in labor intensity due to the rule. We quantify the effects of costs on
employment, and we discuss the effects due to sales and labor intensity
qualitatively. In response to comments, we have added a discussion in
Chapter 10 of the RIA describing a method that could be used to
quantitatively estimate a demand effect on employment, as well as an
illustrative application of that method. The partial quantification of
employment impacts due to increases in the costs of vehicles and parts,
holding labor intensity constant, shows an increase in employment by
1,000 to 5,300 job-years in 2027.\55\ See Section X for further detail
on limitations and assumptions of this analysis.
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    \55\ A job-year is, for example, one year of full-time work for
one person, or one year of half-time work for two people.
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D. EPA Statutory Authority for This Action

    This section briefly summarizes the statutory authority for the
final rule. Title II of the Clean Air Act provides for comprehensive
regulation of mobile sources, authorizing EPA to regulate emissions of
air pollutants from all mobile source categories. Specific Title II
authorities for this final rule include: CAA sections 202, 203, 206,
207, 208, 213, 216, and 301 (42 U.S.C. 7521, 7522, 7525, 7541, 7542,
7547, 7550, and 7601). We discuss some key aspects of these sections in
relation to this final action immediately below (see also Section XIII
of this preamble), as well as in each of the relevant sections later in
this preamble. As noted in Section I.B.2.v, the final rule includes
confidentiality determinations for much of the information collected by
EPA for certification and compliance under Title II; see Section XI.A.
for discussion of

relevant statutory authority for these final rule provisions.
    Statutory authority for the final NOX, PM, HC, and CO
emission standards in this action comes from CAA section 202(a), which
states that ``the Administrator shall by regulation prescribe (and from
time to time revise) . . . standards applicable to the emission of any
air pollutant from any class or classes of new . . . motor vehicle
engines, which in his judgment cause, or contribute to, air pollution
which may reasonably be anticipated to endanger public health or
welfare.'' Standards under CAA section 202(a) take effect after such
period as the Administrator finds necessary to permit the development
and application of the requisite technology, giving appropriate
consideration to the cost of compliance within such period.''
    Section 202(a)(3) further addresses EPA authority to establish
standards for emissions of NOX, PM, HC, and CO from heavy-
duty engines and vehicles. Section 202(a)(3)(A) requires that such
standards ``reflect the greatest degree of emission reduction
achievable through the application of technology which the
Administrator determines will be available for the model year to which
such standards apply, giving appropriate consideration to cost, energy,
and safety factors associated with the application of such
technology.'' Section 202(a)(3)(B) allows EPA to take into account air
quality information in revising such standards. Section 202(a)(3)(C)
provides that standards shall apply for a period of no less than three
model years beginning no earlier than the model year commencing four
years after promulgation. CAA section 202(a)(3)(A) is a technology-
forcing provision and reflects Congress' intent that standards be based
on projections of future advances in pollution control capability,
considering costs and other statutory factors.56 57 CAA
section 202(a)(3) neither requires that EPA consider all the statutory
factors equally nor mandates a specific method of cost-analysis; rather
EPA has discretion in determining the appropriate consideration to give
such factors.\58\
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    \56\ See National Petrochemical & Refiners Association v. EPA,
287 F.3d 1130, 1136 (D.C. Cir. 2002) (explaining that EPA is
authorized to adopt ``technology-forcing'' regulations under CAA
section 202(a)(3)); NRDC v. Thomas, 805 F.2d 410, 428 n.30 (D.C.
Cir. 1986) (explaining that such statutory language that ``seek[s]
to promote technological advances while also accounting for cost
does not detract from their categorization as technology-forcing
standards''); see also Husqvarna AB v. EPA, 254 F.3d 195 (D.C. Cir.
2001) (explaining that CAA sections 202 and 213 have similar
language and are technology-forcing standards).
    \57\ In this context, the term ``technology-forcing'' has a
specific legal meaning and is used to distinguish standards that may
require manufacturers to develop new technologies (or significantly
improve existing technologies) from standards that can be met using
off-the-shelf technology alone. Technology-forcing standards such as
those in this final rule do not require manufacturers to use
specific technologies.
    \58\ See, e.g., Sierra Club v. EPA, 325 F.3d 374, 378 (D.C. Cir.
2003) (explaining that similar technology-forcing language in CAA
section 202(l)(2) ``does not resolve how the Administrator should
weigh all [the statutory] factors in the process of finding the
`greatest emission reduction achievable' ''); Husqvarna AB v. EPA,
254 F.3d 195, 200 (D.C. Cir. 2001) (explaining that under CAA
section 213's similar technology-forcing authority that ``EPA did
not deviate from its statutory mandate or frustrate congressional
will by placing primary significance on the `greatest degree of
emission reduction achievable' '' or by considering cost and other
statutory factors as important but secondary).
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    CAA section 202(d) directs EPA to prescribe regulations under which
the useful life of vehicles and engines are determined and establishes
minimum values of 10 years or 100,000 miles, whichever occurs first,
unless EPA determines that a period of greater duration or mileage is
appropriate. EPA may apply adjustment factors to assure compliance with
requirements in use throughout useful life (CAA section 206(a)). CAA
section 207(a) requires manufacturers to provide emissions-related
warranty, which EPA last updated in its regulations for heavy-duty
engines in 1983 (see 40 CFR 86.085-2).\59\
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    \59\ 48 FR 52170, November 16, 1983.
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    EPA is promulgating the final emission standards pursuant to its
authority under CAA section 202(a), including 202(a)(3)(A). Section II
and Chapter 4 of the RIA describe EPA's analysis of information
regarding heavy-duty engines' contribution to air pollution and how
that pollution adversely impacts public health and welfare. Sections
III and IV discuss our feasibility analysis of the emission standards
and useful life periods in the final rule, with more detail in Chapter
3 of the RIA. Our analysis shows that the final emission standards and
useful life periods are feasible and will result in the greatest
emission reductions achievable for the model years to which they will
apply, pursuant to CAA section 202(a)(3), giving appropriate
consideration to costs, lead time, and other factors. Our analysis of
the final standards includes providing manufacturers with sufficient
time to ensure that emission control components are durable enough for
the longer useful life periods in the final program. In setting the
final emission standards, EPA appropriately assessed the statutory
factors specified in CAA section 202(a)(3)(A), including giving
appropriate consideration to the cost associated with the application
of technology EPA determined will be available for the model year the
final standards apply (i.e., cost of compliance for the manufacturer
associated with the application of such technology). EPA's assessment
of the relevant statutory factors in CAA section 202(a)(3)(A) justify
the final emission standards. We also evaluated additional factors,
including factors to comply with E.O. 12866; our assessment of these
factors lend further support to the final rule.
    As proposed, we are finalizing new emission standards along with
new and revised test procedures for both laboratory-based duty-cycles
and off-cycle testing. Manufacturers demonstrate compliance over
specified duty-cycle test procedures during pre-production testing, as
well as confirmatory testing during production, which is conducted by
EPA or the manufacturer. Test data and other information submitted by
the manufacturer as part of their certification application are the
basis on which EPA issues certificates of conformity pursuant to CAA
section 206. Under CAA section 203, sales of new vehicles are
prohibited unless the vehicle is covered by a certificate of
conformity. Compliance with engine emission standards is required
throughout the regulatory useful life of the engine, not only at
certification but throughout the regulatory useful life in-use in the
real word. In-use engines can be tested for compliance with duty-cycle
and off-cycle standards, with testing over corresponding specific duty-
cycle test procedures and off-cycle test procedures, either on the road
or in the laboratory (see Section III for more discussion on for
testing at various stages in the life of an engine).
    Also as proposed, we are finalizing lengthened regulatory useful
life and emission warranty periods to better reflect the mileages and
time periods over which heavy-duty engines are driven today. These and
other provisions in the final rule are further discussed in the
preamble sections that follow. The proposed rule (87 FR 17414, March
28, 2022) includes additional information relevant to the development
of this rule, including: History of Emissions Standards for Heavy-duty
Engines and Vehicles; Petitions to EPA for Additional NOX
control; the California Heavy-Duty Highway Low NOX Program
Development; and the Advance Notice of Proposed Rulemaking.

