360.
Atkinson, RW; Anderson, HR; Strachan, DP; Bland, JM; Bremner, SA;
Ponce de Leon, A. (1999a). Short-term associations between outdoor
air pollution and visits to accident and emergency departments in
London for respiratory complaints. Eur Respir J 13: 257-265.
ATSDR (Agency for Toxic Substances and Disease Registry). (2006). A
study of ambient air contaminants and asthma in New York City: Part
A and B. Atlanta, GA: U.S. Department of Health and Human Services.
http://permanent.access.gpo.gov/lps88357/ASTHMA_BRONX_FINAL_REPORT.pdf.
Avol, EL; Linn, WS; Peng, RC; Whynot, JD; Shamoo, DA; Little, DE;
Smith, MN; Hackney, JD. (1989). Experimental exposures of young
asthmatic volunteers to 0.3 ppm nitrogen dioxide and to

ambient air pollution. Toxicol Ind Health 5: 1025-1034.
Blackwell, DL; Lucas, JW; Clarke, TC. (2014). Summary health
statistics for U.S. adults: National health interview survey, 2012.
In Vital and health statistics. Hyattsville, MD: National Center for
Health Statistics, U.S. Department of Health and Human Services.
http://www.cdc.gov/nchs/data/series/sr_10/sr10_260.pdf.
Bloom, B; Jones, LI; Freeman, G. (2013). Summary health statistics
for U.S. children: National health interview survey, 2012. In Vital
and health statistics. Hyattsville, MD: National Center for Health
Statistics, U.S. Department of Health and Human Services. http://www.cdc.gov/nchs/data/series/sr_10/sr10_258.pdf.
Brown, JS. (2015). Nitrogen dioxide exposure and airway
responsiveness in individuals with asthma. Inhal Toxicol 27: 1-14.
http://dx.doi.org/10.3109/08958378.2014.979960.
Burnett, RT; Smith-Doiron, M; Stieb, D; Cakmak, S; Brook, JR.
(1999). Effects of particulate and gaseous air pollution on
cardiorespiratory hospitalizations. Arch Environ Health 54: 130-139.
http://dx.doi.org/10.1080/00039899909602248.
Bylin, G; Hedenstierna, G; Lindvall, T; Sundin, B. (1988). Ambient
nitrogen dioxide concentrations increase bronchial responsiveness in
subjects with mild asthma. Eur Respir J 1: 606-612.
Carlsten, C; Dybuncio, A; Becker, A; Chan-Yeung, M; Brauer, M.
(2011). Traffic-related air pollution and incident asthma in a high-
risk birth cohort. Occup Environ Med 68: 291-295. http://dx.doi.org/10.1136/oem.2010.055152.
Clark, NA; Demers, PA; Karr, CJ; Koehoorn, M; Lencar, C; Tamburic,
L; Brauer, M. (2010). Effect of early life exposure to air pollution
on development of childhood asthma. Environ Health Perspect 118:
284-290. http://dx.doi.org/10.1289/ehp.0900916.
Clougherty, JE; Levy, JI; Kubzansky, LD; Ryan, PB; Suglia, SF;
Canner, MJ; Wright, RJ. (2007). Synergistic effects of traffic-
related air pollution and exposure to violence on urban asthma
etiology. Environ Health Perspect 115: 1140-1146. http://dx.doi.org/10.1289/ehp.9863.
Diez Roux, A; Frey HC (2015a). Letter from Drs. Ana Diez Roux, Chair
and H. Christopher Frey, Immediate Past Chair, Clean Air Scientific
Advisory Committee to EPA Administrator Gina McCarthy. CASAC Review
of the EPA's Integrated Science Assessment for Oxides of Nitrogen--
Health Criteria (Second External Review Draft). EPA-CASAC-15-001.
September 9, 2015. Available at: https://yosemite.epa.gov/sab/
sabproduct.nsf/6612DAF24438687B85257EBB0070369C/$File/EPA-CASAC-15-
001+unsigned.pdf.
