controlled human exposure studies demonstrating increased airway
responsiveness in individuals with asthma following ambient-relevant
NO2 exposures. The coherence of this evidence with
epidemiologic findings for asthma hospital admissions and ED visits as
well as lung function decrements and increased pulmonary inflammation
in children with asthma describe a plausible pathway by which
NO2 exposure can cause an asthma exacerbation. The 2016 ISA
for Oxides of Nitrogen also concluded that there is likely to be a
causal relationship between long-term NO2 exposure and
respiratory effects. This conclusion is based on new epidemiologic
evidence for associations of NO2 with asthma development in
children combined with biological plausibility from experimental
studies.
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    \717\ 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 co-pollutant
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.
iv. Sulfur Oxides
    This section provides an overview of the health effects associated
with SO2. Additional information on the health effects of
SO2 can be found in the 2017 Integrated Science Assessment
for Sulfur Oxides--Health Criteria (SOX ISA).\718\ Following
an extensive evaluation of health evidence from animal toxicological,
controlled human exposure, and epidemiologic studies, the EPA has
concluded that there is a causal relationship between respiratory
health effects and short-term exposure to SO2. The immediate
effect of SO2 on the respiratory system in humans is
bronchoconstriction. People with asthma are more sensitive to the
effects of SO2, likely resulting from preexisting
inflammation associated with this disease. In addition to those with
asthma (both children and adults), there is suggestive evidence that
all children and older adults may be at increased risk of
SO2-related health effects. In free-breathing laboratory
studies involving controlled human exposures to SO2,
respiratory effects have consistently been observed following 5-10 min
exposures at SO2 concentrations >=400 ppb in people with
asthma engaged in moderate to heavy levels of exercise, with
respiratory effects occurring at concentrations as low as 200 ppb in
some individuals with asthma. A clear concentration-response
relationship has been demonstrated in these studies following exposures
to SO2 at concentrations between 200 and 1000

ppb, both in terms of increasing severity of respiratory symptoms and
decrements in lung function, as well as the percentage of individuals
with asthma adversely affected. Epidemiologic studies have reported
positive associations between short-term ambient SO2
concentrations and hospital admissions and emergency department visits
for asthma and for all respiratory causes, particularly among children
and older adults (>=65 years). The studies provide supportive evidence
for the causal relationship.
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    \718\ U.S. EPA. Integrated Science Assessment (ISA) for Sulfur
Oxides--Health Criteria (Final Report, Dec 2017). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-17/451, 2017.
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    For long-term SO2 exposure and respiratory effects, the
EPA has concluded that the evidence is suggestive of a causal
relationship. This conclusion is based on new epidemiologic evidence
for positive associations between long-term SO2 exposure and
increases in asthma incidence among children, together with animal
toxicological evidence that provides a pathophysiologic basis for the
development of asthma. However, uncertainty remains regarding the
influence of other pollutants on the observed associations with
SO2 because these epidemiologic studies have not examined
the potential for co-pollutant confounding.
    Consistent associations between short-term exposure to
SO2 and mortality have been observed in epidemiologic
studies, with larger effect estimates reported for respiratory
mortality than for cardiovascular mortality. While this finding is
consistent with the demonstrated effects of SO2 on
respiratory morbidity, uncertainty remains with respect to the
interpretation of these observed mortality associations due to
potential confounding by various copollutants. Therefore, the EPA has
concluded that the overall evidence is suggestive of a causal
relationship between short-term exposure to SO2 and
mortality.
v. Carbon Monoxide
    Information on the health effects of carbon monoxide (CO) can be
found in the January 2010 Integrated Science Assessment for Carbon
Monoxide (CO ISA).\719\ The CO ISA presents conclusions regarding the
presence of causal relationships between CO exposure and categories of
adverse health effects.\720\ This section provides a summary of the
health effects associated with exposure to ambient concentrations of
CO, along with the CO ISA conclusions.\721\
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    \719\ 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.
    \720\ 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.
    \721\ 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 which was often observed in co-pollutant 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.
vi. 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.722 723 A number of

other agencies (National Institute for Occupational Safety and Health,
the International Agency for Research on Cancer, the World Health
Organization, California EPA, and the U.S. Department of Health and
Human Services) made similar hazard classifications prior to 2002. EPA
also concluded in the 2002 Diesel HAD that it was not possible to
calculate a cancer unit risk for diesel exhaust due to limitations in
the exposure data for the occupational groups or the absence of a dose-
response relationship.
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    \722\ 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.
    \723\ 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/m\3\ 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 of the pertinent [diesel exhaust]-
caused noncancer health hazards.'' The Diesel HAD also notes ``that
acute exposure to [diesel exhaust] has been associated with irritation
of the eye, nose, and throat, respiratory symptoms (cough and phlegm),
and neurophysiological symptoms such as headache, lightheadedness,
nausea, vomiting, and numbness or tingling of the extremities.'' The
Diesel HAD 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/m\3\.\724\ 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.
---------------------------------------------------------------------------

    \724\ See Section VI.B.i for discussion of the current
PM2.5 NAAQS standard, and https://www.epa.gov/pm-pollution/national-ambient-air-quality-standards-naaqs-pm.
---------------------------------------------------------------------------

    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, including truck drivers, underground
nonmetal miners, and other diesel motor-related occupations. These
studies reported increased risk of lung cancer related to exposure to
diesel exhaust, with evidence of positive exposure-response
relationships to varying degrees.725 726 727 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.
---------------------------------------------------------------------------

    \725\ 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.
    \726\ 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.
    \727\ 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.'' \728\ This designation was an update from its 1988 evaluation
that considered the evidence to be indicative of a ``probable human
carcinogen.''
---------------------------------------------------------------------------

    \728\ 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.
---------------------------------------------------------------------------

vii. 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, acetaldehyde, acrolein, benzene, 1,3-butadiene,
ethylbenzene, formaldehyde, and naphthalene, which were all identified
as national or regional health effects drivers or contributors in the
2018 AirToxScreen Assessment.729 730
---------------------------------------------------------------------------

    \729\ 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.
    \730\ U.S. EPA (2022) 2018 AirToxScreen Risk Drivers. https://www.epa.gov/AirToxScreen/airtoxscreen-risk-drivers.
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a. Acetaldehyde
    Acetaldehyde is classified in EPA's IRIS database as a probable
human carcinogen, based on nasal tumors in rats, and is considered
toxic by the inhalation, oral, and intravenous routes.\731\ The
inhalation unit risk estimate (URE) in IRIS for acetaldehyde is 2.2 x
10-6 per [micro]g/m3.\732\

Acetaldehyde is reasonably anticipated to be a human carcinogen by the
NTP in the 14th Report on Carcinogens and is classified as possibly
carcinogenic to humans (Group 2B) by the IARC.733 734
---------------------------------------------------------------------------

    \731\ U.S. EPA (1991). Integrated Risk Information System File
of Acetaldehyde. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
electronically at https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=290.
    \732\ U.S. EPA (1991). Integrated Risk Information System File
of Acetaldehyde. This material is available electronically at
https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=290.
    \733\ NTP (National Toxicology Program). 2016. Report on
Carcinogens, Fourteenth Edition.; Research Triangle Park, NC: U.S.
Department of Health and Human Services, Public Health Service.
https://ntp.niehs.nih.gov/go/roc14.
    \734\ International Agency for Research on Cancer (IARC).
(1999). Re-evaluation of some organic chemicals, hydrazine, and
hydrogen peroxide. IARC Monographs on the Evaluation of Carcinogenic
Risk of Chemical to Humans, Vol 71. Lyon, France.
---------------------------------------------------------------------------

    The primary noncancer effects of exposure to acetaldehyde vapors
include irritation of the eyes, skin, and respiratory tract.\735\ In
short-term (4 week) rat studies, degeneration of olfactory epithelium
was observed at various concentration levels of acetaldehyde
exposure.736 737 Data from these studies were used by EPA to
develop an inhalation reference concentration of 9 [micro]g/m\3\. Some
asthmatics have been shown to be a sensitive subpopulation to
decrements in functional expiratory volume (FEV1 test) and
bronchoconstriction upon acetaldehyde inhalation.\738\ Children,
especially those with diagnosed asthma, may be more likely to show
impaired pulmonary function and symptoms of asthma than are adults
following exposure to acetaldehyde.\739\
---------------------------------------------------------------------------

    \735\ U.S. EPA (1991). Integrated Risk Information System File
of Acetaldehyde. This material is available electronically at
https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=290.
    \736\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
electronically at https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=364.
    \737\ Appleman, L.M., R.A. Woutersen, and V.J. Feron. (1982).
Inhalation toxicity of acetaldehyde in rats. I. Acute and subacute
studies. Toxicology. 23: 293-297.
    \738\ Myou, S.; Fujimura, M.; Nishi K.; Ohka, T.; and Matsuda,
T. (1993). Aerosolized acetaldehyde induces histamine-mediated
bronchoconstriction in asthmatics. Am. Rev. Respir.Dis.148(4 Pt 1):
940-943.
    \739\ California OEHHA, 2014. TSD for Noncancer RELs: Appendix
D. Individual, Acute, 8-Hour, and Chronic Reference Exposure Level
Summaries. December 2008 (updated July 2014). https://oehha.ca.gov/media/downloads/crnr/appendixd1final.pdf.
---------------------------------------------------------------------------

b. Acrolein
    EPA most recently evaluated the toxicological and health effects
literature related to acrolein in 2003 and concluded that the human
carcinogenic potential of acrolein could not be determined because the
available data were inadequate. No information was available on the
carcinogenic effects of acrolein in humans, and the animal data
provided inadequate evidence of carcinogenicity.\740\ In 2021, the IARC
classified acrolein as probably carcinogenic to humans.\741\
---------------------------------------------------------------------------

