evidence. This framework employs a five-level hierarchy that
classifies the overall weight of evidence and causality using the
following categorizations: causal relationship, likely to be causal
relationship, suggestive of a causal relationship, inadequate to
infer a causal relationship, and not likely to be a causal
relationship (U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Table 1-3).
    \43\ 78 FR 3086 (January 15, 2013), pages 3103-3104.
    \44\ 77 FR 38890 (June 29, 2012), pages 38906-38911.
---------------------------------------------------------------------------

    The EPA concludes that a causal relationship exists between both
long-

and short-term exposures to PM2.5 and premature mortality
and cardiovascular effects and a likely causal relationship exists
between long- and short-term PM2.5 exposures and respiratory
effects. Further, there is evidence suggestive of a causal relationship
between long-term PM2.5 exposures and other health effects,
including developmental and reproductive effects (e.g., low birth
weight, infant mortality) and carcinogenic, mutagenic, and genotoxic
effects (e.g., lung cancer mortality).\45\
---------------------------------------------------------------------------

    \45\ These causal inferences are based not only on the more
expansive epidemiological evidence available in this review but also
reflect consideration of important progress that has been made to
advance our understanding of a number of potential biologic modes of
action or pathways for PM-related cardiovascular and respiratory
effects (U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, chapter 5).
---------------------------------------------------------------------------

    As summarized in the Final PM NAAQS rule, and discussed extensively
in the 2009 PM ISA, the scientific evidence available since the
completion of the 2006 PM NAAQS review significantly strengthens the
link between long- and short-term exposure to PM2.5 and
premature mortality, while providing indications that the magnitude of
the PM2.5- mortality association with long-term exposures
may be larger than previously estimated.46 47 The strongest
evidence comes from recent studies investigating long-term exposure to
PM2.5 and cardiovascular-related mortality. The evidence
supporting a causal relationship between long-term PM2.5
exposure and mortality also includes consideration of new studies that
demonstrated an improvement in community health following reductions in
ambient fine particles.
---------------------------------------------------------------------------

    \46\ 78 FR 3103-3104 (January 15, 2013).
    \47\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, chapter 6 (Section 6.5)
and chapter 7 (Section 7.6).
---------------------------------------------------------------------------

    Several studies evaluated in the 2009 PM ISA have examined the
association between cardiovascular effects and long-term
PM2.5 exposures in multi-city studies conducted in the U.S.
and Europe. While studies were not available in the 2006 PM NAAQS
review with regard to long-term exposure and cardiovascular-related
morbidity, studies published since then have provided new evidence
linking long-term exposure to PM2.5 with an array of
cardiovascular effects such as heart attacks, congestive heart failure,
stroke, and mortality. This evidence is coherent with studies of short-
term exposure to PM2.5 that have observed associations with
a continuum of effects ranging from subtle changes in indicators of
cardiovascular health to serious clinical events, such as increased
hospitalizations and emergency department visits due to cardiovascular
disease and cardiovascular mortality.\48\
---------------------------------------------------------------------------

    \48\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, chapter 2 (section 2.3.1
and 2.3.2) and chapter 6.
---------------------------------------------------------------------------

    As detailed in the 2009 PM ISA, extended analyses of studies
available in the 2006 PM NAAQS review as well as epidemiological
studies conducted in the U.S. and abroad published since then provide
stronger evidence of respiratory-related morbidity effects associated
with long-term PM2.5 exposure. The strongest evidence for
respiratory-related effects is from studies that evaluated decrements
in lung function growth (in children), increased respiratory symptoms,
and asthma development. The strongest evidence from short-term
PM2.5 exposure studies has been observed for increased
respiratory-related emergency department visits and hospital admissions
for chronic obstructive pulmonary disease (COPD) and respiratory
infections.\49\
---------------------------------------------------------------------------

    \49\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, chapter 2 (section 2.3.1
and 2.3.2) and chapter 6.
---------------------------------------------------------------------------

    The body of scientific evidence detailed in the 2009 PM ISA is
still limited with respect to associations between long-term
PM2.5 exposures and developmental and reproductive effects
as well as cancer, mutagenic, and genotoxic effects, but is somewhat
expanded from the 2006 review. The strongest evidence for an
association between PM2.5 and developmental and reproductive
effects comes from epidemiological studies of low birth weight and
infant mortality, especially due to respiratory causes during the post-
neonatal period (i.e., 1 month to 12 months of age).\50\ With regard to
cancer effects, ``[m]ultiple epidemiologic studies have shown a
consistent positive association between PM2.5 and lung
cancer mortality, but studies have generally not reported associations
between PM2.5 and lung cancer incidence.'' \51\
---------------------------------------------------------------------------

    \50\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, chapter 2 (section 2.3.1
and 2.3.2) and chapter 7.
    \51\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. pg 2-13.
---------------------------------------------------------------------------

    Specific groups within the general population are at increased risk
for experiencing adverse health effects related to PM
exposures.52 53 54 55 The evidence detailed in the 2009 PM
ISA expands our understanding of previously identified at-risk
populations and lifestages (i.e., children, older adults, and
individuals with pre-existing heart and lung disease) and supports the
identification of additional at-risk populations (e.g., persons with
lower socioeconomic status, genetic differences). Additionally, there
is emerging, though still limited, evidence for additional potentially
at-risk populations and lifestages, such as those with diabetes, people
who are obese, pregnant women, and the developing fetus.\56\
---------------------------------------------------------------------------

