SO2 and mortality.
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    \56\ U.S. EPA. (2008). Integrated Science Assessment (ISA) for
Sulfur Oxides--Health Criteria (Final Report). EPA/600/R-08/047F.
Washington, DC: U.S. Environmental Protection Agency.
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d. Current Levels of NO2
    Between 2003 and 2005, national mean concentrations of
NO2 were about 15 parts per billion (ppb) for averaging
periods ranging from a day to a year.\57\ There are two NAAQS for
NO2: an annual standard (53 ppb) and a 1-hour standard (100
ppb). The primary NAAQS for NO2 was revised in January 2010.
EPA completed area designations in January 2012 and there are currently
no nonattainment areas. The designations were based on the existing
community-wide monitoring network. Once the expanded network of
NO2 monitors is fully deployed and three years of air
quality data have been collected, EPA intends to redesignate areas, as
appropriate, based on the air quality data from the new monitoring
network.58 59
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    \57\ U.S. EPA. (2010). Final Regulatory Impact Analysis (RIA)
for the NO2 National Ambient Air Quality Standards
(NAAQS). http://www.epa.gov/ttn/ecas/regdata/RIAs/FinalNO2RIAfulldocument.pdf.
    \58\ U.S. EPA. (2012). Fact Sheet--Air Quality Designations for
the 2010 Primary Nitrogen Dioxide (NO2) National Ambient
Air Quality Standards. http://www.epa.gov/airquality/nitrogenoxides/designations/pdfs/20120120FS.pdf.
    \59\ U.S. Environmental Protection Agency (2013). Revision to
Ambient Nitrogen Dioxide Monitoring Requirements. March 7, 2013.
http://www.epa.gov/airquality/nitrogenoxides/pdfs/20130307fr.pdf.
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4. Carbon Monoxide
    Carbon monoxide (CO) is a colorless, odorless gas emitted from
combustion processes. Nationally and, particularly in urban areas, the
majority of CO emissions to ambient air come from mobile sources.
a. Health Effects of Carbon Monoxide
    Information on the health effects of CO can be found in the EPA
Integrated Science Assessment (ISA) for Carbon Monoxide.\60\ The ISA
concludes that ambient concentrations of CO are associated with a
number of adverse health effects.\61\ This section provides a summary
of the health effects associated with exposure to ambient
concentrations of CO.\62\
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    \60\ U.S. EPA, (2010). Integrated Science Assessment for Carbon
Monoxide (Final Report). U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-09/019F, 2010. Available at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=218686.
    \61\ 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.
    \62\ Personal exposure includes contributions from many sources,
and in many different environments. Total personal exposure to CO
includes both ambient and nonambient components; and both components
may contribute to adverse health effects.
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    Human clinical 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 show 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 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 inconsistent neural
and behavioral effects following low-level CO exposures. The ISA
concludes the evidence is suggestive of a causal relationship with both
short- and long-term exposure to CO and central nervous system effects.
    A number of epidemiologic and animal toxicological studies cited in
the ISA have evaluated associations between CO exposure and birth
outcomes such as preterm birth or cardiac birth defects. The
epidemiologic studies provide limited 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 associations
between perinatal CO exposure and decrements in birth weight, as well
as other developmental outcomes. The ISA concludes these studies are
suggestive of a causal relationship between long-term exposures to CO
and developmental effects and birth outcomes.
    Epidemiologic studies provide evidence of effects on respiratory
morbidity such as changes in pulmonary function, respiratory symptoms,
and hospital admissions associated with ambient CO concentrations. 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 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 ISA concludes that the epidemiologic evidence is
suggestive of a causal relationship between short-term exposures to CO
and mortality. Epidemiologic studies provide evidence of an association
between short-term exposure to CO and mortality, but limited evidence
is available to evaluate cause-specific mortality outcomes associated
with CO exposure. In addition, the attenuation of CO risk estimates
which was often observed in copollutant models contributes to the
uncertainty as to whether CO is acting alone or as an indicator for
other combustion-related pollutants. The ISA also concludes that there
is not likely to be a causal relationship between relevant long-term
exposures to CO and mortality.
5. Mobile Source Air Toxics
    Light-duty vehicle emissions contribute to ambient levels of air
toxics known or suspected as human or animal carcinogens, or that have
noncancer health effects. The population experiences an elevated risk
of cancer and other noncancer health effects from exposure to the class
of pollutants known collectively as ``air toxics.'' \63\ These
compounds include, but are not limited to, benzene, 1,3-butadiene,
formaldehyde, acetaldehyde, acrolein, polycyclic organic matter, and
naphthalene. These compounds were identified as national or regional
risk drivers or contributors in the 2005 National-scale Air Toxics
Assessment and have significant inventory contributions from mobile
sources.\64\
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    \63\ U.S. EPA. (2011) Summary of Results for the 2005 National-
Scale Assessment. www.epa.gov/ttn/atw/nata2005/05pdf/sum_results.pdf.
    \64\ U.S. EPA (2011) 2005 National-Scale Air Toxics Assessment.
http://www.epa.gov/ttn/atw/nata2005.
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a. Health Effects of Air Toxics
i. Benzene
    The EPA's 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.65 66 67 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 as the
unit risk estimate (URE) for benzene.68 69 The International
Agency for Research on Carcinogens (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.70 71
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    \65\ U.S. EPA. (2000). Integrated Risk Information System File
for Benzene. This material is available electronically at: http://www.epa.gov/iris/subst/0276.htm.
    \66\ International Agency for Research on Cancer, IARC
monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29, Some industrial chemicals and dyestuffs,
International Agency for Research on Cancer, World Health
Organization, Lyon, France 1982.
    \67\ 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.
    \68\ A unit risk estimate is defined as the increase in the
lifetime risk of an individual who is exposed for a lifetime to 1
[micro]g/m3 benzene in air.
    \69\ U.S. EPA. (2000). Integrated Risk Information System File
for Benzene. This material is available electronically at: http://www.epa.gov/iris/subst/0276.htm.
    \70\ International Agency for Research on Cancer (IARC). (1987).
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29, Supplement 7, Some industrial chemicals and
dyestuffs, World Health Organization, Lyon, France.
    \71\ U.S. Department of Health and Human Services National
Toxicology Program. (2011). 12th Report on Carcinogens. Available
at: http://ntp.niehs.nih.gov/?objectid=03C9AF75-E1BF-FF40-DBA9EC0928DF8B15.
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    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.72 73 The most
sensitive noncancer effect observed in humans, based on current data,
is the depression of the absolute lymphocyte count in
blood.74 75 EPA's inhalation reference concentration (RfC)
for benzene is 30 [micro]g/m\3\. The RfC is based on suppressed
absolute lymphocyte counts seen in humans under occupational exposure
conditions. In addition, recent work, including studies sponsored by
the Health Effects Institute (HEI), provides evidence that biochemical
responses are occurring at lower levels of benzene exposure than
previously known.76 77 78 79 EPA's IRIS program has