II. Need for Additional Emissions Control

    This final rule will reduce emissions from heavy-duty engines that
contribute to ambient levels of ozone, PM, NOX and CO, which
are all pollutants for which EPA has established health-based NAAQS.
These pollutants are linked to premature death, respiratory illness
(including childhood asthma), cardiovascular problems, and other
adverse health impacts. Many groups are at greater risk than healthy
people from these pollutants, including people with heart or lung
disease, outdoor workers, older adults and children. These pollutants
also reduce visibility and negatively impact ecosystems. This final
rule will also reduce emissions of air toxics from heavy-duty engines.
A more detailed discussion of the health and environmental effects
associated with the pollutants affected by this rule is included in
Sections II.B and II.C and Chapter 4 of the RIA.
    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. We note that there
is substantial evidence that people who live or attend school near
major roadways are more likely to be people of color, Hispanic
ethnicity, and/or low socioeconomic status.
    Across the United States, NOX emissions from heavy-duty
engines are important contributors to concentrations of ozone and
PM2.5 and their resulting threat to public
health.60 61 The emissions modeling done for the final rule
(see Chapter 5 of the RIA) indicates that without these standards,
heavy-duty engines will continue to be one of the largest contributors
to mobile source NOX emissions nationwide in the future,
representing 32 percent of the mobile source NOX in calendar
year 2045.\62\ Furthermore, it is estimated that heavy-duty engines
would represent 90 percent of the onroad NOX inventory in
calendar year 2045.\63\ The emission reductions that will occur from
the final rule are projected to reduce air pollution that is (and is
projected to continue to be) at levels that endanger public health and
welfare. For the reasons discussed in this Section II, EPA concludes
that new standards are warranted to address the emissions of these
pollutants and their contribution to national air pollution. We note
that in the summer of 2016 more than 20 organizations, including state
and local air agencies from across the country, petitioned EPA to
develop more stringent NOX emission standards for on-road
heavy-duty engines.64 65 Among the reasons stated by the
petitioners for such an EPA rulemaking was the need for NOX
emission reductions to reduce adverse health and welfare impacts and to
help areas attain the NAAQS. EPA responded to the petitions on December
20, 2016, noting that an opportunity exists to develop a new national
NOX reduction strategy for heavy-duty highway engines.\66\
We subsequently initiated this rulemaking and issued an Advanced Notice
of Proposed Rulemaking in January 2020.\67\ This final rule culminates
the rulemaking proceeding and is responsive to those petitions.
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    \60\ Zawacki et al., 2018. Mobile source contributions to
ambient ozone and particulate matter in 2025. Atmospheric
Environment, Vol 188, pg 129-141. Available online: https://doi.org/10.1016/j.atmosenv.2018.04.057.
    \61\ Davidson et al., 2020. The recent and future health burden
of the U.S. mobile sector apportioned by source. Environmental
Research Letters. Available online: https://doi.org/10.1088/1748-9326/ab83a8.
    \62\ Sectors other than onroad and nonroad were projected from
2016v1 Emissions Modeling Platform. https://www.epa.gov/air-emissions-modeling/2016v1-platform.
    \63\ U.S. EPA (2020) Motor Vehicle Emission Simulator: MOVES3.
https://www.epa.gov/moves.
    \64\ Brakora, Jessica. ``Petitions to EPA for Revised
NOX Standards for Heavy-Duty Engines'' Memorandum to
Docket EPA-HQ-OAR-2019-0055. December 4, 2019.
    \65\ 87 FR 17414, March 28, 2022.
    \66\ U.S. EPA. 2016. Memorandum in Response to Petition for
Rulemaking to Adopt Ultra-Low NOX Standards for On-
Highway Heavy-Duty Trucks and Engines. Available at https://19january2017snapshot.epa.gov/sites/production/files/2016-12/documents/nox-memorandum-nox-petition-response-2016-12-20.pdf.
    \67\ The Agency published an ANPR on January 21, 2020 to present
EPA's early thinking on this rulemaking and solicit feedback from
stakeholders to inform this proposal (85 FR 3306).
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    Many state and local agencies across the country commented on the
NPRM and have asked the EPA to reduce NOX emissions,
specifically from heavy-duty engines, because such reductions will be a
critical part of many areas' strategies to attain and maintain the
ozone and PM NAAQS. These state and local agencies anticipate
challenges in attaining the NAAQS, maintaining the NAAQS in the future,
and/or preventing nonattainment. Some nonattainment areas have already
been ``bumped up'' to higher classifications because of challenges in
attaining the NAAQS; others say they are struggling to avoid
nonattainment.\68\ Others note that the ozone and PM NAAQS are being
reconsidered so they could be made more stringent in the
future.69 70 Many state and local agencies commented on the
NPRM that heavy-duty vehicles are one of their largest sources of
NOX emissions. They commented that without action to reduce
emissions from heavy-duty vehicles, they will have to adopt other
potentially more burdensome and costly measures to reduce emissions
from other sources under their state or local authority, such as local
businesses. More information on the projected emission reductions and
air quality impacts that will result from this rule is provided in
Sections VI and VII.
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    \68\ For example, in September 2019 several 2008 ozone
nonattainment areas were reclassified from moderate to serious,
including Dallas, Chicago, Connecticut, New York/New Jersey and
Houston, and in January 2020, Denver. Also, on September 15, 2022,
EPA finalized reclassification, bumping up 5 areas in nonattainment
of the 2008 ozone NAAQS from serious to severe and 22 areas in
nonattainment of the 2015 ozone NAAQS from marginal to moderate. The
2008 NAAQS for ozone is an 8-hour standard with a level of 0.075
ppm, which the 2015 ozone NAAQS lowered to 0.070 ppm.
    \69\ https://www.epa.gov/ground-level-ozone-pollution/epa-reconsider-previous-administrations-decision-retain-2015-ozone.
    \70\ https://www.epa.gov/pm-pollution/national-ambient-air-quality-standards-naaqs-pm.
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    In their comments on the NPRM, many nonprofit groups, citizen
groups, individuals, and state, local, and Tribal organizations
emphasized the role that emissions from trucks have in harming
communities and that communities living near truck routes are
disproportionately people of color and those with lower incomes. They
supported additional NOX reductions from heavy-duty vehicles
to address concerns about environmental justice and ensuring that all
communities benefit from improvements in air quality. In addition, many
groups and commenters noted the link between emissions from heavy duty
trucks and harmful health effects, in particular asthma in children.
Commenters also supported additional NOX reductions from
heavy-duty vehicles to address concerns about regional haze, and damage
to terrestrial and aquatic ecosystems. They mentioned the impacts of
NOX emissions on numerous locations, such as the Chesapeake
Bay, Long Island Sound, the Rocky Mountains, Sierra Nevada Mountains,
Appalachian Mountains, Southwestern Desert ecosystems, and other areas.
For further detail regarding these comments and EPA's responses, see
Section 2 of the Response to Comments document for this rulemaking.

A. Background on Pollutants Impacted by This Proposal

1. Ozone
    Ground-level ozone pollution forms in areas with high
concentrations of ambient nitrogen oxides (NOX) and

volatile organic compounds (VOCs) when solar radiation is strong. Major
U.S. sources of NOX are highway and nonroad motor vehicles,
engines, power plants and other industrial sources, with natural
sources, such as soil, vegetation, and lightning, serving as smaller
sources. Vegetation is the dominant source of VOCs in the United
States. Volatile consumer and commercial products, such as propellants
and solvents, highway and nonroad vehicles, engines, fires, and
industrial sources also contribute to the atmospheric burden of VOCs at
ground-level.
    The processes underlying ozone formation, transport, and
accumulation are complex. Ground-level ozone is produced and destroyed
by an interwoven network of free radical reactions involving the
hydroxyl radical (OH), NO, NO2, and complex reaction
intermediates derived from VOCs. Many of these reactions are sensitive
to temperature and available sunlight. High ozone events most often
occur when ambient temperatures and sunlight intensities remain high
for several days under stagnant conditions. Ozone and its precursors
can also be transported hundreds of miles downwind, which can lead to
elevated ozone levels in areas with otherwise low VOC or NOX
emissions. As an air mass moves and is exposed to changing ambient
concentrations of NOX and VOCs, the ozone photochemical
regime (relative sensitivity of ozone formation to NOX and
VOC emissions) can change.
    When ambient VOC concentrations are high, comparatively small
amounts of NOX catalyze rapid ozone formation. Without
available NOX, ground-level ozone production is severely
limited, and VOC reductions would have little impact on ozone
concentrations. Photochemistry under these conditions is said to be
``NOX-limited.'' When NOX levels are sufficiently
high, faster NO2 oxidation consumes more radicals, dampening
ozone production. Under these ``VOC-limited'' conditions (also referred
to as ``NOX-saturated'' conditions), VOC reductions are
effective in reducing ozone, and NOX can react directly with
ozone, resulting in suppressed ozone concentrations near NOX
emission sources. Under these NOX-saturated conditions,
NOX reductions can actually increase local ozone under
certain circumstances, but overall ozone production (considering
downwind formation) decreases. Even in VOC-limited areas,
NOX reductions are not expected to increase ozone levels if
the NOX reductions are sufficiently large--large enough to
become NOX-limited.
    The primary NAAQS for ozone, established in 2015 and retained in
2020, is an 8-hour standard with a level of 0.07 ppm.\71\ EPA announced
that it will reconsider the decision to retain the ozone NAAQS.\72\ The
EPA is also implementing the previous 8-hour ozone primary standard,
set in 2008, at a level of 0.075 ppm. As of August 31, 2022, there were
34 ozone nonattainment areas for the 2008 ozone NAAQS, composed of 141
full or partial counties, with a population of more than 90 million,
and 49 ozone nonattainment areas for the 2015 ozone NAAQS, composed of
212 full or partial counties, with a population of more than 125
million. In total, there are currently, as of August 31, 2022, 57 ozone
nonattainment areas with a population of more than 130 million
people.\73\
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    \71\ https://www.epa.gov/ground-level-ozone-pollution/ozone-national-ambient-air-quality-standards-naaqs.
    \72\ https://www.epa.gov/ground-level-ozone-pollution/epa-reconsider-previous-administrations-decision-retain-2015-ozone.
    \73\ The population total is calculated by summing, without
double counting, the 2008 and 2015 ozone nonattainment populations
contained in the Criteria Pollutant Nonattainment Summary report
(https://www.epa.gov/green-book/green-book-data-download).
---------------------------------------------------------------------------

    States with ozone nonattainment areas are required to take action
to bring those areas into attainment. The attainment date assigned to
an ozone nonattainment area is based on the area's classification. The
attainment dates for areas designated nonattainment for the 2008 8-hour
ozone NAAQS are in the 2015 to 2032 timeframe, depending on the
severity of the problem in each area. Attainment dates for areas
designated nonattainment for the 2015 ozone NAAQS are in the 2021 to
2038 timeframe, again depending on the severity of the problem in each
area.\74\ The final NOX standards will take effect starting
in MY 2027 and will assist areas with attaining the NAAQS and may
relieve areas with already stringent local regulations from some of the
burden associated with adopting additional local controls.\75\ The rule
will also provide assistance to counties with ambient concentrations
near the level of the NAAQS who are working to ensure long-term
attainment or maintenance of the NAAQS.
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    \74\ https://www.epa.gov/ground-level-ozone-pollution/ozone-naaqs-timelines.
    \75\ While not quantified in the air quality modeling analysis
for this rule, elements of the Averaging, Banking, and Trading (ABT)
program could encourage manufacturers to introduce new emission
control technologies prior to the 2027 model year, which may help to
accelerate some emission reductions of the final rule (See Preamble
Section IV.G for more details on the ABT program in the final rule).
In RIA Chapter 5.5 we also include a sensitivity analysis that shows
allowing manufacturers to generate NOX emissions credits
by meeting requirements of the final rule one model year before
required would lead to meaningful, additional reductions in
NOX emissions in the early years of the program compared
to the emissions reductions expected from the final rule (see
preamble Section IV.G.7 and RIA Chapter 5.5 for additional details).
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2. Particulate Matter
    Particulate matter (PM) is a complex mixture of solid particles and
liquid droplets distributed among numerous atmospheric gases which
interact with solid and liquid phases. Particles in the atmosphere
range in size from less than 0.01 to more than 10 micrometers ([mu]m)
in diameter.\76\ Atmospheric particles can be grouped into several
classes according to their aerodynamic diameter and physical sizes.
Generally, the three broad classes of particles include ultrafine
particles (UFPs, generally considered as particles with a diameter less
than or equal to 0.1 [mu]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 [mu]m), and ``thoracic'' particles
(PM10; particles with a nominal mean aerodynamic diameter
less than or equal to 10 [mu]m). 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 greater than 2.5
[mu]m and less than or equal to 10 [mu]m). EPA currently has NAAQS for
PM2.5 and PM10.\77\
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    \76\ U.S. EPA. Policy Assessment (PA) for the Review of the
National Ambient Air Quality Standards for Particulate Matter (Final
Report, 2020). U.S. Environmental Protection Agency, Washington, DC,
EPA/452/R-20/002, 2020.
    \77\ 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 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).
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    Most particles are found in the lower troposphere, where they can
have residence times ranging from a few hours to weeks. Particles are
removed from the atmosphere by wet deposition, such as when they are
carried by rain or snow, or by dry deposition, when particles settle
out of suspension due to gravity. Atmospheric lifetimes are generally
longest for PM2.5, which often remains in the atmosphere for
days to weeks before being removed by wet or dry deposition.\78\ In
contrast,