Diez Roux, A; Frey HC (2015b). Letter from Drs. Ana Diez Roux, Chair
and H. Christopher Frey, Immediate Past Chair, Clean Air Scientific
Advisory Committee to EPA Administrator Gina McCarthy. CASAC Review
of the EPA's Review of the Primary National Ambient Air Quality
Standards for Nitrogen Dioxide: Risk and Exposure Assessment
Planning Document. EPA-CASAC-15-002. September 9, 2015. Available
at: https://yosemite.epa.gov/sab/sabproduct.nsf/
264cb1227d55e02c85257402007446a4/A7922887D5BDD8D485257EBB0071A3AD/
$File/EPA-CASAC-15-002+unsigned.pdf.
Diez Roux, A; Sheppard, E (2017). Letter from Dr. Elizabeth A.
(Lianne) Sheppard, Chair, Clean Air Scientific Advisory Committee to
EPA Administrator E. Scott Pruitt. CASAC Review of the EPA's Policy
Assessment for the Review of the Primary National Ambient Air
Quality Standards for Nitrogen Dioxide (External Review Draft--
September 2016). EPA-CASAC-17-001. March 7, 2017. Available at:
https://yosemite.epa.gov/sab/sabproduct.nsf/
LookupWebProjectsCurrentCASAC/7C2807D0D9BB4CC8852580DD004EBC32/
$File/EPA-CASAC-17-001.pdf.
D[uuml]ring, I; B[auml]chlin, W; Ketzel, M; Baum, A; Friedrich, U;
Wurzler, S. (2011). A new simplified NO/NO2 conversion
model under consideration of direct NO2-emissions. Meteor
Z 20: 67-73. http://dx.doi.org/10.1127/0941-2948/2011/0491.
Folinsbee, LJ. (1992). Does nitrogen dioxide exposure increase
airways responsiveness? Toxicol Ind Health 8: 273-283.
Frey HC (2014a). Letter from Dr. H. Christopher Frey, Clean Air
Scientific Advisory Committee to EPA Administrator Gina McCarthy.
CASAC Review of the EPA's Integrated Science Assessment for Oxides
of Nitrogen--Health Criteria (First External Review Draft). EPA-
CASAC-14-002. June 10, 2014. Available at: https://yosemite.epa.gov/
sab/sabproduct.nsf/15E4619D3CD3409A85257CF30069387D/$File/EPA-CASAC-
14-002+unsigned.pdf.
Frey HC (2014b). Letter from Dr. H. Christopher Frey, Clean Air
Scientific Advisory Committee to EPA Administrator Gina McCarthy.
CASAC Review of the EPA's Integrated Review Plan for the Primary
National Ambient Air Quality Standards for Nitrogen Dioxide
(External Review Draft). EPA-CASAC-14-001. June 10, 2014. Available
at: https://yosemite.epa.gov/sab/sabproduct.nsf/
89989229944F36B085257CF300692E2A/$File/EPA-CASAC-14-
001+unsigned.pdf.
Gehring, U; Gruzieva, O; Agius, RM; Beelen, R; Custovic, A; Cyrys,
J; Eeftens, M; Flexeder, C; Fuertes, E; Heinrich, J; Hoffmann, B; de
Jongste, JC; Kerkhof, M; Kl[uuml]mper, C; Korek, M; M[ouml]lter, A;
Schultz, ES; Simpson, A; Sugiri, D; Svartengren, M; von Berg, A;
Wijga, AH; Pershagen, G; Brunekreef, B. (2013). Air pollution
exposure and lung function in children: the ESCAPE project. Environ
Health Perspect 121: 1357-1364. http://dx.doi.org/10.1289/ehp.1306770.
Goodman, JE; Chandalia, JK; Thakali, S; Seeley, M. (2009). Meta-
analysis of nitrogen dioxide exposure and airway hyper-
responsiveness in asthmatics. Crit Rev Toxicol 39: 719-742. http://dx.doi.org/10.3109/10408440903283641.