not yet evaluated these new data. EPA does not currently have an acute
reference concentration for benzene. The Agency for Toxic Substances
and Disease Registry (ATSDR) Minimal Risk Level (MRL) for acute
exposure to benzene is 29 [micro]g/m\3\ for 1-14 days
exposure.80 81
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    \72\ Aksoy, M. (1989). Hematotoxicity and carcinogenicity of
benzene. Environ. Health Perspect. 82: 193-197.
    \73\ Goldstein, B.D. (1988). Benzene toxicity. Occupational
medicine. State of the Art Reviews. 3: 541-554.
    \74\ 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.
    \75\ 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 http://www.epa.gov/iris/subst/0276.htm.
    \76\ 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.
    \77\ 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.
    \78\ Lan, Qing, Zhang, L., Li, G., Vermeulen, R., et al. (2004).
Hematotoxically in Workers Exposed to Low Levels of Benzene. Science
306: 1774-1776.
    \79\ 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.
    \80\ 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.
    \81\ 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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ii. Formaldehyde
    In 1991, EPA concluded that formaldehyde is a carcinogen based on
nasal tumors in animal bioassays.\82\ An Inhalation Unit Risk for
cancer and a Reference Dose for oral noncancer effects were developed
by the Agency and posted on the Integrated Risk Information System
(IRIS) database. Since that time, the National Toxicology Program (NTP)
and International Agency for Research on Cancer (IARC) have concluded
that formaldehyde is a known human carcinogen.83 84 85
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    \82\ EPA. Integrated Risk Information System. Formaldehyde
(CASRN 50-00-0) http://www.epa.gov/iris/subst/0419/htm.
    \83\ National Toxicology Program, U.S. Department of Health and
Human Services (HHS), 12th Report on Carcinogens, June 10, 2011.
    \84\ IARC Monographs on the Evaluation of Carcinogenic Risks to
Humans Volume 88 (2006): Formaldehyde, 2-Butoxyethanol and 1-tert-
Butoxypropan-2-ol.
    \85\ IARC Mongraphs 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.86 87 88 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.\89\ 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.\90\
Finally, a study of embalmers reported formaldehyde exposures to be
associated with an increased risk of myeloid leukemia but not brain
cancer.\91\
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    \86\ 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.
    \87\ 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.
    \88\ 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.
    \89\ Pinkerton, L.E. 2004. Mortality among a cohort of garment
workers exposed to formaldehyde: an update. Occup. Environ. Med. 61:
193-200.
    \90\ 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.
    \91\ 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 \92\
and supplemented in 2010,\93\ and by the World Health Organization.\94\
These organizations reviewed the literature concerning effects on the
eyes and respiratory system, the primary point of contact for inhaled
formaldehyde, including sensory irritation of eyes and respiratory
tract, pulmonary function, nasal histopathology, and immune system
effects. In addition, research on reproductive and developmental
effects and neurological effects were discussed.
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    \92\ ATSDR. 1999. Toxicological Profile for Formaldehyde, U.S.
Department of Health and Human Services (HHS), July 1999.
    \93\ ATSDR. 2010. Addendum to the Toxicological Profile for
Formaldehyde. U.S. Department of Health and Human Services (HHS),
October 2010.
    \94\ IPCS. 2002. Concise International Chemical Assessment
Document 40. Formaldehyde. World Health Organization.
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    EPA released a draft Toxicological Review of Formaldehyde--
Inhalation Assessment through the IRIS program for peer review by the
National Research Council (NRC) and public comment in June 2010.\95\
The draft assessment reviewed more recent research from animal and
human studies on cancer and other health effects. The NRC released
their review report in April 2011.\96\ The EPA is currently revising
the draft assessment in response to this review.
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    \95\ EPA (U.S. Environmental Protection Agency). 2010.
Toxicological Review of Formaldehyde (CAS No. 50-00-0)--Inhalation
Assessment: In Support of Summary Information on the Integrated Risk
Information System (IRIS). External Review Draft. EPA/635/R-10/002A.
U.S. Environmental Protection Agency, Washington DC [online].
Available: http://cfpub.epa.gov/ncea/irs_drats/recordisplay.cfm?deid=223614.
    \96\ NRC (National Research Council). 2011. Review of the
Environmental Protection Agency's Draft IRIS Assessment of
Formaldehyde. Washington DC: National Academies Press. http://books.nap.edu/openbook.php?record_id=13142.
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iii. 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.\97\ The URE in
IRIS for acetaldehyde is 2.2 x 10-6 per [micro]g/m\3\.\98\
Acetaldehyde is reasonably anticipated to be a human carcinogen by the
U.S. DHHS in the 12th Report on Carcinogens and is classified as
possibly carcinogenic to humans (Group 2B) by the
IARC.99 100 EPA is currently conducting a reassessment of
cancer risk from inhalation exposure to acetaldehyde.
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    \97\ U.S. EPA (1991). Integrated Risk Information System File of
Acetaldehyde. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
electronically at http://www.epa.gov/iris/subst/0290.htm.
    \98\ U.S. EPA (1991). Integrated Risk Information System File of
Acetaldehyde. This material is available electronically at http://www.epa.gov/iris/subst/0290.htm.
    \99\ NTP. (2011). Report on Carcinogens, Twelfth Edition.
Research Triangle Park, NC: U.S. Department of Health and Human
Services, Public Health Service, National Toxicology Program. 499
pp.
    \100\ International Agency for Research on Cancer (IARC).
(1999). Re-evaluation of some organic chemicals, hydrazine, and
hydrogen peroxide. IARC Monographs on the Evaluation of Carcinogenic
Risk of Chemical to Humans, Vol 71. Lyon, France.
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    The primary noncancer effects of exposure to acetaldehyde vapors
include irritation of the eyes, skin, and respiratory tract.\101\ In
short-term (4 week) rat studies, degeneration of olfactory epithelium
was observed at various concentration levels of acetaldehyde
exposure.102 103 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.\104\
The agency is currently conducting a reassessment of the health hazards
from inhalation exposure to acetaldehyde.
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    \101\ U.S. EPA (1991). Integrated Risk Information System File
of Acetaldehyde. This material is available electronically at http://www.epa.gov/iris/subst/0290.htm.
    \102\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
electronically at http://www.epa.gov/iris/subst/0364.htm.
    \103\ 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.
    \104\ 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.
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iv. 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.\105\ The IARC determined in
1995 that acrolein was not classifiable as to its carcinogenicity in
humans.\106\
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    \105\ U.S. EPA. (2003). Integrated Risk Information System File
of Acrolein. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
at http://www.epa.gov/iris/subst/0364.htm.
    \106\ International Agency for Research on Cancer (IARC).
(1995). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, Volume 63. Dry cleaning, some chlorinated
solvents and other industrial chemicals, World Health Organization,
Lyon, France.
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    Lesions to the lungs and upper respiratory tract of rats, rabbits,
and hamsters have been observed after subchronic exposure to
acrolein.\107\ The Agency has developed an RfC for acrolein of 0.02
[micro]g/m\3\ and an RfD of 0.5 [micro]g/kg-day.\108\ EPA is
considering updating the acrolein assessment with data that have become
available since the 2003 assessment was completed.
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    \107\ 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.
    \108\ 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.
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    Acrolein is extremely acrid and irritating to humans when inhaled,
with acute exposure resulting in upper respiratory tract irritation,
mucus hypersecretion and congestion. The intense irritancy of this
carbonyl has been demonstrated during controlled tests in human
subjects, who suffer intolerable eye and nasal mucosal sensory
reactions within minutes of exposure.\109\ 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.\110\ Studies in humans indicate that levels as low as 0.09
ppm (0.21 mg/m\3\) 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 \111\) and demonstration of similar
effects in humans (e.g., reduction in respiratory rate), individuals
with compromised respiratory function (e.g., emphysema, asthma) are
expected to be at increased risk of developing adverse responses to
strong respiratory irritants such as acrolein. EPA does not currently
have an acute reference concentration for acrolein. The available
health effect reference values for acrolein have been summarized by EPA
and include an ATSDR MRL for acute exposure to acrolein of 7 [micro]g/
m\3\ for 1-14 days exposure; and Reference Exposure Level (REL) values
from the California Office of Environmental Health Hazard Assessment
(OEHHA) for one-hour and 8-hour exposures of 2.5 [micro]g/m\3\ and 0.7
[micro]g/m\3\, respectively.\112\
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    \109\ U.S. EPA. (2003) Toxicological review of acrolein in
support of summary information on Integrated Risk Information System
(IRIS) National Center for Environmental Assessment, Washington, DC.
EPA/635/R-03/003. p. 10. Available online at: http://www.epa.gov/ncea/iris/toxreviews/0364tr.pdf.
    \110\ 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: http://www.epa.gov/ncea/iris/toxreviews/0364tr.pdf.
    \111\ 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.
    \112\ 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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v. 1,3-Butadiene
    EPA has characterized 1,3-butadiene as carcinogenic to humans by
inhalation.113 114 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.115 116 117 There
are numerous studies consistently demonstrating that 1,3-butadiene is
metabolized into genotoxic metabolites by experimental animals and
humans. The specific mechanisms of 1,3-butadiene-induced carcinogenesis
are unknown; however, the scientific evidence strongly suggests that
the carcinogenic effects are mediated by genotoxic metabolites. Animal
data suggest that females may be more sensitive than males for cancer
effects associated with 1,3-butadiene exposure; there are insufficient
data in humans from which to draw conclusions about sensitive
subpopulations. The URE for 1,3-butadiene is 3 x 10-5 per
[micro]g/m\3\.\118\ 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.\119\ 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/m\3\).
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    \113\ U.S. EPA. (2002). Health Assessment of 1,3-Butadiene.
Office of Research and Development, National Center for
Environmental Assessment, Washington Office, Washington, DC. Report
No. EPA600-P-98-001F. This document is available electronically at
http://www.epa.gov/iris/supdocs/buta-sup.pdf.
    \114\ U.S. EPA. (2002). ``Full IRIS Summary for 1,3-butadiene
(CASRN 106-99-0)'' Environmental Protection Agency, Integrated Risk
Information System (IRIS), Research and Development, National Center
for Environmental Assessment, Washington, DC http://www.epa.gov/iris/subst/0139.htm.
    \115\ International Agency for Research on Cancer (IARC).
(1999). Monographs on the evaluation of carcinogenic risk of
chemicals to humans, Volume 71, Re-evaluation of some organic
chemicals, hydrazine and hydrogen peroxide and Volume 97 (in
preparation), World Health Organization, Lyon, France.
    \116\ 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.
    \117\ NTP. (2011). Report on Carcinogens, Twelfth Edition.
Research Triangle Park, NC: U.S. Department of Health and Human
Services, Public Health Service, National Toxicology Program. 499
pp.
    \118\ U.S. EPA. (2002). ``Full IRIS Summary for 1,3-butadiene
(CASRN 106-99-0)'' Environmental Protection Agency, Integrated Risk
Information System (IRIS), Research and Development, National Center
for Environmental Assessment, Washington, DC http://www.epa.gov/iris/subst/0139.htm.
    \119\ 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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vi. Ethanol
    EPA is planning to develop an assessment of the health effects of
exposure to ethanol, a compound which is not currently listed on EPA's
IRIS database. Extensive health effects data are available for
ingestion of ethanol, while data on inhalation exposure effects are
sparse. In developing the assessment, EPA is evaluating pharmacokinetic
models as a means of extrapolating across species (animal to human) and
across exposure routes (oral to inhalation) to better characterize the
health hazards and dose-response relationships for low levels of
ethanol exposure in the environment.
vii. Polycyclic Organic Matter
    The term polycyclic organic matter (POM) defines a broad class of
compounds that includes the polycyclic aromatic hydrocarbon compounds
(PAHs). One of these compounds, naphthalene, is discussed separately
below. POM compounds are formed primarily from combustion and are
present in the atmosphere in gas and particulate form. Cancer is the
major concern from exposure to POM. Epidemiologic studies have reported
an increase in lung cancer in humans exposed to diesel exhaust, coke
oven emissions, roofing tar emissions, and cigarette smoke; all of
these mixtures contain POM compounds.120 121 Animal studies
have reported respiratory tract tumors from inhalation exposure to
benzo[a]pyrene and alimentary tract and liver tumors from oral exposure
to benzo[a]pyrene.\122\ In 1997 EPA classified seven PAHs
(benzo[a]pyrene, benz[a]anthracene, chrysene, benzo[b]fluoranthene,
benzo[k]fluoranthene, dibenz[a,h]anthracene, and indeno[1,2,3-
cd]pyrene) as Group B2, probable human carcinogens.\123\ Since that
time, studies have found that maternal exposures to PAHs in a
population of pregnant women were associated with several adverse birth
outcomes, including low birth weight and reduced length at birth, as
well as impaired cognitive development in preschool children (3 years
of age).124 125 These and similar studies are being
evaluated as a part of the ongoing IRIS assessment of health effects
associated with exposure to benzo[a]pyrene.
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    \120\ Agency for Toxic Substances and Disease Registry (ATSDR).
(1995). Toxicological profile for Polycyclic Aromatic Hydrocarbons
(PAHs). Atlanta, GA: U.S. Department of Health and Human Services,
Public Health Service. Available electronically at http://www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=122&tid=25.
    \121\ U.S. EPA (2002). Health Assessment Document for Diesel
Engine Exhaust. EPA/600/8-90/057F Office of Research and
Development, Washington DC. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=29060.
    \122\ International Agency for Research on Cancer (IARC).
(2012). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans, Chemical Agents and Related Occupations. Vol.
100F. Lyon, France.
    \123\ U.S. EPA (1997). Integrated Risk Information System File
of indeno(1,2,3-cd)pyrene. Research and Development, National Center
for Environmental Assessment, Washington, DC. This material is
available electronically at http://www.epa.gov/ncea/iris/subst/0457.htm.
    \124\ Perera, F.P.; Rauh, V.; Tsai, W-Y.; et al. (2002). Effect
of transplacental exposure to environmental pollutants on birth
outcomes in a multiethnic population. Environ Health Perspect. 111:
201-205.
    \125\ Perera, F.P.; Rauh, V.; Whyatt, R.M.; Tsai, W.Y.; Tang,
D.; Diaz, D.; Hoepner, L.; Barr, D.; Tu, Y.H.; Camann, D.; Kinney,
P. (2006). Effect of prenatal exposure to airborne polycyclic
aromatic hydrocarbons on neurodevelopment in the first 3 years of
life among inner-city children. Environ Health Perspect 114: 1287-
1292.
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viii. PAN
    PAN (peroxy acetyl nitrate) has not been evaluated by EPA's IRIS
program. Information regarding the potential carcinogenicity of PAN is
limited. As noted in the EPA air quality criteria document for ozone
and related photochemical oxidants, cytogenetic studies indicate that
PAN is not a potent mutagen, clastogen (a compound that can cause
breaks in chromosomes), or DNA-damaging agent in mammalian cells either
in vivo or in vitro. Some studies suggest that PAN may be a weak
bacterial mutagen at concentrations much higher than exist in present
urban atmospheres.\126\
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    \126\ U.S. EPA. (2006). Air quality criteria for ozone and
related photochemical oxidants (Ozone CD). Research Triangle Park,
NC: National Center for Environmental Assessment; report no. EPA/
600/R-05/004aF-cF.3v. page 5-78. Available at http://cfpub.epa.gov/ncea/.
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    Effects of ground-level smog causing intense eye irritation have
been attributed to photochemical oxidants, including PAN.\127\ Animal
toxicological information on the inhalation effects of the non-ozone
oxidants has been limited to a few studies on PAN. Acute exposure to
levels of PAN can cause changes in lung morphology, behavioral
modifications, weight loss, and susceptibility to pulmonary infections.
Human exposure studies indicate minor pulmonary function effects at
high PAN concentrations, but large inter-individual variability
precludes definitive conclusions.\128\
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    \127\ U.S. EPA (2005). Air Quality Criteria for Ozone and
Related Photochemical Oxidants (Final). U.S. Environmental
Protection Agency, Washington, DC, EPA 600/R-05/004aF-cF, 2006. page
5-63. This document is available in Docket EPA-HQ-OAR-2005-0161.
This document may be accessed electronically at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_cd.html.
    \128\ U.S. EPA (2005). Air Quality Criteria for Ozone and
Related Photochemical Oxidants (Final). U.S. Environmental
Protection Agency, Washington, DC, EPA 600/R-05/004aF-cF, 2006. page
5-78. This document is available in Docket EPA-HQ-OAR-2005-0161.
This document may be accessed electronically at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_cd.html.
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ix. 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.\129\ Chronic
(long term) exposure of workers and rodents to naphthalene has been
reported to cause cataracts and retinal damage.\130\ EPA released an
external review draft of a reassessment of the inhalation
carcinogenicity of naphthalene based on a number of recent animal
carcinogenicity studies.\131\ The draft reassessment completed external
peer review.\132\ Based on external peer review comments received, a
revised draft assessment that considers all routes of exposure, as well
as cancer and noncancer effects, is under development. The external
review draft does not represent official agency opinion and was
released solely for the purposes of external peer review and public
comment. The National Toxicology Program listed naphthalene