atmospheric lifetimes for UFP and PM10-2.5 are
shorter. Within hours, UFP can undergo coagulation and condensation
that lead to formation of larger particles, or can be removed from the
atmosphere by evaporation, deposition, or reactions with other
atmospheric components. PM10-2.5 are also
generally removed from the atmosphere within hours, through wet or dry
deposition.\79\
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    \78\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019. Table 2-
1.
    \79\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019. Table 2-
1.
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    Particulate matter consists of both primary and secondary
particles. Primary particles are emitted directly from sources, such as
combustion-related activities (e.g., industrial activities, motor
vehicle operation, biomass burning), while secondary particles are
formed through atmospheric chemical reactions of gaseous precursors
(e.g., sulfur oxides (SOX), NOX, and VOCs).
    There are two primary NAAQS for PM2.5: An annual
standard (12.0 micrograms per cubic meter ([mu]g/m\3\)) and a 24-hour
standard (35 [mu]g/m\3\), and there are two secondary NAAQS for
PM2.5: An annual standard (15.0 [mu]g/m\3\) and a 24-hour
standard (35 [mu]g/m\3\). The initial PM2.5 standards were
set in 1997 and revisions to the standards were finalized in 2006 and
in December 2012 and then retained in 2020. On June 10, 2021, EPA
announced that it will reconsider the decision to retain the PM
NAAQS.\80\
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    \80\ https://www.epa.gov/pm-pollution/national-ambient-air-quality-standards-naaqs-pm.
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    There are many areas of the country that are currently in
nonattainment for the annual and 24-hour primary PM2.5
NAAQS. As of August 31, 2022, more than 19 million people lived in the
4 areas that are designated as nonattainment for the 1997
PM2.5 NAAQS. Also, as of August 31, 2022, more than 31
million people lived in the 14 areas that are designated as
nonattainment for the 2006 PM2.5 NAAQS and more than 20
million people lived in the 5 areas designated as nonattainment for the
2012 PM2.5 NAAQS. In total, there are currently 15
PM2.5 nonattainment areas with a population of more than 32
million people.\81\ The final NOX standards will take effect
in MY 2027 and will assist areas with attaining the NAAQS and may
relieve areas with already stringent local regulations from some of the
burden associated with adopting additional local controls.\82\ The rule
will also assist counties with ambient concentrations near the level of
the NAAQS who are working to ensure long-term attainment or maintenance
of the PM2.5 NAAQS.
---------------------------------------------------------------------------

    \81\ The population total is calculated by summing, without
double counting, the 1997, 2006 and 2012 PM2.5
nonattainment populations contained in the Criteria Pollutant
Nonattainment Summary report (https://www.epa.gov/green-book/green-book-data-download).
    \82\ While not quantified in the air quality modeling analysis
for this rule, elements of the Averaging, Banking, and Trading (ABT)
program could encourage manufacturers to introduce new emission
control technologies prior to the 2027 model year, which may help to
accelerate some emission reductions of the final rule (See Preamble
Section IV.G for more details on the ABT program in the final rule).
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3. Nitrogen Oxides
    Oxides of nitrogen (NOX) refers to nitric oxide (NO) and
nitrogen dioxide (NO2). Most NO2 is formed in the
air through the oxidation of NO emitted when fuel is burned at a high
temperature. NO2 is a criteria pollutant, regulated for its
adverse effects on public health and the environment, and highway
vehicles are an important contributor to NO2 emissions.
NOX, along with VOCs, are the two major precursors of ozone
and NOX is also a major contributor to secondary
PM2.5 formation. There are two primary NAAQS for
NO2: An annual standard (53 ppb) and a 1-hour standard (100
ppb).\83\ In 2010, EPA established requirements for monitoring
NO2 near roadways expected to have the highest
concentrations within large cities. Monitoring within this near-roadway
network began in 2014, with additional sites deployed in the following
years. At present, there are no nonattainment areas for NO2.
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    \83\ The statistical form of the 1-hour NAAQS for NO2
is the 3-year average of the yearly distribution of 1-hour daily
maximum concentrations.
---------------------------------------------------------------------------

4. Carbon Monoxide
    Carbon monoxide (CO) 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.\84\
There are two primary NAAQS for CO: An 8-hour standard (9 ppm) and a 1-
hour standard (35 ppm). There are currently no CO nonattainment areas;
as of September 27, 2010, all CO nonattainment areas have been
redesignated to attainment. The past designations were based on the
existing community-wide monitoring network. EPA made an addition to the
ambient air monitoring requirements for CO during the 2011 NAAQS
review. Those new requirements called for CO monitors to be operated
near roads in Core Based Statistical Areas (CBSAs) of 1 million or more
persons, in addition to the existing community-based network (76 FR
54294, August 31, 2011).
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    \84\ 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. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=218686. See Section 2.1.
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5. Diesel Exhaust
    Diesel exhaust is 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 [mu]m), of which a significant
fraction is ultrafine particles (<0.1 [mu]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 of the components
present in diesel exhaust ranges from seconds to days.
    Because diesel particulate matter (DPM) is part of overall ambient
PM, varies considerably in composition, and lacks distinct chemical
markers that enable it to be easily distinguished from overall primary
PM, we do not have direct measurements of DPM in the ambient air.\85\
DPM concentrations are

estimated using ambient air quality modeling based on DPM emission
inventories. DPM emission inventories are computed as the exhaust PM
emissions from mobile sources combusting diesel or residual oil fuel.
DPM concentrations were estimated as part of the 2018 national Air
Toxics Screening Assessment (AirToxScreen).\86\ Areas with high
concentrations are clustered in the Northeast and Great Lake States,
with a smaller number of higher concentration locations in Western
states. The highest impacts occur in major urban cores, and are also
distributed throughout the rest of the United States near high truck
traffic, coasts with marine diesel activity, construction sites, and
rail facilities. Approximately half of the average ambient DPM
concentration in the United States can be attributed to heavy-duty
diesel engines, with the remainder attributable to nonroad engines.
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    \85\ DPM in exhaust from a high-load, high-speed engine (e.g.,
heavy-duty truck engines) without aftertreatment such as a diesel
particle filter (DPM) is mostly made of ``soot,'' consisting of
elemental/black carbon (EC/BC), some organic material, and trace
elements. At low loads, DPM in high-speed engine exhaust is mostly
made of organic carbon (OC), with considerably less EC/BC. Low-speed
diesel engines' (e.g., large marine engines) exhaust PM is comprised
of more sulfate and less EC/BC, with OC contributing as well.
    \86\ U.S. EPA (2022) Technical Support Document EPA Air Toxics
Screening Assessment. 2018AirToxScreen TSD. https://www.epa.gov/AirToxScreen/airtoxscreen-technical-support-document.
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6. Air Toxics
    The most recent available data indicate that millions of Americans
live in areas where air toxics pose potential health concerns.\87\ The
levels of air toxics to which people are exposed vary depending on
where people live and work and the kinds of activities in which they
engage, as discussed in detail in EPA's 2007 Mobile Source Air Toxics
Rule.\88\ According to EPA's Air Toxics Screening Assessment
(AirToxScreen) for 2018, mobile sources were responsible for 40 percent
of outdoor anthropogenic toxic emissions and were the largest
contributor to national average cancer and noncancer risk from directly
emitted pollutants.89 90 Mobile sources are also significant
contributors to precursor emissions which react to form air toxics.\91\
Formaldehyde is the largest contributor to cancer risk of all 71
pollutants quantitatively assessed in the 2018 AirToxScreen. Mobile
sources were responsible for 26 percent of primary anthropogenic
emissions of this pollutant in 2018 and are significant contributors to
formaldehyde precursor emissions. Benzene is also a large contributor
to cancer risk, and mobile sources account for about 60 percent of
average exposure to ambient concentrations.
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    \87\ U.S. EPA (2022) Technical Support Document EPA Air Toxics
Screening Assessment. 2017AirToxScreen TSD. https://www.epa.gov/system/files/documents/2022-03/airtoxscreen_2017tsd.pdf.
    \88\ U.S. Environmental Protection Agency (2007). Control of
Hazardous Air Pollutants from Mobile Sources; Final Rule. 72 FR
8434, February 26, 2007.
    \89\ U.S. EPA. (2022) Air Toxics Screening Assessment. https://www.epa.gov/AirToxScreen/2018-airtoxscreen-assessment-results.
    \90\ AirToxScreen also includes estimates of risk attributable
to background concentrations, which includes contributions from
long-range transport, persistent air toxics, and natural sources; as
well as secondary concentrations, where toxics are formed via
secondary formation. Mobile sources substantially contribute to
long-range transport and secondarily formed air toxics.
    \91\ Rich Cook, Sharon Phillips, Madeleine Strum, Alison Eyth &
James Thurman (2020): Contribution of mobile sources to secondary
formation of carbonyl compounds, Journal of the Air & Waste
Management Association, DOI: 10.1080/10962247.2020.1813839.
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B. Health Effects Associated With Exposure to Pollutants Impacted by
This Rule