Hazucha, MJ; Ginsberg, JF; McDonnell, WF; Haak, ED, Jr; Pimmel, RL;
Salaam, SA; House, DE; Bromberg, PA. (1983). Effects of 0.1 ppm
nitrogen dioxide on airways of normal and asthmatic subjects. J Appl
Physiol Respir Environ Exerc Physiol 54: 730-739.
Hinwood, AL; De Klerk, N; Rodriguez, C; Jacoby, P; Runnion, T; Rye,
P; Landau, L; Murray, F; Feldwick, M; Spickett, J. (2006). The
relationship between changes in daily air pollution and
hospitalizations in Perth, Australia 1992-1998: A case-crossover
study. Int J Environ Health Res 16: 27-46. http://dx.doi.org/10.1080/09603120500397680.
Howden, LM; Meyer, JA. (2011). Age and sex composition: 2010. (2010
Census Briefs, C2010BR-03). Washington, DC: U.S. Department of
Commerce, Economics and Statistics Administration, U.S. Census
Bureau. http://www.census.gov/prod/cen2010/briefs/c2010br-03.pdf.
Itano, Y et al. (2014). Estimation of Primary NO2/
NOX Emission Ratio from Road Vehicles Using Ambient
Monitoring Data. Studies in Atm Sci, 1-7.
Ito, K; Mathes, R; Ross, Z; N[aacute]das, A; Thurston, G; Matte, T.
(2011). Fine particulate matter constituents associated with
cardiovascular hospitalizations and mortality in New York City.
Environ Health Perspect 119: 467-473. http://dx.doi.org/10.1289/ehp.1002667.
Jaffe, DH; Singer, ME; Rimm, AA. (2003). Air pollution and emergency
department visits for asthma among Ohio Medicaid recipients, 1991-
1996. Environ Res 91: 21-28. http://dx.doi.org/10.1016/S0013-9351(02)00004-X.
Jenkins, HS; Devalia, JL; Mister, RL; Bevan, AM; Rusznak, C; Davies,
RJ. (1999). The effect of exposure to ozone and nitrogen dioxide on
the airway response of atopic asthmatics to inhaled allergen: Dose-
and time-dependent effects. Am J Respir Crit Care Med 160: 33-39.
http://dx.doi.org/10.1164/ajrccm.160.1.9808119.
Jerrett, M; Shankardass, K; Berhane, K; Gauderman, WJ; K[uuml]nzli,
N; Avol, E; Gilliland, F; Lurmann, F; Molitor, JN; Molitor, JT;
Thomas, DC; Peters, J; McConnell, R. (2008). Traffic-related air
pollution and asthma onset in children: A prospective cohort study
with individual exposure measurement. Environ Health Perspect 116:
1433-1438. http://dx.doi.org/10.1289/ehp.10968.
Jimenez, JL et al. (2000). Remote sensing of NO and NO2
emissions from heavy-duty diesel trucks using tunable diode lasers.
Environ Sci Technol, 2380-2387.
Kleinman, MT; Bailey, RM; Linn, WS; Anderson, KR; Whynot, JD;
Shamoo, DA; Hackney, JD. (1983). Effects of 0.2 ppm nitrogen dioxide
on pulmonary function and response to bronchoprovocation in
asthmatics. J Toxicol Environ Health 12: 815-826. http://dx.doi.org/10.1080/15287398309530472.

Klepeis, NE; Tsang, AM; Behar, JV. (1996). Analysis of the national
human activity pattern survey (NHAPS) respondents from a standpoint
of exposure assessment [EPA Report]. (EPA/600/R-96/074). Washington,
DC: U.S. Environmental Protection Agency. http://exposurescience.org/pub/reports/NHAPS_Report1.pdf#....Local
SettingsTemporary Internet
FilesContent.Outlook3JQ221FPB_Approaches_Population_Tables.docx.
Ko, FWS; Tam, W; Wong, TW; Lai, CKW; Wong, GWK; Leung, TF; Ng, SSS;
Hui, DSC. (2007). Effects of air pollution on asthma hospitalization
rates in different age groups in Hong Kong. Clin Exp Allergy 37:
1312-1319. http://dx.doi.org/10.1111/j.1365-2222.2007.02791.x.