    \740\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
at https://iris.epa.gov/ChemicalLanding/&substance_nmbr=364.
    \741\ International Agency for Research on Cancer (IARC).
(2021). Monographs on the Identification of Carcinogenic Hazards to
humans, Volume 128. Acrolein, Crotonaldehyde, and Arecoline, World
Health Organization, Lyon, France.
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    Lesions to the lungs and upper respiratory tract of rats, rabbits,
and hamsters have been observed after subchronic exposure to
acrolein.\742\ The agency has developed an RfC for acrolein of 0.02
[micro]g/m3 and an RfD of 0.5 [micro]g/kg-day.\743\
---------------------------------------------------------------------------

    \742\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Office of Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
at http://www.epa.gov/iris/subst/0364.htm.
    \743\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Office of Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
at https://iris.epa.gov/ChemicalLanding/&substance_nmbr=364.
---------------------------------------------------------------------------

    Acrolein is extremely acrid and irritating to humans when inhaled,
with acute exposure resulting in upper respiratory tract irritation,
mucus hypersecretion and congestion. The intense irritancy of this
carbonyl has been demonstrated during controlled tests in human
subjects, who suffer intolerable eye and nasal mucosal sensory
reactions within minutes of exposure.\744\ These data and additional
studies regarding acute effects of human exposure to acrolein are
summarized in EPA's 2003 IRIS Human Health Assessment for
acrolein.\745\ Studies in humans indicate that levels as low as 0.09
ppm (0.21 mg/m3) for five minutes may elicit subjective
complaints of eye irritation with increasing concentrations leading to
more extensive eye, nose and respiratory symptoms. Acute exposures in
animal studies report bronchial hyper-responsiveness. Based on animal
data (more pronounced respiratory irritancy in mice with allergic
airway disease in comparison to non-diseased mice \746\) and
demonstration of similar effects in humans (e.g., reduction in
respiratory rate), individuals with compromised respiratory function
(e.g., emphysema, asthma) are expected to be at increased risk of
developing adverse responses to strong respiratory irritants such as
acrolein. EPA does not currently have an acute reference concentration
for acrolein. The available health effect reference values for acrolein
have been summarized by EPA and include an ATSDR MRL for acute exposure
to acrolein of 7 [micro]g/m3 for 1-14 days exposure and
Reference Exposure Level (REL) values from the California Office of
Environmental Health Hazard Assessment (OEHHA) for one-hour and 8-hour
exposures of 2.5 [micro]g/m3 and 0.7 [micro]g/m3,
respectively.\747\
---------------------------------------------------------------------------

    \744\ U.S. EPA. (2003). Toxicological review of acrolein in
support of summary information on Integrated Risk Information System
(IRIS) National Center for Environmental Assessment, Washington, DC.
EPA/635/R-03/003. p. 10. Available online at: https://iris.epa.gov/static/pdfs/0364tr.pdf.
    \745\ U.S. EPA. (2003). Toxicological review of acrolein in
support of summary information on Integrated Risk Information System
(IRIS) National Center for Environmental Assessment, Washington, DC.
EPA/635/R-03/003. Available online at: https://iris.epa.gov/static/pdfs/0364tr.pdf.
    \746\ Morris JB, Symanowicz PT, Olsen JE, et al. (2003).
Immediate sensory nerve-mediated respiratory responses to irritants
in healthy and allergic airway-diseased mice. J Appl Physiol
94(4):1563-1571.
    \747\ U.S. EPA. (2009). Graphical Arrays of Chemical-Specific
Health Effect Reference Values for Inhalation Exposures (Final
Report). U.S. Environmental Protection Agency, Washington, DC, EPA/
600/R-09/061, 2009. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003.
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c. Benzene
    EPA's Integrated Risk Information System (IRIS) database lists
benzene as a known human carcinogen (causing leukemia) by all routes of
exposure and concludes that exposure is associated with additional
health effects, including genetic changes in both humans and animals
and increased proliferation of bone marrow cells in
mice.748 749 750 EPA states in its IRIS database that data
indicate a causal relationship between benzene exposure and acute
lymphocytic leukemia and suggest a relationship between benzene
exposure and chronic non-lymphocytic leukemia and chronic lymphocytic
leukemia. EPA's IRIS documentation for benzene also lists a range of
2.2 x 10-6 to 7.8 x 10-6 per [micro]g/
m3 as the unit risk estimate (URE) for
benzene.751 752 The

International Agency for Research on Cancer (IARC) has determined that
benzene is a human carcinogen, and the U.S. Department of Health and
Human Services (DHHS) has characterized benzene as a known human
carcinogen.753 754
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    \748\ U.S. EPA. (2000). Integrated Risk Information System File
for Benzene. This material is available electronically at: https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=276.
    \749\ International Agency for Research on Cancer. (1982). IARC
monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29, Some industrial chemicals and dyestuffs,
International Agency for Research on Cancer, World Health
Organization, Lyon, France 1982.
    \750\ Irons, R.D.; Stillman, W.S.; Colagiovanni, D.B.; Henry,
V.A. (1992). Synergistic action of the benzene metabolite
hydroquinone on myelopoietic stimulating activity of granulocyte/
macrophage colony-stimulating factor in vitro, Proc. Natl. Acad.
Sci. 89:3691-3695.
    \751\ A unit risk estimate is defined as the increase in the
lifetime risk of cancer of an individual who is exposed for a
lifetime to 1 [micro]g/m3 benzene in air.
    \752\ U.S. EPA. (2000). Integrated Risk Information System File
for Benzene. This material is available electronically at: https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=276.
    \753\ International Agency for Research on Cancer (IARC, 2018.
Monographs on the evaluation of carcinogenic risks to humans, volume
120. World Health Organization--Lyon, France. http://publications.iarc.fr/Book-And-Report-Series/Iarc-Monographs-On-The-Identification-Of-Carcinogenic-Hazards-To-Humans/Benzene-2018.
    \754\ NTP (National Toxicology Program). 2016. Report on
Carcinogens, Fourteenth Edition.; Research Triangle Park, NC: U.S.
Department of Health and Human Services, Public Health Service.
https://ntp.niehs.nih.gov/go/roc14.
---------------------------------------------------------------------------