    Heavy-duty engines emit pollutants that contribute to ambient
concentrations of ozone, PM, NO2, CO, and air toxics. This
section of the preamble discusses the health effects associated with
exposure to these pollutants.
    Additionally, because children have increased vulnerability and
susceptibility for adverse health effects related to air pollution
exposures, EPA's findings regarding adverse effects for children
related to exposure to pollutants that are impacted by this rule are
noted in this section. The increased vulnerability and susceptibility
of children to air pollution exposures may arise because infants and
children generally breathe more relative to their size than adults do,
and consequently may be exposed to relatively higher amounts of air
pollution.\92\ Children also tend to breathe through their mouths more
than adults and their nasal passages are less effective at removing
pollutants, which leads to greater lung deposition of some pollutants,
such as PM.93 94 Furthermore, air pollutants may pose health
risks specific to children because children's bodies are still
developing.\95\ For example, during periods of rapid growth such as
fetal development, infancy, and puberty, their developing systems and
organs may be more easily harmed.96 97 EPA's America's
Children and the Environment is a tool which presents national trends
on air pollutants and other contaminants and environmental health of
children.\98\
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    \92\ EPA (2009) Metabolically-derived ventilation rates: A
revised approach based upon oxygen consumption rates. Washington,
DC: Office of Research and Development. EPA/600/R-06/129F. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=202543.
    \93\ U.S. EPA Integrated Science Assessment for Particulate
Matter (Final Report, 2019). U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-19/188, 2019. Chapter 4 ``Overall
Conclusions'' p. 4-1.
    \94\ Foos, B.; Marty, M.; Schwartz, J.; Bennet, W.; Moya, J.;
Jarabek, A.M.; Salmon, A.G. (2008) Focusing on children's inhalation
dosimetry and health effects for risk assessment: An introduction. J
Toxicol Environ Health 71A: 149-165.
    \95\ Children's environmental health includes conception,
infancy, early childhood and through adolescence until 21 years of
age as described in the EPA Memorandum: Issuance of EPA's 2021
Policy on Children's Health. October 5, 2021. Available at https://www.epa.gov/system/files/documents/2021-10/2021-policy-on-childrens-health.pdf.
    \96\ EPA (2006) A Framework for Assessing Health Risks of
Environmental Exposures to Children. EPA, Washington, DC, EPA/600/R-
05/093F, 2006.
    \97\ U.S. Environmental Protection Agency. (2005). Supplemental
guidance for assessing susceptibility from early-life exposure to
carcinogens. Washington, DC: Risk Assessment Forum. EPA/630/R-03/
003F. https://www3.epa.gov/airtoxics/childrens_supplement_final.pdf.
    \98\ U.S. EPA. America's Children and the Environment. Available
at: https://www.epa.gov/americaschildrenenvironment.
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    Information on environmental effects associated with exposure to
these pollutants is included in Section II.C, and information on
environmental justice is included in Section VII.H. Information on
emission reductions and air quality impacts from this rule are included
in Section VI and VII.
1. Ozone
    This section provides a summary of the health effects associated
with exposure to ambient concentrations of ozone.\99\ The information
in this section is based on the information and conclusions in the
April 2020 Integrated Science Assessment for Ozone (Ozone ISA).\100\
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.\101\ The
following discussion highlights the Ozone ISA's

conclusions pertaining to health effects associated with both short-
term and long-term periods of exposure to ozone.
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    \99\ Human exposure to ozone varies over time due to changes in
ambient ozone concentration and because people move between
locations which have notably different ozone concentrations. Also,
the amount of ozone delivered to the lung is influenced not only by
the ambient concentrations but also by the breathing route and rate.
    \100\ U.S. EPA. Integrated Science Assessment (ISA) for Ozone
and Related Photochemical Oxidants (Final Report). U.S.
Environmental Protection Agency, Washington, DC, EPA/600/R-20/012,
2020.
    \101\ The ISA evaluates evidence and draws conclusions on the
causal 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 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.
---------------------------------------------------------------------------

    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 metabolic effects, including metabolic syndrome
(i.e., changes in insulin or glucose levels, cholesterol levels,
obesity, and blood pressure) and complications due to diabetes are
likely to be causally associated with short-term exposure to ozone. The
evidence is also suggestive of a causal relationship between short-term
exposure to ozone and cardiovascular effects, central nervous system
effects, and total mortality.
    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, metabolic 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 cancer.
    Finally, interindividual 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 and 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.
Recent epidemiologic studies provide generally consistent evidence that
long-term ozone exposure is associated with the development of asthma
in children. Studies comparing age groups reported higher magnitude
associations for short-term ozone exposure and respiratory hospital
admissions and emergency room visits among children than among adults.
Panel studies also provide support for experimental studies with
consistent associations between short-term ozone exposure and lung
function and pulmonary inflammation in healthy children. Additional
children's vulnerability and susceptibility factors are listed in
Section XII of this preamble.
2. Particulate Matter
    Scientific evidence spanning animal toxicological, controlled human
exposure, and epidemiologic studies shows that exposure to ambient PM
is associated with a broad range of health effects. These health
effects are discussed in detail in the Integrated Science Assessment
for Particulate Matter, which was finalized in December 2019 (PM ISA).
In addition, there is a more targeted evaluation of studies published
since the literature cutoff date of the 2019 p.m. ISA in the Supplement
to the Integrated Science Assessment for PM
(Supplement).102 103 The PM ISA characterizes the causal
nature of relationships between PM exposure and broad health categories
(e.g., cardiovascular effects, respiratory effects, etc.) using a
weight-of-evidence approach.\104\ Within this characterization, the PM
ISA summarizes the health effects evidence for short-term (i.e., hours
up to one month) and long-term (i.e., one month to years) exposures to
PM2.5, PM10-2.5, and
ultrafine particles, and concludes that exposures to ambient
PM2.5 are associated with a number of adverse health
effects. The following discussion highlights the PM ISA's conclusions,
and summarizes additional information from the Supplement where
appropriate, pertaining to the health effects evidence for both short-
and long-term PM exposures. Further discussion of PM-related health
effects can also be found in the 2022 Policy Assessment for the review
of the PM NAAQS.\105\
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    \102\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019.
    \103\ U.S. EPA. Supplement to the 2019 Integrated Science
Assessment for Particulate Matter (Final Report, 2022). U.S.
Environmental Protection Agency, Washington, DC, EPA/635/R-22/028,
2022.
    \104\ The causal framework draws upon the assessment and
integration of evidence from across scientific disciplines, spanning
atmospheric chemistry, exposure, dosimetry and health effects
studies (i.e., epidemiologic, controlled human exposure, and animal
toxicological studies), and assess the related uncertainties and
limitations that ultimately influence our understanding of the
evidence. This framework employs a five-level hierarchy that
classifies the overall weight-of-evidence with respect to the causal
nature of relationships between criteria pollutant exposures and
health and welfare effects using the following categorizations:
causal relationship; likely to be causal relationship; suggestive
of, but not sufficient to infer, a causal relationship; inadequate
to infer the presence or absence of a causal relationship; and not
likely to be a causal relationship (U.S. EPA. (2019). Integrated
Science Assessment for Particulate Matter (Final Report). U.S.
Environmental Protection Agency, Washington, DC, EPA/600/R-19/188,
Section P. 3.2.3).
    \105\ U.S. EPA. Policy Assessment (PA) for the Reconsideration
of the National Ambient Air Quality Standards for Particulate Matter
(Final Report, 2022). U.S. Environmental Protection Agency,
Washington, DC, EPA-452/R-22-004, 2022.
---------------------------------------------------------------------------

    EPA has concluded that recent evidence in combination with evidence
evaluated in the 2009 p.m. ISA supports a ``causal relationship''
between both long- and short-term exposures to PM2.5 and
premature mortality and cardiovascular effects and a ``likely to be
causal relationship'' between long- and short-term PM2.5
exposures and respiratory effects.\106\ Additionally, recent
experimental and epidemiologic studies provide evidence supporting a
``likely to be causal relationship'' between long-term PM2.5
exposure and nervous system effects, and long-term PM2.5
exposure and cancer. Because of remaining uncertainties and limitations
in the evidence base, EPA determined a ``suggestive of, but not
sufficient to infer, a causal relationship'' for long-term
PM2.5 exposure and reproductive and developmental effects
(i.e., male/female reproduction and fertility; pregnancy and birth
outcomes), long- and short-term exposures and metabolic effects, and
short-term exposure and nervous system effects.
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    \106\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F.
---------------------------------------------------------------------------

    As discussed extensively in the 2019 p.m. ISA and the Supplement,
recent studies continue to support a ``causal relationship'' between
short- and long-term PM2.5 exposures and
mortality.107 108 For short-term PM2.5 exposure,
multi-city studies, in combination with single- and multi-city studies
evaluated in the 2009 p.m. ISA,

provide evidence of consistent, positive associations across studies
conducted in different geographic locations, populations with different
demographic characteristics, and studies using different exposure
assignment techniques. Additionally, the consistent and coherent
evidence across scientific disciplines for cardiovascular morbidity,
particularly ischemic events and heart failure, and to a lesser degree
for respiratory morbidity, including exacerbations of chronic
obstructive pulmonary disease (COPD) and asthma, provide biological
plausibility for cause-specific mortality and ultimately total
mortality. Recent epidemiologic studies evaluated in the Supplement,
including studies that employed alternative methods for confounder
control, provide additional support to the evidence base that
contributed to the 2019 p.m. ISA conclusion for short-term
PM2.5 exposure and mortality.
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    \107\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019.
    \108\ U.S. EPA. Supplement to the 2019 Integrated Science
Assessment for Particulate Matter (Final Report, 2022). U.S.
Environmental Protection Agency, Washington, DC, EPA/635/R-22/028,
2022.
---------------------------------------------------------------------------