Kota, SH et al. (2013). Simulating near-road reactive dispersion of
gaseous air pollutants using a three-dimensional eulerian model. Sci
Total Environ, Simulating near-road reactive dispersion of gaseous
air pollutants using a three-dimensional eulerian model.
Li, S; Batterman, S; Wasilevich, E; Wahl, R; Wirth, J; Su, FC;
Mukherjee, B. (2011). Association of daily asthma emergency
department visits and hospital admissions with ambient air
pollutants among the pediatric Medicaid population in Detroit: Time-
series and time-stratified case-crossover analyses with threshold
effects. Environ Res 111: 1137-1147. http://dx.doi.org/10.1016/j.envres.2011.06.002.
Linn, WS; Szlachcic, Y; Gong, H, Jr; Kinney, PL; Berhane, KT.
(2000). Air pollution and daily hospital admissions in metropolitan
Los Angeles. Environ Health Perspect 108: 427-434.
MacIntyre, EA; Gehring, U; M[ouml]lter, A; Fuertes, E; Kl[uuml]mper,
C; Kr[auml]mer, U; Quass, U; Hoffmann, B; Gascon, M; Brunekreef, B;
Koppelman, GH; Beelen, R; Hoek, G; Birk, M; de Jongste, JC; Smit,
HA; Cyrys, J; Gruzieva, O; Korek, M; Bergstr[ouml]m, A; Agius, RM;
de Vocht, F; Simpson, A; Porta, D; Forastiere, F; Badaloni, C;
Cesaroni, G; Esplugues, A; Fern[aacute]ndez-Somoano, A; Lerxundi, A;
Sunyer, J; Cirach, M; Nieuwenhuijsen, MJ; Pershagen, G; Heinrich, J.
(2014). Air pollution and respiratory infections during early
childhood: an analysis of 10 European birth cohorts within the
ESCAPE Project. Environ Health Perspect 122: 107-113. http://dx.doi.org/10.1289/ehp.1306755.
McConnell, R; Islam, T; Shankardass, K; Jerrett, M; Lurmann, F;
Gilliland, F; Gauderman, J; Avol, E; K[uuml]nzli, N; Yao, L; Peters,
J; Berhane, K. (2010). Childhood incident asthma and traffic-related
air pollution at home and school. Environ Health Perspect 118: 1021-
1026. http://dx.doi.org/10.1289/ehp.0901232.
Migliaretti, G; Cadum, E; Migliore, E; Cavallo, F. (2005). Traffic
air pollution and hospital admission for asthma: a case-control
approach in a Turin (Italy) population. Int Arch Occup Environ
Health 78: 164-169. http://dx.doi.org/ 10.1007/s00420-004-0569-3.
Nishimura, KK; Galanter, JM; Roth, LA; Oh, SS; Thakur, N; Nguyen,
EA; Thyne, S; Farber, HJ; Serebrisky, D; Kumar, R; Brigino-
Buenaventura, E; Davis, A; LeNoir, MA; Meade, K; Rodriguez-Cintron,
W; Avila, PC; Borrell, LN; Bibbins-Domingo, K; Rodriguez-Santana,
JR; Sen, S; Lurmann, F; Balmes, JR; Burchard, EG. (2013). Early-life
air pollution and asthma risk in minority children: The GALA II and
SAGE II studies. Am J Respir Crit Care Med 188: 309-318. http://dx.doi.org/10.1164/rccm.201302-0264OC.
Orehek, J; Massari, JP; Gayrard, P; Grimaud, C; Charpin, J. (1976).
Effect of short-term, low-level nitrogen dioxide exposure on
bronchial sensitivity of asthmatic patients. J Clin Invest 57: 301-
307. http://dx.doi.org/10.1172/JCI108281.
Ortman, JM; Velkoff, VA; Hogan, H. (2014). An aging nation: The
older population in the United States (pp. 1-28). (P25-1140). United
States Census Bureau. http://www.census.gov/library/publications/2014/demo/p25-1140.html.