    A number of adverse noncancer health effects, including blood
disorders such as preleukemia and aplastic anemia, have also been
associated with long-term exposure to benzene.755 756 The
most sensitive noncancer effect observed in humans, based on current
data, is the depression of the absolute lymphocyte count in
blood.757 758 EPA's inhalation reference concentration (RfC)
for benzene is 30 [micro]g/m3. The RfC is based on
suppressed absolute lymphocyte counts seen in humans under occupational
exposure conditions. In addition, studies sponsored by the Health
Effects Institute (HEI) provide evidence that biochemical responses
occur at lower levels of benzene exposure than previously
known.759 760 761 762 EPA's IRIS program has not yet
evaluated these new data. EPA does not currently have an acute
reference concentration for benzene. The Agency for Toxic Substances
and Disease Registry (ATSDR) Minimal Risk Level (MRL) for acute
inhalation exposure to benzene is 29 [micro]g/m3 for 1-14
days exposure.763 764
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    \755\ Aksoy, M. (1989). Hematotoxicity and carcinogenicity of
benzene. Environ. Health Perspect. 82: 193-197. EPA-HQ-OAR-2011-
0135.
    \756\ Goldstein, B.D. (1988). Benzene toxicity. Occupational
medicine. State of the Art Reviews. 3: 541-554.
    \757\ Rothman, N., G.L. Li, M. Dosemeci, W.E. Bechtold, G.E.
Marti, Y.Z. Wang, M. Linet, L.Q. Xi, W. Lu, M.T. Smith, N. Titenko-
Holland, L.P. Zhang, W. Blot, S.N. Yin, and R.B. Hayes. (1996).
Hematotoxicity among Chinese workers heavily exposed to benzene. Am.
J. Ind. Med. 29: 236-246.
    \758\ U.S. EPA (2002). Toxicological Review of Benzene
(Noncancer Effects). Environmental Protection Agency, Integrated
Risk Information System (IRIS), Research and Development, National
Center for Environmental Assessment, Washington DC. This material is
available electronically at https://cfpub.epa.gov/ncea/iris/iris_documents/documents/toxreviews/0276tr.pdf.
    \759\ Qu, O.; Shore, R.; Li, G.; Jin, X.; Chen, C.L.; Cohen, B.;
Melikian, A.; Eastmond, D.; Rappaport, S.; Li, H.; Rupa, D.;
Suramaya, R.; Songnian, W.; Huifant, Y.; Meng, M.; Winnik, M.; Kwok,
E.; Li, Y.; Mu, R.; Xu, B.; Zhang, X.; Li, K. (2003). HEI Report
115, Validation & Evaluation of Biomarkers in Workers Exposed to
Benzene in China.
    \760\ Qu, Q., R. Shore, G. Li, X. Jin, L.C. Chen, B. Cohen, et
al. (2002). Hematological changes among Chinese workers with a broad
range of benzene exposures. Am. J. Industr. Med. 42: 275-285.
    \761\ Lan, Qing, Zhang, L., Li, G., Vermeulen, R., et al.
(2004). Hematotoxically in Workers Exposed to Low Levels of Benzene.
Science 306: 1774-1776.
    \762\ Turtletaub, K.W. and Mani, C. (2003). Benzene metabolism
in rodents at doses relevant to human exposure from Urban Air.
Research Reports Health Effect Inst. Report No.113.
    \763\ U.S. Agency for Toxic Substances and Disease Registry
(ATSDR). (2007). Toxicological profile for benzene. Atlanta, GA:
U.S. Department of Health and Human Services, Public Health Service.
http://www.atsdr.cdc.gov/ToxProfiles/tp3.pdf.
    \764\ A minimal risk level (MRL) is defined as an estimate of
the daily human exposure to a hazardous substance that is likely to
be without appreciable risk of adverse noncancer health effects over
a specified duration of exposure.
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    There is limited information from two studies regarding an
increased risk of adverse effects to children whose parents have been
occupationally exposed to benzene.765 766 Data from animal
studies have shown benzene exposures result in damage to the
hematopoietic (blood cell formation) system during
development.767 768 769 Also, key changes related to the
development of childhood leukemia occur in the developing fetus.\770\
Several studies have reported that genetic changes related to eventual
leukemia development occur before birth. For example, there is one
study of genetic changes in twins who developed T cell leukemia at nine
years of age.\771\
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    \765\ Corti, M; Snyder, CA. (1996) Influences of gender,
development, pregnancy and ethanol consumption on the hematotoxicity
of inhaled 10 ppm benzene. Arch Toxicol 70:209-217.
    \766\ McKinney P.A.; Alexander, F.E.; Cartwright, R.A.; et al.
(1991) Parental occupations of children with leukemia in west
Cumbria, north Humberside, and Gateshead. Br Med J 302:681-686.
    \767\ Keller, KA; Snyder, CA. (1986) Mice exposed in utero to
low concentrations of benzene exhibit enduring changes in their
colony forming hematopoietic cells. Toxicology 42:171-181.
    \768\ Keller, KA; Snyder, CA. (1988) Mice exposed in utero to 20
ppm benzene exhibit altered numbers of recognizable hematopoietic
cells up to seven weeks after exposure. Fundam Appl Toxicol 10:224-
232.
    \769\ Corti, M; Snyder, CA. (1996) Influences of gender,
development, pregnancy and ethanol consumption on the hematotoxicity
of inhaled 10 ppm benzene. Arch Toxicol 70:209-217.
    \770\ U.S. EPA. (2002). Toxicological Review of Benzene
(Noncancer Effects). National Center for Environmental Assessment,
Washington, DC. Report No. EPA/635/R-02/001F. https://cfpub.epa.gov/ncea/iris/iris_documents/documents/toxreviews/0276tr.pdf.
    \771\ Ford, AM; Pombo-de-Oliveira, MS; McCarthy, KP; MacLean,
JM; Carrico, KC; Vincent, RF; Greaves, M. (1997) Monoclonal origin
of concordant T-cell malignancy in identical twins. Blood 89:281-
285.
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d. 1,3-Butadiene
    EPA has characterized 1,3-butadiene as carcinogenic to humans by
inhalation.772 773 The IARC has determined that 1,3-
butadiene is a human carcinogen, and the U.S. DHHS has characterized
1,3-butadiene as a known human carcinogen.774 775 776 777
There are numerous studies consistently demonstrating that 1,3-
butadiene is metabolized into genotoxic metabolites by experimental
animals and humans. The specific mechanisms of 1,3-butadiene-induced
carcinogenesis are unknown; however, the scientific evidence strongly
suggests that the carcinogenic effects are mediated by genotoxic
metabolites. Animal data suggest that females may be more sensitive
than males for cancer effects associated with 1,3-butadiene exposure;
there are insufficient data in humans from which to draw conclusions
about sensitive subpopulations. The URE for 1,3-butadiene is 3 x
10-5 per [micro]g/m3.\778\ 1,3-butadiene also
causes a variety of reproductive and developmental effects in mice; no
human data on these effects are available. The most sensitive effect
was ovarian atrophy observed in a lifetime bioassay of female
mice.\779\ Based on this critical effect and the benchmark
concentration methodology, an RfC for chronic health effects was

