occur naturally in the atmosphere, human activities have changed their
atmospheric concentrations. From the pre-industrial era (i.e., ending
about 1750) to 2016, concentrations of these greenhouse gases have
increased globally by 44, 163, and 22%, respectively.\597\ The Draft
Environmental Impact Analysis (DEIS) accompanying today's notice
discusses potential impacts of greenhouse gases at greater length, and
also summaries analysis quantifying some of these impacts (e.g.,
average temperatures) for each of the considered regulatory
alternatives.
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    \597\ Impacts and U.S. emissions of GHGs are discussed at
greater length in EPA's 2018 Inventory of U.S. Greenhouse Gas
Emissions and Sinks (EPA 430-R-18-003) (Apr. 12, 2018), available at
https://www.epa.gov/sites/production/files/2018-01/documents/2018_complete_report.pdf.
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(a) CAFE Standards

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[GRAPHIC] [TIFF OMITTED] TP24AU18.242

(b) CO2 Standards

[GRAPHIC] [TIFF OMITTED] TP24AU18.243

[GRAPHIC] [TIFF OMITTED] TP24AU18.244

2. How would the proposal impact emissions of criteria and toxic
pollutants?
    Although this proposal focuses on standards for fuel economy and
CO2, it will also have an impact on criteria and air toxic
pollutant emissions, although as discussed above, it is expected that
incremental impacts on criteria and air toxic pollutant emissions would
be too small to observe under any of the regulatory alternatives under
consideration. Nevertheless, the following sections detail the criteria
pollutant and air toxic inventory impacts of this proposal; the
methodology used to calculate those impacts; the health and
environmental effects associated with the criteria and toxic air
pollutants that are being impacted by this proposal; the potential
impact of this proposal on concentrations of criteria and air toxic
pollutants in the ambient air; and other

unquantified health and environmental effects.
    Today's analysis reflects the combined result of several underlying
impacts, all discussed above. CAFE and CO2 standards are
estimated to impacts new vehicle prices, fuel economy levels, and
CO2 emission rates. These changes are estimated to impact
the size and composition of the new vehicle fleet and to impact the
retention of older vehicles (i.e., vehicle survival and scrappage) that
tend to have higher criteria and toxic pollutant emission rates. Along
with the rebound effect, these lead to changes in the overall amount of
highway travel and the distribution among different vehicles in the on-
road fleet. Vehicular emissions depend on the overall amount of highway
travel and the distribution of that travel among different vehicles,
and emissions from ``upstream'' processes (e.g., petroleum refining,
electricity generation) depend on the total consumption of different
types of fuels for light-duty vehicles.
(a) Impacts
    In addition to affecting fuel consumption and emissions of
greenhouse gases, this rule would influence ``non-GHG'' pollutants,
i.e., ``criteria'' air pollutants and their precursors, and air toxics.
The proposal would affect emissions of carbon monoxide (CO), fine
particulate matter (PM2.5), sulfur dioxide (SOX),
volatile organic compounds (VOC), nitrogen oxides (NOX),
benzene, 1,3-butadiene, formaldehyde, acetaldehyde, and acrolein.
Consistent with the evaluation conducted for the Environmental Impact
Statement accompanying this NPRM, the agency analyzed criteria air
pollutant impacts in 2025 and 2035 (as a representation of future
program impacts). Estimates of these non-GHG emission impacts are shown
by pollutant in Table VII-80 through Table VII-87 and are broken down
by the two drivers of these changes: (a) ``downstream'' emission
changes, reflecting the estimated effects of VMT rebound (discussed in
Chapter 8.7 of the PRIA), changes in vehicle fleet age, changes in
vehicle emission standards, and changes in fuel consumption; and (b)
``upstream'' emission increases because of increased refining and
distribution of motor vehicle gasoline relative to the baseline.
Program impacts on criteria and toxics emissions are discussed below,
followed by individual discussions of the methodology used to calculate
each of these three sources of impacts.\598\
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    \598\ The agencies have employed the same methodology in this
rulemaking to estimate the effect of each alternative on emissions
of PM and other criteria pollutants emissions as they have
previously applied in the other rulemakings under the National
Program. Briefly, emissions from vehicle use are estimated for each
calendar year of the analysis period by applying emission rates per
vehicle-mile of travel to estimates of VMT for cars and light trucks
produced during each model year making up the vehicle fleet. These
emission rates are derived from EPA's Motor Vehicle Emissions
Simulator (MOVES); they reflect normal increases in vehicles'
emission rates as they age and accumulate mileage, as well as
adopted and pending vehicle emission standards and regulations on
fuel composition. ``Upstream'' emissions from crude oil production,
fuel refining, and fuel distribution are estimated from the total
energy content of fuels produced and consumed (gasoline, diesel,
ethanol, and electricity), using separate emission factors per unit
of fuel energy for each phase of fuel production and distribution
derived from Argonne National Laboratories' Greenhouse Gases and
Regulated Emissions in Transportation (GREET) fuel cycle model. This
procedure accounts for differences in domestic emissions associated
with refining fuel from imported and domestically-supplied crude
petroleum, as well as from importing fuel that has been refined
outside the U.S. Economic damages caused by emissions from vehicle
use and from fuel production and distribution are monetized using
different per-ton values, which reflect differences in the locations
where emissions occur and resulting variation in population exposure
to their potential adverse health effects. However, we note that in
some other rules affecting tailpipe emissions of criteria
pollutants, EPA has employed more detailed methods for estimating
emissions associated with different phases of fuel production and
distribution, and has also used more detailed estimates of their
per-ton health damage costs that reflect variation in population
exposure to emissions occurring during different phases of fuel
production and distribution. The agencies will consider whether to
employ these more detailed procedures in their analysis supporting
the final rule.
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    As shown in Table VII-80, it is estimated in 2025 the light duty
vehicle CAFE scenarios would result in reductions of NOX,
VOC, and CO, and increases in PM2.5 and SOx.\599\ For
NOx, VOC, and CO, it is estimated net reductions result from
lower downstream, or tailpipe emissions in the scenarios evaluated.
This is a result of reduced VMT rebound as well as fewer older vehicles
in the scenarios as compared to the baseline. Because the scenarios
result in greater fuel consumption than the baseline, however, upstream
emissions associated with fuel refining and distribution increase for
all pollutants in all scenarios as compared to the baseline. Tailpipe
emissions reductions for NOx, VOC, and CO more than compensate for this
increase in 2025. PM2.5 and SOx, tailpipe
emissions reductions are not great enough to compensate for increased
emissions from fuel refining and distribution and therefore an overall
increase in total PM2.5 and SOx is seen in 2025.
Similar results can be seen in Table VII-81 which shows results for the
CO2 target scenarios.
---------------------------------------------------------------------------

    \599\ While estimates for CY 2025 and 2035 are shown here,
estimates through 2050 are shown in PRIA Chapter 5.
---------------------------------------------------------------------------

    In 2035, Table VII-82 shows decreases in total CO result from all
CAFE scenarios, while NOX, VOC, SO2, and
PM2.5 increase. Tailpipe CO emissions reductions more than
offset increases in upstream CO emissions. For NOX, VOC,
SO2, and PM2.5 however, upstream emissions
increases are not offset by tailpipe NOX, VOC,
SO2, and PM2.5 emissions reductions. Similar
results can be seen in the CO2 target scenarios for 2035
shown in Table VII-83, with the exception that NOX emission
decrease for scenarios 1-4 and increase for scenarios 5-8. For all
criteria pollutants, the overall impact of the proposed program would
be small compared to total U.S. inventories across all sectors.

[GRAPHIC] [TIFF OMITTED] TP24AU18.245

[GRAPHIC] [TIFF OMITTED] TP24AU18.246

    As shown in Table VII-84 through Table VII-87, it is estimated that
the proposed program would result in small changes for air toxic
emissions compared to total U.S. inventories across all sectors. In
2025, it is estimated the scenarios evaluated would reduce total
acetaldehyde, acrolein, benzene, butadiene, and formaldehyde, toxics as
compared to the baseline. This result is caused by greater VMT rebound
miles assumed in the augural scenario and fewer rebound VMT in
scenarios 1-8, and fewer older vehicles in the scenarios as compared to
the baseline. Similarly, in 2035, acetaldehyde, benzene, butadiene,
acrolein, and formaldehyde would all be reduced as compared to the
baseline. As is the case with criteria emissions, upstream toxic
emissions generally increase in the evaluated scenarios as compared to
the baseline because of the greater amount of gasoline and diesel being
refined and distributed.

[GRAPHIC] [TIFF OMITTED] TP24AU18.247

[GRAPHIC] [TIFF OMITTED] TP24AU18.248

(b) Methodology
    For the downstream analysis, emission factors in grams per mile for
VOC, CO, NOX, PM2.5, and air toxics by vehicle
model year and age were taken from the current version of the EPA
``Motor Vehicle Emission Simulator'' (MOVES2014a) and multiplied in the
CAFE model by assumed VMT to estimate mass VOC, CO, NOX,
PM2.5, and air toxics emissions. Additional emissions from
light duty cars and trucks attributable to the rebound effect were also
calculated using the CAFE model. A more complete discussion of the
inputs, methodology, and results is contained in PRIA Chapter 6. This
proposal also assumes implementation of EPA's Tier 3 emission
standards.\600\ For a more detailed description of the method used to
estimate emissions, please refer to pages 104-106 of the CAFE model
documentation.
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    \600\ See 79 FR 23414 (April 28, 2014). EPA's Tier 3 emissions
standards included standards for vehicle emissions and the sulfur
content of gasoline.
---------------------------------------------------------------------------

    For the purposes of this emission analysis, it is assumed that all
gasoline in the timeframe of the analysis is blended with 10% ethanol
(E10). While electric vehicles have zero tailpipe

emissions, it is assumed that manufacturers will plan for these
vehicles in their regulatory compliance strategy for non-GHG emissions
standards, and will not over-comply with those standards. Because the
Tier 3 emissions standards are fleet-average standards (for all
pollutants except formaldehyde and PM2.5), it is assumed
that if a manufacturer introduces EVs into its fleet, that it would
correspondingly compensate through changes to vehicles elsewhere in its
fleet, rather than meet an overall lower fleet-average emissions level.
Consequently, no tailpipe pollutant benefit (other than CO2,
formaldehyde, and PM2.5) is assumed. The analysis does not
estimate evaporative emissions from light-duty vehicles. Other factors
which may impact downstream non-GHG emissions, but are not estimated in
this analysis, include the potential for decreased criteria pollutant
emissions because of increased air conditioner efficiency; reduced
refueling emissions because of less frequent refueling events and
reduced annual refueling volumes resulting from the CO2
standards; and increased hot soak evaporative emissions because of the
likely increase in number of trips associated with VMT rebound modeled
in this proposal. In all, these additional analyses would likely result
in small changes relative to the national inventory.
    To determine the impacts of increased fuel production on upstream
emissions, the impact of increased gasoline consumption by light-duty
vehicles on the extraction and transportation of crude oil, refining of
crude oil, and distribution and storage of finished gasoline was
estimated. To assess the resulting increases in domestic emissions, the
fraction of increased gasoline consumption that would be supplied by
additional domestic refining of gasoline, and the fraction of that
gasoline that would be refined from domestic crude oil was estimated.
Using NEMS, it was estimated that 50% of increased gasoline consumption
would be supplied by increased domestic refining and that 90% of this
additional refining would use imported crude petroleum. Emission
factors for most upstream emission sources are based on the DOE Argonne
National Laboratory's GREET 2017 model,\601\ but emission factors
developed by EPA were relied on for the air toxics estimated in this
analysis: benzene, 1,3-butadiene, acetaldehyde, acrolein, and
formaldehyde. These emission factors came from the MOVES 2014a model
and were incorporated into the CAFE model.
---------------------------------------------------------------------------

    \601\ Greenhouse Gas, Regulated Emissions, and Energy Use in
Transportation model (GREET), U.S. Department of Energy, Argonne
National Laboratory, https://greet.es.anl.gov/.
---------------------------------------------------------------------------

    Emission factors for electricity upstream emissions were also based
on GREET 2017. GREET allows the user to either select a region of the
country for the electricity upstream emissions or to use the U.S.
average of electricity emissions. The regional emission factors reflect
the specific mix of fuels used to generate electricity in the selected
region. The U.S. mix provides an average of electricity-related
emissions (in grams per million Btu) in the U.S. in a given calendar
year. The GREET 2017 U.S. mix emission factors were used for the
analysis. In order to capture projected changes in upstream emissions
over time, upstream emission factors for gasoline, diesel, and
electricity were taken from the GREET 2017 model in five year
increments, beginning in 1995 and ending in 2040.
    For the downstream analysis of emissions, there are a number of
uncertainties associated with the method, such as: Emission factors are
based on samples of tested vehicles and these samples may not represent
average emissions for the full in-use fleet; and there is considerable
uncertainty in estimating total vehicle use (VMT). For the upstream
analysis of emissions, there are uncertainties related to the
projection of emissions associated with fossil fuel extraction,
refining, and mode split for transportation of fuels. In addition,
projections for electricity-related upstream emissions are based on
assumptions about the fuels and technologies used to generate
electricity which may not represent actual conditions through 2050.