Peel, JL; Tolbert, PE; Klein, M; Metzger, KB; Flanders, WD; Todd, K;
Mulholland, JA; Ryan, PB; Frumkin, H. (2005). Ambient air pollution
and respiratory emergency department visits. Epidemiology 16: 164-
174. http://dx.doi.org/10.1097/01.ede.0000152905.42113.db.
Reddel, HK; Taylor, DR; Bateman, ED; Boulet, LP; Boushey, HA; Busse,
WW; Casale, TB; Chanez, P; Enright, PL; Gibson, PG; de Jongste, JC;
Kerstjens, HA; Lazarus, SC; Levy, ML; O'Byrne, PM; Partridge, MR;
Pavord, ID; Sears, MR; Sterk, PJ; Stoloff, SW; Sullivan, SD;
Szefler, SJ; Thomas, MD; Wenzel, SE. (2009). An official American
Thoracic Society/European Respiratory Society statement: Asthma
control and exacerbations: Standardizing endpoints for clinical
asthma trials and clinical practice. Am J Respir Crit Care Med 180:
59-99. http://dx.doi.org/10.1164/rccm.200801-060ST.
Richmond-Bryant, J; Reff, A. (2012). Air pollution retention within
a complex of urban street canyons: A two-city comparison. Atmos
Environ 49: 24-32. http://dx.doi.org/10.1016/j.atmosenv.2011.12.036.
Richmond-Bryant, J et al. (2016). Estimation of on-road
NO2 concentrations, NO2/NOX ratios,
and related roadway gradients from near-road monitoring data.
Submitted to Air Quality, Atm and Health.
Riedl, MA; Diaz-Sanchez, D; Linn, WS; Gong, H, Jr; Clark, KW;
Effros, RM; Miller, JW; Cocker, DR; Berhane, KT. (2012). Allergic
inflammation in the human lower respiratory tract affected by
exposure to diesel exhaust [HEI] (pp. 5-43; discussion 45-64). (ISSN
1041-5505 Research Report 165). Boston, MA: Health Effects
Institute. http://pubs.healtheffects.org/view.php?id=373.
Roger, LJ; Horstman, DH; McDonnell, W; Kehrl, H; Ives, PJ; Seal, E;
Chapman, R; Massaro, E. (1990). Pulmonary function, airway
responsiveness, and respiratory symptoms in asthmatics following
exercise in NO2. Toxicol Ind Health 6: 155-171. http://dx.doi.org/10.1177/074823379000600110.
Rowangould, GM. (2013). A census of the US near-roadway population:
Public health and environmental justice considerations. Transport
Res Transport Environ 25: 59-67. http://dx.doi.org/10.1016/j.trd.2013.08.003.
Samet, J (2008a). Letter from Dr. Jonathan M. Samet, Chair, Clean
Air Scientific Advisory Committee to EPA Administrator Stephen
Johnson. Clean Air Scientific Advisory Committee's (CASAC) Peer
Review of Draft Chapter 8 of EPA's Risk and Exposure Assessment to
Support the Review of the NO2 Primary National Ambient
Air Quality Standard. EPA-CASAC-09-001. October 28, 2008. Available
at: http://yosemite.epa.gov/sab/sabproduct.nsf/
264cb1227d55e02c85257402007446a4/87D38275673D66B8852574F00069D45E/
$File/EPA-CASAC-09-001-unsigned.pdf.
Samet, J (2008b). Letter from Dr. Jonathan M. Samet, Chair, Clean
Air Scientific Advisory Committee to EPA Administrator Stephen
Johnson. Clean Air Scientific Advisory Committee's (CASAC) Review
comments on EPA's Risk and Exposure Assessment to Support the Review
of the NO2 Primary National Ambient Air Quality Standard.
EPA-CASAC-09-003. December 16, 2008. Available at: http://
yosemite.epa.gov/sab/sabproduct.nsf/
264cb1227d55e02c85257402007446a4/9C4A540D86BFB67A852575210074A7AE/
$File/EPA-CASAC-09-003-unsigned.pdf.