    The 2019 p.m. ISA concluded a ``causal relationship'' between long-
term PM2.5 exposure and mortality. In addition to reanalyses
and extensions of the American Cancer Society (ACS) and Harvard Six
Cities (HSC) cohorts, multiple new cohort studies conducted in the
United States and Canada consisting of people employed in a specific
job (e.g., teacher, nurse), and that apply different exposure
assignment techniques, provide evidence of positive associations
between long-term PM2.5 exposure and mortality. Biological
plausibility for mortality due to long-term PM2.5 exposure
is provided by the coherence of effects across scientific disciplines
for cardiovascular morbidity, particularly for coronary heart disease,
stroke, and atherosclerosis, and for respiratory morbidity,
particularly for the development of COPD. Additionally, recent studies
provide evidence indicating that as long-term PM2.5
concentrations decrease there is an increase in life expectancy. Recent
cohort studies evaluated in the Supplement, as well as epidemiologic
studies that conducted accountability analyses or employed alternative
methods for confounder controls, support and extend the evidence base
that contributed to the 2019 p.m. ISA conclusion for long-term
PM2.5 exposure and mortality.
    A large body of studies examining both short- and long-term
PM2.5 exposure and cardiovascular effects builds on the
evidence base evaluated in the 2009 p.m. ISA. The strongest evidence
for cardiovascular effects in response to short-term PM2.5
exposures is for ischemic heart disease and heart failure. The evidence
for short-term PM2.5 exposure and cardiovascular effects is
coherent across scientific disciplines and supports a continuum of
effects ranging from subtle changes in indicators of cardiovascular
health to serious clinical events, such as increased emergency
department visits and hospital admissions due to cardiovascular disease
and cardiovascular mortality. For long-term PM2.5 exposure,
there is strong and consistent epidemiologic evidence of a relationship
with cardiovascular mortality. This evidence is supported by
epidemiologic and animal toxicological studies demonstrating a range of
cardiovascular effects including coronary heart disease, stroke,
impaired heart function, and subclinical markers (e.g., coronary artery
calcification, atherosclerotic plaque progression), which collectively
provide coherence and biological plausibility. Recent epidemiologic
studies evaluated in the Supplement, as well as studies that conducted
accountability analyses or employed alternative methods for confounder
control, support and extend the evidence base that contributed to the
2019 p.m. ISA conclusion for both short- and long-term PM2.5
exposure and cardiovascular effects.
    Studies evaluated in the 2019 p.m. ISA continue to provide evidence
of a ``likely to be causal relationship'' between both short- and long-
term PM2.5 exposure and respiratory effects. Epidemiologic
studies provide consistent evidence of a relationship between short-
term PM2.5 exposure and asthma exacerbation in children and
COPD exacerbation in adults, as indicated by increases in emergency
department visits and hospital admissions, which is supported by animal
toxicological studies indicating worsening allergic airways disease and
subclinical effects related to COPD. Epidemiologic studies also provide
evidence of a relationship between short-term PM2.5 exposure
and respiratory mortality. However, there is inconsistent evidence of
respiratory effects, specifically lung function declines and pulmonary
inflammation, in controlled human exposure studies. With respect to
long term PM2.5 exposure, epidemiologic studies conducted in
the United States and abroad provide evidence of a relationship with
respiratory effects, including consistent changes in lung function and
lung function growth rate, increased asthma incidence, asthma
prevalence, and wheeze in children; acceleration of lung function
decline in adults; and respiratory mortality. The epidemiologic
evidence is supported by animal toxicological studies, which provide
coherence and biological plausibility for a range of effects including
impaired lung development, decrements in lung function growth, and
asthma development.
    Since the 2009 p.m. ISA, a growing body of scientific evidence
examined the relationship between long-term PM2.5 exposure
and nervous system effects, resulting for the first time in a causality
determination for this health effects category of a ``likely to be
causal relationship.'' The strongest evidence for effects on the
nervous system come from epidemiologic studies that consistently report
cognitive decrements and reductions in brain volume in adults. The
effects observed in epidemiologic studies in adults are supported by
animal toxicological studies demonstrating effects on the brain of
adult animals including inflammation, morphologic changes, and
neurodegeneration of specific regions of the brain. There is more
limited evidence for neurodevelopmental effects in children, with some
studies reporting positive associations with autism spectrum disorder
and others providing limited evidence of an association with cognitive
function. While there is some evidence from animal toxicological
studies indicating effects on the brain (i.e., inflammatory and
morphological changes) to support a biologically plausible pathway for
neurodevelopmental effects, epidemiologic studies are limited due to
their lack of control for potential confounding by copollutants, the
small number of studies conducted, and uncertainty regarding critical
exposure windows.
    Building off the decades of research demonstrating mutagenicity,
DNA damage, and other endpoints related to genotoxicity due to whole PM
exposures, recent experimental and epidemiologic studies focusing
specifically on PM2.5 provide evidence of a relationship
between long-term PM2.5 exposure and cancer. Epidemiologic
studies examining long-term PM2.5 exposure and lung cancer
incidence and mortality provide evidence of generally positive
associations in cohort studies spanning different populations,
locations, and exposure assignment techniques. Additionally, there is
evidence of positive associations with lung cancer incidence and
mortality in analyses limited to never smokers. In addition,
experimental and epidemiologic studies of genotoxicity, epigenetic
effects, carcinogenic potential, and that PM2.5 exhibits
several characteristics of

carcinogens provide biological plausibility for cancer development.
This collective body of evidence contributed to the conclusion of a
``likely to be causal relationship.''
    For the additional health effects categories evaluated for
PM2.5 in the 2019 p.m. ISA, experimental and epidemiologic
studies provide limited and/or inconsistent evidence of a relationship
with PM2.5 exposure. As a result, the 2019 p.m. ISA
concluded that the evidence is ``suggestive of, but not sufficient to
infer a causal relationship'' for short-term PM2.5 exposure
and metabolic effects and nervous system effects, and long-term
PM2.5 exposures and metabolic effects as well as
reproductive and developmental effects.
    In addition to evaluating the health effects attributed to short-
and long-term exposure to PM2.5, the 2019 p.m. ISA also
conducted an extensive evaluation as to whether specific components or
sources of PM2.5 are more strongly related with health
effects than PM2.5 mass. An evaluation of those studies
resulted in the 2019 p.m. ISA concluding that ``many PM2.5
components and sources are associated with many health effects, and the
evidence does not indicate that any one source or component is
consistently more strongly related to health effects than
PM2.5 mass.'' \109\
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    \109\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019.
---------------------------------------------------------------------------

    For both PM10-2.5 and UFPs, for all health effects
categories evaluated, the 2019 p.m. ISA concluded that the evidence was
``suggestive of, but not sufficient to infer, a causal relationship''
or ``inadequate to determine the presence or absence of a causal
relationship.'' For PM10-2.5, although a Federal Reference
Method (FRM) was instituted in 2011 to measure PM10-2.5
concentrations nationally, the causality determinations reflect that
the same uncertainty identified in the 2009 p.m. ISA persists with
respect to the method used to estimate PM10-2.5
concentrations in epidemiologic studies. Specifically, across
epidemiologic studies, different approaches are used to estimate
PM10-2.5 concentrations (e.g., direct measurement of
PM10-2.5, difference between PM10 and
PM2.5 concentrations), and it remains unclear how well
correlated PM10-2.5 concentrations are both spatially and
temporally across the different methods used.
    For UFPs, which have often been defined as particles <0.1 [micro]m,
the uncertainty in the evidence for the health effect categories
evaluated across experimental and epidemiologic studies reflects the
inconsistency in the exposure metric used (i.e., particle number
concentration, surface area concentration, mass concentration) as well
as the size fractions examined. In epidemiologic studies the size
fraction examined can vary depending on the monitor used and exposure
metric, with some studies examining number count over the entire
particle size range, while experimental studies that use a particle
concentrator often examine particles up to 0.3 [micro]m. Additionally,
due to the lack of a monitoring network, there is limited information
on the spatial and temporal variability of UFPs within the United
States, as well as population exposures to UFPs, which adds uncertainty
to epidemiologic study results.
    The 2019 p.m. ISA cites extensive evidence indicating that ``both
the general population as well as specific populations and life stages
are at risk for PM2.5-related health effects.'' \110\ For
example, in support of its ``causal'' and ``likely to be causal''
determinations, the ISA cites substantial evidence for (1) PM-related
mortality and cardiovascular effects in older adults; (2) PM-related
cardiovascular effects in people with pre-existing cardiovascular
disease; (3) PM-related respiratory effects in people with pre-existing
respiratory disease, particularly asthma exacerbations in children; and
(4) PM-related impairments in lung function growth and asthma
development in children. The ISA additionally notes that stratified
analyses (i.e., analyses that directly compare PM-related health
effects across groups) provide strong evidence for racial and ethnic
differences in PM2.5 exposures and in the risk of
PM2.5-related health effects, specifically within Hispanic
and non-Hispanic Black populations, with some evidence of increased
risk for populations of low socioeconomic status. Recent studies
evaluated in the Supplement support the conclusion of the 2019 p.m. ISA
with respect to disparities in both PM2.5 exposure and
health risk by race and ethnicity and provide additional support for
disparities for populations of lower socioeconomic status.\111\
Additionally, evidence spanning epidemiologic studies that conducted
stratified analyses, experimental studies focusing on animal models of
disease or individuals with pre-existing disease, dosimetry studies, as
well as studies focusing on differential exposure suggest that
populations with pre-existing cardiovascular or respiratory disease,
populations that are overweight or obese, populations that have
particular genetic variants, and current/former smokers could be at
increased risk for adverse PM2.5-related health effects. The
2022 Policy Assessment for the review of the PM NAAQS also highlights
that factors that may contribute to increased risk of PM2.5-
related health effects include lifestage (children and older adults),
pre-existing diseases (cardiovascular disease and respiratory disease),
race/ethnicity, and socioeconomic status.\112\
---------------------------------------------------------------------------

    \110\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019.
    \111\ U.S. EPA. Supplement to the 2019 Integrated Science
Assessment for Particulate Matter (Final Report, 2022). U.S.
Environmental Protection Agency, Washington, DC, EPA/635/R-22/028,
2022.
    \112\ U.S. EPA. Policy Assessment (PA) for the Reconsideration
of the National Ambient Air Quality Standards for Particulate Matter
(Final Report, 2022). U.S. Environmental Protection Agency,
Washington, DC, EPA-452/R-22-004, 2022, p. 3-53.
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3. 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 (ISA for Oxides of
Nitrogen).\113\ 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 consists of 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 emergency department 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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    \113\ 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 that 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. Carbon Monoxide
    Information on the health effects of CO can be found in the January
2010 Integrated Science Assessment for Carbon Monoxide (CO ISA).\114\
The CO ISA presents conclusions regarding the presence of causal
relationships between CO exposure and categories of adverse health
effects.\115\ This section provides a summary of the health effects
associated with exposure to ambient concentrations of CO, along with
the CO ISA conclusions.\116\
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    \114\ 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. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=218686.
    \115\ The ISA evaluates the health evidence associated with
different health 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 definitions of these levels of evidence, please
refer to Section 1.6 of the ISA.
    \116\ Personal exposure includes contributions from many
sources, and in many different environments. Total personal exposure
to CO includes both ambient and non-ambient components; and both
components may contribute to adverse health effects.
---------------------------------------------------------------------------

    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 that 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 that 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 that 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.
5. 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.117 118 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.
---------------------------------------------------------------------------

    \117\ U.S. EPA. (1999). Guidelines for Carcinogen Risk
Assessment. Review Draft. NCEA-F-0644, July. Washington, DC: U.S.
EPA. Retrieved on March 19, 2009 from http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54932.
    \118\ 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. 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.
    Noncancer 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 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 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 notes 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.\119\ 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.
---------------------------------------------------------------------------

    \119\ See Section II.A.2 for discussion of the current
PM2.5 NAAQS standard.
---------------------------------------------------------------------------