E. Health Effects of Non-GHG Pollutants

    This section discusses health effects associated with exposure to
some of the criteria and air toxic pollutants impacted by the proposed
vehicle standards.
1. Particulate Matter
(a) Background
    Particulate matter is a highly complex mixture of solid particles
and liquid droplets distributed among numerous atmospheric gases which
interact with solid and liquid phases. Particles range in size from
those smaller than 1 nanometer (10-9 meter) to more than 100
micrometers ([micro]m, or 10-6 meter) in diameter (for reference, a
typical strand of human hair is 70 [micro]m in diameter and a grain of
salt is approximately 100 [micro]m). Atmospheric particles can be
grouped into several classes according to their aerodynamic and
physical sizes. Generally, the three broad classes of particles include
ultrafine particles (UFPs, generally considered as particulates with a
diameter less than or equal to 0.1 [micro]m [typically based on
physical size, thermal diffusivity or electrical mobility]), ``fine''
particles (PM2.5; particles with a nominal mean aerodynamic
diameter less than or equal to 2.5 [micro]m), and ``thoracic''
particles (PM10; particles with a nominal mean aerodynamic
diameter less than or equal to 10 [micro]m).\602\ Particles that fall
within the size range between PM2.5 and PM10, are
referred to as ``thoracic coarse particles'' (PM10-2.5,
particles with a nominal mean aerodynamic diameter less than or equal
to 10 [micro]m and greater than 2.5 [micro]m). EPA currently has
standards that regulate PM2.5 and PM10.\603\
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    \602\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Figure 3-1.
    \603\ Regulatory definitions of PM size fractions, and
information on reference and equivalent methods for measuring PM in
ambient air, are provided in 40 CFR parts 50, 53, and 58. With
regard to national ambient air quality standards (NAAQS) which
provide protection against health and welfare effects, the 24-hour
PM10 standard provides protection against effects
associated with short-term exposure to thoracic coarse particles
(i.e., PM10-2.5).
---------------------------------------------------------------------------

    Particles span many sizes and shapes and may consist of hundreds of
different chemicals. Particles are emitted directly from sources and
are also formed through atmospheric chemical reactions; the former are
often referred to as ``primary'' particles, and the latter as
``secondary'' particles. Particle concentration and composition varies
by time of year and location, and, in addition to differences in source
emissions, is affected by several weather-related factors, such as
temperature, clouds, humidity, and wind. A further layer of complexity
comes from particles' ability to shift between solid/liquid and gaseous
phases, which is influenced by concentration and meteorology,
especially temperature.
    Fine particles are produced primarily by combustion processes and
by transformations of gaseous emissions (e.g., sulfur oxides
(SOX), oxides of nitrogen, and volatile organic compounds
(VOC)) in the atmosphere. The chemical and physical properties of
PM2.5 may vary greatly with time, region, meteorology, and
source category. Thus, PM2.5 may include a complex mixture
of different components including sulfates, nitrates, organic
compounds, elemental carbon and metal compounds. These particles can
remain in the atmosphere for days

to weeks and travel hundreds to thousands of kilometers.
(b) Health Effects of PM
    Scientific studies show exposure to ambient PM is associated with a
broad range of health effects. These health effects are discussed in
detail in the 2009 Integrated Science Assessment for Particulate Matter
(PM ISA), which was used as the basis of the 2012 NAAQS.\604\ The PM
ISA summarizes health effects evidence for short- and long-term
exposures to PM2.5, PM10-2.5, and ultrafine
particles.\605\ The PM ISA concludes that human exposures to ambient
PM2.5 are associated with a number of adverse health effects
and characterizes the weight of evidence for broad health categories
(e.g., cardiovascular effects, respiratory effects, etc.).\606\ The
discussion below highlights the PM ISA's conclusions pertaining to
health effects associated with both short- and long-term PM exposures.
Further discussion of health effects associated with PM can also be
found in the rulemaking documents for the most recent review of the PM
NAAQS completed in 2012.607 608
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    \604\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F.
    \605\ The ISA also evaluated evidence for individual PM
components but did not reach causal determinations for components.
    \606\ The causal framework draws upon the assessment and
integration of evidence from across epidemiological, controlled
human exposure, and toxicological studies, and the related
uncertainties that ultimately influence our understanding of the
evidence. This framework employs a five-level hierarchy that
classifies the overall weight of evidence and causality using the
following categorizations: Causal relationship, likely to be causal
relationship, suggestive of a causal relationship, inadequate to
infer a causal relationship, and not likely to be a causal
relationship (U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Table 1-3).
    \607\ 78 FR 3103-3104 (Jan. 15, 2013).
    \608\ 77 FR 38906-38911 (June 29, 2012).
---------------------------------------------------------------------------

    EPA has concluded that ``a causal relationship exists'' between
both long- and short-term exposures to PM2.5 and premature
mortality and cardiovascular effects and that ``a causal relationship
is likely to exist'' between long- and short-term PM2.5
exposures and respiratory effects. Further, there is evidence
``suggestive of a causal relationship'' between long-term
PM2.5 exposures and other health effects, including
developmental and reproductive effects (e.g., low birth weight, infant
mortality) and carcinogenic, mutagenic, and genotoxic effects (e.g.,
lung cancer mortality).\609\
---------------------------------------------------------------------------

    \609\ These causal inferences are based not only on the more
expansive epidemiological evidence available in this review but also
reflect consideration of important progress that has been made to
advance our understanding of a number of potential biologic modes of
action or pathways for PM-related cardiovascular and respiratory
effects (U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Chapter 5).
---------------------------------------------------------------------------

    As summarized in the final rule promulgating the 2012 PM NAAQS, and
discussed extensively in the 2009 PM ISA, the available scientific
evidence significantly strengthens the link between long- and short-
term exposure to PM2.5 and mortality, while providing
indications that the magnitude of the PM2.5-mortality
association with long-term exposures may be larger than previously
estimated.610 611 The strongest evidence comes from recent
studies investigating long-term exposure to PM2.5 and
cardiovascular-related mortality. The evidence supporting a causal
relationship between long-term PM2.5 exposure and mortality
also includes consideration of studies that demonstrated an improvement
in community health following reductions in ambient fine particles.
---------------------------------------------------------------------------

    \610\ 78 FR 3103-3104 (Jan. 15, 2013).
    \611\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Chapter 6 (Section 6.5)
and Chapter 7 (Section 7.6).
---------------------------------------------------------------------------

    The 2009 PM ISA examined the association between cardiovascular
effects and long-term PM2.5 exposures in multi-city
epidemiological studies conducted in the U.S. and Europe. These studies
have provided new evidence linking long-term exposure to
PM2.5 with an array of cardiovascular effects such as heart
attacks, congestive heart failure, stroke, and mortality. This evidence
is coherent with epidemiological studies of effects associated with
short-term exposure to PM2.5 that have observed associations
with a continuum of effects ranging from subtle changes in indicators
of cardiovascular health to serious clinical events, such as increased
hospitalizations and emergency department visits due to cardiovascular
disease and cardiovascular mortality.\612\
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    \612\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Chapter 2 (Section 2.3.1
and 2.3.2) and Chapter 6.
---------------------------------------------------------------------------

    As detailed in the 2009 PM ISA, extended analyses of seminal
epidemiological studies, as well as more recent epidemiological studies
conducted in the U.S. and abroad, provide strong evidence of
respiratory-related morbidity effects associated with long-term
PM2.5 exposure. The strongest evidence for respiratory-
related effects is from studies that evaluated decrements in lung
function growth (in children), increased respiratory symptoms, and
asthma development. The strongest evidence from short-term
PM2.5 exposure studies has been observed for increased
respiratory-related emergency department visits and hospital admissions
for chronic obstructive pulmonary disease (COPD) and respiratory
infections.\613\
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    \613\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Chapter 2 (Section 2.3.1
and 2.3.2) and Chapter 6.
---------------------------------------------------------------------------

    The body of scientific evidence detailed in the 2009 PM ISA is
still limited with respect to associations between long-term
PM2.5 exposures and developmental and reproductive effects
as well as cancer, mutagenic, and genotoxic effects. The strongest
evidence for an association between PM2.5 and developmental
and reproductive effects comes from epidemiological studies of low
birth weight and infant mortality, especially due to respiratory causes
during the post-neonatal period (i.e., 1 month to 12 months of
age).\614\ With regard to cancer effects, ``[m]ultiple epidemiologic
studies have shown a consistent positive association between
PM2.5 and lung cancer mortality, but studies have generally
not reported associations between PM2.5 and lung cancer
incidence.'' \615\
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    \614\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Chapter 2 (Section 2.3.1
and 2.3.2) and Chapter 7.
    \615\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. pg 2-13.
---------------------------------------------------------------------------

    In addition to evaluating the health effects attributed to short-
and long-term exposure to PM2.5, the 2009 PM ISA also
evaluated whether specific components or sources of PM2.5
are more strongly associated with specific health effects. The 2009 PM
ISA concluded that ``many [components] of PM can be linked with
differing health effects, and the evidence is not yet sufficient to
allow differentiation of those [components] or sources that are more
closely related to specific health outcomes.'' \616\
---------------------------------------------------------------------------

    \616\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. pg 2-26.
---------------------------------------------------------------------------

    For PM10-2.5, the 2009 PM ISA concluded that available
evidence was ``suggestive of a causal relationship'' between short-term
exposures to PM10-2.5 and cardiovascular effects (e.g.,
hospital admissions and Emergency Department (ED) visits, changes in

cardiovascular function), respiratory effects (e.g., ED visits and
hospital admissions, increase in markers of pulmonary inflammation),
and premature mortality. The scientific evidence was ``inadequate to
infer a causal relationship'' between long-term exposure to
PM10-2.5 and various health effects.617 618 619
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    \617\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Section 2.3.4 and Table
2-6.
    \618\ 78 FR 3167-3168 (Jan. 15, 2013).
    \619\ 77 FR 38947-38951 (June 29, 2012).
---------------------------------------------------------------------------

    For UFPs, the 2009 PM ISA concluded that the evidence was
``suggestive of a causal relationship'' between short-term exposures
and cardiovascular effects, including changes in heart rhythm and
vasomotor function (the ability of blood vessels to expand and
contract). It also concluded that there was evidence ``suggestive of a
causal relationship'' between short-term exposure to UFPs and
respiratory effects, including lung function and pulmonary
inflammation, with limited and inconsistent evidence for increases in
ED visits and hospital admissions. Scientific evidence was ``inadequate
to infer a causal relationship'' between short-term exposure to UFPs
and additional health effects including premature mortality as well as
long-term exposure to UFPs and all health outcomes
evaluated.620 621
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    \620\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Section 2.3.5 and Table
2-6.
    \621\ 78 FR 3121 (Jan. 15, 2013).
---------------------------------------------------------------------------

    The 2009 PM ISA conducted an evaluation of specific groups within
the general population potentially at increased risk for experiencing
adverse health effects related to PM
exposures.622 623 624 625 The evidence detailed in the 2009
PM ISA expands our understanding of previously identified at-risk
populations and lifestages (i.e., children, older adults, and
individuals with pre-existing heart and lung disease) and supports the
identification of additional at-risk populations (e.g., persons with
lower socioeconomic status, genetic differences). Additionally, there
is emerging, though still limited, evidence for additional potentially
at-risk populations and lifestages, such as those with diabetes, people
who are obese, pregnant women, and the developing fetus.\626\
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    \622\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Chapter 8 and Chapter 2.
    \623\ 77 FR 38890 (June 29, 2012).
    \624\ 78 FR 3104 (Jan. 15, 2013).
    \625\ U.S. EPA. (2011). Policy Assessment for the Review of the
PM NAAQS. U.S. Environmental Protection Agency, Washington, DC, EPA/
452/R-11-003. Section 2.2.1.
    \626\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Chapter 8 and Chapter 2
(Section 2.4.1).
---------------------------------------------------------------------------

2. Ozone
(a) Background
    Ground-level ozone pollution is typically formed through reactions
involving VOC and NOX in the lower atmosphere in the
presence of sunlight. These pollutants, often referred to as ozone
precursors, are emitted by many types of sources, such as highway and
nonroad motor vehicles and engines, power plants, chemical plants,
refineries, makers of consumer and commercial products, industrial
facilities, and smaller area sources.
    The science of ozone formation, transport, and accumulation is
complex. Ground-level ozone is produced and destroyed in a cyclical set
of chemical reactions, many of which are sensitive to temperature and
sunlight. When ambient temperatures and sunlight levels remain high for
several days and the air is relatively stagnant, ozone and its
precursors can build up and result in more ozone than typically occurs
on a single high-temperature day. Ozone and its precursors can be
transported hundreds of miles downwind from precursor emissions,
resulting in elevated ozone levels even in areas with low local VOC or
NOX emissions.
(b) Health Effects of Ozone
    This section provides a summary of the health effects associated
with exposure to ambient concentrations of ozone.\627\ The information
in this section is based on the information and conclusions in the
February 2013 Integrated Science Assessment for Ozone (Ozone ISA),
which formed the basis for EPA's revision to the primary and secondary
standards in 2015.\628\ The Ozone ISA concludes that human exposures to
ambient concentrations of ozone are associated with a number of adverse
health effects and characterizes the weight of evidence for these
health effects.\629\ The discussion below highlights the Ozone ISA's
conclusions pertaining to health effects associated with both short-
term and long-term periods of exposure to ozone.
---------------------------------------------------------------------------