as ``reasonably anticipated to be a human carcinogen'' in 2004 on the
basis of bioassays reporting clear evidence of carcinogenicity in rats
and some evidence of carcinogenicity in mice.\133\ 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.\134\
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    \129\ 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 http://www.epa.gov/iris/subst/0436.htm.
    \130\ 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 http://www.epa.gov/iris/subst/0436.htm.
    \131\ 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 http://www.epa.gov/iris/subst/0436.htm.
    \132\ 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.
    \133\ NTP. (2011). Report on Carcinogens, Twelfth Edition.
Research Triangle Park, NC: U.S. Department of Health and Human
Services, Public Health Service, National Toxicology Program. 499
pp.
    \134\ International Agency for Research on Cancer (IARC).
(2002). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans. Vol. 82. Lyon, France.
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    Naphthalene also causes a number of chronic non-cancer effects in
animals, including abnormal cell changes and growth in respiratory and
nasal tissues.\135\ The current EPA IRIS assessment includes noncancer
data on hyperplasia and metaplasia in nasal tissue that form the basis
of the inhalation RfC of 3 [micro]g/m\3\.\136\ The ATSDR MRL for acute
exposure to naphthalene is 0.6 mg/kg/day.
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    \135\ 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 http://www.epa.gov/iris/subst/0436.htm.
    \136\ 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 http://www.epa.gov/iris/subst/0436.htm.
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x. Other Air Toxics
    In addition to the compounds described above, other compounds in
gaseous hydrocarbon and PM emissions from light-duty vehicles would be
affected by this proposal. Mobile source air toxic compounds that would
potentially be impacted include ethylbenzene, propionaldehyde, toluene,
and xylene. Information regarding the health effects of these compounds
can be found in EPA's IRIS database.\137\
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    \137\ U.S. EPA Integrated Risk Information System (IRIS)
database is available at: www.epa.gov/iris.
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b. Current Levels of Air Toxics
    The majority of Americans continue to be exposed to ambient
concentrations of air toxics at levels which have the potential to
cause adverse health effects.\138\ The levels of air toxics to which
people are exposed vary depending on where people live and work and the
kinds of activities in which they engage, as discussed in detail in
U.S. EPA's most recent Mobile Source Air Toxics Rule.\139\ According to
the National Air Toxic Assessment (NATA) for 2005,\140\ mobile sources
were responsible for 43 percent of outdoor toxic emissions and over 50
percent of the cancer risk and noncancer hazard associated with primary
emissions. Mobile sources are also large contributors to precursor
emissions which react to form secondary concentrations of air toxics.
Formaldehyde is the largest contributor to cancer risk of all 80
pollutants quantitatively assessed in the 2005 NATA. Mobile sources
were responsible for over 40 percent of primary emissions of this
pollutant in 2005, and are major contributors to formaldehyde precursor
emissions. Benzene is also a large contributor to cancer risk, and
mobile sources account for over 70 percent of ambient exposure. Over
the years, EPA has implemented a number of mobile source and fuel
controls which have resulted in VOC reductions, which also reduced
formaldehyde, benzene and other air toxic emissions.
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    \138\ U.S. Environmental Protection Agency (2007). Control of
Hazardous Air Pollutants from Mobile Sources; Final Rule. 72 FR
8434, February 26, 2007.
    \139\ U. S. Environmental Protection Agency (2007). Control of
Hazardous Air Pollutants from Mobile Sources; Final Rule. 72 FR
8434, February 26, 2007.
    \140\ U.S. EPA. (2011). 2005 National-Scale Air Toxics
Assessment. http://www.epa.gov/ttn/atw/nata2005/.
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6. Near-Roadway Pollution
    Locations in close proximity to major roadways generally have
elevated concentrations of many air pollutants emitted from motor
vehicles. Hundreds of such studies have been published in peer-reviewed
journals, concluding that concentrations of CO, NO, NO2,
benzene, aldehydes, particulate matter, black carbon, and many other
compounds are elevated in ambient air within approximately 300-600
meters (about 1,000-2,000 feet) of major roadways. Highest
concentrations of most pollutants emitted directly by motor vehicles
are found at locations within 50 meters (about 165 feet) of the edge of
a roadway's traffic lanes.
    A recent large-scale review of air quality measurements in 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.\141\ These pollutants showed a large
reduction in concentrations within 100 meters downwind of the roadway.
Pollutants that showed more gradual reductions with distance from
roadways included benzene, NO2, PM2.5, and
PM10. In the review article, results varied based on the
method of statistical analysis used to determine the trend.
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    \141\ 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.
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    For pollutants with relatively high background concentrations
relative to near-road concentrations, detecting concentration gradients
can be difficult. For example, many aldehydes have high background
concentrations as a result of photochemical breakdown of precursors
from many different organic compounds. This can make detection of
gradients around roadways and other primary emission sources difficult.
However, several studies have measured aldehydes in multiple weather
conditions, and found higher concentrations of many carbonyls downwind
of roadways.142 143 These findings suggest a substantial
roadway source of these carbonyls.
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    \142\ Liu, W.; Zhang, J.; Kwon, J.l; et al. (2006).
Concentrations and source characteristics of airborne carbonyl
compounds measured outside urban residences. J Air Waste Manage
Assoc 56: 1196-1204.
    \143\ 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 http://dx.doi.org.
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    In the past 15 years, many studies have been published with results
showing 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.\144\ In
addition, numerous studies have found adverse health effects associated
with spending time in traffic, such as commuting or walking along high-
traffic roadways. 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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    \144\ In the widely-used PubMed database of health publications,
between January 1, 1990 and August 18, 2011, 605 publications
contained the keywords ``traffic, pollution, epidemiology,'' with
approximately half the studies published after 2007.
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    Numerous reviews of this body of health literature have been
published as well. In 2010, an expert panel of the Health Effects
Institute (HEI) published a review of hundreds of exposure,
epidemiology, and toxicology studies.\145\ The panel rated how the
evidence for each type of health outcome supported a conclusion of a
causal association with traffic-

associated air pollution as either ``sufficient,'' ``suggestive but not
sufficient,'' or ``inadequate and insufficient.'' The panel categorized
evidence of a causal association for exacerbation of childhood asthma
as ``sufficient.'' The panel categorized evidence of a causal
association for new onset asthma as between ``sufficient'' and as
``suggestive but not sufficient.'' ``Suggestive of a causal
association'' was how the panel categorized evidence linking traffic-
associated air pollutants with exacerbation of adult respiratory
symptoms and lung function decrement. It categorized as ``inadequate
and insufficient'' evidence of a causal relationship between traffic-
related air pollution and health care utilization for respiratory
problems, new onset adult asthma, chronic obstructive pulmonary disease
(COPD), nonasthmatic respiratory allergy, and cancer in adults and
children. Other literature reviews have been published with conclusions
similar to the HEI panel's.146 147 148 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).149 150 151 152
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    \145\ Health Effects Institute Panel on the Health Effects of
Traffic-Related Air Pollution. (2010). Traffic-related air
pollution: a critical review of the literature on emissions,
exposure, and health effects. HEI Special Report 17. Available at
http://www.healtheffects.org.
    \146\ Boothe, V.L.; Shendell, D.G. (2008). Potential health
effects associated with residential proximity to freeways and primay
roads: review of scientific literature, 1999-2006. J Environ Health
70: 33-41.
    \147\ 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.
    \148\ Raaschou-Nielsen, O.; Reynolds, P. (2006). Air pollution
and childhood cancer: a review of the epidemiological literature.
Int J Cancer 118: 2920-9.
    \149\ 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.
    \150\ Franco-Suglia, S.; Gryparis, A.; Wright, R.O.; et al.
(2007). Association of black carbon with cognition among children in
a prospective birth cohort study. Am J Epidemiol. doi: 10.1093/aje/
kwm308. [Online at http://dx.doi.org].
    \151\ 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.
    \152\ 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.
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    In addition to health outcomes, particularly cardiopulmonary
effects, conclusions of numerous studies suggest mechanisms by which
traffic-related air pollution affects health. Numerous studies indicate
that near-roadway exposures increase systemic inflammation, affecting
organ systems, including blood vessels and
lungs.153 154 155 156 Long-term exposures in near-road
environments have been associated with inflammation-associated
conditions, such as atherosclerosis and asthma.157 158 159
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    \153\ Riediker, M. (2007). Cardiovascular effects of fine
particulate matter components in highway patrol officers. Inhal
Toxicol 19: 99-105. doi: 10.1080/08958370701495238 Available at
http://dx.doi.org.
    \154\ Alexeef, S.E.; Coull, B.A.; Gryparis, A.; et al. (2011).
Medium-term exposure to traffic-related air pollution and markers of
inflammation and endothelial function. Environ Health Perspect 119:
481-486. doi:10.1289/ehp.1002560 Available at http://dx.doi.org.
    \155\ Eckel. S.P.; Berhane, K.; Salam, M.T.; et al. (2011).
Traffic-related pollution exposure and exhaled nitric oxide in the
Children's Health Study. Environ Health Perspect (IN PRESS).
doi:10.1289/ehp.1103516. Available at http://dx.doi.org.
    \156\ 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].
    \157\ Adar, S.D.; Klein, R.; Klein, E.K.; et al. (2010). Air
pollution and the microvasculatory: a cross-sectional assessment of
in vivo retinal images in the population-based Multi-Ethnic Study of
Atherosclerosis. PLoS Med 7(11): E1000372. doi:10.1371/
journal.pmed.1000372. Available at http://dx.doi.org.
    \158\ Kan, H.; Heiss, G.; Rose, K.M.; et al. (2008). Proxpective
analysis of traffic exposure as a risk factor for incident coronary
heart disease: the Atherosclerosis Risk in Communities (ARIC) study.
Environ Health Perspect 116: 1463-1468. doi:10.1289/ehp.11290.
Available at http://dx.doi.org.
    \159\ 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.160 161 162
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    \160\ 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 (In press)
    \161\ 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.
    \162\ 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. According to the 2009 American
Housing Survey, over 22 million homes (17.0 percent of all U.S. housing
units) were located within 300 feet of an airport, railroad, or highway
with four or more lanes. This corresponds to a population of more than
50 million U.S. residents in close proximity to high-traffic roadways
or other transportation sources. As discussed in Section III,
populations near major roads have higher fractions of minority
residents and lower socioeconomic status. Furthermore, on average,
Americans spend more than an hour traveling each day, bringing nearly
all residents into a high-exposure microenvironment for part of the
day.
    EPA continues to research near-road air quality, including the
types of pollutants found in high concentrations near major roads and
health problems associated with the mixture of pollutants near roads.
7. Environmental Impacts of Motor Vehicles and Fuels
a. Plant and Ecosystem Effects of Ozone
    Elevated ozone levels contribute to environmental effects, with
impacts to plants and ecosystems being of most concern. Ozone can
produce both acute and chronic injury in sensitive species depending on
the concentration level and the duration of the exposure. Ozone effects
also tend to accumulate over the growing season of the plant, so that
even low concentrations experienced for a longer duration have the
potential to create chronic stress on vegetation. Ozone damage to
plants includes visible injury to leaves and impaired photosynthesis,
both of which can lead to reduced plant growth and reproduction,
resulting in reduced crop yields, forestry production, and use of
sensitive ornamentals in landscaping. In addition, the impairment of
photosynthesis, the process by which the plant makes carbohydrates (its
source of energy and food), can lead to a subsequent reduction in root
growth and carbohydrate storage below ground, resulting in other, more
subtle plant and ecosystems impacts.
    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 forest
and other natural vegetation can potentially lead to species shifts and
loss from the affected ecosystems, resulting in a loss or reduction in
associated ecosystem goods and services. Lastly, 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. The final
2006 Ozone Air Quality Criteria Document presents more detailed
information on ozone effects on vegetation and ecosystems.