    Since 2002, several new studies have been published which continue
to report increased lung cancer risk associated with occupational
exposure to diesel exhaust from older engines. Of particular note since
2011 are three new epidemiology studies that 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.120 121 122 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 reinforce 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 (i.e., heavy-duty highway engines from 2007
and later model years) since the newer engines have large reductions in
the emission constituents compared to older technology diesel engines.
---------------------------------------------------------------------------

    \120\ Garshick, Eric, Francine Laden, Jaime E. Hart, Mary E.
Davis, Ellen A. Eisen, and Thomas J. Smith. 2012. Lung cancer and
elemental carbon exposure in trucking industry workers.
Environmental Health Perspectives 120(9): 1301-1306.
    \121\ 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.
    \122\ Olsson, Ann 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.'' \123\ This designation was an update from its 1988 evaluation
that considered the evidence to be indicative of a ``probable human
carcinogen.''
---------------------------------------------------------------------------

    \123\ 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].
---------------------------------------------------------------------------

6. Air Toxics
    Heavy-duty engine emissions contribute to ambient levels of air
toxics that are known or suspected human or animal carcinogens, or that
have noncancer health effects. These compounds include, but are not
limited to, benzene, formaldehyde, acetaldehyde, and naphthalene. These
compounds were identified as national or regional cancer risk drivers
or contributors in the 2018 AirToxScreen Assessment and have
significant inventory contributions from mobile
sources.124 125 Chapter 4 of the RIA includes additional
information on the health effects associated with exposure to each of
these pollutants.
---------------------------------------------------------------------------

    \124\ U.S. EPA (2022) Technical Support Document EPA Air Toxics
Screening Assessment. 2017AirToxScreen TSD. https://www.epa.gov/system/files/documents/2022-03/airtoxscreen_2017tsd.pdf.
    \125\ U.S. EPA (2022) 2018 AirToxScreen Risk Drivers. https://www.epa.gov/AirToxScreen/airtoxscreen-risk-drivers.
---------------------------------------------------------------------------

7. 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 studies have been published in peer-reviewed
journals, concluding that concentrations of CO, CO2, NO,
NO2, benzene, aldehydes, PM, black carbon, and many other
compounds are elevated in ambient air within approximately

300-600 meters (about 1,000-2,000 feet) of major roadways. The highest
concentrations of most pollutants emitted directly by motor vehicles
are found at locations within 50 meters (about 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,
UFPs, metals, elemental carbon (EC), NO, NOX, and several
VOCs.\126\ 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 reviewing the
literature, Karner et al., (2010) reported that results varied based on
the method of statistical analysis used to determine the gradient in
pollutant concentration. More recent studies continue to show
significant concentration gradients of traffic-related air pollution
around major
roads.127 128 129 130 131 132 133 134 135 136
There is evidence that EPA's regulations for vehicles have lowered the
near-road concentrations and gradients.\137\ Starting in 2010, EPA
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). The monitoring data for NO2 indicate
that in urban areas, monitors near roadways often report the highest
concentrations of NO2.\138\ More recent studies of traffic-
related air pollutants continue to report sharp gradients around
roadways, particularly within several hundred meters.139 140
---------------------------------------------------------------------------

    \126\ Karner, A.A.; Eisinger, D.S.; Niemeier, D.A. (2010). Near-
roadway air quality: synthesizing the findings from real-world data.
Environ Sci Technol 44: 5334-5344.
    \127\ McDonald, B.C.; McBride, Z.C.; Martin, E.W.; Harley, R.A.
(2014) High-resolution mapping of motor vehicle carbon dioxide
emissions. J. Geophys. Res. Atmos.,119, 5283-5298, doi:10.1002/
2013JD021219.
    \128\ Kimbrough, S.; Baldauf, R.W.; Hagler, G.S.W.; Shores,
R.C.; Mitchell, W.; Whitaker, D.A.; Croghan, C.W.; Vallero, D.A.
(2013) Long-term continuous measurement of near-road air pollution
in Las Vegas: seasonal variability in traffic emissions impact on
air quality. Air Qual Atmos Health 6: 295-305. DOI 10.1007/s11869-
012-0171-x.
    \129\ Kimbrough, S.; Palma, T.; Baldauf, R.W. (2014) Analysis of
mobile source air toxics (MSATs)--Near-road VOC and carbonyl
concentrations. Journal of the Air & Waste Management Association,
64:3, 349-359, DOI: 10.1080/10962247.2013.863814.
    \130\ Kimbrough, S.; Owen, R.C.; Snyder, M.; Richmond-Bryant, J.
(2017) NO to NO2 Conversion Rate Analysis and
Implications for Dispersion Model Chemistry Methods using Las Vegas,
Nevada Near-Road Field Measurements. Atmos Environ 165: 23-24.
    \131\ Hilker, N.; Wang, J.W.; Jong, C-H.; Healy, R.M.; Sofowote,
U.; Debosz, J.; Su, Y.; Noble, M.; Munoz, A.; Doerkson, G.; White,
L.; Audette, C.; Herod, D.; Brook, J.R.; Evans, G.J. (2019) Traffic-
related air pollution near roadways: discerning local impacts from
background. Atmos. Meas. Tech., 12, 5247-5261. https://doi.org/10.5194/amt-12-5247-2019.
    \132\ Grivas, G.; Stavroulas, I.; Liakakou, E.; Kaskaoutis,
D.G.; Bougiatioti, A.; Paraskevopoulou, D.; Gerasopoulos, E.;
Mihalopoulos, N. (2019) Measuring the spatial variability of black
carbon in Athens during wintertime. Air Quality, Atmosphere & Health
(2019) 12:1405-1417. https://doi.org/10.1007/s11869-019-00756-y.
    \133\ Apte, J.S.; Messier, K.P.; Gani, S.; Brauer, M.;
Kirchstetter, T.W.; Lunden, M.M.; Marshall, J.D.; Portier, C.J.;
Vermeulen, R.C.H.; Hamburg, S.P. (2017) High-Resolution Air
Pollution Mapping with Google Street View Cars: Exploiting Big Data.
Environ Sci Technol 51: 6999-7008. https://doi.org/10.1021/acs.est.7b00891.
    \134\ Dabek-Zlotorzynska, E.; Celo, V.; Ding, L.; Herod, D.;
Jeong, C-H.; Evans, G.; Hilker, N. (2019) Characteristics and
sources of PM2.5 and reactive gases near roadways in two
metropolitan areas in Canada. Atmos Environ 218: 116980. https://doi.org/10.1016/j.atmosenv.2019.116980.
    \135\ Apte, J.S.; Messier, K.R.; Gani, S.; et al. (2017) High-
resolution air pollution mapping with Google Street View cars:
exploiting big data. Environ Sci Technol 51: 6999-7018, [Online at
https://doi.org/10.1021/acs.est.7b00891].
    \136\ Gu, P.; Li, H.Z.; Ye, Q.; et al. (2018) Intercity
variability of particulate matter is driven by carbonaceous sources
and correlated with land-use variables. Environ Sci Technol 52: 52:
11545-11554. [Online at http://dx.doi.org/10.1021/acs.est.8b03833].
    \137\ Sarnat, J.A.; Russell, A.; Liang, D.; Moutinho, J.L.;
Golan, R.; Weber, R.; Gao, D.; Sarnat, S.; Chang, H.H.; Greenwald,
R.; Yu, T. (2018) Developing Multipollutant Exposure Indicators of
Traffic Pollution: The Dorm Room Inhalation to Vehicle Emissions
(DRIVE) Study. Health Effects Institute Research Report Number 196.
[Online at: https://www.healtheffects.org/publication/developing-multipollutant-exposure-indicators-traffic-pollution-dorm-room-inhalation].
    \138\ Gantt, B; Owen, R.C.; Watkins, N. (2021) Characterizing
nitrogen oxides and fine particulate matter near major highways in
the United States using the National Near-road Monitoring Network.
Environ Sci Technol 55: 2831-2838. [Online at https://doi.org/10.1021/acs.est.0c05851].
    \139\ Apte, J.S.; Messier, K.R.; Gani, S.; et al. (2017) High-
resolution air pollution mapping with Google Street View cars:
exploiting big data. Environ Sci Technol 51: 6999-7018, [Online at
https://doi.org/10.1021/acs.est.7b00891].
    \140\ Gu, P.; Li, H.Z.; Ye, Q.; et al. (2018) Intercity
variability of particulate matter is driven by carbonaceous sources
and correlated with land-use variables. Environ Sci Technol 52: 52:
11545-11554. [Online at http://dx.doi.org/10.1021/acs.est.8b03833].
---------------------------------------------------------------------------

    For pollutants with relatively high background concentrations
relative to near-road concentrations, detecting concentration gradients
can be difficult. For example, many carbonyls have high background
concentrations as a result of photochemical breakdown of precursors
from many different organic compounds. However, several studies have
measured carbonyls in multiple weather conditions and found higher
concentrations of many carbonyls downwind of
roadways.141 142 These findings suggest a substantial
roadway source of these carbonyls.
---------------------------------------------------------------------------

    \141\ Liu, W.; Zhang, J.; Kwon, J.l.; et l. (2006).
Concentrations and source characteristics of airborne carbonyl
compounds measured outside urban residences. J Air Waste Manage
Assoc 56: 1196-1204.
    \142\ 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/system/files/Cahill149.pdf.
---------------------------------------------------------------------------

    In the past 30 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.\143\ In
addition, numerous studies have found adverse health effects associated
with spending time in traffic, such as commuting or walking along high-
traffic roadways, including studies among
children.144 145 146 147 The health outcomes with the
strongest evidence linking them with traffic-associated air pollutants
are respiratory effects, particularly in asthmatic children, and
cardiovascular effects. Commenters on the NPRM stressed the importance
of consideration of the impacts of traffic-related air pollution,
especially NOX, on children's health.
---------------------------------------------------------------------------

    \143\ In the widely-used PubMed database of health publications,
between January 1, 1990 and December 31, 2021, 1,979 publications
contained the keywords ``traffic, pollution, epidemiology,'' with
approximately half the studies published after 2015.
    \144\ 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 Perspect 115:1192-1196.
    \145\ 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 J Med
351: 1721-1730.
    \146\ 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. Am J Cardiol 104: 665-670.
    \147\ 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. Environ
Health Perspect 115: 507-512.
---------------------------------------------------------------------------