Samet, J (2009). Letter from Dr. Jonathan M. Samet, Chair, Clean Air
Scientific Advisory Committee to EPA Administrator Lisa P. Jackson.
Comments and Recommendations Concerning EPA's Proposed Rule for the
Revision of the National Ambient Air Quality Standards (NAAQS) for
Nitrogen Dioxide. EPA-CASAC-09-014. September 9, 2009. Available at:
http://yosemite.epa.gov/sab/sabproduct.nsf/
264cb1227d55e02c85257402007446a4/0067573718EDA17F8525762C0074059E/
$File/EPA-CASAC-09-014-unsigned.pdf.
Son, JY; Lee, JT; Park, YH; Bell, ML. (2013). Short-term effects of
air pollution on hospital admissions in Korea. Epidemiology 24: 545-
554. http://dx.doi.org/10.1097/EDE.0b013e3182953244.
Stieb, DM; Szyszkowicz, M; Rowe, BH; Leech, JA. (2009). Air
pollution and emergency department visits for cardiac and
respiratory conditions: A multi-city time-series analysis. Environ
Health 8. http://dx.doi.org/10.1186/1476-069X-8-25.
Strand, V; Svartengren, M; Rak, S; Barck, C; Bylin, G. (1998).
Repeated exposure to an ambient level of NO2 enhances asthmatic
response to a nonsymptomatic allergen dose. Eur Respir J 12: 6-12.
http://dx.doi.org/10.1183/09031936.98.12010006.
Strickland, MJ; Darrow, LA; Klein, M; Flanders, WD; Sarnat, JA;
Waller, LA; Sarnat, SE; Mulholland, JA; Tolbert, PE. (2010). Short-
term associations between ambient air pollutants and pediatric

asthma emergency department visits. Am J Respir Crit Care Med 182:
307-316. http://dx.doi.org/10.1164/rccm.200908-1201OC.
Tunnicliffe, WS; Burge, PS; Ayres, JG. (1994). Effect of domestic
concentrations of nitrogen dioxide on airway responses to inhaled
allergen in asthmatic patients. Lancet 344: 1733-1736. http://dx.doi.org/10.1016/s0140-6736(94)92886-x.
U.S. EPA (1971). Air Quality Criteria for Nitrogen Oxides. U.S.
Environmental Protection Agency. Air Pollution Control Office,
Washington, DC January 1971. Air Pollution Control Office
Publication No. AP-84.
U.S. EPA (1993). Air Quality Criteria for Oxides of Nitrogen. Office
of Health and Environmental Assessment, Environmental Criteria and
Assessment Office. Research Triangle Park, NC. EPA-600/8-91-049aF-
cF, August 1993. Available at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=40179.
U.S. EPA (1995). Review of the National Ambient Air Quality
Standards for Nitrogen Oxides: Assessment of Scientific and
Technical Information, OAQPS Staff Paper. U.S. EPA, Office of Air
Quality Planning and Standards, Research Triangle Park, NC. EPA-452/
R-95-005, September 1995. Available at: http://www.epa.gov/ttn/naaqs/standards/nox/data/noxsp1995.pdf.
U.S. EPA (2008a). Integrated Science Assessment for Oxides of
Nitrogen--Health Criteria. U.S. EPA, National Center for
Environmental Assessment and Office, Research Triangle Park, NC.
EPA/600/R-08/071. July 2008. Available at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=194645.
U.S. EPA (2008b). Risk and Exposure Assessment to Support the Review
of the NO2 Primary National Ambient Air Quality Standard. U.S. EPA,
Office of Air Quality Planning and Standards. Research Triangle
Park, NC. EPA 452/R-08-008a/b. November 2008. Available at: http://www.epa.gov/ttn/naaqs/standards/nox/s_nox_cr_rea.html.
U.S. EPA (2011). Policy Assessment for the Review of the Particulate
Matter National Ambient Air Quality Standards. Office of Air Quality
Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, NC. EPA 452/R-11-003. April 2011. Available
at: https://www3.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pa.html.