b. Visibility
    Visibility can be defined as the degree to which the atmosphere is
transparent to visible light.\163\ Visibility impairment is caused by
light scattering and absorption by suspended particles and gases.
Visibility is important because it has direct significance to people's
enjoyment of daily activities in all parts of the country. Individuals
value good visibility for the well-being it provides them directly,
where they live and work, and in places where they enjoy recreational
opportunities. Visibility is also highly valued in significant natural
areas, such as national parks and wilderness areas, and special
emphasis is given to protecting visibility in these areas. For more
information on visibility see the final 2009 PM ISA.\164\
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    \163\ 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 Web site at http://www.nap.edu/books/0309048443/html/.
    \164\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F.
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    EPA is pursuing a two-part strategy to address visibility
impairment. First, EPA developed the regional haze program which was
put in place in July 1999 to protect the visibility in Mandatory Class
I Federal areas.\165\ There are 156 national parks, forests and
wilderness areas categorized as Mandatory Class I Federal areas.\166\
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. Second, EPA has concluded that PM2.5 causes
adverse effects on visibility in other areas that are not protected by
the Regional Haze Rule, depending on PM2.5 concentrations
and other factors that control their visibility impact effectiveness
such as dry chemical composition and relative humidity (i.e., an
indicator of the water composition of the particles). EPA revised the
PM2.5 standards in December 2012 and established a target
level of protection that is expected to be met through attainment of
the existing secondary standards for PM2.5.
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    \165\ 64 FR 35714 (July 1, 1999).
    \166\ 62 FR 38680-38681 (July 18, 1997).
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i. Current Visibility Levels
    As mentioned in Section II.B.2.c, millions of people live in
nonattainment areas for the PM2.5 NAAQS. These populations,
as well as large numbers of individuals who travel to these areas, are
likely to experience visibility impairment. In addition, while
visibility trends have improved in mandatory class I federal areas, the
most recent data show that these areas continue to suffer from
visibility impairment. In summary, visibility impairment is experienced
throughout the U.S., in multi-state regions, urban areas, and remote
mandatory class I federal areas.
c. Atmospheric Deposition
    Wet and dry deposition of ambient particulate matter delivers a
complex mixture of metals (e.g., mercury, zinc, lead, nickel, aluminum,
cadmium), organic compounds (e.g., polycyclic organic matter, dioxins,
furans) and inorganic compounds (e.g., nitrate, sulfate) to terrestrial
and aquatic ecosystems. The chemical form of the compounds deposited
depends on a variety of factors including ambient conditions (e.g.,
temperature, humidity, oxidant levels) and the sources of the material.
Chemical and physical transformations of the compounds occur in the
atmosphere as well as the media onto which they deposit. These
transformations in turn influence the fate, bioavailability and
potential toxicity of these compounds. Atmospheric deposition has been
identified as a key component of the environmental and human health
hazard posed by several pollutants including mercury, dioxin and
PCBs.\167\
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    \167\ U.S. EPA. (2000). Deposition of Air Pollutants to the
Great Waters: Third Report to Congress. Office of Air Quality
Planning and Standards. EPA-453/R-00-0005.
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    Adverse impacts on water quality can occur when atmospheric
contaminants deposit to the water surface or when material deposited on
the land enters a waterbody through runoff. Potential impacts of
atmospheric deposition to waterbodies include those related to both
nutrient and toxic inputs. Adverse effects to human health and welfare
can occur from the addition of excess nitrogen via atmospheric
deposition. The nitrogen-nutrient enrichment contributes to toxic algae
blooms and zones of depleted oxygen, which can lead to fish kills,
frequently in coastal waters. Deposition of heavy metals or other
toxics may lead to the human ingestion of contaminated fish, impairment
of drinking water, damage to freshwater and marine ecosystem
components, and limits to recreational uses. Several studies have been
conducted in U.S. coastal waters and in the Great Lakes Region in which
the role of ambient PM deposition and runoff is
investigated.168 169 170 171 172
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    \168\ U.S. EPA. (2004). National Coastal Condition Report II.
Office of Research and Development/Office of Water. EPA-620/R-03/
002.
    \169\ Gao, Y., E.D. Nelson, M.P. Field, et al. (2002).
Characterization of atmospheric trace elements on PM2.5
particulate matter over the New York-New Jersey harbor estuary.
Atmos. Environ. 36: 1077-1086.
    \170\ Kim, G., N. Hussain, J.R. Scudlark, and T.M. Church.
(2000). Factors influencing the atmospheric depositional fluxes of
stable Pb, 210Pb, and 7Be into Chesapeake Bay. J. Atmos. Chem. 36:
65-79.
    \171\ Lu, R., R.P. Turco, K. Stolzenbach, et al. (2003). Dry
deposition of airborne trace metals on the Los Angeles Basin and
adjacent coastal waters. J. Geophys. Res. 108(D2, 4074): AAC 11-1 to
11-24.
    \172\ Marvin, C.H., M.N. Charlton, E.J. Reiner, et al. (2002).
Surficial sediment contamination in Lakes Erie and Ontario: A
comparative analysis. J. Great Lakes Res. 28(3): 437-450.
---------------------------------------------------------------------------

    Atmospheric deposition of nitrogen and sulfur contributes to
acidification, altering biogeochemistry and affecting animal and plant
life in terrestrial and aquatic ecosystems across the United States.
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 nutritional value of preferred prey species,
threatening biodiversity 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 include a
decline in sensitive forest tree species, such as red spruce (Picea
rubens) and sugar maple (Acer saccharum), and a loss of biodiversity of
fishes, zooplankton, and macro invertebrates.
    In addition to the role nitrogen deposition plays in acidification,
nitrogen deposition also leads to nutrient enrichment and altered
biogeochemical cycling. 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. For a broader
explanation of the topics treated here, refer to the description in
Section 6.3.2 of the RIA.
    Adverse impacts on soil chemistry and plant life have been observed
for areas heavily influenced by atmospheric

deposition of nutrients, metals and acid species, resulting in species
shifts, loss of biodiversity, forest decline, damage to forest
productivity and reductions in ecosystem services. Potential impacts
also include adverse effects to human health through ingestion of
contaminated vegetation or livestock (as in the case for dioxin
deposition), reduction in crop yield, and limited use of land due to
contamination.
    Atmospheric deposition of pollutants can reduce the aesthetic
appeal of buildings and culturally important articles through soiling,
and can contribute directly (or in conjunction with other pollutants)
to structural damage by means of corrosion or erosion. Atmospheric
deposition may affect materials principally by promoting and
accelerating the corrosion of metals, by degrading paints, and by
deteriorating building materials such as concrete and limestone.
Particles contribute to these effects because of their electrolytic,
hygroscopic, and acidic properties, and their ability to adsorb
corrosive gases (principally sulfur dioxide).
i. Current Nitrogen and Sulfur Deposition
    Over the past two decades, the EPA has undertaken numerous efforts
to reduce nitrogen and sulfur deposition across the U.S. Analyses of
long-term monitoring data for the U.S. show that deposition of both
nitrogen and sulfur compounds has decreased over the last 17 years. The
data show that reductions were more substantial for sulfur compounds
than for nitrogen compounds. In the eastern U.S., where data are most
abundant, total sulfur deposition decreased by about 44 percent between
1990 and 2007, while total nitrogen deposition decreased by 25 percent
over the same time frame.\173\ These numbers are generated by the U.S.
national monitoring network and they likely underestimate nitrogen
deposition because neither ammonia nor organic nitrogen is measured.
Although total nitrogen and sulfur deposition has decreased over time,
many areas continue to be negatively impacted by deposition. Deposition
of inorganic nitrogen and sulfur species routinely measured in the U.S.
between 2005 and 2007 were as high as 9.6 kilograms of nitrogen per
hectare (kg N/ha) averaged over three years and 20.8 kilograms of
sulfur per hectare (kg S/ha) averaged over three years.\174\
---------------------------------------------------------------------------