calculated at 0.9 ppb (approximately 2 [micro]g/m3).
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    \772\ U.S. EPA. (2002). Health Assessment of 1,3-Butadiene.
Office of Research and Development, National Center for
Environmental Assessment, Washington Office, Washington, DC. Report
No. EPA600-P-98-001F. This document is available electronically at
https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=54499.
    \773\ U.S. EPA. (2002) ``Full IRIS Summary for 1,3-butadiene
(CASRN 106-99-0)'' Environmental Protection Agency, Integrated Risk
Information System (IRIS), Research and Development, National Center
for Environmental Assessment, Washington, DC https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=139.
    \774\ International Agency for Research on Cancer (IARC).
(1999). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, Volume 71, Re-evaluation of some organic
chemicals, hydrazine and hydrogen peroxide, World Health
Organization, Lyon, France.
    \775\ International Agency for Research on Cancer (IARC).
(2008). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, 1,3-Butadiene, Ethylene Oxide and Vinyl Halides
(Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide) Volume 97, World
Health Organization, Lyon, France.
    \776\ NTP (National Toxicology Program). 2016. Report on
Carcinogens, Fourteenth Edition.; Research Triangle Park, NC: U.S.
Department of Health and Human Services, Public Health Service.
https://ntp.niehs.nih.gov/go/roc14.
    \777\ International Agency for Research on Cancer (IARC).
(2012). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, Volume 100F chemical agents and related
occupations, World Health Organization, Lyon, France.
    \778\ U.S. EPA. (2002). ``Full IRIS Summary for 1,3-butadiene
(CASRN 106-99-0)'' Environmental Protection Agency, Integrated Risk
Information System (IRIS), Research and Development, National Center
for Environmental Assessment, Washington, DC https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=139.
    \779\ Bevan, C.; Stadler, J.C.; Elliot, G.S.; et al. (1996).
Subchronic toxicity of 4-vinylcyclohexene in rats and mice by
inhalation. Fundam. Appl. Toxicol. 32:1-10.
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e. Ethylbenzene
    EPA's inhalation RfC for ethylbenzene is 1 mg/m3. This conclusion
on a weight of evidence determination and RfC is contained in the 1991
IRIS file for ethylbenzene.\780\ The RfC is based on developmental
effects. A study in rabbits found reductions in live rabbit kits per
litter at 1000 ppm. In addition, a study on rats found an increased
incidence of supernumerary and rudimentary ribs at 1000 ppm and
elevated incidence of extra ribs at 100 ppm. In 1988, EPA concluded
that data were inadequate to give a weight of evidence characterization
for carcinogenic effects. EPA released an IRIS Assessment Plan for
Ethylbenzene in 2017,\781\ and EPA will be releasing the Systematic
Review Protocol for ethylbenzene in 2023.\782\
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    \780\ U.S. EPA. (1991). Integrated Risk Information System File
for Ethylbenzene. This material is available electronically at:
https://iris.epa.gov/ChemicalLanding/&substance_nmbr=51.
    \781\ U.S. EPA (2017). IRIS Assessment Plan for Ethylbenzene.
EPA/635/R-17/332. This document is available electronically at:
https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=337468.
    \782\ U.S. EPA (2022). IRIS Program Outlook. June, 2022. This
material is available electronically at: https://www.epa.gov/system/files/documents/2022-06/IRIS%20Program%20Outlook_June22.pdf.
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    California EPA completed a cancer risk assessment for ethylbenzene
in 2007 and developed an inhalation unit risk estimate of 2.5 x
10-6.\783\ This value was based on incidence of kidney
cancer in male rats. California EPA also developed a chronic inhalation
noncancer reference exposure level (REL) of 2000 [micro]g/
m3, based on nephrotoxicity and body weight reduction in
rats, liver cellular alterations, necrosis in mice, and hyperplasia of
the pituitary gland in mice.\784\
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    \783\ California OEHHA, 2007. Adoption of a Unit Risk Value for
Ethylbenzene. This material is available electronically at: https://oehha.ca.gov/air/report-hot-spots/adoption-unit-risk-value-ethylbenzene.
    \784\ California OEHHA, 2008. Technical Supporting Document for
Noncancer RELs, Appendix D3. This material is available
electronically at: https://oehha.ca.gov/media/downloads/crnr/appendixd3final.pdf.
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    ATSDR developed a chronic inhalation Minimal Risk Level (MRL) for
ethylbenzene of 0.06 ppm based on renal effects and an acute MRL of 5
ppm based on auditory effects.
f. Formaldehyde
    In 1991, EPA concluded that formaldehyde is a Class B1 probable
human carcinogen based on limited evidence in humans and sufficient
evidence in animals.\785\ An inhalation URE for cancer and a reference
dose for oral noncancer effects were developed by EPA and posted on the
IRIS database. Since that time, the NTP and IARC have concluded that
formaldehyde is a known human carcinogen.786 787 788
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    \785\ EPA. Integrated Risk Information System. Formaldehyde
(CASRN 50-00-0) https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=419.
    \786\ NTP (National Toxicology Program). 2016. Report on
Carcinogens, Fourteenth Edition.; Research Triangle Park, NC: U.S.
Department of Health and Human Services, Public Health Service.
https://ntp.niehs.nih.gov/go/roc14.
    \787\ IARC Monographs on the Evaluation of Carcinogenic Risks to
Humans Volume 88 (2006): Formaldehyde, 2-Butoxyethanol and 1-tert-
Butoxypropan-2-ol.
    \788\ IARC Monographs on the Evaluation of Carcinogenic Risks to
Humans Volume 100F (2012): Formaldehyde.
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    The conclusions by IARC and NTP reflect the results of
epidemiologic research published since 1991 in combination with
previous animal, human and mechanistic evidence. Research conducted by
the National Cancer Institute reported an increased risk of
nasopharyngeal cancer and specific lymphohematopoietic malignancies
among workers exposed to formaldehyde.789 790 791 A National
Institute of Occupational Safety and Health study of garment workers
also reported increased risk of death due to leukemia among workers
exposed to formaldehyde.\792\ Extended follow-up of a cohort of British
chemical workers did not report evidence of an increase in
nasopharyngeal or lymphohematopoietic cancers, but a continuing
statistically significant excess in lung cancers was reported.\793\
Finally, a study of embalmers reported formaldehyde exposures to be
associated with an increased risk of myeloid leukemia but not brain
cancer.\794\
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    \789\ Hauptmann, M.; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.;
Blair, A. 2003. Mortality from lymphohematopoetic malignancies among
workers in formaldehyde industries. Journal of the National Cancer
Institute 95: 1615-1623.
    \790\ Hauptmann, M.; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.;
Blair, A. 2004. Mortality from solid cancers among workers in
formaldehyde industries. American Journal of Epidemiology 159: 1117-
1130.
    \791\ Beane Freeman, L. E.; Blair, A.; Lubin, J. H.; Stewart, P.
A.; Hayes, R. B.; Hoover, R. N.; Hauptmann, M. 2009. Mortality from
lymphohematopoietic malignancies among workers in formaldehyde
industries: The National Cancer Institute cohort. J. National Cancer
Inst. 101: 751-761.
    \792\ Pinkerton, L. E. 2004. Mortality among a cohort of garment
workers exposed to formaldehyde: an update. Occup. Environ. Med. 61:
193-200.
    \793\ Coggon, D, EC Harris, J Poole, KT Palmer. 2003. Extended
follow-up of a cohort of British chemical workers exposed to
formaldehyde. J National Cancer Inst. 95:1608-1615.
    \794\ Hauptmann, M.; Stewart P. A.; Lubin J. H.; Beane Freeman,
L. E.; Hornung, R. W.; Herrick, R. F.; Hoover, R. N.; Fraumeni, J.
F.; Hayes, R. B. 2009. Mortality from lymphohematopoietic
malignancies and brain cancer among embalmers exposed to
formaldehyde. Journal of the National Cancer Institute 101:1696-
1708.
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    Health effects of formaldehyde in addition to cancer were reviewed
by the Agency for Toxics Substances and Disease Registry in 1999,
supplemented in 2010, and by the World Health
Organization.795 796 797 These organizations reviewed the
scientific literature concerning health effects linked to formaldehyde
exposure to evaluate hazards and dose response relationships and
defined exposure concentrations for minimal risk levels (MRLs). The
health endpoints reviewed included sensory irritation of eyes and
respiratory tract, reduced pulmonary function, nasal histopathology,
and immune system effects. In addition, research on reproductive and
developmental effects and neurological effects was discussed along with
several studies that suggest that formaldehyde may increase the risk of
asthma--particularly in the young.
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    \795\ ATSDR. 1999. Toxicological Profile for Formaldehyde, U.S.
Department of Health and Human Services (HHS), July 1999.
    \796\ ATSDR. 2010. Addendum to the Toxicological Profile for
Formaldehyde. U.S. Department of Health and Human Services (HHS),
October 2010.
    \797\ IPCS. 2002. Concise International Chemical Assessment
Document 40. Formaldehyde. World Health Organization.
---------------------------------------------------------------------------

    In June 2010, EPA released a draft Toxicological Review of
Formaldehyde--Inhalation Assessment through the IRIS program for peer
review by the National Research Council (NRC) and public comment.\798\
That draft assessment reviewed more recent research from animal and
human studies on cancer and other health effects. The NRC released
their review report in April 2011.\799\ EPA's draft assessment, which
addresses NRC recommendations, was suspended in 2018.\800\ The draft
assessment was unsuspended in March 2021, and an external review draft
was released in