    \627\ Human exposure to ozone varies over time due to changes in
ambient ozone concentration and because people move between
locations which have notable different ozone concentrations. Also,
the amount of ozone delivered to the lung is not only influenced by
the ambient concentrations but also by the individuals breathing
route and rate.
    \628\ U.S. EPA. Integrated Science Assessment of Ozone and
Related Photochemical Oxidants (Final Report). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-10/076F, 2013. The ISA
is available at http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492#Download.
    \629\ The ISA evaluates evidence and draws conclusions on the
causal nature of relationship between relevant pollutant exposures
and health effects, assigning one of five ``weight of evidence''
determinations: Causal relationship, likely to be a causal
relationship, suggestive of, but not sufficient to infer, a causal
relationship, inadequate to infer a causal relationship, and not
likely to be a causal relationship. For more information on these
levels of evidence, please refer to Table II in the Preamble of the
ISA.
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    For short-term exposure to ozone, the Ozone ISA concludes that
respiratory effects, including lung function decrements, pulmonary
inflammation, exacerbation of asthma, respiratory-related hospital
admissions, and mortality, are causally associated with ozone exposure.
It also concludes that cardiovascular effects, including decreased
cardiac function and increased vascular disease, and total mortality
are likely to be causally associated with short-term exposure to ozone,
and that evidence is suggestive of a causal relationship between
central nervous system effects and short-term exposure to ozone.
    For long-term exposure to ozone, the Ozone ISA concludes that
respiratory effects, including new onset asthma, pulmonary inflammation
and injury, are likely to be causally related with ozone exposure. The
Ozone ISA characterizes the evidence as suggestive of a causal
relationship for associations between long-term ozone exposure and
cardiovascular effects, reproductive and developmental effects, central
nervous system effects and total mortality. The evidence is inadequate
to infer a causal relationship between chronic ozone exposure and
increased risk of lung cancer.
    Finally, inter-individual variation in human responses to ozone
exposure can result in some groups being at increased risk for
detrimental effects in response to exposure. In addition, some groups
are at increased risk of exposure due to their activities, such as
outdoor workers or children. The Ozone ISA identified several groups
that are at increased risk for ozone-related health effects. These
groups are people with asthma, children and older adults, individuals
with reduced intake of certain nutrients (i.e., Vitamins C and E),
outdoor workers, and individuals having certain genetic variants
related to oxidative metabolism or inflammation. Ozone exposure during
childhood can have lasting effects through adulthood. Such effects
include altered function of the

respiratory and immune systems. Children absorb higher doses
(normalized to lung surface area) of ambient ozone, compared to adults,
due to their increased time spent outdoors, higher ventilation rates
relative to body size, and a tendency to breathe a greater fraction of
air through the mouth. Children also have a higher asthma prevalence
compared to adults.
3. Nitrogen Oxides
(a) Background
    Oxides of nitrogen (NOX) refers to nitric oxide and
nitrogen dioxide (NO2). For the NOX NAAQS,
NO2 is the indicator. Most NO2 is formed in the
air through the oxidation of nitric oxide (NO) emitted when fuel is
burned at a high temperature. NOX is also a major
contributor to secondary PM2.5 formation. NOX and
VOC are the two major precursors of ozone.
(b) Health Effects of Nitrogen Oxides
    The most recent review of the health effects of oxides of nitrogen
completed by EPA can be found in the 2016 Integrated Science Assessment
for Oxides of Nitrogen--Health Criteria (Oxides of Nitrogen ISA).\630\
The primary source of NO2 is motor vehicle emissions, and
ambient NO2 concentrations tend to be highly correlated with
other traffic-related pollutants. Thus, a key issue in characterizing
the causality of NO2-health effect relationships was
evaluating the extent to which studies supported an effect of
NO2 that is independent of other traffic-related pollutants.
EPA concluded that the findings for asthma exacerbation integrated from
epidemiologic and controlled human exposure studies provided evidence
that is sufficient to infer a causal relationship between respiratory
effects and short-term NO2 exposure. The strongest evidence
supporting an independent effect of NO2 exposure comes from
controlled human exposure studies demonstrating increased airway
responsiveness in individuals with asthma following ambient-relevant
NO2 exposures. The coherence of this evidence with
epidemiologic findings for asthma hospital admissions and ED visits as
well as lung function decrements and increased pulmonary inflammation
in children with asthma describe a plausible pathway by which
NO2 exposure can cause an asthma exacerbation. The 2016 ISA
for Oxides of Nitrogen also concluded that there is likely to be a
causal relationship between long-term NO2 exposure and
respiratory effects. This conclusion is based on new epidemiologic
evidence for associations of NO2 with asthma development in
children combined with biological plausibility from experimental
studies.
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    \630\ U.S. EPA. Integrated Science Assessment for Oxides of
Nitrogen--Health Criteria (2016 Final Report). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-15/068, 2016.
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    In evaluating a broader range of health effects, the 2016 ISA for
Oxides of Nitrogen concluded evidence is ``suggestive of, but not
sufficient to infer, a causal relationship'' between short-term
NO2 exposure and cardiovascular effects and mortality and
between long-term NO2 exposure and cardiovascular effects
and diabetes, birth outcomes, and cancer. In addition, the scientific
evidence is inadequate (insufficient consistency of epidemiologic and
toxicological evidence) to infer a causal relationship for long-term
NO2 exposure with fertility, reproduction, and pregnancy, as
well as with postnatal development. A key uncertainty in understanding
the relationship between these non-respiratory health effects and
short- or long-term exposure to NO2 is copollutant
confounding, particularly by other roadway pollutants. The available
evidence for non-respiratory health effects does not adequately address
whether NO2 has an independent effect or whether it
primarily represents effects related to other or a mixture of traffic-
related pollutants.
    The 2016 ISA for Oxides of Nitrogen concluded that people with
asthma, children, and older adults are at increased risk for
NO2-related health effects. In these groups and lifestages,
NO2 is consistently related to larger effects on outcomes
related to asthma exacerbation, for which there is confidence in the
relationship with NO2 exposure.
4. Sulfur Oxides
(a) Background
    Sulfur dioxide (SO2), a member of the sulfur oxide
(SOX) family of gases, is formed from burning fuels
containing sulfur (e.g., coal or oil derived), extracting gasoline from
oil, or extracting metals from ore. SO2 and its gas phase
oxidation products can dissolve in water droplets and further oxidize
to form sulfuric acid which reacts with ammonia to form sulfates, which
are important components of ambient PM.
(b) Health Effects of SO2
    Information on the health effects of SO2 can be found in
the 2008 Integrated Science Assessment for Sulfur Oxides--Health
Criteria (SOX ISA).\631\ Short-term peaks (5-10 minutes) of
SO2 have long been known to cause adverse respiratory health
effects, particularly among individuals with asthma. In addition to
those with asthma (both children and adults), potentially at-risk
lifestages include all children and the elderly. During periods of
elevated ventilation, asthmatics may experience symptomatic
bronchoconstriction within minutes of exposure. Following an extensive
evaluation of health evidence from epidemiologic and laboratory
studies, EPA concluded that there is a causal relationship between
respiratory health effects and short-term exposure to SO2.
Separately, based on an evaluation of the epidemiologic evidence of
associations between short-term exposure to SO2 and
mortality, EPA concluded that the overall evidence is suggestive of a
causal relationship between short-term exposure to SO2 and
mortality.
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    \631\ U.S. EPA. (2008). Integrated Science Assessment (ISA) for
Sulfur Oxides--Health Criteria (Final Report). EPA/600/R-08/047F.
Washington, DC: U.S. Environmental Protection Agency.
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5. Carbon Monoxide
(a) Background
    Carbon monoxide is a colorless, odorless gas emitted from
combustion processes. Nationally, particularly in urban areas, the
majority of CO emissions to ambient air come from mobile sources.\632\
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    \632\ U.S. EPA, (2010). Integrated Science Assessment for Carbon
Monoxide (Final Report). U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-09/019F, 2010. Available at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=218686. See Section
2.1.
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(b) Health Effects of Carbon Monoxide
    Information on the health effects of CO can be found in the January
2010 Integrated Science Assessment for Carbon Monoxide (CO ISA)
associated with the 2010 evaluation of the NAAQS.\633\ The CO ISA
presents conclusions regarding the presence of causal relationships
between CO exposure and categories of adverse health effects. This
section provides a summary of the health effects associated with
exposure to ambient concentrations of CO, along with the ISA
conclusions.\634\
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    \633\ U.S. EPA, (2010). Integrated Science Assessment for Carbon
Monoxide (Final Report). U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-09/019F, 2010. Available at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=218686.
    \634\ Personal exposure includes contributions from many sources
and in many different environments. Total personal exposure to CO
includes both ambient and nonambient components; both components may
contribute to adverse health effects.

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    Controlled human exposure studies of subjects with coronary artery
disease show a decrease in the time to onset of exercise-induced angina
(chest pain) and electrocardiogram changes following CO exposure. In
addition, epidemiologic studies observed associations between short-
term CO exposure and cardiovascular morbidity, particularly increased
emergency room visits and hospital admissions for coronary heart
disease (including ischemic heart disease, myocardial infarction, and
angina). Some epidemiologic evidence is also available for increased
hospital admissions and emergency room visits for congestive heart
failure and cardiovascular disease as a whole. The CO ISA concludes
that a causal relationship is likely to exist between short-term
exposures to CO and cardiovascular morbidity. It also concludes that
available data are inadequate to conclude that a causal relationship
exists between long-term exposures to CO and cardiovascular morbidity.
    Animal studies show various neurological effects with in-utero CO
exposure. Controlled human exposure studies report central nervous
system and behavioral effects following low-level CO exposures,
although the findings have not been consistent across all studies. The
CO ISA concludes the evidence is suggestive of a causal relationship
with both short- and long-term exposure to CO and central nervous
system effects.
    A number of studies cited in the CO ISA have evaluated the role of
CO exposure in birth outcomes such as preterm birth or cardiac birth
defects. There is limited epidemiologic evidence of a CO-induced effect
on preterm births and birth defects, with weak evidence for a decrease
in birth weight. Animal toxicological studies have found perinatal CO
exposure to affect birth weight, as well as other developmental
outcomes. The CO ISA concludes the evidence is suggestive of a causal
relationship between long-term exposures to CO and developmental
effects and birth outcomes.
    Epidemiologic studies provide evidence of associations between
short-term CO concentrations and respiratory morbidity such as changes
in pulmonary function, respiratory symptoms, and hospital admissions. A
limited number of epidemiologic studies considered copollutants such as
ozone, SO2, and PM in two-pollutant models and found that CO
risk estimates were generally robust, although this limited evidence
makes it difficult to disentangle effects attributed to CO itself from
those of the larger complex air pollution mixture. Controlled human
exposure studies have not extensively evaluated the effect of CO on
respiratory morbidity. Animal studies at levels of 50-100 ppm CO show
preliminary evidence of altered pulmonary vascular remodeling and
oxidative injury. The CO ISA concludes that the evidence is suggestive
of a causal relationship between short-term CO exposure and respiratory
morbidity, and inadequate to conclude that a causal relationship exists
between long-term exposure and respiratory morbidity.
    Finally, the CO ISA concludes that the epidemiologic evidence is
suggestive of a causal relationship between short-term concentrations
of CO and mortality. Epidemiologic evidence suggests an association
exists between short-term exposure to CO and mortality, but limited
evidence is available to evaluate cause-specific mortality outcomes
associated with CO exposure. In addition, the attenuation of CO risk
estimates which was often observed in copollutant models contributes to
the uncertainty as to whether CO is acting alone or as an indicator for
other combustion-related pollutants. The CO ISA also concludes that
there is not likely to be a causal relationship between relevant long-
term exposures to CO and mortality.
6. Diesel Exhaust
(a) Background
    Diesel exhaust consists of a complex mixture composed of
particulate matter, carbon dioxide, oxygen, nitrogen, water vapor,
carbon monoxide, nitrogen compounds, sulfur compounds and numerous low-
molecular-weight hydrocarbons. A number of these gaseous hydrocarbon
components are individually known to be toxic, including aldehydes,
benzene and 1,3-butadiene. The diesel particulate matter present in
diesel exhaust consists mostly of fine particles (<2.5 [micro]m), of
which a significant fraction is ultrafine particles (< 0.1 [micro]m).
These particles have a large surface area which makes them an excellent
medium for adsorbing organics, and their small size makes them highly
respirable. Many of the organic compounds present in the gases and on
the particles, such as polycyclic organic matter, are individually
known to have mutagenic and carcinogenic properties.
    Diesel exhaust varies significantly in chemical composition and
particle sizes between different engine types (heavy-duty, light-duty),
engine operating conditions (idle, acceleration, deceleration), and
fuel formulations (high/low sulfur fuel). Also, there are emissions
differences between on-road and nonroad engines because the nonroad
engines are generally of older technology. After being emitted in the
engine exhaust, diesel exhaust undergoes dilution as well as chemical
and physical changes in the atmosphere. The lifetime for some of the
compounds present in diesel exhaust ranges from hours to days.
(b) Health Effects of Diesel Exhaust
    In EPA's 2002 Diesel Health Assessment Document (Diesel HAD),
exposure to diesel exhaust was classified as likely to be carcinogenic
to humans by inhalation from environmental exposures, in accordance
with the revised draft 1996/1999 EPA cancer
guidelines.635 636 A number of other agencies (National
Institute for Occupational Safety and Health, the International Agency
for Research on Cancer, the World Health Organization, California EPA,
and the U.S. Department of Health and Human Services) made similar
hazard classifications prior to 2002. EPA also concluded in the 2002
Diesel HAD that it was not possible to calculate a cancer unit risk for
diesel exhaust due to limitations in the exposure data for the
occupational groups or the absence of a dose-response relationship.
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    \635\ U.S. EPA. (March 2005). Guidelines for Carcinogen Risk
Assessment EPA/630/P-03/001F, https://www.epa.gov/risk/guidelines-carcinogen-risk-assessment (Last accessed July 2018).
    \636\ U.S. EPA (2002). Health Assessment Document for Diesel
Engine Exhaust. EPA/600/8-90/057F Office of Research and
Development, Washington, DC. Retrieved on March 17, 2009 from http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=29060 (last accessed
July 2018). pp. 1-1 1-2.
---------------------------------------------------------------------------