    \173\ U.S. EPA. (2012). U.S. EPA's Report on the Environment.
Data accessed online February 15, 2012 at: http://cfpub.epa.gov/eroe/index.cfm?fuseaction=detail.viewPDF&ch=46&lShowInd=0&subtop=341&lv=list.listByChapter&r=216610.
    \174\ U.S. EPA. (2012). U.S. EPA's Report on the Environment.
Data accessed online February 15, 2012 at: http://cfpub.epa.gov/eroe/index.cfm?fuseaction=detail.viewPDF&ch=46&lShowInd=0&subtop=341&lv=list.listByChapter&r=216610.
---------------------------------------------------------------------------

d. Environmental Effects of Air Toxics
    Emissions from producing, transporting and combusting fuel
contribute to ambient levels of pollutants that contribute to adverse
effects on vegetation. Volatile organic compounds, some of which are
considered air toxics, have long been suspected to play a role in
vegetation damage.\175\ In laboratory experiments, a wide range of
tolerance to VOCs has been observed.\176\ 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.\177\
---------------------------------------------------------------------------

    \175\ U.S. EPA. (1991). Effects of organic chemicals in the
atmosphere on terrestrial plants. EPA/600/3-91/001.
    \176\ 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.
    \177\ 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.
---------------------------------------------------------------------------

    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 nitrogen oxides.178 179 180
---------------------------------------------------------------------------

    \178\ Viskari E-L. (2000). Epicuticular wax of Norway spruce
needles as indicator of traffic pollutant deposition. Water, Air,
and Soil Pollut. 121:327-337.
    \179\ Ugrekhelidze D, F Korte, G Kvesitadze. (1997). Uptake and
transformation of benzene and toluene by plant leaves. Ecotox.
Environ. Safety 37:24-29.
    \180\ 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.
---------------------------------------------------------------------------

III. How would this proposal reduce emissions and air pollution?

A. Effects of the Proposed Vehicle and Fuel Changes on Mobile Source
Emissions

    The vehicle and fuel standards that EPA is proposing would
significantly reduce the tailpipe and evaporative emissions of light-
and heavy-duty vehicles in several ways, as described in this section.
In addition, the proposed gasoline sulfur standard would reduce
emissions of SO2 from existing gasoline-powered vehicles and
equipment. As described in Section II, all of these emission reductions
would in turn improve air quality nationwide and reduce the health
effects associated with air pollution from mobile sources.
    As with the Tier 2 program, EPA is proposing to implement closely-
coordinated requirements for both automakers and refiners in the same
rulemaking action. The proposed vehicle emission standards and gasoline
sulfur standards represent a ``systems approach'' to reducing vehicle-
related exhaust and evaporative emissions. By recognizing the
relationships among the various sources of emissions addressed by this
proposed rule, we have been able to integrate the provisions into a
single, coordinated program.
1. How do vehicles produce the emissions addressed in this proposal?
    The degree to which vehicles produce exhaust and evaporative
emissions depends on the design and functionality of the engine and the
associated exhaust and evaporative emission controls, in concert with
the properties of the fuel on which the vehicle is operating. In the
following paragraphs, we discuss how light- and heavy-duty vehicles
produce each of these types of emissions, both from the tailpipe and
from the fuel system.
a. Tailpipe (Exhaust) Emissions
    Which pollutants are emitted at the vehicle's tailpipe and their
quantities depend on how the fuel is combusted in the engine and how
the resulting gases are treated in the exhaust system. Historically,
much of tailpipe emission control has focused on hydrocarbon compounds
(HC) and NOX. The portion of hydrocarbons that is methane is
minimally reactive in forming ozone. Thus, for emission control
purposes, the focus is generally on non-methane hydrocarbons (NMHC),
which are also expressed as non-methane organic gases (NMOG) in order
to account for oxygenates (usually ethanol) now usually present in the
fuel.
    Tailpipe hydrocarbon emissions also include several toxic
pollutants, including benzene, acetaldehyde, and formaldehyde. To
varying degrees, the mass emissions of these pollutants are reduced
along with other hydrocarbons by the catalytic converter and improved
engine controls.

    Light- and heavy-duty gasoline vehicles also emit PM and CO. PM
forms directly as a combustion product (primarily as elemental carbon,
usually called soot) and also indirectly as semi-volatile hydrocarbon
compounds that form particles in the exhaust system or soon after
exiting the tailpipe. CO is a product of incomplete fuel combustion.
    When operating properly, modern exhaust emission controls
(centering on the catalytic convertor) can reduce much of the HC
(including toxics), NOX and CO exiting the engine. However,
tailpipe emissions are increased during periods of vehicle startup, as
catalytic convertors must warm up to be effective; during subsequent
operation due to the interference of sulfur in the gasoline; during
high load operating events, as the catalyst is overwhelmed or its
operation is modified to protect against permanent damage; and as a
vehicle ages, as the catalyst degrades in performance due to the
effects of high temperature operation and contaminants in the fuel and
lubricating oil.
b. Evaporative Emissions
    Gasoline vehicles also produce vapors in the fuel tank and fuel
system that can be released as evaporative emissions. These vapors are
primarily the lighter, more volatile hydrocarbon compounds in the
gasoline, which, like exhaust hydrocarbons, contribute to
concentrations of VOCs in the atmosphere.
    As discussed in Section IV below, vehicle evaporative (``evap'')
control systems are designed to block or capture vapors as they are
generated. Vapors are generated in the vehicle fuel tank and fuel
system (and released to the atmosphere if not adequately controlled) as
fuel heats up due to ambient temperature increase and/or vehicle
operation. Fuel vapors are also released when they permeate through
hose material, when they leak at connections or due to damaged
components, and during refueling events.
    In general, the evap emission controls on current vehicles (and
that would be improved under this proposed rule) consist of a canister
filled with activated charcoal and connected by hoses to the fuel
system. The hoses direct generated vapors to the canister, which
collects the vapors on the carbon and stores them until the system
experiences a ``purge'' event. During purge, the engine draws fresh air
through the canister, carrying vapors released by the carbon to the
engine to be combusted and restoring the capacity of the canister.
Evaporative emissions occur when vapors are emitted to the atmosphere
because the evap system is compromised, the carbon canister is
overwhelmed, or vapors permeate or leak. As such, evaporative emission
controls also involve proper material selection for fuel system
components, careful design of these components, and onboard diagnostics
to check the system for failure.
2. How would the proposed changes to gasoline sulfur content affect
vehicle emissions?
    Gasoline vehicles depend to a great degree on catalytic converters
to reduce levels of pollutants in their exhaust, including NMOG and
NOX, as well as PM (specifically, the volatile hydrocarbon
fraction), CO, and most air toxics. The presence of sulfur in gasoline
has a strong impact on these emissions, particularly NOX,
due to its impact on proper catalyst operation.
    Sulfur naturally occurs in crude oil and thus in gasoline. In
vehicle catalytic converters, the precious metals that catalyze the
reactions that convert the pollutants become significantly less
efficient when sulfur is deposited (adsorbed) onto them. The Tier 2
rulemaking required refiners to take steps to reduce sulfur levels in
gasoline by approximately 90 percent, to an average of 30 ppm. At the
time there were indications that sulfur reductions below 30 ppm may
continue to provide additional emission benefits. However, the data was
insufficient to quantify the benefits to the existing fleet, and the
Tier 2 vehicle standards could be achieved without lowering sulfur
further. As a result, to minimize the cost of the Tier 2 program, the
sulfur standard was not further reduced below 30 ppm.
    As discussed in Section IV.A.6, subsequent research provides a
compelling case that even this level of sulfur degrades the emission
performance of vehicles on the road today, and inhibits necessary
further reductions in vehicle emissions performance, which depend on
optimum catalyst performance to reach emission targets. A study
conducted by EPA and the auto industry in support of the Mobile Source
Air Toxics (MSAT) rule found significant reductions in NOX,
CO and total HC when nine Tier 2 vehicles were tested on low sulfur
fuel, relative to 32-ppm fuel.\181\ In particular, the study found a
nearly 50 percent increase in NOX when sulfur was increased
from 6 ppm to 32 ppm. Another recent study by Umicore showed reductions
of 41 percent for NOX and 17 percent for HC on a PZEV
operating on fuel with 33-ppm and 3-ppm fuel.\182\
---------------------------------------------------------------------------

    \181\ Regulatory Impact Analysis for the Control of Hazardous
Air Pollutants from Mobile Sources Final Rule, EPA 420-R-07-002,
Chapter 6.
    \182\ Ball D., Clark D., Moser D. (2011). Effects of Fuel Sulfur
on FTP NOx Emissions from a PZEV 4 Cylinder Application. SAE 2011
World Congress Paper 2011-01-0300.
---------------------------------------------------------------------------

    A larger study recently completed by EPA confirmed these results,
showing significant reductions in FTP-composite NOX (23
percent), CO (12 percent) and total HC (13 percent) on the 5-ppm fuel,
relative to 28-ppm fuel. For NOX, the majority of overall
reductions were driven by large reductions on warmed-up periods of the
test cycle (Bag 2), which showed a 59 percent reduction between 28 and
5-ppm fuel, consistent with the role of sulfur in catalyst degradation
discussed above. Applying individual bag reductions to in-use activity
patterns from EPA emission models suggests an overall NOX
reduction of nearly 40 percent on the road.
    Based on these studies, the benefits of the proposed Tier 3 sulfur
standard are significant in two ways: they enable vehicles designed to
the proposed Tier 3 tailpipe exhaust standards to meet these standards
for the duration of their useful life, and they facilitate immediate
emission reductions from all the vehicles on the road at the time the
sulfur controls are implemented.

B. How would emissions be reduced?

    The proposed standards would reduce emissions of VOC,
NOX (including NO2), direct PM2.5, CO,
SO2, and air toxics. The proposed sulfur standards would
reduce emissions from the on-road fleet immediately upon
implementation, so to reflect these early reductions, we present
emission reductions in calendar year 2017. The proposed vehicle
standards would begin to reduce emissions as the cleaner cars and
trucks begin to enter the fleet in model year 2017. The magnitude of
reduction would grow as more Tier 3 vehicles enter the fleet.
Therefore, we also present emission reductions in calendar year 2030,
when model year 2017 and later cars and trucks contribute nearly 90
percent of fleet-wide vehicle miles travelled. Although 2030 is the
farthest year that is feasible for air quality modeling, the full
reduction of the vehicle program would be realized after 2030, when the
fleet has fully turned over to Tier 3 vehicles. In Chapter 7 of the
RIA, we present emission reductions projected in 2050, as well as
additional calendar years between 2017 and 2030.
    Emission reductions are estimated on an annual basis, for all 50
U.S. states