April 2022.\801\ This draft assessment is now undergoing review by the
National Academy of Sciences.\802\
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    \798\ EPA (U.S. Environmental Protection Agency). 2010.
Toxicological Review of Formaldehyde (CAS No. 50-00-0)--Inhalation
Assessment: In Support of Summary Information on the Integrated Risk
Information System (IRIS). External Review Draft. EPA/635/R-10/002A.
U.S. Environmental Protection Agency, Washington DC [online].
Available: http://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=223614.
    \799\ NRC (National Research Council). 2011. Review of the
Environmental Protection Agency's Draft IRIS Assessment of
Formaldehyde. Washington DC: National Academies Press. http://books.nap.edu/openbook.php?record_id=13142.
    \800\ U.S. EPA (2018). See https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=419.
    \801\ U.S. EPA. IRIS Toxicological Review of Formaldehyde-
Inhalation (Interagency Science Consultation Draft, 2021). U.S.
Environmental Protection Agency, Washington, DC, EPA/635/R-21/286,
2021.
    \802\ For additional information, see: https://www.nationalacademies.org/our-work/review-of-epas-2021-draft-formaldehyde-assessment.
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g. Naphthalene
    Naphthalene is found in small quantities in gasoline and diesel
fuels. Naphthalene emissions have been measured in larger quantities in
both gasoline and diesel exhaust compared with evaporative emissions
from mobile sources, indicating it is primarily a product of
combustion.
    Acute (short-term) exposure of humans to naphthalene by inhalation,
ingestion, or dermal contact is associated with hemolytic anemia and
damage to the liver and the nervous system.\803\ Chronic (long term)
exposure of workers and rodents to naphthalene has been reported to
cause cataracts and retinal damage.\804\ Children, especially neonates,
appear to be more susceptible to acute naphthalene poisoning based on
the number of reports of lethal cases in children and infants
(hypothesized to be due to immature naphthalene detoxification
pathways).\805\ EPA released an external review draft of a reassessment
of the inhalation carcinogenicity of naphthalene based on a number of
recent animal carcinogenicity studies.\806\ The draft reassessment
completed external peer review.\807\ Based on external peer review
comments received, EPA is developing a revised draft assessment that
considers inhalation and oral routes of exposure, as well as cancer and
noncancer effects.\808\ The external review draft does not represent
official agency opinion and was released solely for the purposes of
external peer review and public comment. The NTP listed naphthalene as
``reasonably anticipated to be a human carcinogen'' in 2004 on the
basis of bioassays reporting clear evidence of carcinogenicity in rats
and some evidence of carcinogenicity in mice.\809\ California EPA has
released a new risk assessment for naphthalene, and the IARC has
reevaluated naphthalene and re-classified it as Group 2B: possibly
carcinogenic to humans.\810\
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    \803\ U.S. EPA. 1998. Toxicological Review of Naphthalene
(Reassessment of the Inhalation Cancer Risk), Environmental
Protection Agency, Integrated Risk Information System, Research and
Development, National Center for Environmental Assessment,
Washington, DC. This material is available electronically at https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=56434.
    \804\ U.S. EPA. 1998. Toxicological Review of Naphthalene
(Reassessment of the Inhalation Cancer Risk), Environmental
Protection Agency, Integrated Risk Information System, Research and
Development, National Center for Environmental Assessment,
Washington, DC. This material is available electronically at https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=56434.
    \805\ U.S. EPA. (1998). Toxicological Review of Naphthalene
(Reassessment of the Inhalation Cancer Risk), Environmental
Protection Agency, Integrated Risk Information System, Research and
Development, National Center for Environmental Assessment,
Washington, DC. This material is available electronically at https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=56434.
    \806\ U.S. EPA. (1998). Toxicological Review of Naphthalene
(Reassessment of the Inhalation Cancer Risk), Environmental
Protection Agency, Integrated Risk Information System, Research and
Development, National Center for Environmental Assessment,
Washington, DC. This material is available electronically at https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=56434.
    \807\ Oak Ridge Institute for Science and Education. (2004).
External Peer Review for the IRIS Reassessment of the Inhalation
Carcinogenicity of Naphthalene. August 2004. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=84403.
    \808\ U.S. EPA. (2018) See: https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=436.
    \809\ NTP (National Toxicology Program). 2016. Report on
Carcinogens, Fourteenth Edition.; Research Triangle Park, NC: U.S.
Department of Health and Human Services, Public Health Service.
https://ntp.niehs.nih.gov/go/roc14.
    \810\ International Agency for Research on Cancer (IARC).
(2002). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans. Vol. 82. Lyon, France.
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    Naphthalene also causes a number of non-cancer effects in animals
following chronic and less-than-chronic exposure, including abnormal
cell changes and growth in respiratory and nasal tissues.\811\ The
current EPA IRIS assessment includes noncancer data on hyperplasia and
metaplasia in nasal tissue that form the basis of the inhalation RfC of
3 [micro]g/m3.\812\ The ATSDR MRL for acute and intermediate duration
oral exposure to naphthalene is 0.6 mg/kg/day based on maternal
toxicity in a developmental toxicology study in rats.\813\ ATSDR also
derived an ad hoc reference value of 6 x 10-2 mg/m3 for acute (<=24-
hour) inhalation exposure to naphthalene in a Letter Health
Consultation dated March 24, 2014 to address a potential exposure
concern in Illinois.\814\ The ATSDR acute inhalation reference value
was based on a qualitative identification of an exposure level
interpreted not to cause pulmonary lesions in mice. More recently, EPA
developed acute RfCs for 1-, 8-, and 24-hour exposure scenarios; the
<=24-hour reference value is 2 x 10x2 mg/m3.\815\ EPA's acute RfCs are
based on a systematic review of the literature, benchmark dose modeling
of naphthalene-induced nasal lesions in rats, and application of a PBPK
(physiologically based pharmacokinetic) model.
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    \811\ U. S. EPA. (1998). Toxicological Review of Naphthalene,
Environmental Protection Agency, Integrated Risk Information System,
Research and Development, National Center for Environmental
Assessment, Washington, DC. This material is available
electronically at https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=56434.
    \812\ U.S. EPA. (1998). Toxicological Review of Naphthalene.
Environmental Protection Agency, Integrated Risk Information System
(IRIS), Research and Development, National Center for Environmental
Assessment, Washington, DC https://cfpub.epa.gov/ncea/iris_drafts/recordisplay.cfm?deid=56434.
    \813\ ATSDR. Toxicological Profile for Naphthalene, 1-
Methylnaphthalene, and 2-Methylnaphthalene (2005). https://www.atsdr.cdc.gov/ToxProfiles/tp67-p.pdf.
    \814\ ATSDR. Letter Health Consultation, Radiac Abrasives, Inc.,
Chicago, Illinois (2014). https://www.atsdr.cdc.gov/HAC/pha/RadiacAbrasives/Radiac%20Abrasives,%20Inc.%20_%20LHC%20(Final)%20_%2003-24-
2014%20(2)_508.pdf.
    \815\ U. S. EPA. Derivation of an acute reference concentration
for inhalation exposure to naphthalene. Report No. EPA/600/R-21/292.
https://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=355035.
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viii. 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, particulate matter, 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,
ultrafine particles, metals, elemental carbon (EC), NO, NOX,
and several VOCs.\816\ 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.817 818 819 820 821;
822 823 824 There is evidence that EPA's regulations for
vehicles have lowered the near-road concentrations and gradients.\825\
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.\826\ More recent studies of traffic-related air
pollutants continue to report sharp gradients around roadways,
particularly within several hundred meters.827 828
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    \816\ 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.
    \817\ 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.
    \818\ 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.
    \819\ 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.
    \820\ 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.
    \821\ 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.
    \822\ 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.
    \823\ 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.
    \824\ 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.
    \825\ 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].
    \826\ 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].
    \827\ 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.
    \828\ 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].
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    For pollutants with relatively high background concentrations
relative to near-road concentrations, detecting concentration gradients
can be difficult. For example, many 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.829 830 These findings suggest a substantial
roadway source of these carbonyls.
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    \829\ 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.
    \830\ 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.
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    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.\831\ 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.832 833 834 835 The health outcomes with the
strongest evidence linking them with traffic-associated air pollutants
are respiratory effects, particularly in asthmatic children, and
cardiovascular effects.
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    \831\ 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.
    \832\ 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.
    \833\ 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.
    \834\ 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.
    \835\ 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.
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    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.\836\ 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.\837\ 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'.838 839 840 841 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.\842\ The U.S. Department of
Health and Human Services' National Toxicology Program published a
monograph including a systematic review of traffic-related air
pollution and its impacts on hypertensive disorders of pregnancy. The
National Toxicology Program concluded that exposure to traffic-related
air pollution is ``presumed to be a hazard to pregnant women'' for
developing hypertensive disorders of pregnancy.\843\
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    \836\ 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/publication/systematic-review-and-meta-analysis-selected-health-effects-long-term-exposure-traffic] This more recent review focused on health
outcomes related to birth effects, respiratory effects,
cardiometabolic effects, and mortality.
    \837\ 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].
    \838\ 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.
    \839\ 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.
    \840\ 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.
    \841\ Raaschou-Nielsen, O.; Reynolds, P. (2006). Air pollution
and childhood cancer: a review of the epidemiological literature.
Int J Cancer 118: 2920-9.
    \842\ Boothe, VL.; 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.
    \843\ 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).844 845 846 847 848
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    \844\ 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.
    \845\ 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. https://doi.org/10.1093/aje/kwm308.
    \846\ Power, M.C.; Weisskopf, M.G.; Alexeef, SE; et al. (2011).
Traffic-related air pollution and cognitive function in a cohort of
older men. Environ Health Perspect 2011: 682-687.
    \847\ 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.
    \848\ 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.849 850 851 852 Additionally, long-term exposures in
near-road environments have been associated with inflammation-
associated conditions, such as atherosclerosis and
asthma.853 854 855
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    \849\ Riediker, M. (2007). Cardiovascular effects of fine
particulate matter components in highway patrol officers. Inhal
Toxicol 19: 99-105. doi: 10.1080/08958370701495238.
    \850\ Alexeef, SE; 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.
    \851\ 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.
    \852\ 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].
    \853\ 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. https://doi.org/10.1371/journal.pmed.1000372.
    \854\ 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. https://doi.org/10.1289/ehp.11290.
    \855\ 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 respiratory associations in
children experiencing chronic social stress, such as in violent
neighborhoods or in homes with high family
stress.856 857 858
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    \856\ 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.
    \857\ 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.
    \858\ 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.
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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. Every two years from 1997 to
2009 and in 2011, the U.S. Census Bureau's American Housing Survey
(AHS) conducted a survey that includes whether housing units are within
300 feet of an ``airport, railroad, or highway with four or more
lanes.'' \859\ The 2013 AHS was the last AHS that included that
question. 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.
---------------------------------------------------------------------------

    \859\ 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.\860\ 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 (about 650 feet) of these freight routes.861 862
In addition, as described in Section VI.D.2, 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.