U.S. EPA (2014a). Integrated Review Plan for the Primary National
Ambient Air Quality Standards for Nitrogen Dioxide. U.S. EPA,
National Center for Environmental Assessment and Office of Air
Quality Planning and Standards, Research Triangle Park, NC. EPA-452/
R-14-003. June 2014. Available at: http://www.epa.gov/ttn/naaqs/standards/nox/data/201406finalirpprimaryno2.pdf.
U.S. EPA (2014b). Policy Assessment for the Review of the Ozone
National Ambient Air Quality Standards. Office of Air Quality
Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, NC. EPA 452/R-14-006. August 2014. Available
at: https://www3.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pa.html.
U.S. EPA (2015a). Preamble to the Integrated Science Assessments.
U.S. EPA, Washington, DC, EPA/600/R-15/067. November 2015. Available
at: https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=310244.
U.S. EPA (2015b). Review of the Primary National Ambient Air Quality
Standards for Nitrogen Dioxide: Risk and Exposure Assessment
Planning Document. U.S. EPA, Office of Air Quality Planning and
Standards, Research Triangle Park, NC. EPA-452/D-15-001. May 13,
2015. Available at: https://www3.epa.gov/ttn/naaqs/standards/nox/data/20150504reaplanning.pdf.
U.S. EPA (2016a). Integrated Science Assessment for Oxides of
Nitrogen--Health Criteria (2016 Final Report). U.S. EPA, National
Center for Environmental Assessment, Research Triangle Park, NC.
EPA/600/R-15/068. January 2016. Available at: https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=310879.
U.S. EPA (2016b). Integrated Review Plan for the National Ambient
Air Quality Standards for Particulate Matter. U.S. EPA, National
Center for Environmental Assessment and Office of Air Quality
Planning and Standards, Research Triangle Park, NC. EPA/452/R-16/
005. December 2016. Available at: https://www3.epa.gov/ttn/naaqs/standards/pm/data/201612-final-integrated-review-plan.pdf.
U.S. EPA (2017a). Policy Assessment for the Review of the Primary
National Ambient Air Quality Standards for Oxides of Nitrogen U.S.
EPA, National Center for Environmental Assessment, Research Triangle
Park, NC. EPA-452/R-17-003. April 2017. Available at: https://www.epa.gov/sites/production/files/2017-04/documents/policy_assessment_for_the_review_of_the_no2_naaqs_-_final_report.pdf.
U.S. EPA (2017b). Integrated Review Plan for the Secondary National
Ambient Air Quality Standards for Ecological Effects of Oxides of
Nitrogen, Oxides of Sulfur, and Particulate Matter U.S. EPA,
National Center for Environmental Assessment, Research Triangle
Park, NC. EPA-452/R-17-002. January 2017. Available at: http://ofmpub.epa.gov/eims/eimscomm.getfile?p_download_id=530335.
Villeneuve, PJ; Chen, L; Rowe, BH; Coates, F. (2007). Outdoor air
pollution and emergency department visits for asthma among children
and adults: A case-crossover study in northern Alberta, Canada.
Environ Health 6: 40. http://dx.doi.org/10.1186/1476-069X-6-40.
Witten, A; Solomon, C; Abbritti, E; Arjomandi, M; Zhai, W; Kleinman,
M; Balmes, J. (2005). Effects of nitrogen dioxide on allergic airway
responses in subjects with asthma. J Occup Environ Med 47: 1250-
1259. http://dx.doi.org/10.1097/01.jom.0000177081.62204.8d.
Wong, CM; Yang, L; Thach, TQ; Chau, PY; Chan, KP; Thomas, GN; Lam,
TH; Wong, TW; Hedley, AJ; Peiris, JS. (2009). Modification by
influenza on health effects of air pollution in Hong Kong. Environ
Health Perspect 117: 248-253. http://dx.doi.org/10.1289/ehp.11605.

List of Subjects in 40 CFR Part 50

    Environmental protection, Air pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.

    Dated: July 14, 2017.
E. Scott Pruitt,
Administrator.
[FR Doc. 2017-15591 Filed 7-25-17; 8:45 am]
BILLING CODE 6560-50-P