    In the absence of a cancer unit risk, the Diesel HAD sought to
provide additional insight into the significance of the diesel exhaust
cancer hazard by estimating possible ranges of risk that might be
present in the population. An exploratory analysis was used to
characterize a range of possible lung cancer risk. The outcome was that
environmental risks of cancer from long-term diesel exhaust exposures
could plausibly range from as low as 10-5 to as high as 10-3. Because
of uncertainties, the analysis acknowledged that the risks could be
lower than 10-5, and a zero risk from diesel exhaust exposure could not
be ruled out.
    Non-cancer health effects of acute and chronic exposure to diesel
exhaust emissions are also of concern to EPA. EPA derived a diesel
exhaust reference

concentration (RfC) from consideration of four well-conducted chronic
rat inhalation studies showing adverse pulmonary effects. The RfC is 5
[micro]g/m3 for diesel exhaust measured as diesel particulate matter.
This RfC does not consider allergenic effects such as those associated
with asthma or immunologic or the potential for cardiac effects. There
was emerging evidence in 2002, discussed in the Diesel HAD, that
exposure to diesel exhaust can exacerbate these effects, but the
exposure-response data were lacking at that time to derive an RfC based
on these then-emerging considerations. The EPA Diesel HAD states,
``With [diesel particulate matter] being a ubiquitous component of
ambient PM, there is an uncertainty about the adequacy of the existing
[diesel exhaust] noncancer database to identify all of the pertinent
[diesel exhaust]-caused noncancer health hazards.'' The Diesel HAD also
notes ``that acute exposure to [diesel exhaust] has been associated
with irritation of the eye, nose, and throat, respiratory symptoms
(cough and phlegm), and neurophysiological symptoms such as headache,
lightheadedness, nausea, vomiting, and numbness or tingling of the
extremities.'' The Diesel HAD noted that the cancer and noncancer
hazard conclusions applied to the general use of diesel engines then on
the market and as cleaner engines replace a substantial number of
existing ones, the applicability of the conclusions would need to be
reevaluated.
    It is important to note that the Diesel HAD also briefly summarizes
health effects associated with ambient PM and discusses EPA's then-
annual PM2.5 NAAQS of 15 [micro]g/m3. In 2012, EPA revised
the annual PM2.5 NAAQS to 12 [micro]g/m3. There is a large
and extensive body of human data showing a wide spectrum of adverse
health effects associated with exposure to ambient PM, of which diesel
exhaust is an important component. The PM2.5 NAAQS is
designed to provide protection from the noncancer health effects and
premature mortality attributed to exposure to PM2.5. The
contribution of diesel PM to total ambient PM varies in different
regions of the country and also, within a region, from one area to
another. The contribution can be high in near-roadway environments, for
example, or in other locations where diesel engine use is concentrated.
    Since 2002, several new studies have been published which continue
to report increased lung cancer risk with occupational exposure to
diesel exhaust from older engines. Of particular note since 2011 are
three new epidemiology studies which have examined lung cancer in
occupational populations, for example, truck drivers, underground
nonmetal miners and other diesel motor-related occupations. These
studies reported increased risk of lung cancer with exposure to diesel
exhaust with evidence of positive exposure-response relationships to
varying degrees.\637\ \638\ \639\ These newer studies (along with
others that have appeared in the scientific literature) add to the
evidence EPA evaluated in the 2002 Diesel HAD and further reinforces
the concern that diesel exhaust exposure likely poses a lung cancer
hazard. The findings from these newer studies do not necessarily apply
to newer technology diesel engines b the newer engines have large
reductions in the emission constituents compared to older technology
diesel engines.
---------------------------------------------------------------------------

    \637\ Garshick, E., Laden, F., Hart, J.E., Davis, M.E., Eisen,
E.A., & Smith T.J. 2012. Lung cancer and elemental carbon exposure
in trucking industry workers. Environmental Health Perspectives.
120(9): 1301-1306.
    \638\ Silverman, D.T., Samanic, C.M., Lubin, J.H., Blair, A.E.,
Stewart, P.A., Vermeulen, R., & Attfield, M.D. (2012). The diesel
exhaust in miners study: a nested case-control study of lung cancer
and diesel exhaust. Journal of the National Cancer Institute.
    \639\ Olsson, A.C., et al. ``Exposure to diesel motor exhaust
and lung cancer risk in a pooled analysis from case-control studies
in Europe and Canada.'' American Journal of Respiratory and Critical
Care Medicine 183(7). (2011): 941-948.
---------------------------------------------------------------------------

    In light of the growing body of scientific literature evaluating
the health effects of exposure to diesel exhaust, in June 2012 the
World Health Organization's International Agency for Research on Cancer
(IARC), a recognized international authority on the carcinogenic
potential of chemicals and other agents, evaluated the full range of
cancer-related health effects data for diesel engine exhaust. IARC
concluded that diesel exhaust should be regarded as ``carcinogenic to
humans.'' \640\ This designation was an update from its 1988 evaluation
that considered the evidence to be indicative of a ``probable human
carcinogen.''
---------------------------------------------------------------------------

    \640\ IARC [International Agency for Research on Cancer].
(2013). Diesel and gasoline engine exhausts and some nitroarenes.
IARC Monographs Volume 105. [Online at http://monographs.iarc.fr/ENG/Monographs/vol105/index.php].
---------------------------------------------------------------------------

7. Air Toxics
(a) Background
    Light-duty vehicle emissions contribute to ambient levels of air
toxics that are known or suspected human or animal carcinogens, or that
have noncancer health effects. The population experiences an elevated
risk of cancer and other noncancer health effects from exposure to the
class of pollutants known collectively as ``air toxics.'' \641\ These
compounds include, but are not limited to, benzene, 1,3-butadiene,
formaldehyde, acetaldehyde, acrolein, polycyclic organic matter, and
naphthalene. These compounds were identified as national or regional
risk drivers or contributors in the 2011 National-scale Air Toxics
Assessment and have significant inventory contributions from mobile
sources.\642\
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    \641\ U.S. EPA. (2015) Summary of Results for the 2011 National-
Scale Assessment. http://www3.epa.gov/sites/production/files/2015-12/documents/2011-nata-summary-results.pdf.
    \642\ U.S. EPA (2015) 2011 National Air Toxics Assessment.
http://www3.epa.gov/national-air-toxics-assessment/2011-national-air-toxics-assessment.
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(b) Benzene
    EPA's Integrated Risk Information System (IRIS) database lists
benzene as a known human carcinogen (causing leukemia) by all routes of
exposure and concludes that exposure is associated with additional
health effects, including genetic changes in both humans and animals
and increased proliferation of bone marrow cells in mice.\643\ \644\
\645\ EPA states in its IRIS database that data indicate a causal
relationship between benzene exposure and acute lymphocytic leukemia
and suggest a relationship between benzene exposure and chronic non-
lymphocytic leukemia and chronic lymphocytic leukemia. EPA's IRIS
documentation for benzene also lists a range of 2.2 x 10-6 to 7.8 x 10-
6 per [micro]g/m3 as the unit risk estimate (URE) for benzene.\646\
\647\ The International Agency for Research on Cancer (IARC) has
determined that benzene is a human carcinogen and the U.S. Department
of Health and Human Services (DHHS) has characterized benzene as a
known human carcinogen.\648 649\
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    \643\ U.S. EPA. (2000). Integrated Risk Information System File
for Benzene. This material is available electronically at: https://www.epa.gov/iris (Last accessed July 2018)
    \644\ International Agency for Research on Cancer, IARC
monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29, some industrial chemicals and dyestuffs,
International Agency for Research on Cancer, World Health
Organization, Lyon, France 1982.
    \645\ Irons, R.D.; Stillman, W.S.; Colagiovanni, D.B.; Henry,
V.A. (1992). Synergistic action of the benzene metabolite
hydroquinone on myelopoietic stimulating activity of granulocyte/
macrophage colony-stimulating factor in vitro, Proc. Natl. Acad.
Sci. 89:3691-3695.
    \646\ A unit risk estimate is defined as the increase in the
lifetime risk of an individual who is exposed for a lifetime to 1
[micro]g/m3 benzene in air.
    \647\ U.S. EPA. (2000). Integrated Risk Information System File
for Benzene. This material is available electronically at: http://www3.epa.gov/iris/subst/0276.htm.
    \648\ International Agency for Research on Cancer (IARC).
(1987). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, Volume 29, Supplement 7, Some industrial
chemicals and dyestuffs, World Health Organization, Lyon, France.
    \649\ NTP. (2014). 13th Report on Carcinogens. Research Triangle
Park, NC: U.S. Department of Health and Human Services, Public
Health Service, National Toxicology Program.

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    A number of adverse noncancer health effects including blood
disorders, such as pre-leukemia and aplastic anemia, have also been
associated with long-term exposure to benzene. The most sensitive
noncancer effect observed in humans, based on current data, is the
depression of the absolute lymphocyte count in blood. EPA's inhalation
reference concentration (RfC) for benzene is 30 [micro]g/m3. The RfC is
based on suppressed absolute lymphocyte counts seen in humans under
occupational exposure conditions. In addition, recent work, including
studies sponsored by the Health Effects Institute, provides evidence
that biochemical responses are occurring at lower levels of benzene
exposure than previously known.\650\ \651\ \652\ \653\ EPA's IRIS
program has not yet evaluated these new data. EPA does not currently
have an acute reference concentration for benzene. The Agency for Toxic
Substances and Disease Registry (ATSDR) Minimal Risk Level (MRL) for
acute exposure to benzene is 29 [micro]g/m3 for 1-14 days exposure.
---------------------------------------------------------------------------