863 864  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. 865 866 867  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.
868 869 870 871
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    \860\ 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.
    \861\ 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/.
    \862\ The same analysis estimated the population living within
100 meters of a FAF4 truck route is 41 million.
    \863\ EPA. (2011) Exposure Factors Handbook: 2011 Edition.
Chapter 16. Online at https://www.epa.gov/expobox/about-exposure-factors-handbook.
    \864\ It is not yet possible to estimate the long-term impact of
growth in telework associated with the COVID-19 pandemic on travel
behavior. There were notable changes during the pandemic. For
example, according to the 2021 American Time Use Survey, a greater
fraction of workers did at least part of their work at home (38%) as
compared with the 2019 survey (24%). [Online at https://www.bls.gov/news.release/atus.nr0.htm.]
    \865\ 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.]
    \866\ 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.]
    \867\ 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 351: https://doi.org/10.1097/01.ede.0000249409.81050.46.]
    \868\ 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.]
    \869\ 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.]
    \870\ Austin, W.; Heutel, G.; Kreisman, D. (2019) School bus
emissions, student health and academic performance. Econ Edu Rev 70:
108-12.
    \871\ Adar, S.D.; D.Souza, J.; Sheppard, L.; et al. (2015)
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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    As described in Section VI.D.2, we estimate that about 10 million
students attend schools within 200 meters of major roads. 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.872 873 However, this evidence
was judged to be weak due to limitations in the assessment methods.
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    \872\ 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.]
    \873\ Gartland, N; Aljofi, H.E.; Dienes, K.; Munford, L.A.;
Theakston, A.L.; van Tongeren, M. (2022) The effects of traffic air
pollution in and around schools on executive function and academic
performance in children: a rapid review. Int J Environ Res Public
Health 10: 749. [Online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8776123.]
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3. Welfare Effects Associated With Exposure to Non-GHG Pollutants
    This section discusses the environmental effects associated with
non-GHG pollutants affected by this rule, specifically particulate
matter, ozone, NOX, SOX, and air toxics.
i. Visibility
    Visibility can be defined as the degree to which the atmosphere is
transparent to visible light.\874\ 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.\875\
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    \874\ 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.
    \875\ 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.\876\ However, 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.\877\
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    \876\ 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.
    \877\ Hand, JL; Prenni, AJ; Copeland, S; Schichtel, BA; Malm,
WC. (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.\878\ In 1999, EPA finalized the regional
haze program to protect the visibility in Mandatory Class I Federal
areas.\879\ There are 156 national parks, forests and wilderness areas
categorized as Mandatory Class I Federal areas.\880\ 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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    \878\ See CAA Section 169(a).
    \879\ 64 FR 35714, July 1, 1999.
    \880\ 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.\881\
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    \881\ On June 10, 2021, EPA announced that it will reconsider
the decision to retain the PM NAAQS. https://www.epa.gov/pm-pollution/national-ambient-air-quality-standards-naaqs-pm.
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ii. Ozone Effects on Ecosystems
    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. Ozone effects
that begin at small spatial scales, such as the leaf of an individual
plant, when they occur at sufficient magnitudes (or to a sufficient
degree) 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.\882\ In those sensitive species,\883\ 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.884 885 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.\886\ 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,\887\ 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.\888\ 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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    \882\ 73 FR 16486, March 27, 2008.
    \883\ 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.
    \884\ 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.
    \885\ 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.
    \886\ 73 FR 16492, March 27, 2008.
    \887\ 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.
    \888\ 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.\889\ 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.\890\ The 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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    \889\ 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.
    \890\ 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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iii. 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.\891\ It is clear from the body of evidence that oxides of
nitrogen, oxides of sulfur, and particulate matter 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 U.S. 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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    \891\ 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
nitrogen can alter species assemblages and cause eutrophication. In
terrestrial systems nitrogen 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.
    The sensitivity of terrestrial and aquatic ecosystems to
acidification from nitrogen and sulfur 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.\892\ 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 (as monuments and building facings), and surface
coatings (paints).\893\ 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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    \892\ 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.
    \893\ 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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iv. Welfare Effects Associated With Air Toxics
    Emissions from producing, transporting, and combusting fuel
contribute to ambient levels of pollutants that contribute to adverse
effects on vegetation. VOCs, some of which are considered air toxics,
have long been suspected to play a role in vegetation damage.\894\ In
laboratory experiments, a wide range of tolerance to VOCs has been
observed.\895\ Decreases in harvested seed pod weight have been
reported for the more sensitive plants, and some studies have reported
effects on seed germination, flowering, and fruit ripening. Effects of
individual VOCs or their role in conjunction with other stressors
(e.g., acidification, drought, temperature extremes) have not been well
studied. In a recent study of a mixture of VOCs including ethanol and
toluene on herbaceous plants, significant effects on seed production,
leaf water content, and photosynthetic efficiency were reported for
some plant species.\896\
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    \894\ U.S. EPA. (1991). Effects of organic chemicals in the
atmosphere on terrestrial plants. EPA/600/3-91/001.
    \895\ Cape JN, ID Leith, J Binnie, J Content, M Donkin, M
Skewes, DN Price AR Brown, AD Sharpe. (2003). Effects of VOCs on
herbaceous plants in an open-top chamber experiment. Environ.
Pollut. 124:341-343.
    \896\ Cape JN, ID Leith, J Binnie, J Content, M Donkin, M
Skewes, DN Price AR Brown, AD Sharpe. (2003). Effects of VOCs on
herbaceous plants in an open-top chamber experiment. Environ.
Pollut. 124:341-343.
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    Research suggests an adverse impact of vehicle exhaust on plants,
which has in some cases been attributed to aromatic compounds and in
other cases to NOX.897 898 899 The impacts of
VOCs on plant reproduction may have long-term implications for
biodiversity and survival of native species near major roadways. Most
of the studies of the impacts of VOCs on vegetation have focused on
short-term exposure, and few studies have focused on long-term effects
of VOCs on vegetation and the potential for metabolites of these
compounds to affect herbivores or insects.
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    \897\ Viskari E-L. (2000). Epicuticular wax of Norway spruce
needles as indicator of traffic pollutant deposition. Water, Air,
and Soil Pollut. 121:327-337.
    \898\ Ugrekhelidze D, F Korte, G Kvesitadze. (1997). Uptake and
transformation of benzene and toluene by plant leaves. Ecotox.
Environ. Safety 37:24-29.
    \899\ Kammerbauer H, H Selinger, R Rommelt, A Ziegler-Jons, D
Knoppik, B Hock. (1987). Toxic components of motor vehicle emissions
for the spruce Picea abies. Environ. Pollut. 48:235-243.
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C. Air Quality Impacts of Non-GHG Pollutants

    Section V of the preamble presents projections of the changes in
criteria pollutant and air toxics emissions due to the proposed
standards. However, the atmospheric chemistry related to ambient
concentrations of PM2.5, ozone and air toxics is very
complex, and evaluating air quality impacts of this proposed rule based
solely on emissions changes is difficult. Photochemical air quality
modeling is necessary to accurately project levels of most criteria and
air toxic pollutants, including ozone and PM. Air quality models use
mathematical and numerical techniques to simulate the physical and
chemical processes that affect air pollutants as they disperse and
react in the atmosphere. Based on inputs of meteorological data and
source information, these models are designed to characterize primary
pollutants that are emitted directly into the atmosphere and secondary
pollutants that are formed through complex chemical reactions within
the atmosphere. Photochemical air quality models have become widely
recognized and routinely utilized tools in regulatory analysis for
assessing the impacts of control strategies. Because of the length of
time needed to prepare the necessary emissions inventories, in addition
to the processing time associated with the modeling itself, we do not
have air quality modeling results available for this proposed rule.

D. Environmental Justice

    EPA's 2016 ``Technical Guidance for Assessing Environmental Justice
in Regulatory Analysis'' provides recommendations on conducting the
highest quality analysis feasible, recognizing that data limitations,
time and resource constraints, and analytic challenges will vary by
media and regulatory context.\900\ When assessing the potential for
disproportionately high and adverse health or environmental impacts of
regulatory actions on populations with potential EJ concerns, the EPA
strives to answer three broad questions: (1) Is there evidence of
potential environmental justice (EJ) concerns in the baseline (the
state of the world absent the regulatory action)? Assessing the
baseline will allow the EPA to determine whether pre-existing
disparities are associated with the pollutant(s) under consideration
(e.g., if the effects of the pollutant(s) are more concentrated in some
population groups); (2) Is there evidence of potential EJ concerns for
the regulatory option(s) under consideration? Specifically, how are the
pollutant(s) and its effects distributed for the regulatory options
under consideration?; and (3) Do the regulatory option(s) under
consideration exacerbate or mitigate EJ concerns relative to the
baseline? It is not always possible to quantitatively assess these
questions.
---------------------------------------------------------------------------

    \900\ ``Technical Guidance for Assessing Environmental Justice
in Regulatory Analysis.'' Epa.gov, Environmental Protection Agency,
https://www.epa.gov/sites/production/files/2016-06/documents/ejtg_5_6_16_v5.1.pdf. (June 2016).
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    In this section, we discuss the EJ impacts of the proposed
CO2 emission standards from the anticipated reduction of
GHGs (Section VI.D.1). EPA did not consider any potential
disproportionate impacts of vehicle emissions in selecting the proposed
CO2 emission standards, but we view mitigation of
disproportionate impacts of vehicle GHG emissions as one element of
protecting public health consistent with CAA section 202. We also
discuss potential additional EJ impacts from the non-GHG (criteria
pollutants and air toxics) emissions changes we estimate would result
from compliance with the proposed CO2 emission standards
(Section VI.D.2). EPA requests comment on the EJ impact analysis
presented in this proposal.
1. GHG Impacts
    In 2009, under the Endangerment and Cause or Contribute Findings
for Greenhouse Gases Under Section 202(a) of the Clean Air Act
(``Endangerment Finding''), the Administrator considered