    Numerous reviews of this body of health literature have been
published. In a 2022 final report, an expert panel of the Health
Effects Institute (HEI) employed a systematic review focusing on
selected health endpoints related to exposure to traffic-related air
pollution.\148\ The HEI panel concluded

that there was a high level of confidence in evidence between long-term
exposure to traffic-related air pollution and health effects in adults,
including all-cause, circulatory, and ischemic heart disease
mortality.\149\ The panel also found that there is a moderate-to-high
level of confidence in evidence of associations with asthma onset and
acute respiratory infections in children and lung cancer and asthma
onset in adults. This report follows on an earlier expert review
published by HEI in 2010, where it found strongest evidence for asthma-
related traffic impacts. Other literature reviews have been published
with conclusions generally similar to the HEI
panels'.150 151 152 153 Additionally, 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.\154\ The U.S. Department of Health and Human Services'
National Toxicology Program (NTP) published a monograph including a
systematic review of traffic-related air pollution and its impacts on
hypertensive disorders of pregnancy. The NTP concluded that exposure to
traffic-related air pollution is ``presumed to be a hazard to pregnant
women'' for developing hypertensive disorders of pregnancy.\155\
---------------------------------------------------------------------------

    \148\ HEI Panel on the Health Effects of Long-Term Exposure to
Traffic-Related Air Pollution (2022) Systematic review and meta-
analysis of selected health effects of long-term exposure to
traffic-related air pollution. Health Effects Institute Special
Report 23. [Online at https://www.healtheffects.org/system/files/hei-special-report-23_1.pdf.] This more recent review focused on
health outcomes related to birth effects, respiratory effects,
cardiometabolic effects, and mortality.
    \149\ Boogaard, H.; Patton. A.P.; Atkinson, R.W.; Brook, J.R.;
Chang, H.H.; Crouse, D.L.; Fussell, J.C.; Hoek, G.; Hoffman, B.;
Kappeler, R.; Kutlar Joss, M.; Ondras, M.; Sagiv, S.K.; Somoli, E.;
Shaikh, R.; Szpiro, A.A.; Van Vliet E.D.S.; Vinneau, D.; Weuve, J.;
Lurmann, F.W.; Forastiere, F. (2022) Long-term exposure to traffic-
related air pollution and selected health outcomes: a systematic
review and meta-analysis. Environ Intl 164: 107262. [Online at
https://doi.org/10.1016/j.envint.2022.107262].
    \150\ 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. J Environ
Health 70: 33-41.
    \151\ 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.
    \152\ Sun, X.; Zhang, S.; Ma, X. (2014) No association between
traffic density and risk of childhood leukemia: a meta-analysis.
Asia Pac J Cancer Prev 15: 5229-5232.
    \153\ Raaschou-Nielsen, O.; Reynolds, P. (2006). Air pollution
and childhood cancer: a review of the epidemiological literature.
Int J Cancer 118: 2920-9.
    \154\ 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. Am J Prev Med 46: 413-422.
    \155\ National Toxicology Program (2019) NTP Monograph on the
Systematic Review of Traffic-related Air Pollution and Hypertensive
Disorders of Pregnancy. NTP Monograph 7. https://ntp.niehs.nih.gov/ntp/ohat/trap/mgraph/trap_final_508.pdf.
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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).156 157 158 159 160
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    \156\ Volk, H.E.; Hertz-Picciotto, I.; Delwiche, L.; et al.
(2011). Residential proximity to freeways and autism in the CHARGE
study. Environ Health Perspect 119: 873-877.
    \157\ 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. Am J Epidemiol. doi: 10.1093/aje/
kwm308. [Online at http://dx.doi.org].
    \158\ 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. Environ Health Perspect 2011: 682-687.
    \159\ Wu, J.; Wilhelm, M.; Chung, J.; et al. (2011). Comparing
exposure assessment methods for traffic-related air pollution in and
adverse pregnancy outcome study. Environ Res 111: 685-6692.
    \160\ Stenson, C.; Wheeler, A.J.; Carver, A.; et al. (2021) The
impact of traffic-related air pollution on child and adolescent
academic performance: a systematic review. Environ Intl 155: 106696
[Online at https://doi.org/10.1016/j.envint.2021.106696].
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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. For example, numerous
studies indicate that near-roadway exposures may increase systemic
inflammation, affecting organ systems, including blood vessels and
lungs.161 162 163 164 Additionally, long-term exposures in
near-road environments have been associated with inflammation-
associated conditions, such as atherosclerosis and
asthma.165 166 167
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    \161\ Riediker, M. (2007). Cardiovascular effects of fine
particulate matter components in highway patrol officers. Inhal
Toxicol 19: 99-105. doi: 10.1080/08958370701495238.
    \162\ 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. Environ Health Perspect 119:
481-486. doi:10.1289/ehp.1002560.
    \163\ Eckel. S.P.; Berhane, K.; Salam, M.T.; et al. (2011).
Residential Traffic-related pollution exposure and exhaled nitric
oxide in the Children's Health Study. Environ Health Perspect.
doi:10.1289/ehp.1103516.
    \164\ 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].
    \165\ Adar, S.D.; Klein, R.; Klein, E.K.; et al. (2010). Air
pollution and the microvasculature: 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.
    \166\ 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.
Environ Health Perspect 116: 1463-1468. doi:10.1289/ehp.11290.
Available at http://dx.doi.org.
    \167\ McConnell, R.; Islam, T.; Shankardass, K.; et al. (2010).
Childhood incident asthma and traffic-related air pollution at home
and school. Environ Health Perspect 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 adverse health associations in
children experiencing chronic social stress, such as in violent
neighborhoods or in homes with low incomes or high family
stress.168 169 170 171
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    \168\ Islam, T.; Urban, R.; Gauderman, W.J.; et al. (2011).
Parental stress increases the detrimental effect of traffic exposure
on children's lung function. Am J Respir Crit Care Med.
    \169\ 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. Environ Health
Perspect 115: 1140-1146.
    \170\ 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. Environ Health Perspect
116: 970-5.
    \171\ Long, D.; Lewis, D.; Langpap, C. (2021) Negative traffic
externalities and infant health: the role of income heterogeneity
and residential sorting. Environ and Resource Econ 80: 637-674.
[Online at https://doi.org/10.1007/s10640-021-00601-w].
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    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. The 2013 U.S. Census Bureau's
American Housing Survey (AHS) was the last AHS that included whether
housing units were within 300 feet of an ``airport, railroad, or
highway with four or more lanes.'' \172\ The 2013 survey reports that
17.3 million housing units, or 13 percent of all housing units in the
United States, were in such areas. Assuming that populations and
housing units are in the same locations, this corresponds to a
population of more than 41 million U.S. residents in close proximity to
high-traffic roadways or other transportation sources. According to the
Central Intelligence Agency's World Factbook, based on data collected
between 2012-2014, the United States had 6,586,610 km of roadways,
293,564 km of railways, and 13,513 airports. As such, highways
represent the overwhelming majority of transportation facilities
described by this factor in the AHS.
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    \172\ The variable was known as ``ETRANS'' in the questions
about the neighborhood.

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    EPA also conducted a study to estimate the number of people living
near truck freight routes in the United States.\173\ Based on a
population analysis using the U.S. Department of Transportation's
(USDOT) Freight Analysis Framework 4 (FAF4) and population data from
the 2010 decennial census, an estimated 72 million people live within
200 meters of these freight routes.174 175 In addition,
relative to the rest of the population, people of color and those with
lower incomes are more likely to live near FAF4 truck routes. They are
also more likely to live in metropolitan areas. The EPA's Exposure
Factor Handbook also indicates that, 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.\176\
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    \173\ U.S. EPA (2021). Estimation of Population Size and
Demographic Characteristics among People Living Near Truck Routes in
the Conterminous United States. Memorandum to the Docket.
    \174\ FAF4 is a model from the USDOT's Bureau of Transportation
Statistics (BTS) and Federal Highway Administration (FHWA), which
provides data associated with freight movement in the U.S. It
includes data from the 2012 Commodity Flow Survey (CFS), the Census
Bureau on international trade, as well as data associated with
construction, agriculture, utilities, warehouses, and other
industries. FAF4 estimates the modal choices for moving goods by
trucks, trains, boats, and other types of freight modes. It includes
traffic assignments, including truck flows on a network of truck
routes. https://ops.fhwa.dot.gov/freight/freight_analysis/faf/.
    \175\ The same analysis estimated the population living within
100 meters of a FAF4 truck route is 41 million.
    \176\ EPA. (2011) Exposure Factors Handbook: 2011 Edition.
Chapter 16. Online at https://www.epa.gov/sites/production/files/2015-09/documents/efh-Chapter16.pdf.
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    As described in Section VII.H.1, we estimate that about 10 million
students attend schools within 200 meters of major roads.\177\ Research
into the impact of traffic-related air pollution on school performance
is tentative. A review of this literature found some evidence that
children exposed to higher levels of traffic-related air pollution show
poorer academic performance than those exposed to lower levels of
traffic-related air pollution.\178\ However, this evidence was judged
to be weak due to limitations in the assessment methods.
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    \177\ Pedde, M.; Bailey, C. (2011) Identification of Schools
within 200 Meters of U.S. Primary and Secondary Roads. Memorandum to
the docket.
    \178\ Stenson, C.; Wheeler, A.J.; Carver, A.; et al. (2021) The
impact of traffic-related air pollution on child and adolescent
academic performance: a systematic review. Environ Intl 155: 106696.
[Online at https://doi.org/10.1016/j.envint.2021.106696].
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    While near-roadway studies focus on residents near roads or others
spending considerable time near major roads, the duration of commuting
results in another important contributor to overall exposure to
traffic-related air pollution. Studies of health that address time
spent in transit have found evidence of elevated risk of cardiac
impacts.179 180 181 Studies have also found that school bus
emissions can increase student exposures to diesel-related air
pollutants, and that programs that reduce school bus emissions may
improve health and reduce school absenteeism.182 183 184 185
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    \179\ Riediker, M.; Cascio, W.E.; Griggs, T.R.; et al. (2004)
Particulate matter exposure in cars is associated with
cardiovascular effects in healthy young men. Am J Respir Crit Care
Med 169. [Online at https://doi.org/10.1164/rccm.200310-1463OC].
    \180\ Peters, A.; von Klot, S.; Heier, M.; et al. (2004)
Exposure to traffic and the onset of myocardial infarction. New Engl
J Med 1721-1730. [Online at https://doi.org/10.1056/NEJMoa040203].
    \181\ Adar, S.D.; Gold, D.R.; Coull, B.A.; (2007) Focused
exposure to airborne traffic particles and heart rate variability in
the elderly. Epidemiology 18: 95-103 [Online at: https://doi.org/10.1097/01.ede.0000249409.81050.46].
    \182\ Sabin, L.; Behrentz, E.; Winer, A.M.; et al.
Characterizing the range of children's air pollutant exposure during
school bus commutes. J Expo Anal Environ Epidemiol 15: 377-387.
[Online at https://doi.org/10.1038/sj.jea.7500414].
    \183\ Li, C.; N, Q.; Ryan, P.H.; School bus pollution and
changes in the air quality at schools: a case study. J Environ Monit
11: 1037-1042. [https://doi.org/10.1039/b819458k].
    \184\ Austin, W.; Heutel, G.; Kreisman, D. (2019) School bus
emissions, student health and academic performance. Econ Edu Rev 70:
108-12.
    \185\ Adar, S.D.; D. Souza, J.; Sheppard, L.; Adopting clean
fuels and technologies on school buses. Pollution and health impacts
in children. Am J Respir Crit Care Med 191. [Online at http://doi.org/10.1164/rccm.201410-1924OC].
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C. Environmental Effects Associated With Exposure to Pollutants
Impacted by This Rule