    \650\ Qu, O.; Shore, R.; Li, G.; Jin, X.; Chen, C.L.; Cohen, B.;
Melikian, A.; Eastmond, D.; Rappaport, S.; Li, H.; Rupa, D.;
Suramaya, R.; Songnian, W.; Huifant, Y.; Meng, M.; Winnik, M.; Kwok,
E.; Li, Y.; Mu, R.; Xu, B.; Zhang, X.; Li, K. (2003). HEI Report
115, Validation & Evaluation of Biomarkers in Workers Exposed to
Benzene in China.
    \651\ Qu, Q., R. Shore, G. Li, X. Jin, L.C. Chen, B. Cohen, et
al. (2002). Hematological changes among Chinese workers with a broad
range of benzene exposures. American. Journal of Industrial
Medicine. 42: 275-285.
    \652\ Lan, Qing, Zhang, L., Li, G., Vermeulen, R., et al.
(2004). Hematotoxically in Workers Exposed to Low Levels of Benzene.
Science 306: 1774-1776.
    \653\ Turtletaub, K.W. and Mani, C. (2003). Benzene metabolism
in rodents at doses relevant to human exposure from Urban Air.
Research Reports Health Effect Inst. Report No.113.
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(c) 1,3-Butadiene
    EPA has characterized 1,3-butadiene as carcinogenic to humans by
inhalation.\654 655\ The IARC has determined that 1,3-butadiene is a
human carcinogen and the U.S. DHHS has characterized 1,3-butadiene as a
known human carcinogen.\656\ \657\ \658\ There are numerous studies
consistently demonstrating that 1,3-butadiene is metabolized into
genotoxic metabolites by experimental animals and humans. The specific
mechanisms of 1,3-butadiene-induced carcinogenesis are unknown;
however, the scientific evidence strongly suggests that the
carcinogenic effects are mediated by genotoxic metabolites. Animal data
suggest that females may be more sensitive than males for cancer
effects associated with 1,3-butadiene exposure; there are insufficient
data in humans from which to draw conclusions about sensitive
subpopulations. The URE for 1,3-butadiene is 3 x 10-5 per
[micro]g/m\3\.\659\ 1,3-butadiene also causes a variety of reproductive
and developmental effects in mice; no human data on these effects are
available. The most sensitive effect was ovarian atrophy observed in a
lifetime bioassay of female mice.\660\ Based on this critical effect
and the benchmark concentration methodology, an RfC for chronic health
effects was calculated at 0.9 ppb (approximately 2 [micro]g/m3).
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    \654\ U.S. EPA. (2002). Health Assessment of 1,3-Butadiene.
Office of Research and Development, National Center for
Environmental Assessment, Washington Office, Washington, DC. Report
No. EPA600-P-98-001F. This document is available electronically at
http://www3.epa.gov/iris/supdocs/buta-sup.pdf.
    \655\ U.S. EPA. (2002). ``Full IRIS Summary for 1,3-butadiene
(CASRN 106-99-0)'' Environmental Protection Agency, Integrated Risk
Information System (IRIS), Research and Development, National Center
for Environmental Assessment, Washington, DC http://www3.epa.gov/iris/subst/0139.htm.
    \656\ International Agency for Research on Cancer (IARC).
(1999). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, Volume 71, Re-evaluation of some organic
chemicals, hydrazine and hydrogen peroxide and Volume 97 (in
preparation), World Health Organization, Lyon, France.
    \657\ International Agency for Research on Cancer (IARC).
(2008). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, 1,3-Butadiene, Ethylene Oxide and Vinyl Halides
(Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide) Volume 97, World
Health Organization, Lyon, France.
    \658\ NTP. (2014). 13th Report on Carcinogens. Research Triangle
Park, NC: U.S. Department of Health and Human Services, Public
Health Service, National Toxicology Program.
    \659\ U.S. EPA. (2002). ``Full IRIS Summary for 1,3-butadiene
(CASRN 106-99-0)'' Environmental Protection Agency, Integrated Risk
Information System (IRIS), Research and Development, National Center
for Environmental Assessment, Washington, DC https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=139 (Last accessed
July 10, 2018).
    \660\ Bevan, C.; Stadler, J.C.; Elliot, G.S.; et al. (1996).
Subchronic toxicity of 4-vinylcyclohexene in rats and mice by
inhalation. Fundamental Applied Toxicology. 32:1-10.
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(d) Formaldehyde
    In 1991, EPA concluded that formaldehyde is a carcinogen based on
nasal tumors in animal bioassays.\661\ An Inhalation URE for cancer and
a Reference Dose for oral noncancer effects were developed by the
agency and posted on the IRIS database. Since that time, the National
Toxicology Program (NTP) and International Agency for Research on
Cancer (IARC) have concluded that formaldehyde is a known human
carcinogen.\662\ \663\
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    \661\ EPA. Integrated Risk Information System. Formaldehyde
(CASRN 50-00-0) https://cfpub.epa.gov/ncea/iris/iris_documents/documents/subst/0419_summary.pdf (Last accessed July 2018).
    \662\ NTP. (2014). 13th Report on Carcinogens. Research Triangle
Park, NC: U.S. Department of Health and Human Services, Public
Health Service, National Toxicology Program.
    \663\ IARC Monographs on the Evaluation of Carcinogenic Risks to
Humans Volume 100F (2012): Formaldehyde.
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    The conclusions by IARC and NTP reflect the results of
epidemiologic research published since 1991 in combination with
previous animal, human and mechanistic evidence. Research conducted by
the National Cancer Institute reported an increased risk of
nasopharyngeal cancer and specific lymph hematopoietic malignancies
among workers exposed to formaldehyde.\664\ \665\ \666\ A National
Institute of Occupational Safety and Health study of garment workers
also reported increased risk of death due to leukemia among workers
exposed to formaldehyde.\667\ Extended follow-up of a cohort of British
chemical workers did not report evidence of an increase in
nasopharyngeal or lymph hematopoietic cancers, but a continuing
statistically significant excess in lung cancers was reported.\668\
Finally, a study of embalmers reported formaldehyde exposures to be
associated with an increased risk of myeloid leukemia but not brain
cancer.\669\
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    \664\ Hauptmann, M., Lubin, J. H., Stewart, P. A., Hayes, R. B.,
& Blair, A. 2003. Mortality from lymphohematopoetic malignancies
among workers in formaldehyde industries. Journal of the National
Cancer Institute 95: 1615-1623.
    \665\ Hauptmann, M., Lubin, J. H., Stewart, P. A., Hayes, R. B.,
& Blair, A. 2004. Mortality from solid cancers among workers in
formaldehyde industries. American Journal of Epidemiology 159: 1117-
1130.
    \666\ Beane Freeman, L. E., Blair, A., Lubin, J. H., Stewart, P.
A., Hayes, R. B., Hoover, R. N., & Hauptmann, M. 2009. Mortality
from lymph hematopoietic malignancies among workers in formaldehyde
industries: The National Cancer Institute cohort. Journal of the
National Cancer Institute. 101: 751-761.
    \667\ Pinkerton, L. E. 2004. Mortality among a cohort of garment
workers exposed to formaldehyde: an update. Occupational
Environmental Medicine 61: 193-200.
    \668\ Coggon, D., Harris, E. C. Poole, J., & Palmer, K. T. 2003.
Extended follow-up of a cohort of British chemical workers exposed
to formaldehyde. Journal of the National Cancer Institute. 95:1608-
1615.
    \669\ Hauptmann, M., Stewart P. A., Lubin J. H., Beane Freeman,
L. E., Hornung, R. W., Herrick, R. F., Hoover, R. N., Fraumeni, J.
F., & Hayes, R. B. 2009. Mortality from lymph hematopoietic
malignancies and brain cancer among embalmers exposed to
formaldehyde. Journal of the National Cancer Institute 101:1696-
1708.
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    Health effects of formaldehyde in addition to cancer were reviewed
by the Agency for Toxics Substances and

Disease Registry in 1999,\670\ supplemented in 2010,\671\ and by the
World Health Organization.\672\ These organizations reviewed the
scientific literature concerning health effects linked to formaldehyde
exposure to evaluate hazards and dose response relationships and
defined exposure concentrations for minimal risk levels (MRLs). The
health endpoints reviewed included sensory irritation of eyes and
respiratory tract, reduced pulmonary function, nasal histopathology,
and immune system effects. In addition, research on reproductive and
developmental effects and neurological effects were discussed along
with several studies that suggest that formaldehyde may increase the
risk of asthma, particularly in the young.
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    \670\ ATSDR. 1999. Toxicological Profile for Formaldehyde, U.S.
Department of Health and Human Services (HHS), July 1999.
    \671\ ATSDR. 2010. Addendum to the Toxicological Profile for
Formaldehyde. U.S. Department of Health and Human Services (HHS),
October 2010.
    \672\ IPCS. 2002. Concise International Chemical Assessment
Document 40. Formaldehyde. World Health Organization.
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    EPA released a draft Toxicological Review of Formaldehyde--
Inhalation Assessment through the IRIS program for peer review by the
National Research Council (NRC) and public comment in June 2010.\673\
The draft assessment reviewed more recent research from animal and
human studies on cancer and other health effects. The NRC released
their review report in April 2011.\674\ EPA is currently developing a
revised draft assessment in response to this review.
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    \673\ EPA (U.S. Environmental Protection Agency). 2010.
Toxicological Review of Formaldehyde (CAS No. 50-00-0)--Inhalation
Assessment: In Support of Summary Information on the Integrated Risk
Information System (IRIS). External Review Draft. EPA/635/R-10/002A.
U.S. Environmental Protection Agency, Washington DC [online].
Available: http://cfpub.epa.gov/ncea/irs_drats/recordisplay.cfm?deid=223614.
    \674\ NRC (National Research Council). 2011. Review of the
Environmental Protection Agency's Draft IRIS Assessment of
Formaldehyde. Washington DC: National Academies Press. http://books.nap.edu/openbook.php?record_id=13142.
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(e) Acetaldehyde
    Acetaldehyde is classified in EPA's IRIS database as a probable
human carcinogen, based on nasal tumors in rats, and is considered
toxic by the inhalation, oral, and intravenous routes.\675\ The URE in
IRIS for acetaldehyde is 2.2 x 10\-6\ per [micro]g/m\3\.\676\
Acetaldehyde is reasonably anticipated to be a human carcinogen by the
U.S. DHHS in the 13th Report on Carcinogens and is classified as
possibly carcinogenic to humans (Group 2B) by the IARC.\677\ \678\
Acetaldehyde is currently listed on the IRIS Program Multi-Year Agenda
for reassessment within the next few years.
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    \675\ U.S. EPA (1991). Integrated Risk Information System File
of Acetaldehyde. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
electronically at http://www3.epa.gov/iris/subst/0290.htm.
    \676\ U.S. EPA (1991). Integrated Risk Information System File
of Acetaldehyde. This material is available electronically at http://www3.epa.gov/iris/subst/0290.htm.
    \677\ NTP. (2014). 13th Report on Carcinogens. Research Triangle
Park, NC: U.S. Department of Health and Human Services, Public
Health Service, National Toxicology Program.
    \678\ International Agency for Research on Cancer (IARC).
(1999). Re-evaluation of some organic chemicals, hydrazine, and
hydrogen peroxide. IARC Monographs on the Evaluation of Carcinogenic
Risk of Chemical to Humans, Vol 71. Lyon, France.
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    The primary noncancer effects of exposure to acetaldehyde vapors
include irritation of the eyes, skin, and respiratory tract.\679\ In
short-term (four week) rat studies, degeneration of olfactory
epithelium was observed at various concentration levels of acetaldehyde
exposure.\680\ \681\ Data from these studies were used by EPA to
develop an inhalation reference concentration of 9 [micro]g/m\3\. Some
asthmatics have been shown to be a sensitive subpopulation to
decrements in functional expiratory volume (FEV1 test) and
bronchoconstriction upon acetaldehyde inhalation.\682\
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    \679\ U.S. EPA (1991). Integrated Risk Information System File
of Acetaldehyde. This material is available electronically at http://www3.epa.gov/iris/subst/0290.htm.
    \680\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
electronically at http://www3.epa.gov/iris/subst/0364.htm.
    \681\ Appleman, L.M., Woutersen, R. A., & Feron, V. J. (1982).
Inhalation toxicity of acetaldehyde in rats. I. Acute and subacute
studies. Toxicology. 23: 293-297.
    \682\ Myou, S., Fujimura, M., Nishi, K., Ohka, T., & Matsuda, T.
(1993) Aerosolized acetaldehyde induces histamine-mediated
bronchoconstriction in asthmatics. Am. Rev. Respir. Dis. 148(4 Pt
1): 940-943.
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(f) Acrolein
    EPA most recently evaluated the toxicological and health effects
literature related to acrolein in 2003 and concluded that the human
carcinogenic potential of acrolein could not be determined because the
available data were inadequate. No information was available on the
carcinogenic effects of acrolein in humans and the animal data provided
inadequate evidence of carcinogenicity.\683\ The IARC determined in
1995 that acrolein was not classifiable as to its carcinogenicity in
humans.\684\
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    \683\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
at http://www3.epa.gov/iris/subst/0364.htm.
    \684\ International Agency for Research on Cancer (IARC).
(1995). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, Volume 63. Dry cleaning, some chlorinated
solvents and other industrial chemicals, World Health Organization,
Lyon, France.
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    Lesions to the lungs and upper respiratory tract of rats, rabbits,
and hamsters have been observed after subchronic exposure to
acrolein.\685\ The agency has developed an RfC for acrolein of 0.02
[micro]g/m\3\ and an RfD of 0.5 [micro]g/kg-day.\686\
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    \685\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Office of Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
at http://www3.epa.gov/iris/subst/0364.htm.
    \686\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Office of Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
at http://www3.epa.gov/iris/subst/0364.htm.
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    Acrolein is extremely acrid and irritating to humans when inhaled,
with acute exposure resulting in upper respiratory tract irritation,
mucus hypersecretion and congestion. The intense irritancy of this
carbonyl has been demonstrated during controlled tests in human
subjects, who suffer intolerable eye and nasal mucosal sensory
reactions within minutes of exposure.\687\ These data and additional
studies regarding acute effects of human exposure to acrolein are
summarized in EPA's 2003 Toxicological Review of Acrolein.\688\ Studies
in humans indicate that levels as low as 0.09 ppm (0.21 mg/m3) for five
minutes may elicit subjective complaints of eye irritation with
increasing concentrations leading to more extensive eye, nose and
respiratory symptoms. Acute exposures in animal studies report
bronchial hyper-responsiveness. Based on animal data (more pronounced
respiratory irritancy in mice with allergic airway disease in
comparison to non-diseased mice \689\) and demonstration of similar
effects in humans (e.g., reduction in