how climate change threatens the health and welfare of the U.S.
population. As part of that consideration, she also considered risks to
people of color and low-income individuals and communities, finding
that certain parts of the U.S. population may be especially vulnerable
based on their characteristics or circumstances. These groups include
economically and socially disadvantaged communities; individuals at
vulnerable life stages, such as the elderly, the very young, and
pregnant or nursing women; those already in poor health or with
comorbidities; the disabled; those experiencing homelessness, mental
illness, or substance abuse; and Indigenous or other populations
dependent on one or limited resources for subsistence due to factors
including but not limited to geography, access, and mobility.
    Scientific assessment reports produced over the past decade by the
U.S. Global Change Research Program (USGCRP), 901 902 the
Intergovernmental Panel on Climate Change IPCC),
903 904 905 906 and the National Academies of Science,
Engineering, and Medicine 907 908 add more evidence that the
impacts of climate change raise potential environmental justice
concerns. These reports conclude that poorer or predominantly non-White
communities can be especially vulnerable to climate change impacts
because they tend to have limited adaptive capacities, are more
dependent on climate-sensitive resources such as local water and food
supplies, or have less access to social and information resources. Some
communities of color, specifically populations defined jointly by
ethnic/racial characteristics and geographic location, may be uniquely
vulnerable to climate change health impacts in the United States. In
particular, the 2016 scientific assessment on the Impacts of Climate
Change on Human Health \909\ found with high confidence that
vulnerabilities are place- and time-specific, life stages and ages are
linked to immediate and future health impacts, and social determinants
of health are linked to greater extent and severity of climate change-
related health impacts. The GHG emission reductions from this proposal
would contribute to efforts to reduce the probability of severe impacts
related to climate change.
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    \901\ USGCRP, 2018: Impacts, Risks, and Adaptation in the United
States: Fourth National Climate Assessment, Volume II [Reidmiller,
D.R., C.W. Avery, D.R. Easterling, K.E. Kunkel, K.L.M. Lewis, T.K.
Maycock, and B.C. Stewart (eds.)]. U.S. Global Change Research
Program, Washington, DC, USA, 1515 pp. doi: 10.7930/NCA4.2018.
    \902\ USGCRP, 2016: The Impacts of Climate Change on Human
Health in the United States: A Scientific Assessment. Crimmins, A.,
J. Balbus, J.L. Gamble, C.B. Beard, J.E. Bell, D. Dodgen, R.J.
Eisen, N. Fann, M.D. Hawkins, S.C. Herring, L. Jantarasami, D.M.
Mills, S. Saha, M.C. Sarofim, J. Trtanj, and L. Ziska, Eds. U.S.
Global Change Research Program, Washington, DC, 312 pp. http://dx.doi.org/10.7930/J0R49NQX.
    \903\ Oppenheimer, M., M. Campos, R.Warren, J. Birkmann, G.
Luber, B. O'Neill, and K. Takahashi, 2014: Emergent risks and key
vulnerabilities. In: Climate Change 2014: Impacts, Adaptation, and
Vulnerability. Part A: Global and Sectoral Aspects. Contribution of
Working Group II to the Fifth Assessment Report of the
Intergovernmental Panel on Climate Change [Field, C.B., V.R. Barros,
D.J. Dokken, K.J. Mach, M.D. Mastrandrea, T.E. Bilir, M. Chatterjee,
K.L. Ebi, Y.O. Estrada, R.C. Genova, B. Girma, E.S. Kissel, A.N.
Levy, S. MacCracken, P.R. Mastrandrea, and L.L.White (eds.)].
Cambridge University Press, Cambridge, United Kingdom and New York,
NY, USA, pp. 1039-1099.
    \904\ Porter, J.R., L. Xie, A.J. Challinor, K. Cochrane, S.M.
Howden, M.M. Iqbal, D.B. Lobell, and M.I. Travasso, 2014: Food
security and food production systems. In: Climate Change 2014:
Impacts, Adaptation, and Vulnerability. Part A: Global and Sectoral
Aspects. Contribution of Working Group II to the Fifth Assessment
Report of the Intergovernmental Panel on Climate Change [Field,
C.B., V.R. Barros, D.J. Dokken, K.J. Mach, M.D. Mastrandrea, T.E.
Bilir, M. Chatterjee, K.L. Ebi, Y.O. Estrada, R.C. Genova, B. Girma,
E.S. Kissel, A.N. Levy, S. MacCracken, P.R. Mastrandrea, and
L.L.White (eds.)]. Cambridge University Press, Cambridge, United
Kingdom and New York, NY, USA, pp. 485-533.
    \905\ Smith, K.R., A.Woodward, D. Campbell-Lendrum, D.D. Chadee,
Y. Honda, Q. Liu, J.M. Olwoch, B. Revich, and R. Sauerborn, 2014:
Human health: impacts, adaptation, and co-benefits. In: Climate
Change 2014: Impacts, Adaptation, and Vulnerability. Part A: Global
and Sectoral Aspects. Contribution of Working Group II to the Fifth
Assessment Report of the Intergovernmental Panel on Climate Change
[Field, C.B., V.R. Barros, D.J. Dokken, K.J. Mach, M.D. Mastrandrea,
T.E. Bilir, M. Chatterjee, K.L. Ebi, Y.O. Estrada, R.C. Genova, B.
Girma, E.S. Kissel,A.N. Levy, S. MacCracken, P.R. Mastrandrea, and
L.L.White (eds.)]. Cambridge University Press, Cambridge, United
Kingdom and New York, NY, USA, pp. 709-754.
    \906\ IPCC, 2018: Global Warming of 1.5[deg]C.An IPCC Special
Report on the impacts of global warming of 1.5[deg]C above pre-
industrial levels and related global greenhouse gas emission
pathways, in the context of strengthening the global response to the
threat of climate change, sustainable development, and efforts to
eradicate poverty [Masson-Delmotte, V., P. Zhai, H.-O. P[ouml]rtner,
D. Roberts, J. Skea, P.R. Shukla, A. Pirani, W. Moufouma-Okia, C.
P[eacute]an, R. Pidcock, S. Connors, J.B.R. Matthews, Y. Chen, X.
Zhou, M.I. Gomis, E. Lonnoy, T. Maycock, M. Tignor, and T.
Waterfield (eds.)]. In Press.
    \907\ National Research Council. 2011. America's Climate
Choices. Washington, DC: The National Academies Press. https://doi.org/10.17226/12781.
    \908\ National Academies of Sciences, Engineering, and Medicine.
2017. Communities in Action: Pathways to Health Equity. Washington,
DC: The National Academies Press. https://doi.org/10.17226/24624.
    \909\ USGCRP, 2016: The Impacts of Climate Change on Human
Health in the United States: A Scientific Assessment. Crimmins, A.,
J. Balbus, J.L. Gamble, C.B. Beard, J.E. Bell, D. Dodgen, R.J.
Eisen, N. Fann, M.D. Hawkins, S.C. Herring, L. Jantarasami, D.M.
Mills, S. Saha, M.C. Sarofim, J. Trtanj, and L. Ziska, Eds. U.S.
Global Change Research Program, Washington, DC, 312 pp. http://dx.doi.org/10.7930/J0R49NQX.
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i. Effects on Specific Populations of Concern
    Individuals living in socially and economically vulnerable
communities, such as those living at or below the poverty line or who
are experiencing homelessness or social isolation, are at greater risk
of health effects from climate change. This is also true with respect
to people at vulnerable life stages, specifically women who are pre-
and perinatal or are nursing; in utero fetuses; children at all stages
of development; and the elderly. Per the Fourth National Climate
Assessment (NCA4), ``Climate change affects human health by altering
exposures to heat waves, floods, droughts, and other extreme events;
vector-, food- and waterborne infectious diseases; changes in the
quality and safety of air, food, and water; and stresses to mental
health and well-being.'' \910\ Many health conditions such as
cardiopulmonary or respiratory illness and other health impacts are
associated with and exacerbated by an increase in GHGs and climate
change outcomes, which is problematic as these diseases occur at higher
rates within vulnerable communities. Importantly, negative public
health outcomes include those that are physical in nature, as well as
mental, emotional, social, and economic.
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    \910\ Ebi, K.L., J.M. Balbus, G. Luber, A. Bole, A. Crimmins, G.
Glass, S. Saha, M.M. Shimamoto, J. Trtanj, and J.L. White-Newsome,
2018: Human Health. In Impacts, Risks, and Adaptation in the United
States: Fourth National Climate Assessment, Volume II [Reidmiller,
D.R., C.W. Avery, D.R. Easterling, K.E. Kunkel, K.L.M. Lewis, T.K.
Maycock, and B.C. Stewart (eds.)]. U.S. Global Change Research
Program, Washington, DC, USA, pp. 539-571. doi: 10.7930/
NCA4.2018.CH14.
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    To this end, the scientific assessment literature, including the
aforementioned reports, demonstrates that there are myriad ways in
which these populations may be affected at the individual and community
levels. Individuals face differential exposure to criteria pollutants,
in part due to the proximities of highways, trains, factories, and
other major sources of pollutant-emitting sources to less-affluent
residential areas. Outdoor workers, such as construction or utility
crews and agricultural laborers, who frequently are comprised of
already at-risk groups, are exposed to poor air quality and extreme
temperatures without relief. Furthermore, people in communities with EJ
concerns face greater housing, clean water, and food insecurity and
bear disproportionate economic impacts and health burdens associated
with climate change effects. They have less or limited access to
healthcare and affordable, adequate