plus the District of Columbia, Puerto Rico and the U.S. Virgin Islands.
The reductions were estimated using a version of EPA's MOVES model
updated for this analysis, as described in detail in Chapter 7 of the
RIA. This version of MOVES includes our most recent data on how vehicle
emissions are affected by changes in sulfur, ethanol, and other fuel
properties. We estimated emission reductions compared to a reference
case that assumed partial RFS2 implementation by 2017, with full
implementation in 2022 and beyond. The ethanol scenarios used for the
reference and control cases were the ``post-EPAct/EISA'' scenario
defined in Chapter 7 of the RIA, reflecting a mix of E10 and E15 in
2017, and E15 only in 2030. The reference case also assumed
continuation of the Tier 2 vehicle program indefinitely, and an average
sulfur level of 30 ppm (10 ppm in California).
    As discussed throughout this preamble, implementation of the
proposed Tier 3 standards is aligned with the 2017 LD GHG standards to
achieve significant criteria pollutant and GHG emissions reductions
while providing regulatory certainty and compliance efficiency to the
auto and oil industries. The 2017 LD GHG standards were still in a
preliminary state of development (pre-proposal) at the time we
finalized our assumptions for the Tier 3 emissions, air quality, and
cost analyses, so we were not able to reflect them in these analyses.
However, we continue to expect vehicle criteria pollutant performance
to be neutral under the GHG program, because exhaust and evaporative
emissions are not proportional to the amount of fuel burned; rather,
our standards are expressed on a per-mile basis, not on a per-gallon
basis. Vehicle criteria emissions are almost exclusively controlled by
a vehicle's emissions aftertreatment system and not by the efficiency
of the engine.
    The majority of the NMOG that is emitted from a gasoline engine is
generated during cold start, before the catalyst is lit off, and
NOX is often created during higher load operation.
Optimizing catalyst efficiency, minimizing thermal parasitics,
minimizing fuel system leaks, and lower gasoline sulfur will be key
enablers for all vehicles to meet the Tier 3 standards, regardless of
the vehicle's fuel efficiency. Because we do not expect the increase in
fuel efficiency to result in lower criteria pollutant emissions, we did
not claim in the 2017 LD GHG rule any reductions attributable to the
ability of vehicles to meet lower criteria emission levels (see 77 FR
62899-62901, October 15, 2012). In other words, in the 2017 LD GHG
rule, we assumed that, absent the proposed Tier 3 standards, the light-
duty fleet would continue to meet the Tier 2 standards. Thus, we
believe that the inclusion of the light-duty GHG standards in our cost
and benefit analyses for the proposed Tier 3 standards would have had
little or no impact on the results or our conclusions, as discussed in
Sections 7.1.2 and <IP_ADDRESS>.1 of the draft RIA. Nevertheless, for the
final rulemaking we will include the LD GHG requirements in the
analysis.
    The analysis described here does account for the following national
onroad rules:

 Tier 2 Motor Vehicle Emissions Standards and Gasoline Sulfur
Control Requirements (65 FR 6698, February 10, 2000)
 Heavy-Duty Engine and Vehicle Standards and Highway Diesel
Fuel Sulfur Control Requirements (66 FR 5002, January 18, 2001)
 Mobile Source Air Toxics Rule (72 FR 8428, February 26, 2007)
 Regulation of Fuels and Fuel Additives: Changes to Renewable
Fuel Standard Program (75 FR 14670, March 26, 2010)
 Light-Duty Vehicle Greenhouse Gas Emission Standards and
Corporate Average Fuel Economy Standards for 2012-2016 (75 FR 25324,
May 7, 2010)
The analysis also accounts for many other national rules and standards.
In addition, the modeling accounts for state and local rules including
local fuel standards, Inspection/Maintenance programs, Stage II
refueling controls, the National Low Emission Vehicle Program (NLEV),
and the section 177 states LEV and LEVII programs. See the Tier 3
emissions modeling TSD for more detail.

    A summary of emission reductions projected to result from Tier 3,
relative to the reference case, is shown in calendar years 2017 and
2030 for NOX, VOC, direct PM2.5, CO,
SO2, and total air toxics in Table III-1. For many
pollutants, the immediate reductions in 2017 are significant; for
example, combined NOX and VOC emissions would be reduced by
over 300,000 tons. By 2030, combined NOX and VOC emissions
would be reduced by roughly 750,000 tons, one quarter of the onroad
inventory. Many of the modeled air toxics would be significantly
reduced as well, including benzene, 1,3-butadiene, acetaldehyde,
acrolein and ethanol (ranging from 20 to nearly 40 percent of the
national onroad inventory by 2030). The relative reduction in overall
emissions would continue to increase beyond 2030 as more of the fleet
continues to turn over to Tier 3 vehicles; for example, by 2050, when
nearly all of the fleet would have turned over to Tier 3 standards, we
estimate the Tier 3 program would reduce onroad emissions of
NOX and VOC nearly 40 percent from the level of emissions
projected without Tier 3 controls.

                  Table III-1--Estimated Emission Reductions from the Proposed Tier 3 Standards
                                          [Annual U.S. short tons] \a\
----------------------------------------------------------------------------------------------------------------
                                                               2017                            2030
                                                ----------------------------------------------------------------
                                                                    Percent of                      Percent of
                                                      Tons            onroad           Tons           onroad
                                                                    inventory                        inventory
----------------------------------------------------------------------------------------------------------------
NOX............................................         284,381              8           524,790              28
VOC............................................          44,782              3           226,028              23
CO.............................................         746,683              4         5,765,362              30
Direct PM2.5...................................             121              0.1           7,458              10
Benzene........................................           1,625              4             8,582              36
SO2............................................          16,261             51            17,267              51
1,3-Butadiene..................................             322              5             1,087              37
Formaldehyde...................................             727              3             2,707              12
Acetaldehyde...................................             762              3             4,414              26
Acrolein.......................................              23              1               184              15

Ethanol........................................           2,684              2            27,821              24
----------------------------------------------------------------------------------------------------------------
\a\ This analysis assumed emissions reductions from the Tier 3 vehicle standards would occur in all states. For
  the final rule we will account for LEV III vehicle standards in states that have subsequently adopted it.

    Reductions for each pollutant are discussed in the following
sections, focusing on the contribution of program elements to the total
reductions summarized above.
1. NOX
    The proposed sulfur standards would significantly reduce
NOX emissions immediately upon implementation of the
program. As discussed above, recent research on the impact of sulfur on
Tier 2 technology vehicles shows the potential for significant
reductions in NOX emissions from the existing fleet of Tier
2 vehicles by lowering sulfur levels to 10 ppm. Prior research shows
that NOX emissions would also be expected to decrease from
the fleet of older (pre-Tier 2) light-duty vehicles as well as heavy-
duty gasoline vehicles,\183\ although at to a lesser extent than for
Tier 2 vehicles.
---------------------------------------------------------------------------

    \183\ Rao, V. (2001) Fuel Sulfur Effects on Exhaust Emissions:
Recommendations for MOBILE6, EPA420-R-01-039.
---------------------------------------------------------------------------

    Table III-2 shows the reduction in NOX emissions, in
annual short tons, projected in calendar years 2017 and 2030. The
reductions are split into those attributable to the introduction of low
sulfur fuel in the pre-Tier 3 fleet (defined for this analysis as model
years prior to 2017); and reductions attributable to vehicle standards
enabled by low sulfur fuel (model year 2017 and later). As shown, upon
implementation of the proposed sulfur standards, total onroad
NOX emissions are projected to drop 8 percent. This is
primarily due to large reductions from Tier 2 gasoline vehicles, which
contribute about one-quarter of the NOX emissions from the
on-road fleet in 2017. The relative reduction grows as cleaner vehicles
turn over into the fleet. By 2030, we project that the reduction in
overall onroad NOX inventory would be close to 30 percent.

        Table III-2--Projected NOX Reductions From Tier 3 Program
                         [Annual U.S. Tons] \a\
------------------------------------------------------------------------
                                               2017            2030
------------------------------------------------------------------------
Total reduction.........................         284,381         524,790
Reduction from pre-Tier 3 fleet due to           264,653          66,286
 sulfur standard........................
Reduction from Tier 3 fleet due to                19,728         458,504
 vehicle and sulfur standards...........
Percent reduction in onroad NOX                       8%             28%
 emissions..............................
------------------------------------------------------------------------
\a\ This analysis assumed emissions reductions from the Tier 3 vehicle
  standards would occur in all states. For the final rule we will
  account for LEV III vehicle standards in states that have subsequently
  adopted it.

2. VOC
    Table III-3 shows the reduction in VOC emissions, in annual short
tons, projected in calendar years 2017 and 2030 resulting from the
proposed standards. In 2017, as with NOX, we project
reductions from the pre-Tier 3 fleet with the proposed fuel standards.
By 2030 the reduction in overall onroad VOC emissions would be over 20
percent, the majority of this from the Tier 3 fleet. The proposed
evaporative standards are projected to account for roughly one quarter
of the overall vehicle program reduction in 2030.

        Table III-3--Projected VOC Reductions From Tier 3 Program
                         [Annual U.S. tons] \a\
------------------------------------------------------------------------
                                               2017            2030
------------------------------------------------------------------------
Total reduction.........................          44,782         226,028
Reduction from pre-Tier 3 fleet due to            39,561          13,739
 sulfur standard........................
Reduction from Tier 3 fleet due to                 5,222         212,289
 vehicle and sulfur standards...........
Exhaust.................................          41,433         168,264
Evaporative.............................           3,349          57,764
Percent reduction in onroad VOC                       3%             23%
 emissions..............................
------------------------------------------------------------------------
\a\ This analysis assumed emissions reductions from the Tier 3 vehicle
  standards would occur in all states. For the final rule we will
  account for LEV III vehicle standards in states that have subsequently
  adopted it.

3. CO
    Table III-4 shows the reductions for CO, broken down by pre- and
post-Tier 3 in the manner described for NOX and VOC above.
Based on research showing sizeable CO reductions from lower sulfur
fuel, the immediate reductions in the onroad fleet from sulfur control
are also significant. The CO exhaust standards are projected to reduce
onroad CO emissions 30 percent by 2030.

        Table III-4--Projected CO Reductions From Tier 3 Program
                           [Annual U.S. tons]
------------------------------------------------------------------------
                                               2017            2030
------------------------------------------------------------------------
Total reduction.........................         746,683       5,765,362
Reduction from pre-Tier 3 fleet due to           608,502         139,074
 sulfur standard........................
Reduction from Tier 3 fleet due to               138,181       5,626,288
 vehicle and sulfur standards...........
Percent reduction in onroad CO emissions              4%             30%
------------------------------------------------------------------------
\a\ This analysis assumed emissions reductions from the Tier 3 vehicle
  standards would occur in all states. For the final rule we will
  account for LEV III vehicle standards in states that have subsequently
  adopted it.

4. Direct PM2.5
    Reductions in direct emissions of PM2.5 are projected to
result solely from the proposed vehicle tailpipe standards, so
meaningful reductions are realized mainly as the fleet turns over. By
2030, we project a reduction of about 7,500 tons annually, which
represents approximately 10 percent of the onroad direct
PM2.5 inventory. However, since the PM standards are mainly
focused on improving engine durability through the end of a vehicle's
useful life, the relative reduction in onroad emissions is projected to
grow to 17 percent with full fleet turnover in 2050. Reductions in
NOX and VOC emissions would also reduce secondary PM
formation, which is quantified as part of the air quality analysis
described in Section III.C.
5. Air Toxics
    Emissions of air toxics also would be reduced by the proposed
sulfur, exhaust and evaporative standards. Air toxics are generally a
subset of compounds making up VOC, so the reduction trends tend to
track the VOC reductions presented above. Table III-5 presents
reductions for certain key air toxics, and Table III-6 presents
reductions for the sum of 71 different toxic compounds.