respiratory rate), individuals with compromised respiratory function
(e.g., emphysema, asthma) are expected to be at increased risk of
developing adverse responses to strong respiratory irritants such as
acrolein. EPA does not currently have an acute reference concentration
for acrolein. The available health effect reference values for acrolein
have been summarized by EPA and include an ATSDR MRL for acute exposure
to acrolein of 7 [micro]g/m\3\ for 1-14 days' exposure; and Reference
Exposure Level (REL) values from the California Office of Environmental
Health Hazard Assessment (OEHHA) for one-hour and 8-hour exposures of
2.5 [micro]g/m\3\ and 0.7 [micro]g/m\3\, respectively.\690\
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    \687\ U.S. EPA. (2003) Toxicological review of acrolein in
support of summary information on Integrated Risk Information System
(IRIS) National Center for Environmental Assessment, Washington, DC.
EPA/635/R-03/003. p. 10. Available online at: http://www3.epa.gov/ncea/iris/toxreviews/0364tr.pdf.
    \688\ U.S. EPA. (2003) Toxicological review of acrolein in
support of summary information on Integrated Risk Information System
(IRIS) National Center for Environmental Assessment, Washington, DC.
EPA/635/R-03/003. Available online at: https://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=51977 (Last accessed July 10 2018).
    \689\ Morris, J. B., Symanowicz, P. T., Olsen, J. E., et al.
(2003). Immediate sensory nerve-mediated respiratory responses to
irritants in healthy and allergic airway-diseased mice. Journal of
Applied Physiology. 94(4):1563-1571.
    \690\ U.S. EPA. (2009). Graphical Arrays of Chemical-Specific
Health Effect Reference Values for Inhalation Exposures (Final
Report). U.S. Environmental Protection Agency, Washington, DC, EPA/
600/R-09/061, 2009. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003 (last accessed July 10 2018).
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(g) Polycyclic Organic Matter
    The term polycyclic organic matter (POM) defines a broad class of
compounds that includes the polycyclic aromatic hydrocarbon compounds
(PAHs). One of these compounds, naphthalene, is discussed separately
below. POM compounds are formed primarily from combustion and are
present in the atmosphere in gas and particulate form. Cancer is the
major concern from exposure to POM. Epidemiologic studies have reported
an increase in lung cancer in humans exposed to diesel exhaust, coke
oven emissions, roofing tar emissions, and cigarette smoke; all of
these mixtures contain POM compounds.\691\ \692\ Animal studies have
reported respiratory tract tumors from inhalation exposure to
benzo[a]pyrene and alimentary tract and liver tumors from oral exposure
to benzo[a]pyrene.\693\ In 1997 EPA classified seven PAHs
(benzo[a]pyrene, benz[a]anthracene, chrysene, benzo[b]fluoranthene,
benzo[k]fluoranthene, dibenz[a,h]anthracene, and indeno[1,2,3-
cd]pyrene) as Group B2, probable human carcinogens.\694\ Since that
time, studies have found that maternal exposures to PAHs in a
population of pregnant women were associated with several adverse birth
outcomes, including low birth weight and reduced length at birth, as
well as impaired cognitive development in preschool children (three
years of age).\695\ \696\ These and similar studies are being evaluated
as a part of the ongoing IRIS reassessment of health effects associated
with exposure to benzo[a]pyrene.
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    \691\ Agency for Toxic Substances and Disease Registry (ATSDR).
(1995). Toxicological profile for Polycyclic Aromatic Hydrocarbons
(PAHs). Atlanta, GA: U.S. Department of Health and Human Services,
Public Health Service. Available electronically at http://www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=122&tid=25.
    \692\ U.S. EPA (2002). Health Assessment Document for Diesel
Engine Exhaust. EPA/600/8-90/057F Office of Research and
Development, Washington DC. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=29060 (last accessed July 10 2018).
    \693\ International Agency for Research on Cancer (IARC).
(2012). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans, Chemical Agents and Related Occupations. Vol.
100F. Lyon, France.
    \694\ U.S. EPA (1997). Integrated Risk Information System File
of indeno (1,2,3-cd) pyrene. Research and Development, National
Center for Environmental Assessment, Washington, DC. This material
is available electronically at https://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=2776 (Last accessed July 10 2018).
    \695\ Perera, F. P., Rauh, V., Tsai, W. Y., et al. (2002).
Effect of transplacental exposure to environmental pollutants on
birth outcomes in a multiethnic population. Environmental Health
Perspectives. 111: 201-205.
    \696\ Perera, F. P., Rauh, V., Whyatt, R. M., Tsai, W. Y., Tang,
D., Diaz, D., Hoepner, L., Barr, D., Tu, Y. H., Camann, D., &
Kinney, P. (2006). Effect of prenatal exposure to airborne
polycyclic aromatic hydrocarbons on neurodevelopment in the first 3
years of life among inner-city children. Environmental Health
Perspectives. 114: 1287-1292.
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(h) Naphthalene
    Naphthalene is found in small quantities in gasoline and diesel
fuels. Naphthalene emissions have been measured in larger quantities in
both gasoline and diesel exhaust compared with evaporative emissions
from mobile sources, indicating it is primarily a product of
combustion. Acute (short-term) exposure of humans to naphthalene by
inhalation, ingestion, or dermal contact is associated with hemolytic
anemia and damage to the liver and the nervous system.\697\ Chronic
(long term) exposure of workers and rodents to naphthalene has been
reported to cause cataracts and retinal damage.\698\ EPA released an
external review draft of a reassessment of the inhalation
carcinogenicity of naphthalene based on a number of recent animal
carcinogenicity studies. The draft reassessment completed external peer
review.\699\ Based on external peer review comments received, a revised
draft assessment that considers all routes of exposure, as well as
cancer and noncancer effects, is under development. The external review
draft does not represent official agency opinion and was released
solely for the purposes of external peer review and public comment. The
National Toxicology Program listed naphthalene as ``reasonably
anticipated to be a human carcinogen'' in 2004 on the basis of
bioassays reporting clear evidence of carcinogenicity in rats and some
evidence of carcinogenicity in mice.\700\ California EPA has released a
new risk assessment for naphthalene, and the IARC has reevaluated
naphthalene and re-classified it as Group 2B: Possibly carcinogenic to
humans.\701\
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    \697\ U. S. EPA. 1998. Toxicological Review of Naphthalene
(Reassessment of the Inhalation Cancer Risk), Environmental
Protection Agency, Integrated Risk Information System, Research and
Development, National Center for Environmental Assessment,
Washington, DC. This material is available electronically at https://cfpub.epa.gov/ncea/iris/iris_documents/documents/toxreviews/0436tr.pdf (last accessed July 10 2018).
    \698\ U. S. EPA. 1998. Toxicological Review of Naphthalene
(Reassessment of the Inhalation Cancer Risk), Environmental
Protection Agency, Integrated Risk Information System, Research and
Development, National Center for Environmental Assessment,
Washington, DC. This material is available electronically at https://cfpub.epa.gov/ncea/iris/iris_documents/documents/toxreviews/0436tr.pdf (last accessed July 10 2018)
    \699\ Oak Ridge Institute for Science and Education. (2004).
External Peer Review for the IRIS Reassessment of the Inhalation
Carcinogenicity of Naphthalene. August 2004. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=84403.
    \700\ NTP. (2014). 13th Report on Carcinogens. U.S. Department
of Health and Human Services, Public Health Service, National
Toxicology Program.
    \701\ International Agency for Research on Cancer (IARC).
(2002). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans. Vol. 82. Lyon, France.
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    Naphthalene also causes a number of chronic non-cancer effects in
animals, including abnormal cell changes and growth in respiratory and
nasal tissues. The current EPA IRIS assessment includes noncancer data
on hyperplasia and metaplasia in nasal tissue that form the basis of
the inhalation RfC of 3 [micro]g/m\3\.\702\ The ATSDR MRL for acute
exposure to naphthalene is 0.6 mg/kg/day.
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    \702\ U.S. EPA. (1998). Toxicological Review of Naphthalene.
Environmental Protection Agency, Integrated Risk Information System
(IRIS), Research and Development, National Center for Environmental
Assessment, Washington, DC https://cfpub.epa.gov/ncea/iris/iris_documents/documents/toxreviews/0436tr.pdf (last accessed July
10 2018).
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(i) Other Air Toxics
    In addition to the compounds described above, other compounds in
gaseous hydrocarbon and PM emissions from motor vehicles will be
affected by this action. Mobile source air toxic compounds that will
potentially be impacted include ethylbenzene, propionaldehyde, toluene,
and xylene. Information regarding the health effects of these compounds
can be found in EPA's IRIS database.\703\
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    \703\ U.S. EPA Integrated Risk Information System (IRIS)
database is available at: https://www.epa.gov/iris (last accessed
July 10 2018)

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(j) Exposure and Health Effects Associated With Traffic
    Locations in close proximity to major roadways generally have
elevated concentrations of many air pollutants emitted from motor
vehicles. Hundreds of such studies have been published in peer-reviewed
journals, concluding that concentrations of CO, NO, NO2,
benzene, aldehydes, particulate matter, black carbon, and many other
compounds are elevated in ambient air within approximately 300-600
meters (approximately 1,000-2,000 feet) of major roadways. Highest
concentrations of most pollutants emitted directly by motor vehicles
are found at locations within 50 meters (approximately 165 feet) of the
edge of a roadway's traffic lanes.
    A large-scale review of air quality measurements in the vicinity of
major roadways between 1978 and 2008 concluded that the pollutants with
the steepest concentration gradients in vicinities of roadways were CO,
ultrafine particles, metals, elemental carbon (EC), NO, NOX,
and several VOCs.\704\ These pollutants showed a large reduction in
concentrations within 100 meters downwind of the roadway. Pollutants
that showed more gradual reductions with distance from roadways
included benzene, NO2, PM2.5, and
PM10. In the review article, results varied based on the
method of statistical analysis used to determine the trend.
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    \704\ Karner, A. A., Eisinger, D. S., & Niemeier, D. A. (2010).
Near-roadway air quality: synthesizing the findings from real-world
data. Environmental Science Technology. 44: 5334-5344.
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    For pollutants with relatively high background concentrations
relative to near-road concentrations, detecting concentration gradients
can be difficult. For example, many aldehydes have high background
concentrations as a result of photochemical breakdown of precursors
from many different organic compounds. This can make detection of
gradients around roadways and other primary emission sources difficult.
However, several studies have measured aldehydes in multiple weather
conditions and found higher concentrations of many carbonyls downwind
of roadways.\705\ \706\ These findings suggest a substantial roadway
source of these carbonyls.
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    \705\ Liu, W., Zhang, J., Kwon, J. et al. (2006). Concentrations
and source characteristics of airborne carbonyl comlbs measured
outside urban residences. Journal of the Air Waste Management
Assocication 56: 1196-1204.
    \706\ Cahill, T. M., Charles, M. J., & Seaman, V. Y. (2010).
Development and application of a sensitive method to determine
concentrations of acrolein and other carbonyls in ambient air.
Health Effects Institute Research Report 149.Available at https://www.healtheffects.org/publication/development-and-application-sensitive-method-determine-concentrations-acrolein-and-other (last
accessed July 10 2018)
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    In the past 15 years, many studies have been published with results
reporting that populations who live, work, or go to school near high-
traffic roadways experience higher rates of numerous adverse health
effects, compared to populations far away from major roads.\707\ In
addition, numerous studies have found adverse health effects associated
with spending time in traffic, such as commuting or walking along high-
traffic roadways; however, it is difficult to fully control for
confounding in such studies.\708\ \709\ \710\ \711\ The health outcomes
with the strongest evidence linking them with traffic-associated air
pollutants are respiratory effects, particularly in asthmatic children,
and cardiovascular effects.
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    \707\ In the widely-used PubMed database of health publications,
between January 1, 1990 and August 18, 2011, 605 publications
contained the keywords ``traffic, pollution, epidemiology,'' with
approximately half the studies published after 2007.
    \708\ Laden, F., Hart, J. E., Smith, T. J., Davis, M. E., &
Garshick, E. (2007) Cause-specific mortality in the unionized U.S.
trucking industry. Environmental Health Perspectives 115:1192-1196.
    \709\ Peters, A., von Klot, S., Heier, M., Trentinaglia, I.,
H[ouml]rmann, A., Wichmann, H. E., & L[ouml]wel, H. (2004) Exposure
to traffic and the onset of myocardial infarction. New England
Journal of Medicine. 351: 1721-1730.
    \710\ Zanobetti, A., Stone, P. H., Spelzer, F. E., Schwartz, J.
D., Coull, B. A., Suh, H. H., Nearling, B. D., Mittleman, M. A.,
Verrier, R. L., & Gold, D. R. (2009) T-wave alternans, air pollution
and traffic in high-risk subjects. American Journal of Cardiology.
104: 665-670.
    \711\ Dubowsky Adar, S., Adamkiewicz, G., Gold, D. R., Schwartz,
J., Coull, B. A., & Suh, H. (2007) Ambient and microenvironmental
particles and exhaled nitric oxide before and after a group bus
trip. Environmental Health Perspectives. 115: 507-512.
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    Numerous reviews of this body of health literature have been
published as well. In 2010, an expert panel of the Health Effects
Institute (HEI) published a review of hundreds of exposure,
epidemiology, and toxicology studies.\712\ The panel rated how the
evidence for each type of health outcome supported a conclusion of a
causal association with traffic-associated air pollution as either
``sufficient,'' ``suggestive but not sufficient,'' or ``inadequate and
insufficient.'' The panel categorized evidence of a causal association
for exacerbation of childhood asthma as ``sufficient.'' The panel
categorized evidence of a causal association for new onset asthma as
between ``sufficient'' and ``suggestive but not sufficient.''
``Suggestive of a causal association'' was how the panel categorized
evidence linking traffic-associated air pollutants with exacerbation of
adult respiratory symptoms and lung function decrement. It categorized
as ``inadequate and insufficient'' evidence of a causal relationship
between traffic-related air pollution and health care utilization for
respiratory problems, new onset adult asthma, chronic obstructive
pulmonary disease (COPD), nonasthmatic respiratory allergy, and cancer
in adults and children. Other literature reviews have been published
with conclusions generally similar to the HEI panel's.\713\ \714\ \715\
\716\ However, in 2014, researchers from the U.S. Centers for Disease
Control and Prevention (CDC) published a systematic review and meta-
analysis of studies evaluating the risk of childhood leukemia
associated with traffic exposure and reported positive associations
between ``postnatal'' proximity to traffic and leukemia risks, but no
such association for ``prenatal'' exposures.\717\
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    \712\ Health Effects Institute Panel on the Health Effects of
Traffic-Related Air Pollution. (2010). Traffic-related air
pollution: A critical review of the literature on emissions,
exposure, and health effects. HEI Special Report 17. Available at
http://www.healtheffects.org.
    \713\ Boothe, V. L. & Shendell, D. G. (2008). Potential health
effects associated with residential proximity to freeways and
primary roads: review of scientific literature, 1999-2006. Journal
of Environmental Health. 70: 33-41.
    \714\ Salam, M. T., Islam, T., & Gilliland, F. D. (2008). Recent
evidence for adverse effects of residential proximity to traffic
sources on asthma. Curr Opin Pulm Med 14: 3-8.
    \715\ Sun, X., Zhang, S., & Ma, X. (2014) No association between
traffic density and risk of childhood leukemia: a meta-analysis.
Asia Pacific Journal of Cancer Prevention. 15: 5229-5232.
    \716\ Raaschou-Nielsen, O. & Reynolds, P. (2006). Air pollution
and childhood cancer: A review of the epidemiological literature.
International Journal of Cancer. 118: 2920-9.
    \717\ Boothe, V. L., Boehmer, T. K., Wendel, A. M., & Yip, F. Y.
(2014) Residential traffic exposure and childhood leukemia: a
systematic review and meta-analysis. American Journal of
Preventative Medicine. 46: 413-422.
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    Health outcomes with few publications suggest the possibility of
other effects still lacking sufficient evidence to draw definitive
conclusions. Among these outcomes with a small number of positive
studies are neurological impacts (e.g., autism and reduced cognitive
function) and reproductive outcomes (e.g., preterm