    This section discusses the environmental effects associated with
pollutants affected by this rule, specifically PM, ozone,
NOX and air toxics.
1. Visibility
    Visibility can be defined as the degree to which the atmosphere is
transparent to visible light.\186\ Visibility impairment is caused by
light scattering and absorption by suspended particles and gases. It is
dominated by contributions from suspended particles except under
pristine conditions. 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 2019 p.m.
ISA.\187\
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    \186\ 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 https://www.nap.edu/catalog/2097/protecting-visibility-in-national-parks-and-wilderness-areas.
    \187\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019.
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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 provisions have resulted in
substantial improvements in visibility and will continue to do so in
the future. Nationally, 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.\188\ However between 1990 and 2018, in the western part
of the country, changes in total light extinction were smaller, and the
contribution of particulate organic matter to atmospheric light
extinction was increasing due to increasing wildfire emissions.\189\
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    \188\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019.
    \189\ Hand, J.L.; Prenni, A.J.; Copeland, S.; Schichtel, B.A.;
Malm, W.C. (2020). Thirty years of the Clean Air Act Amendments:
Impacts on haze in remote regions of the United States (1990-2018).
Atmos Environ 243: 117865.
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    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.\190\ In 1999, EPA finalized the regional
haze program to protect the visibility in Mandatory Class I Federal
areas.\191\ There are 156 national parks, forests and wilderness areas
categorized as Mandatory Class I Federal areas.\192\ 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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    \190\ See CAA section 169(a).
    \191\ 64 FR 35714, July 1, 1999.
    \192\ 62 FR 38680-38681, July 18, 1997.

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    EPA has also concluded that PM2.5 causes 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). The secondary (welfare-based) PM NAAQS provide protection
against visibility effects. In recent PM NAAQS reviews, EPA evaluated a
target level of protection for visibility impairment that is expected
to be met through attainment of the existing secondary PM standards.
2. Plant and Ecosystem Effects of Ozone
    The welfare effects of ozone include effects on ecosystems, which
can be observed across a variety of scales, i.e., subcellular,
cellular, leaf, whole plant, population and ecosystem. When ozone
effects that begin at small spatial scales, such as the leaf of an
individual plant, occur at sufficient magnitudes (or to a sufficient
degree), they can result in effects being propagated along a continuum
to higher and higher levels of biological organization. For example,
effects at the individual plant level, such as altered rates of leaf
gas exchange, growth and reproduction, can, when widespread, result in
broad changes in ecosystems, such as productivity, carbon storage,
water cycling, nutrient cycling, and community composition.
    Ozone can produce both acute and chronic injury in sensitive plant
species depending on the concentration level and the duration of the
exposure.\193\ In those sensitive species,\194\ effects from repeated
exposure to ozone throughout the growing season of the plant can tend
to accumulate, so even relatively low concentrations experienced for a
longer duration have the potential to create chronic stress on
vegetation.195 196 Ozone damage to sensitive plant 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.\197\ 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,\198\ 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.\199\ In addition
to ozone effects on vegetation, newer evidence suggests that ozone
affects interactions between plants and insects by altering chemical
signals (e.g., floral scents) that plants use to communicate to other
community members, such as attraction of pollinators.
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    \193\ 73 FR 16486, March 27, 2008.
    \194\ 73 FR 16491, March 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.
    \195\ U.S. EPA. Integrated Science Assessment (ISA) for Ozone
and Related Photochemical Oxidants (Final Report). U.S.
Environmental Protection Agency, Washington, DC, EPA/600/R-20/012,
2020.
    \196\ 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.
    \197\ 73 FR 16492, March 27, 2008.
    \198\ 73 FR 16493-16494, March 27, 2008. Ozone impacts could be
occurring in areas where plant species sensitive to ozone have not
yet been studied or identified.
    \199\ 73 FR 16490-16497, March 27, 2008.
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    The Ozone ISA presents more detailed information on how ozone
affects vegetation and ecosystems.200 201 The Ozone ISA
reports causal and likely causal relationships between ozone exposure
and a number of welfare effects and characterizes the weight of
evidence for different effects associated with ozone.\202\ The Ozone
ISA concludes that visible foliar injury effects on vegetation, reduced
vegetation growth, reduced plant reproduction, reduced productivity in
terrestrial ecosystems, reduced yield and quality of agricultural
crops, alteration of below-ground biogeochemical cycles, and altered
terrestrial community composition are causally associated with exposure
to ozone. It also concludes that increased tree mortality, altered
herbivore growth and reproduction, altered plant-insect signaling,
reduced carbon sequestration in terrestrial ecosystems, and alteration
of terrestrial ecosystem water cycling are likely to be causally
associated with exposure to ozone.
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    \200\ U.S. EPA. Integrated Science Assessment (ISA) for Ozone
and Related Photochemical Oxidants (Final Report). U.S.
Environmental Protection Agency, Washington, DC, EPA/600/R-20/012,
2020.
    \201\ U.S. EPA. Integrated Science Assessment (ISA) for Ozone
and Related Photochemical Oxidants (Final Report). U.S.
Environmental Protection Agency, Washington, DC, EPA/600/R-20/012,
2020.
    \202\ 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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3. Atmospheric Deposition
    The Integrated Science Assessment for Oxides of Nitrogen, Oxides of
Sulfur, and Particulate Matter--Ecological Criteria documents the
ecological effects of the deposition of these criteria air
pollutants.\203\ It is clear from the body of evidence that
NOX, oxides of sulfur (SOX), and PM contribute to
total nitrogen (N) and sulfur (S) deposition. In turn, N and S
deposition cause either nutrient enrichment or acidification depending
on the sensitivity of the landscape or the species in question. Both
enrichment and acidification are characterized by an alteration of the
biogeochemistry and the physiology of organisms, resulting in harmful
declines in biodiversity in terrestrial, freshwater, wetland, and
estuarine ecosystems in the United States. Decreases in biodiversity
mean that some species become relatively less abundant and may be
locally extirpated. In addition to the loss of unique living species,
the decline in total biodiversity can be harmful because biodiversity
is an important determinant of the stability of ecosystems and their
ability to provide socially valuable ecosystem services.
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    \203\ U.S. EPA. Integrated Science Assessment (ISA) for Oxides
of Nitrogen, Oxides of Sulfur and Particulate Matter Ecological
Criteria (Final Report). U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-20/278, 2020.
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    Terrestrial, wetland, freshwater, and estuarine ecosystems in the
United States are affected by N enrichment/eutrophication caused by N
deposition. These effects have been consistently documented across the
United States for hundreds of species. In aquatic systems increased N
can alter species assemblages and cause eutrophication. In terrestrial
systems N loading can lead to loss of nitrogen-sensitive lichen
species, decreased biodiversity of grasslands, meadows and other
sensitive habitats, and increased potential for invasive species. For a
broader explanation of the topics treated here, refer to the
description in Chapter 4 of the RIA.
    The sensitivity of terrestrial and aquatic ecosystems to
acidification from N and S deposition is predominantly governed by
geology. Prolonged exposure to excess nitrogen and sulfur

deposition in sensitive areas acidifies lakes, rivers, and soils.
Increased acidity in surface waters creates inhospitable conditions for
biota and affects the abundance and biodiversity of fishes,
zooplankton, and macroinvertebrates and ecosystem function. Over time,
acidifying deposition also removes essential nutrients from forest
soils, depleting the capacity of soils to neutralize future acid
loadings and negatively affecting forest sustainability. Major effects
in forests include a decline in sensitive tree species, such as red
spruce (Picea rubens) and sugar maple (Acer saccharum).
    Building materials including metals, stones, cements, and paints
undergo natural weathering processes from exposure to environmental
elements (e.g., wind, moisture, temperature fluctuations, sunlight,
etc.). Pollution can worsen and accelerate these effects. Deposition of
PM is associated with both physical damage (materials damage effects)
and impaired aesthetic qualities (soiling effects). Wet and dry
deposition of PM can physically affect materials, adding to the effects
of natural weathering processes, by potentially promoting or
accelerating the corrosion of metals, by degrading paints, and by
deteriorating building materials such as stone, concrete, and
marble.\204\ The effects of PM are exacerbated by the presence of
acidic gases and can be additive or synergistic due to the complex
mixture of pollutants in the air and surface characteristics of the
material. Acidic deposition has been shown to have an effect on
materials including zinc/galvanized steel and other metal, carbonate
stone (such as monuments and building facings), and surface coatings
(paints).\205\ The effects on historic buildings and outdoor works of
art are of particular concern because of the uniqueness and
irreplaceability of many of these objects. In addition to aesthetic and
functional effects on metals, stone, and glass, altered energy
efficiency of photovoltaic panels by PM deposition is also becoming an
important consideration for impacts of air pollutants on materials.
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    \204\ U.S. EPA. Integrated Science Assessment (ISA) for
Particulate Matter (Final Report, 2019). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-19/188, 2019.
    \205\ Irving, P.M., e.d. 1991. Acid Deposition: State of Science
and Technology, Volume III, Terrestrial, Materials, Health, and
Visibility Effects, The U.S. National Acid Precipitation Assessment
Program, Chapter 24, page 24-76.
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4. Environmental Effects of Air Toxics
    Emissions from producing, transporting, and combusting fuel
contribute to ambient levels of pollutants that contribute to adverse