                            Table III-5--Reductions for Certain Individual Compounds
                                               [Annual U.S. tons]
----------------------------------------------------------------------------------------------------------------
                                                                      Percent                         Percent
                                                   Tons reduced    reduction in    Tons reduced    reduction in
                                                      in 2017         onroad          in 2030         onroad
                                                                     emissions                       emissions
----------------------------------------------------------------------------------------------------------------
Acetaldehyde....................................             762               3           4,414              26
Formaldehyde....................................             727               3           2,707              12
Acrolein........................................              23               1             184              15
1,3-Butadiene...................................             322               5           1,087              37
Benzene.........................................           1,625               4           8,581              36
Naphthalene.....................................              96               2             420              17
Ethanol.........................................           2,684               2          27,821              24
----------------------------------------------------------------------------------------------------------------
\a\ This analysis assumed emissions reductions from the Tier 3 vehicle standards would occur in all states. For
  the final rule we will account for LEV III vehicle standards in states that have subsequently adopted it.

    The totals shown in Table III-6 represent the sum of 71 species
including the toxics in Table III-5, 15 polycyclic aromatic hydrocarbon
(PAH) compounds in gas and particle phase, and additional gaseous
compounds such as toluene, xylenes, styrene, hexane, 2,2,4-
trimethylpentane, n-hexane, and propionaldehyde (Appendix 7A in the
draft RIA). As shown, in 2030 the overall onroad inventory of total
toxics would be reduced by over 20 percent, with nearly one third of
the vehicle program reductions coming from the proposed evaporative
standards.

        Table III-6--Reductions in Total Mobile Source Air Toxics
                           [Annual U.S. Tons]
------------------------------------------------------------------------
                                               2017            2030
------------------------------------------------------------------------
Total reduction.........................          15,156          89,685
Reduction from pre-Tier 3 fleet due to            12,452           5,022
 sulfur standard........................
Reduction from Tier 3 fleet due to                 2,683          84,663
 vehicle and sulfur standards...........
Exhaust.................................          13,748          64,144
Evaporative.............................           1,408          25,541
Percent reduction in onroad toxics                    3%            23%
 emissions..............................
------------------------------------------------------------------------
\a\ This analysis assumed emissions reductions from the Tier 3 vehicle
  standards would occur in all states. For the final rule we will
  account for LEV III vehicle standards in states that have subsequently
  adopted it.

6. SO2
    SO2 emissions from mobile sources are a direct function
of sulfur in the fuel, and reducing sulfur in gasoline would result in
immediate reductions in SO2 from the on and off-road fleet.
The reductions, shown in Table III-7, are a function of the sulfur
level and fuel consumption. This is reflected in the relative
contribution of on-road vehicles and off-road equipment, where off-road
gasoline consumption accounts for approximately 5 percent of overall
gasoline use.\184\
---------------------------------------------------------------------------

    \184\ U.S. Energy Information Administration (2011), Annual
Energy Outlook 2011, DOE/EIA-0383 (2011).

        Table III-7--Projected SO2 Reductions From Tier 3 Program
                           [Annual U.S. Tons]
------------------------------------------------------------------------
                                               2017            2030
------------------------------------------------------------------------
Total reduction.........................          16,261          17,267
Reduction from onroad vehicles due to             15,494          16,370
 sulfur standard........................
Reduction from off-road equipment due to             767             897
 sulfur standard........................
Percent reduction in onroad SO2                      51%             51%
 emissions..............................
------------------------------------------------------------------------

 7. Greenhouse Gases
    Reductions in nitrous oxide (N2O) emissions and methane
(CH4) emissions, both potent greenhouse gas emissions, are
projected for gasoline cars and trucks due to the proposed sulfur and
tailpipe standards. A study conducted by the University of California
at Riverside found a 29 percent reduction in N2O emissions
over the FTP when sulfur was reduced from 30 to 5 ppm,\185\ while EPA
research described in Section IV.A on sulfur effects found a 25 percent
reduction in CH4 emissions when sulfur was reduced from 28
to 5 ppm. Several studies have established correlations between
reductions in tailpipe NOX emissions and reductions in
N2O from gasoline cars and trucks,186 187 188 as
well as correlations between reductions in tailpipe HC emissions and
reductions in CH4.189 190 One such study
(Behrentz et al.) reported an N2O: NOX ratio of
0.095  0.035, and supported the application of
N2O: NOX ratios to NOX emissions as a
reasonable method for estimating N2O emission inventories.
As detailed in RIA Chapter 7.3, a range of N2O reductions is
bounded by applying this ratio to NOX reductions projected
for this proposal (from Table III-1), and applying the UC Riverside
sulfur results to MOVES N2O inventories for pre-Tier 3
vehicles. Using a 100-year global warming potential of 298 for
N2O according to the 2007 IPCC AR4,\191\ the range of
reductions calculated for N2O is from 2.9 to 7.3 million
metric tons of carbon dioxide equivalent (MMTCO2e) in 2017,
growing to 12.3 to 13.5 MMTCO2e in 2030. MOVES can be used
to directly estimate CH4 reductions from the sulfur and
vehicle standards, estimating an additional 0.1 MMTCO2e
reduction in 2017, growing to 0.5 MMTCO2e in 2030. The range of total
GHG reductions from the Tier 3 rule is 3.0 to 7.4 MMTCO2e in
2017, growing to 12.8 to 14.0 MMTCO2e in 2030.
---------------------------------------------------------------------------

    \185\ Huai, et al. (2004) Estimates of the emission rates of
nitrous oxide from light-duty vehicles using different chassis
dynamometer test cycles Atmospheric Environment 6621-6629.
    \186\ Michaels, H. (1998) Emissions of Nitrous Oxide from
Highway Mobile Sources, U.S. EPA EPA420-R-98-009.
    \187\ Behrentz, et al. (2004), Measurements of nitrous oxide
emissions from light-duty motor vehicles: a pilot study Atmospheric
Environment 4291-4303.
    \188\ Meffert, et. al (2000) Analysis of Nitrous Oxide Emissions
from Light Duty Passenger Cars, SAE 2000-01-1952.
    \189\ Meszler, D. (2004), Light Duty Vehicle Methane and Nitrous
Oxide Emissions: Greenhouse Gas Impacts Study for Northeast States
Center for a Clean Air Future.
    \190\ Graham, L. Greenhouse Gas Emissions from 1997-2005 Model
Year Light Duty Vehicles Environment Canada ERMD Report 04-
44.
    \191\ The global warming potentials (GWP) used in this rule are
consistent with the 100-year time frame values in the 2007
Intergovernmental Panel on Climate Change (IPCC) Fourth Assessment
Report (AR4). At this time, the 1996 IPCC Second Assessment Report
(SAR) 100-year GWP values are used in the official U.S. greenhouse
gas inventory submission to the United Nations Framework Convention
on Climate Change (per the reporting requirements under that
international convention, which were last updated in 2006).
N2O has a 100-year GWP of 298 and CH4 has a
100-year GWP of 25 according to the 2007 IPCC AR4.
---------------------------------------------------------------------------

    These reductions would be offset to some degree by CO2
emissions associated with higher energy use required in the process of
removing sulfur within the refinery. To assess the potential refinery
permitting implications of the Tier 3 proposal, we calculated the
CO2 emission impacts on a refinery-by-refinery basis. We
used the projected refinery-specific changes from our refinery-by-
refinery modeling (see Chapter 5 of the draft RIA) to estimate changes
in process energy and then applied emission factors that correspond to
those changes. The results showed an increase of up to 4.6
MMTCO2e in 2017 for all U.S. refineries complying with the
lower sulfur standards assuming that the proposed sulfur standards are
fully phased-in.\192\ The actual increase is expected to be
considerably lower, since this is a permitting analysis and refineries
will not be operating at their permit capacity. The actual increase
will also be a function of several factors, including technology
options selected by the refineries and the projected use of averaging,
banking and trading in avoiding the need for investments at some
refineries. As a result, 4.6 MMTCO2e represents an upper-
bound estimate of the possible increase in refinery CO2
emissions due to the need for additional process heat and hydrogen
production to enable the additional hydrotreating required.
---------------------------------------------------------------------------

    \192\ Keller, P. (February, 2013). New Source Review Permitting
Impact Analysis for Proposed Tier 3 Gasoline Program. Memorandum to
the docket.
---------------------------------------------------------------------------

    In 2017, the range of potential decrease in CH4 and
N2O emissions overlaps with the range of projected increase
in CO2 from refinery processes, suggesting that a net
increase or decrease in GHG emissions cannot be quantified with
certainty. However, we estimate the program would result in net GHG
reductions as the program continues into the future, as shown by our
2030 estimates.
    We do not expect the Tier 3 vehicle standards to result in any
discernible changes in vehicle CO2 emissions or fuel
economy. Emissions of the pollutants that we have designed the program
to address--NMOG, NOX, and PM--are not a function of the
amount of fuel consumed, since manufacturers need to design their
catalytic emission control systems to reduce these emissions regardless
of their engine-out levels. However, there may be some slight reduction
of vehicle mass if manufacturers explore lighter exhaust manifold
materials in order to reduce thermal mass and promote earlier catalyst
light-off. EPA invites comments on any potential impacts of the
proposed Tier 3 program on vehicle CO2 emissions and fuel
economy.