birth, low birth weight).\718\ \719\ \720\ \721\
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    \718\ Volk, H. E., Hertz-Picciotto, I., Delwiche, L., et al.
(2011). Residential proximity to freeways and autism in the CHARGE
study. Environmental Health Perspectives. 119: 873-877.
    \719\ Franco-Suglia, S., Gryparis, A., Wright, R. O., et al.
(2007). Association of black carbon with cognition among children in
a prospective birth cohort study. American Journal of Epidemiology.
doi: 10.1093/aje/kwm308. [Online at http://dx.doi.org].
    \720\ Power, M. C., Weisskopf, M. G., Alexeef, S. E., et al.
(2011). Traffic-related air pollution and cognitive function in a
cohort of older men. Environmental Health Perspectives. 2011: 682-
687.
    \721\ Wu, J., Wilhelm, M., Chung, J., et al. (2011). Comparing
exposure assessment methods for traffic-related air pollution in and
adverse pregnancy outcome study. Environmental Research. 111: 685-
6692.
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    In addition to health outcomes, particularly cardiopulmonary
effects, conclusions of numerous studies suggest mechanisms by which
traffic-related air pollution affects health. Numerous studies indicate
that near-roadway exposures may increase systemic inflammation,
affecting organ systems, including blood vessels and lungs.\722\ \723\
\724\ \725\ Long-term exposures in near-road environments have been
associated with inflammation-associated conditions, such as
atherosclerosis and asthma.\726\ \727\ \728\
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    \722\ Riediker, M. (2007). Cardiovascular effects of fine
particulate matter components in highway patrol officers. Inhal
Toxicol 19: 99-105. doi: 10.1080/08958370701495238 Available at
http://dx.doi.org.
    \723\ Alexeef, S. E., Coull, B. A., Gryparis, A., et al. (2011).
Medium-term exposure to traffic-related air pollution and markers of
inflammation and endothelial function. Environmental Health
Perspectives. 119: 481-486. doi:10.1289/ehp.1002560 Available at
http://dx.doi.org.
    \724\ Eckel, S. P., Berhane, K., Salam, M. T., et al. (2011).
Traffic-related pollution exposure and exhaled nitric oxide in the
Children's Health Study. Environmental Health Perspectives. (IN
PRESS). doi:10.1289/ehp.1103516. Available at http://dx.doi.org.
    \725\ Zhang, J., McCreanor, J. E., Cullinan, P., et al. (2009).
Health effects of real-world exposure diesel exhaust in persons with
asthma. Res Rep Health Effects Inst 138. [Online at http://www.healtheffects.org].
    \726\ Adar, S. D., Klein, R., Klein, E. K., et al. (2010). Air
pollution and the microvasculatory: a cross-sectional assessment of
in vivo retinal images in the population-based Multi-Ethnic Study of
Atherosclerosis. PLoS Med 7(11): E1000372. doi:10.1371/
journal.pmed.1000372. Available at http://dx.doi.org.
    \727\ Kan, H., Heiss, G., Rose, K. M., et al. (2008).
Prospective analysis of traffic exposure as a risk factor for
incident coronary heart disease: the Atherosclerosis Risk in
Communities (ARIC) study. Environmental Health Perspectives. 116:
1463-1468. doi:10.1289/ehp.11290. Available at http://dx.doi.org.
    \728\ McConnell, R., Islam, T., Shankardass, K., et al. (2010).
Childhood incident asthma and traffic-related air pollution at home
and school. Environmental Health Perspectives. 1021-1026.
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    Several studies suggest that some factors may increase
susceptibility to the effects of traffic-associated air pollution.
Several studies have found stronger respiratory associations in
children experiencing chronic social stress, such as in violent
neighborhoods or in homes with high family stress.\729\ \730\ \731\
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    \729\ Islam, T., Urban, R., Gauderman, W. J., et al. (2011).
Parental stress increases the detrimental effect of traffic exposure
on children's lung function. American Journal of Respiratory
Critical Care Medicine. (In press).
    \730\ Clougherty, J. E., Levy, J. I., Kubzansky, L. D., et al.
(2007). Synergistic effects of traffic-related air pollution and
exposure to violence on urban asthma etiology. Environmental Health
Perspectives. 115: 1140-1146.
    \731\ Chen, E., Schrier, H. M., Strunk, R. C., et al. (2008).
Chronic traffic-related air pollution and stress interact to predict
biologic and clinical outcomes in asthma. Environmental Health
Perspectives. 116: 970-5.
---------------------------------------------------------------------------

    The risks associated with residence, workplace, or schools near
major roads are of potentially high public health significance due to
the large population in such locations. According to the 2009 American
Housing Survey, more than 22 million homes (17% of all U.S. housing
units) were located within 300 feet of an airport, railroad, or highway
with four or more lanes. This corresponds to a population of more than
50 million U.S. residents in close proximity to high-traffic roadways
or other transportation sources. Based on 2010 Census data, a 2013
publication estimated that 19% of the U.S. population (more than 59
million people) lived within 500 meters of roads with at least 25,000
annual average daily traffic (AADT), while about 3.2% of the population
lived within 100 meters (about 300 feet) of such roads.\732\ Another
2013 study estimated that 3.7% of the U.S. population (about 11.3
million people) lived within 150 meters (about 500 feet) of interstate
highways or other freeways and expressways.\733\ On average,
populations near major roads have higher fractions of minority
residents and lower socioeconomic status. Furthermore, on average,
Americans spend more than an hour traveling each day, bringing nearly
all residents into a high-exposure microenvironment for part of the
day.
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    \732\ Rowangould, G. M. (2013) A census of the U.S. near-roadway
population: public health and environmental justice considerations.
Transportation Research Part D 25: 59-67.
    \733\ Boehmer, T. K., Foster, S. L., Henry, J. R., Woghiren-
Akinnifesi, E. L., & Yip, F. Y. (2013) Residential proximity to
major highways--United States, 2010. Morbidity and Mortality Weekly
Report 62 (3); 46-50.
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    In light of these concerns, EPA has required through the NAAQS
process that air quality monitors be placed near high-traffic roadways
for determining concentrations of CO, NO2, and
PM2.5 (in addition to those existing monitors located in
neighborhoods and other locations farther away from pollution sources).
Near-roadway monitors for NO2 begin operation between 2014
and 2017 in Core Based Statistical Areas (CBSAs) with population of at
least 500,000. Monitors for CO and PM2.5 begin operation
between 2015 and 2017. These monitors will further our understanding of
exposure in these locations.
    EPA and DOT continue to research near-road air quality, including
the types of pollutants found in high concentrations near major roads
and health problems associated with the mixture of pollutants near
roads.
8. Environmental Justice
    Environmental justice (EJ) is a principle asserting that all people
deserve fair treatment and meaningful involvement with respect to
environmental laws, regulations, and policies. EPA seeks to provide the
same degree of protection from environmental health hazards for all
people. DOT shares this goal and is informed about the potential
environmental impacts of its rulemakings through its NEPA process (see
NHTSA's DEIS). As referenced below, numerous studies have found that
some environmental hazards are more prevalent in areas where non-white,
Hispanic and people with low socioeconomic status (SES) represent a
higher fraction of the population compared with the general population.
In addition, compared to non-Hispanic whites, some subpopulations
defined by race and ethnicity have been shown to have greater levels of
some health conditions during some life stages. For example, in 2014,
about 13% of Black, non-Hispanic and 24% of Puerto Rican children were
estimated to currently have asthma, compared with eight percent of
white, non-Hispanic children.\734\
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    \734\ http://www.cdc.gov/asthma/most_recent_data.htm.
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    As discussed in the DEIS, concentrations of many air pollutants are
elevated near high-traffic roadways. If minority populations and low-
income populations disproportionately live near such roads, then an
issue of EJ may be present. We reviewed existing scholarly literature
examining the potential for disproportionate exposure among people with
low SES, and we conducted our own evaluation of two national datasets:
The U.S. Census Bureau's American Housing Survey for calendar year 2009
and the U.S. Department of Education's database of school locations.
    Publications that address EJ issues generally report that
populations living near major roadways (and other types of

transportation infrastructure) tend to be composed of larger fractions
of nonwhite residents. People living in neighborhoods near such sources
of air pollution also tend to be lower in income than people living
elsewhere. Numerous studies evaluating the demographics and
socioeconomic status of populations or schools near roadways have found
that they include a greater percentage of minority residents, as well
as lower SES (indicated by variables such as median household income).
Locations in these studies include Los Angeles, CA; Seattle, WA; Wayne
County, MI; Orange County, FL; and California \735\ \736\ \737\ \738\
\739\ \740\ Such disparities may be due to multiple factors.\741\
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    \735\ Marshall, J. D. (2008) Environmental inequality: air
pollution exposures in California's South Coast Air Basin.
    \736\ Su, J. G., Larson, T., Gould, T., Cohen, M., & Buzzelli,
M. (2010) Transboundary air pollution and environmental justice:
Vancouver and Seattle compared. GeoJournal 57: 595-608. doi:10.1007/
s10708-009-9269-6 [Online at http://dx.doi.org].
    \737\ Chakraborty, J. & Zandbergen, P. A. (2007) Children at
risk: measuring racial/ethnic disparities in potential exposure to
air pollution at school and home. Journal of Epidemiol Community
Health 61: 1074-1079. doi: 10.1136/jech.2006.054130 [Online at
http://dx.doi.org].
    \738\ Green, R. S., Smorodinsky, S., Kim, J. J., McLaughlin, R.,
& Ostro, B. (2003) Proximity of California public schools to busy
roads. Environmental Health Perspectives. 112: 61-66. doi:10.1289/
ehp.6566 [http://dx.doi.org].
    \739\ Wu, Y. & Batterman, S. A. (2006) Proximity of schools in
Detroit, Michigan to automobile and truck traffic. Journal of
Exposure Science & Environmental Epidemiology. doi:10.1038/
sj.jes.7500484 [Online at http://dx.doi.org].
    \740\ Su, J. G., Jerrett, M., de Nazelle, A., & Wolch, J. (2011)
Does exposure to air pollution in urban parks have socioeconomic,
racial, or ethnic gradients? Environmental Research. 111: 319-328.
    \741\ Depro, B. & Timmins, C. (2008) Mobility and environmental
equity: do housing choices determine exposure to air pollution?
North Caroline State University Center for Environmental and
Resource Economic Policy
---------------------------------------------------------------------------