health or homeowner insurance. Finally, resiliency and adaptation are
more difficult for economically vulnerable communities; they have less
liquidity, individually and collectively, to move or to make the types
of infrastructure or policy changes to limit or reduce the hazards they
face. They frequently are less able to self-advocate for resources that
would otherwise aid in building resilience and hazard reduction and
mitigation.
    The assessment literature cited in EPA's 2009 and 2016 Endangerment
and Cause or Contribute Findings, as well as Impacts of Climate Change
on Human Health, also concluded that certain populations and life
stages, including children, are most vulnerable to climate-related
health effects.\911\ The assessment literature produced from 2016 to
the present strengthens these conclusions by providing more detailed
findings regarding related vulnerabilities and the projected impacts
youth may experience. These assessments--including the NCA4 and The
Impacts of Climate Change on Human Health in the United States (2016)--
describe how children's unique physiological and developmental factors
contribute to making them particularly vulnerable to climate change.
Impacts to children are expected from heat waves, air pollution,
infectious and waterborne illnesses, and mental health effects
resulting from extreme weather events. In addition, children are among
those especially susceptible to allergens, as well as health effects
associated with heat waves, storms, and floods. Additional health
concerns may arise in low-income households, especially those with
children, if climate change reduces food availability and increases
prices, leading to food insecurity within households.
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    \911\ 74 FR 66496, December 15, 2009; 81 FR 54422, August 15,
2016.
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    The Impacts of Climate Change on Human Health \912\ also found that
some communities of color, low-income groups, people with limited
English proficiency, and certain immigrant groups (especially those who
are undocumented) live with many of the factors that contribute to
their vulnerability to the health impacts of climate change. While
difficult to isolate from related socioeconomic factors, race appears
to be an important factor in vulnerability to climate-related stress,
with elevated risks for mortality from high temperatures reported for
Black or African American individuals compared to White individuals
after controlling for factors such as air conditioning use. Moreover,
people of color are disproportionately exposed to air pollution based
on where they live, and disproportionately vulnerable due to higher
baseline prevalence of underlying diseases such as asthma, so climate
exacerbations of air pollution are expected to have disproportionate
effects on these communities.
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    \912\ USGCRP, 2016: The Impacts of Climate Change on Human
Health in the United States: A Scientific Assessment. Crimmins, A.,
J. Balbus, J.L. Gamble, C.B. Beard, J.E. Bell, D. Dodgen, R.J.
Eisen, N. Fann, M.D. Hawkins, S.C. Herring, L. Jantarasami, D.M.
Mills, S. Saha, M.C. Sarofim, J. Trtanj, and L. Ziska, Eds. U.S.
Global Change Research Program, Washington, DC, 312 pp. http://dx.doi.org/10.7930/J0R49NQX.
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    Native American Tribal communities possess unique vulnerabilities
to climate change, particularly those impacted by degradation of
natural and cultural resources within established reservation
boundaries and threats to traditional subsistence lifestyles. Tribal
communities whose health, economic well-being, and cultural traditions
depend upon the natural environment will likely be affected by the
degradation of ecosystem goods and services associated with climate
change. The IPCC indicates that losses of customs and historical
knowledge may cause communities to be less resilient or adaptable.\913\
The NCA4 noted that while Indigenous peoples are diverse and will be
impacted by the climate changes universal to all Americans, there are
several ways in which climate change uniquely threatens Indigenous
peoples' livelihoods and economies.\914\ In addition, there can
institutional barriers to their management of water, land, and other
natural resources that could impede adaptive measures.
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    \913\ Porter et al., 2014: Food security and food production
systems.
    \914\ Jantarasami, L.C., R. Novak, R. Delgado, E. Marino, S.
McNeeley, C. Narducci, J. Raymond-Yakoubian, L. Singletary, and K.
Powys Whyte, 2018: Tribes and Indigenous Peoples. In Impacts, Risks,
and Adaptation in the United States: Fourth National Climate
Assessment, Volume II [Reidmiller, D.R., C.W. Avery, D.R.
Easterling, K.E. Kunkel, K.L.M. Lewis, T.K. Maycock, and B.C.
Stewart (eds.)]. U.S. Global Change Research Program, Washington,
DC, USA, pp. 572-603. doi: 10.7930/NCA4.2018.CH15.
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    For example, Indigenous agriculture in the Southwest is already
being adversely affected by changing patterns of flooding, drought,
dust storms, and rising temperatures leading to increased soil erosion,
irrigation water demand, and decreased crop quality and herd sizes. The
Confederated Tribes of the Umatilla Indian Reservation in the Northwest
have identified climate risks to salmon, elk, deer, roots, and
huckleberry habitat. Housing and sanitary water supply infrastructure
are vulnerable to disruption from extreme precipitation events.
    NCA4 noted that Indigenous peoples often have disproportionately
higher rates of asthma, cardiovascular disease, Alzheimer's, diabetes,
and obesity, which can all contribute to increased vulnerability to
climate-driven extreme heat and air pollution events. These factors
also may be exacerbated by stressful situations, such as extreme
weather events, wildfires, and other circumstances.
    NCA4 and IPCC Fifth Assessment Report also highlighted several
impacts specific to Alaskan Indigenous Peoples. Permafrost thaw will
lead to more coastal erosion, exacerbated risks of winter travel, and
damage to buildings, roads, and other infrastructure--these impacts on
archaeological sites, structures, and objects will lead to a loss of
cultural heritage for Alaska's Indigenous people. In terms of food
security, the NCA4 discussed reductions in suitable ice conditions for
hunting, warmer temperatures impairing the use of traditional ice
cellars for food storage, and declining shellfish populations due to
warming and acidification. While the NCA also noted that climate change
provided more opportunity to hunt from boats later in the fall season
or earlier in the spring, the assessment found that the net impact was
an overall decrease in food security.
    In addition, the U.S. Pacific Islands and the indigenous
communities that live there are also uniquely vulnerable to the effects
of climate change due to their remote location and geographic
isolation. They rely on the land, ocean, and natural resources for
their livelihoods, but they face challenges in obtaining energy and
food supplies that need to be shipped in at high costs. As a result,
they face higher energy costs than the rest of the nation and depend on
imported fossil fuels for electricity generation and diesel. These
challenges exacerbate the climate impacts that the Pacific Islands are
experiencing. NCA4 notes that Indigenous peoples of the Pacific are
threatened by rising sea levels, diminishing freshwater availability,
and negative effects to ecosystem services that threaten these
individuals' health and well-being.
2. Non-GHG Impacts
    In Section V.B., in addition to GHG emissions impacts, we also
discuss potential additional impacts to emissions of non-GHGs (i.e.,
criteria and air toxic pollutants) that we estimate would result from
compliance with the proposed GHG emission standards. This section
VI.D.2 describes evidence that communities with EJ concerns are
disproportionately impacted by the non-GHG emissions affected by this
rule.

Numerous studies have found that environmental hazards such as air
pollution are more prevalent in areas where people of color and low-
income populations represent a higher fraction of the population
compared with the general population.915 916 917 Consistent
with this evidence, a recent study found that most anthropogenic
sources of PM2.5, including industrial sources and light-
and heavy-duty vehicle sources, disproportionately affect people of
color.\918\ In addition, compared to non-Hispanic Whites, some other
racial groups experience greater levels of health problems during some
life stages. For example, in 2018-2020, about 12 percent of non-
Hispanic Black; 9 percent of non-Hispanic American Indian/Alaska
Native; and 7 percent of Hispanic children were estimated to currently
have asthma, compared with 6 percent of non-Hispanic White
children.\919\ Nationally, on average, non-Hispanic Black and Non-
Hispanic American Indian or Alaska Native people also have lower than
average life expectancy based on 2019 data, the latest year for which
CDC estimates are available.\920\
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    \915\ Rowangould, G.M. (2013) A census of the near-roadway
population: public health and environmental justice considerations.
Trans Res D 25: 59-67. http://dx.doi.org/10.1016/j.trd.2013.08.003.
    \916\ Marshall, J.D., Swor, K.R.; Nguyen, N.P (2014)
Prioritizing environmental justice and equality: diesel emissions in
Southern California. Environ Sci Technol 48: 4063-4068. https://doi.org/10.1021/es405167f.
    \917\ Marshall, J.D. (2008) Environmental inequality: air
pollution exposures in California's South Coast Air Basin. Atmos
Environ 21: 5499-5503. https://doi.org/10.1016/j.atmosenv.2008.02.005.
    \918\ C. W. Tessum, D. A. Paolella, S. E. Chambliss, J. S. Apte,
J. D. Hill, J. D. Marshall, PM2.5 polluters
disproportionately and systemically affect people of color in the
United States. Sci. Adv. 7, eabf4491 (2021).
    \919\ http://www.cdc.gov/asthma/most_recent_data.htm.
    \920\ Arias, E. Xu, J. (2022) United States Life Tables, 2019.
National Vital Statistics Report, Volume 70, Number 19. [Online at
https://www.cdc.gov/nchs/data/nvsr/nvsr70/nvsr70-19.pdf].
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    We discuss near-roadway issues in Section VI.D.2.i and upstream
sources in Section VI.D.2.ii.
i. Near-Roadway Analysis
    As described in Section VI.B of this preamble, concentrations of
many air pollutants are elevated near high-traffic roadways. We
recently conducted an analysis of the populations within the CONUS
living in close proximity to truck freight routes as identified in
USDOT's FAF4.\921\ 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
United States \922\ Relative to the rest of the population, people
living near FAF4 truck routes are more likely to be people of color and