C. How would air pollution be reduced?

    Reductions in emissions of NOX, VOC, PM2.5
and air toxics expected as a result of the proposed Tier 3 standards
are projected to lead to significant decreases in ambient
concentrations of ozone, PM2.5, and air toxics. The results
of our air quality modeling of the impacts of the Tier 3 proposal are
summarized in the following section. The air quality modeling predicts
significant improvements in ozone concentrations due to the proposed
Tier 3 standards. Ambient PM2.5 and NO2
concentrations are also expected to improve as a result of the proposed
Tier 3 program. Decreases in ambient concentrations of air toxics are
projected with the proposed standards, including notable nationwide
reductions in benzene concentrations. Our air quality modeling also
predicts improvements in visibility and sulfur deposition, as well as
substantial decreases in nitrogen deposition as a result of the
proposed standards.
1. Ozone
    The air quality modeling done for this proposal projects that in
2017, with all current controls in effect but excluding the emissions
changes expected to occur as a result of this proposed action or any
other additional controls, at least 40 counties, with a projected
population of almost 50 million people, would have projected design
values above the level of the 2008 8-hour ozone standard of 75 ppb.
Even in 2030 the modeling projects that in the absence of additional
controls there would be 12 counties with a population of almost 32
million people with projected design values above the level of the 2008
8-hour ozone standard of 75 ppb. Since the emission changes from this
proposal go into effect during the period when some areas are still
working to attain the ozone NAAQS, the projected emission changes would
help state and local agencies in their effort to attain and maintain
the ozone standard.
    Air quality modeling indicates ozone design value concentrations
would decrease dramatically in many areas of the country as a result of
this action and in some places those decreases would be enough to
change the projected design values from being above the NAAQS to being
below the NAAQS. The decreases in ozone design values are likely due to
projected tailpipe reductions in NOX and VOCs from
reductions in fuel sulfur and engine controls.
    In 2017, the majority of the design value decreases are between 0.5
and 1.0 ppb. The projected population-weighted average design value
concentration without the proposed rule is 71.3 ppb in 2017. The
proposed rule would also reduce the projected ozone design values in
three counties from above the level of the standard to below. These
three counties are Bucks County in Pennsylvania, Arlington County in
Virginia and St Louis County in Missouri. The projected population in
these three counties in 2017 is almost 2 million people. In 2030, the
proposed rule would result in larger decreases in ozone design values,
with the majority of counties projecting decreases of between 1.0 and
1.5 ppb, and over 200 more counties with decreases greater than 1.5
ppb. The projected population-weighted average design value
concentration without the proposed rule is 66.7 ppb in 2030. There are
also two more counties whose projected design values would be reduced
from above the level of the ozone standard to below by the proposed
rule in 2030. These counties are Hudson County in New Jersey and
Brazoria County in Texas. The projected population in these two
counties in 2030 is over 1 million people.
    Table III-8 and Table III-9 show the average change in 2017 and
2030 8-hour ozone design values for: (1) All counties with 2005
baseline design values, (2) counties with 2005 baseline design values
that exceeded the 2008 ozone standard, (3) counties with 2005 baseline
design values that did not exceed the 2008 standard, but were within 10
percent of it, (4) counties with 2017/2030 design values that exceeded
the 2008 ozone standard, and (5) counties with 2017/2030 design values
that did not exceed the standard, but were within 10 percent of it.
Counties within 10 percent of the standard are intended to reflect
counties that although not violating the standards, will also be
impacted by changes in ozone as they work to ensure long-term
maintenance of the ozone NAAQS. All of these metrics show a decrease in
2017 and 2030, indicating in five different ways the overall
improvement in air quality.
    On a population-weighted basis, the average modeled future-year 8-
hour ozone design values are projected to decrease by 0.47 ppb in 2017
and 1.55 ppb in 2030. On a population-weighted basis design values in
those counties that are projected to be above the 2008 ozone standard
in 2017 and 2030 are projected to decrease by 0.30 and 1.62 ppb
respectively due to the proposed standards.

                 Table III-8--Average Change in Projected 8-Hour Ozone Design Value in 2017 \c\
----------------------------------------------------------------------------------------------------------------
                                                                                Change in 2017
                           Average \a\                            Number of U.S.       2020        design value
                                                                     counties     population \b\       (ppb)
----------------------------------------------------------------------------------------------------------------
All.............................................................             676     238,026,106           -0.50
All, population-weighted........................................  ..............  ..............           -0.47
Counties whose 2005 base year is violating the 2008 8-hour ozone             393     176,910,535           -0.56
 standard.......................................................
Counties whose 2005 base year is violating the 2008 8-hour ozone  ..............  ..............           -0.51
 standard, population-weighted..................................
Counties whose 2005 base year is within 10 percent of the 2008 8-            201      40,516,171           -0.47
 hour ozone standard............................................
Counties whose 2005 base year is within 10 percent of the 2008 8- ..............  ..............           -0.42
 hour ozone standard, population-weighted.......................
Counties whose 2017 control case is violating the 2008 8-hour                 37      47,659,433           -0.35
 ozone standard.................................................
Counties whose 2017 control case is violating the 2008 8-hour     ..............  ..............           -0.30
 ozone standard, population-weighted............................
Counties whose 2017 control case is within 10 percent of the                 124      68,625,934           -0.51
 2008 8-hour ozone standard.....................................
Counties whose 2017 control case is within 10 percent of the      ..............  ..............           -0.49
 2008 8-hour ozone standard, population-weighted................
----------------------------------------------------------------------------------------------------------------
\a\ Averages are over counties with 2005 modeled design values.
\b\ Population numbers based on Woods & Poole data. Woods & Poole Economics, Inc. 2001. Population by Single
  Year of Age CD.
\c\ This analysis assumed emissions reductions from Tier 3 vehicle standards would occur in all states and did
  not account for emission reductions associated with LEV III vehicle standards in California and other states
  that have subsequently adopted it. The analysis for the final rule will account for LEV III vehicle standards.

                 Table III-9--Average Change in Projected 8-Hour Ozone Design Value in 2030 \c\
----------------------------------------------------------------------------------------------------------------
                                                                                Change in 2030
                           Average\a\                             Number of U.S.       2030        design value
                                                                     counties     population \b\       (ppb)
----------------------------------------------------------------------------------------------------------------
All.............................................................             676     261,497,900           -1.35
All, population-weighted........................................  ..............  ..............           -1.55
Counties whose 2005 base year is violating the 2008 8-hour ozone             393     194,118,748           -1.54
 standard.......................................................
Counties whose 2005 base year is violating the 2008 8-hour ozone  ..............  ..............           -1.69
 standard, population-weighted..................................
Counties whose 2005 base year is within 10 percent of the 2008 8-            201      44,436,103           -1.18
 hour ozone standard............................................
Counties whose 2005 base year is within 10 percent of the 2008 8- ..............  ..............           -1.25
 hour ozone standard, population-weighted.......................
Counties whose 2030 control case is violating the 2008 8-hour                 10      30,619,714           -1.49
 ozone standard.................................................
Counties whose 2030 control case is violating the 2008 8-hour     ..............  ..............           -1.62
 ozone standard, population-weighted............................
Counties whose 2030 control case is within 10 percent of the                  40      21,541,863           -1.37
 2008 8-hour ozone standard.....................................
Counties whose 2030 control case is within 10 percent of the      ..............  ..............           -1.50
 2008 8-hour ozone standard, population-weighted................
----------------------------------------------------------------------------------------------------------------
\a\ Averages are over counties with 2005 modeled design values.
\b\ Population numbers based on Woods & Poole data. Woods & Poole Economics, Inc. 2001. Population by Single
  Year of Age CD.
\c\ This analysis assumed emissions reductions from Tier 3 vehicle standards would occur in all states and did
  not account for emission reductions associated with LEV III vehicle standards in California and other states
  that have subsequently adopted it. The analysis for the final rule will account for LEV III vehicle standards.

2. Particulate Matter
    The air quality modeling conducted for this proposal projects that
in 2030, with all current controls in effect but excluding the
emissions changes expected to occur as a result of this proposal or any
other additional controls, at least 14 counties, with a projected
population of over 28 million people, would have projected design
values above the level of the annual standard of 12 [micro]g/
m3 and at least 21 counties, with a projected population of
over 31 million people, would have projected design values above the
level of the 24-hour standard of 35 [mu]g/m3. \193\ Since
the emission changes from this proposed action would go into effect
during the period when some areas are still working to attain the
PM2.5 NAAQS, the projected emission changes would be useful
to state and local agencies in their effort to attain and maintain the
PM2.5 standard.
---------------------------------------------------------------------------

    \193\ The projections from the modeling analysis for the Tier 3
proposal differ from what was presented in the recent PM NAAQS RIA
(http://www.epa.gov/pm/actions.html). The differences in modeling
between the analyses stem primarily from the difference in modeling
platform and the different years being evaluated (2020 vs. 2030).
---------------------------------------------------------------------------

    The proposed rule would reduce 24-hour and annual PM2.5
design values in 2030. Annual PM2.5 design values in the
majority of modeled counties would decrease by between 0.01 and 0.05
[micro]g/m3 and in over 100 additional counties design
values are projected to decrease by greater than 0.05 [mu]g/
m3. The projected population-weighted average design value
concentration without the proposed rule is 9.5 [micro]g/m3
in 2030. The average modeled future-year annual PM2.5 design
values in 2030 decrease by 0.06 [micro]g/m3 on a population-
weighted basis. Design values in those counties that are projected to
be above the annual PM2.5 standard in 2030 decrease even
more, by 0.11 [micro]g/m\3\ on a population-weighted basis, due to the
proposed standards. In addition, the average modeled future-year 24-
hour PM2.5 design values in 2030 decrease by 0.20 [micro]g/
m3 on a population-weighted basis. The projected population-
weighted average design value concentration without the proposed rule
is 24.3 [micro]g/m3 in 2030. The decreases in
PM2.5 design values are likely due to the projected tailpipe
reductions in primary PM2.5, NOX and VOCs. The
proposed rule has little impact on PM2.5 design values for
the majority of counties in 2017, although our air quality modeling
underestimated the PM decreases that would result from this proposal
(see Section <IP_ADDRESS> of the draft RIA for more detail).
    Table III-10 and Table III-11 present the average change in 2030
annual and 24-hour PM2.5 design values for: (1) All counties
with 2005 baseline design values, (2) counties with 2005 baseline
design values that exceeded the PM2.5 standard, (3) counties
with 2005 baseline design values that did not exceed the standard, but
were within 10 percent of it, (4) counties with 2030 design values that
exceeded the PM2.5 standard, and (5) counties with 2030
design values that did not exceed the standard, but were within 10
percent of it. Counties within 10 percent of the standard are intended
to reflect counties that although not violating the standards, will
also be impacted by changes in PM2.5 as they work to ensure
long-term maintenance of the annual and/or 24-hour PM2.5
NAAQS. All of these metrics show a decrease in 2030. On a population-
weighted basis, there is a 0.06 [micro]g/m3 decrease in the
average modeled future-year annual PM2.5 design values in
2030 and a decrease of 0.11 [micro]g/m\3\ in those counties that are
projected to be above the annual PM2.5 standard in 2030. In
addition, the average population-weighted modeled future-year 24-hour
PM2.5 design values are projected to decrease by 0.20
[micro]g/m3 due to the proposed standards and design values
in those counties that are projected to be above the 24-hour
PM2.5 standard in 2030 would decrease by 0.32 [micro]g/
m3.

                Table III-10--Average Change in Projected Annual PM2.5 Design Values in 2030 \c\
----------------------------------------------------------------------------------------------------------------
                                                                                Change in 2030
                           Average \a\                            Number of U.S.       2030        design value
                                                                     counties       Population     ([mu]g/m\3\)
----------------------------------------------------------------------------------------------------------------
All.............................................................             576     247,415,381           -0.05

All, population-weighted........................................  ..............  ..............           -0.06
Counties whose 2005 base year is violating the annual PM2.5                  314     152,109,569           -0.05
 standard.......................................................
Counties whose 2005 base year is violating the annual PM2.5       ..............  ..............           -0.07
 standard, population-weighted..................................
Counties whose 2005 base year is within 10 percent of the annual              83      31,863,376           -0.05
 PM2.5 standard.................................................
Counties whose 2005 base year is within 10 percent of the annual  ..............  ..............           -0.05
 PM2.5 standard, population-weighted............................
Counties whose 2030 control case is violating the annual PM2.5                14      28,624,758           -0.11
 standard \d\...................................................
Counties whose 2030 control case is violating the annual PM2.5    ..............  ..............           -0.10
 standard, population-weighted \d\..............................
Counties whose 2030 control case is within 10 percent of the                  28      23,840,272           -0.07
 annual PM2.5 standard..........................................