    People with low SES often live in neighborhoods with multiple
environmental stressors and higher rates of health risk factors,
including reduced health insurance coverage rates, higher smoking and
drug use rates, limited access to fresh food, visible neighborhood
violence, and elevated rates of obesity and some diseases such as
asthma, diabetes, and ischemic heart disease. Although questions
remain, several studies find stronger associations between air
pollution and health in locations with such chronic neighborhood
stress, suggesting that populations in these areas may be more
susceptible to the effects of air pollution.\742\ \743\ \744\ \745\
Household-level stressors such as parental smoking and relationship
stress also may increase susceptibility to the adverse effects of air
pollution.\746\ \747\
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    \742\ Clougherty, J. E. & Kubzansky, L. D. (2009) A framework
for examining social stress and susceptibility to air pollution in
respiratory health. Environmental Health Perspectives. 117: 1351-
1358. Doi:10.1289/ehp.0900612 [Online at http://dx.doi.org].
    \743\ Clougherty, J. E., Levy, J. I., Kubzansky, L. D., Ryan, P.
B., Franco Suglia, S., Jacobson Canner, M., & Wright, R. J. (2007)
Synergistic effects of traffic-related air pollution and exposure to
violence on urban asthma etiology. Environmental Health
Perspectives. 115: 1140-1146. doi:10.1289/ehp.9863 [Online at http://dx.doi.org].
    \744\ Finkelstein, M. M., Jerrett, M., DeLuca, P., Finkelstein,
N., Verma, D. K., Chapman, K., & Sears, M. R. (2003) Relation
between income, air pollution and mortality: A cohort study.
Canadian Medical Association Journal. 169: 397-402.
    \745\ Shankardass, K., McConnell, R., Jerrett, M., Milam, J.,
Richardson, J., & Berhane, K. (2009) Parental stress increases the
effect of traffic-related air pollution on childhood asthma
incidence. Proc National Academy of Science. 106: 12406-12411.
doi:10.1073/pnas.0812910106 [Online at http://dx.doi.org].
    \746\ Lewis, A. S., Sax, S. N., Wason, S. C. & Campleman, S. L
(2011) Non-chemical stressors and cumulative risk assessment: an
overview of current initiatives and potential air pollutant
interactions. International Journal of Environmental Research in
Public Health. 8: 2020-2073. Doi:10.3390/ijerph8062020 [Online at
http://dx.doi.org].
    \747\ Rosa, M. J., Jung, K. H., Perzanowski, M. S., Kelvin, E.
A., Darling, K.W., Camann, D. E., Chillrud, S. N., Whyatt, R. M.,
Kinney, P. L., Perera, F. P., & Miller, R. L. (2010) Prenatal
exposure to polycyclic aromatic hydrocarbons, environmental tobacco
smoke and asthma. Respiratory Medicine. (In press). doi:10.1016/
j.rmed.2010.11.022 [Online at http://dx.doi.org].
---------------------------------------------------------------------------

    Two national databases were analyzed that allowed evaluation of
whether homes and schools were located near a major road and whether
disparities in exposure may be occurring in these environments. The
American Housing Survey (AHS) includes descriptive statistics of over
70,000 housing units across the nation. The study survey is conducted
every two years by the U.S. Census Bureau. The second database we
analyzed was the U.S. Department of Education's Common Core of Data,
which includes enrollment and location information for schools across
the U.S.
    In analyzing the 2009 AHS, the focus was on whether or not a
housing unit was located within 300 feet of ``4-or-more lane highway,
railroad, or airport.'' \748\ Whether there were differences between
households in such locations compared with those in locations farther
from these same transportation facilities was analyzed.\749\ Other
variables, such as land use category, region of country, and housing
type were included.
---------------------------------------------------------------------------

    \748\ This variable primarily represents roadway proximity.
According to the Central Intelligence Agency's World Factbook, in
2010, the United States had 6,506,204 km or roadways, 224,792 km of
railways, and 15,079 airports. Highways thus represent the
overwhelming majority of transportation facilities described by this
factor in the AHS.
    \749\ Bailey, C. (2011) Demographic and Social Patterns in
Housing Units Near Large Highways and other Transportation Sources.
Memorandum to docket.
---------------------------------------------------------------------------

    In examining schools near major roadways, the Common Core of Data
(CCD) from the U.S. Department of Education, which includes information
on all public elementary and secondary schools and school districts
nationwide, was examined.\750\ To determine school proximities to major
roadways, a geographic information system (GIS) to map each school and
roadways based on the U.S. Census's TIGER roadway file was used.\751\
Non-white students were found to be overrepresented at schools within
200 meters of the largest roadways, and schools within 200 meters of
the largest roadways also had higher than expected numbers of students
eligible for free or reduced-price lunches. For example, Black students
represent 22% of students at schools located within 200 meters of a
primary road, whereas Black students represent 17% of students in all
U.S. schools. Hispanic students represent 30% of students at schools
located within 200 meters of a primary road, whereas Hispanic students
represent 22% of students in all U.S. schools.
---------------------------------------------------------------------------

    \750\ http://nces.ed.gov/ccd/.
    \751\ Pedde, M. & Bailey, C. (2011) Identification of Schools
within 200 Meters of U.S. Primary and Secondary Roads. Memorandum to
the docket.
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    Overall, there is substantial evidence that people who live or
attend school near major roadways are more likely to be non-white,
Hispanic ethnicity, and/or low SES. The emission reductions from these
proposed standards will likely result in widespread air quality
improvements, but the impact on pollution levels in close proximity to
roadways will be most direct. Thus, these proposed standards will
likely help in mitigating the disparity in racial, ethnic, and
economically based exposures.
9. Environmental Effects of Non-GHG Pollutants
(a) Visibility
    Visibility can be defined as the degree to which the atmosphere is
transparent to visible light.\752\ Visibility impairment is caused by
light scattering and absorption by suspended particles and gases.
Visibility is important because it has direct significance to people's
enjoyment of daily activities in all parts of the country. Individuals
value good visibility for the well-being it provides

them directly, where they live and work, and in places where they enjoy
recreational opportunities. Visibility is also highly valued in
significant natural areas, such as national parks and wilderness areas,
and special emphasis is given to protecting visibility in these areas.
For more information on visibility see the final 2009 PM ISA.\753\
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    \752\ National Research Council, (1993). Protecting Visibility
in National Parks and Wilderness Areas. National Academy of Sciences
Committee on Haze in National Parks and Wilderness Areas. National
Academy Press, Washington, DC. This book can be viewed on the
National Academy Press website at http://www.nap.edu/books/0309048443/html/.
    \753\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F.
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    EPA is working to address visibility impairment. Reductions in air
pollution from implementation of various programs associated with the
Clean Air Act Amendments of 1990 (CAAA) provisions have resulted in
substantial improvements in visibility and will continue to do so in
the future. Because trends in haze are closely associated with trends
in particulate sulfate and nitrate due to the relationship between
their concentration and light extinction, visibility trends have
improved as emissions of SO2 and NOX have
decreased over time due to air pollution regulations such as the Acid
Rain Program.\754\
---------------------------------------------------------------------------

    \754\ U.S. EPA. 2009 Final Report: Integrated Science Assessment
for Particulate Matter. U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-08/139F, 2009.
---------------------------------------------------------------------------

    In the Clean Air Act Amendments of 1977, Congress recognized
visibility's value to society by establishing a national goal to
protect national parks and wilderness areas from visibility impairment
caused by manmade pollution.\755\ In 1999, EPA finalized the regional
haze program to protect the visibility in Mandatory Class I Federal
areas.\756\ There are 156 national parks, forests and wilderness areas
categorized as Mandatory Class I Federal areas.\757\ These areas are
defined in CAA Section 162 as those national parks exceeding 6,000
acres, wilderness areas and memorial parks exceeding 5,000 acres, and
all international parks which were in existence on August 7, 1977.
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    \755\ See Section 169(a) of the Clean Air Act.
    \756\ 64 FR 35714 (July 1, 1999).
    \757\ 62 FR 38680-38681 (July 18, 1997).
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    EPA has also concluded that PM2.5 can cause adverse
effects on visibility in other areas that are not targeted by the
Regional Haze Rule, such as urban areas, depending on PM2.5
concentrations and other factors such as dry chemical composition and
relative humidity (i.e., an indicator of the water composition of the
particles).\758\ In December 2012, EPA revised the primary (health-
based) PM2.5 standards in order to increase public health
protection. As part of that same review, the EPA generally retained the
secondary (welfare-based) PM2.5 standards, concluding that
the target level of protection against PM-related visibility impairment
would be achieved in areas meeting the existing secondary standards for
PM2.5.
---------------------------------------------------------------------------

    \758\ 78 FR 3226, January 15, 2013.
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(b) Plant and Ecosystem Effects of Ozone
    The welfare effects of ozone can be observed across a variety of
scales, i.e. subcellular, cellular, leaf, whole plant, population and
ecosystem. Ozone can produce both acute and chronic injury in sensitive
species depending on the concentration level and the duration of the
exposure.\759\ In those sensitive species,\760\ effects from repeated
exposure to ozone throughout the growing season of the plant tend to
accumulate, so that even low concentrations experienced for a longer
duration have the potential to create chronic stress on
vegetation.\761\ Ozone damage to sensitive species includes impaired
photosynthesis and visible injury to leaves. The impairment of
photosynthesis, the process by which the plant makes carbohydrates (its
source of energy and food), can lead to reduced crop yields, timber
production, and plant productivity and growth. Impaired photosynthesis
can also lead to a reduction in root growth and carbohydrate storage
below ground, resulting in other, more subtle plant and ecosystems
impacts.\762\ These latter impacts include increased susceptibility of
plants to insect attack, disease, harsh weather, interspecies
competition and overall decreased plant vigor. The adverse effects of
ozone on areas with sensitive species could potentially lead to species
shifts and loss from the affected ecosystems,\763\ resulting in a loss
or reduction in associated ecosystem goods and services. Additionally,
visible ozone injury to leaves can result in a loss of aesthetic value
in areas of special scenic significance like national parks and
wilderness areas and reduced use of sensitive ornamentals in
landscaping.\764\
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    \759\ 73 FR 16486 (Mar. 27, 2008).
    \760\ 73 FR 16491 (Mar. 27, 2008). Only a small percentage of
all the plant species growing within the U.S. (over 43,000 species
have been catalogued in the USDA PLANTS database) have been studied
with respect to ozone sensitivity.
    \761\ The concentration at which ozone levels overwhelm a
plant's ability to detoxify or compensate for oxidant exposure
varies. Thus, whether a plant is classified as sensitive or tolerant
depends in part on the exposure levels being considered. Chapter 9,
Section 9.3.4 of U.S. EPA, 2013 Integrated Science Assessment for
Ozone and Related Photochemical Oxidants. Office of Research and
Development/National Center for Environmental Assessment. U.S.
Environmental Protection Agency. EPA 600/R-10/076F.
    \762\ 73 FR 16492 (Mar. 27, 2008).
    \763\ 73 FR 16493-16494 (Mar. 27, 2008). Ozone impacts could be
occurring in areas where plant species sensitive to ozone have not
yet been studied or identified.
    \764\ 73 FR 16490-16497 (Mar. 27, 2008).
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    The most recent Integrated Science Assessment (ISA) for Ozone
presents more detailed information on how ozone affects vegetation and
ecosystems.\765\ The ISA concludes that ambient concentrations of ozone
are associated with a number of adverse welfare effects and
characterizes the weight of evidence for different effects associated
with ozone.\766\ The ISA concludes that visible foliar injury effects
on some vegetation, reduced vegetation growth, reduced productivity in
terrestrial ecosystems, reduced yield and quality of some agricultural
crops, and alteration of below-ground biogeochemical cycles are
causally associated with exposure to ozone. It also concludes that
reduced carbon sequestration in terrestrial ecosystems, alteration of
terrestrial ecosystem water cycling, and alteration of terrestrial
community composition are likely to be causally associated with
exposure to ozone.
---------------------------------------------------------------------------

    \765\ U.S. EPA. Integrated Science Assessment of Ozone and
Related Photochemical Oxidants (Final Report). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-10/076F, 2013. The ISA
is available at http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492#Download.
    \766\ The Ozone ISA evaluates the evidence associated with
different ozone related health and welfare effects, assigning one of
five ``weight of evidence'' determinations: Causal relationship,
likely to be a causal relationship, suggestive of a causal
relationship, inadequate to infer a causal relationship, and not
likely to be a causal relationship. For more information on these
levels of evidence, please refer to Table II of the ISA.
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(c) Atmospheric Deposition
    Wet and dry deposition of ambient particulate matter delivers a
complex mixture of metals (e.g., mercury, zinc, lead, nickel, aluminum,
and cadmium), organic compounds (e.g., polycyclic organic matter,
dioxins, and furans), and inorganic compounds (e.g., nitrate, sulfate)
to terrestrial and aquatic ecosystems. The chemical form of the
compounds deposited depends on a variety of factors including ambient
conditions (e.g., temperature, humidity, oxidant levels) and the
sources of the material. Chemical and physical transformations of the
compounds occur in the atmosphere as well as the media onto which they
deposit. These transformations in turn influence the fate,
bioavailability and potential toxicity of these compounds.
    Adverse impacts to human health and the environment can occur when