    \52\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Chapter 8 and Chapter 2.
    \53\ 77 FR 38890 (June 29, 2012).
    \54\ 78 FR 3104 (January 15, 2013).
    \55\ U.S. EPA. (2011). Policy Assessment for the Review of the
PM NAAQS. U.S. Environmental Protection Agency, Washington, DC, EPA/
452/R-11-003. section 2.2.1.
    \56\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Chapter 8 and Chapter 2
(Section 2.4.1).
---------------------------------------------------------------------------

    For PM10-2.5, the 2009 PM ISA concluded that available
evidence was suggestive of a causal relationship between short-term
exposures to PM10-2.5 and cardiovascular effects (e.g.,
hospital admissions and ED visits, changes in cardiovascular function),
respiratory effects (e.g, ED visits and hospital admissions, increase
in markers of pulmonary inflammation), and premature mortality. Data
were inadequate to draw conclusions regarding the relationships between
long-term exposure to PM10-2.5 and various health
effects.57 58 59
---------------------------------------------------------------------------

    \57\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Section 2.3.4 and Table
2-6.
    \58\ 78 FR 3167-8 (January 15, 2013).
    \59\ 77 FR 38947-51 (June 29, 2012).
---------------------------------------------------------------------------

    For ultrafine particles, the 2009 PM ISA concluded that the
evidence was suggestive of a causal relationship between short-term
exposures and cardiovascular effects, including changes in heart rhythm
and vasomotor function (the ability of blood vessels to expand and
contract). It also concluded that there was evidence suggestive of a
causal relationship between short-term exposure to ultrafine particles
and respiratory effects, including lung function and pulmonary
inflammation,

with limited and inconsistent evidence for increases in ED visits and
hospital admissions. Data were inadequate to draw conclusions regarding
the relationship between short-term exposure to ultrafine particle and
additional health effects including premature mortality as well as
long-term exposure to ultrafine particles and all health outcomes
evaluated.60 61
---------------------------------------------------------------------------

    \60\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F. Section 2.3.5 and Table
2-6.
    \61\ 78 FR 3121 (January 15, 2013).
---------------------------------------------------------------------------

c. Current and Projected Concentrations of PM2.5
    There are two primary NAAQS for PM2.5: an annual
standard (12.0 micrograms per cubic meter ([mu]g/m\3\)) and a 24-hour
standard (35 [mu]g/m\3\), and two secondary NAAQS for PM2.5:
an annual standard (15.0 [mu]g/m\3\) and a 24-hour standard (35 [mu]g/
m\3\). The initial PM2.5 standards were set in 1997 and
revisions to the standards were finalized in 2006 and in December 2012.
The December 2012 rule revised the level of the primary annual
PM2.5 standard from 15.0 [mu]g/m\3\ to 12.0 [mu]g/m\3\.\62\
---------------------------------------------------------------------------

    \62\ U.S. EPA (2012). National Ambient Air Quality Standards for
Particulate Matter. http://www.epa.gov/PM/2012/finalrule.pdf. 78 FR
3164.
---------------------------------------------------------------------------

    There are many areas of the country that are currently in
nonattainment for the annual and 24-hour PM2.5 NAAQS. Our
modeling without the Tier 3 controls projects that in the future we
will continue to have many areas that will have ambient
PM2.5 concentrations above the level of the NAAQS (see
Section III.C.2). States will need to meet the 2006 24-hour standards
in the 2015-2019 timeframe and the 2012 primary annual standard in the
2021-2025 timeframe. The emission reductions and improvements in
ambient PM2.5 concentrations from this action, which will
take effect starting in 2017, will be helpful to states as they work to
attain and maintain the PM2.5 NAAQS.
    In 2005 the EPA designated 39 nonattainment areas for the 1997
PM2.5 NAAQS.\63\ As of December 5, 2013, over 68 million
people lived in the 24 areas that are still designated as nonattainment
for the 1997 annual PM2.5 NAAQS. These PM2.5
nonattainment areas are comprised of 135 full or partial counties. EPA
anticipates making initial area designation decisions for the 2012
primary annual PM2.5 NAAQS in December 2014, with those
designations likely becoming effective in early 2015.\64\ On November
13, 2009 and February 3, 2011, the EPA designated 32 nonattainment
areas for the 2006 24-hour PM2.5 NAAQS.\65\ As of December
5, 2013, 28 of these areas remain designated as nonattainment, and they
are composed of 104 full or partial counties with a population of over
65 million. In total, there are currently 39 PM2.5
nonattainment areas with a population of over 84 million people.\66\
---------------------------------------------------------------------------

    \63\ 70 FR 19844 (April 14, 2005).
    \64\ U.S. EPA (2012). Fact Sheet: Implementing the Standards.
http://www.epa.gov/airquality/particlepollution/2012/decfsimp.pdf.
    \65\ 74 FR 58688 (November 13, 2009) and 76 FR 6056 (February 3,
2011).
    \66\ Data come from Summary Nonattainment Area Population
Exposure Report, current as of July 31, 2013 at: http://www.epa.gov/oar/oaqps/greenbk/popexp.html and contained in Docket EPA-HQ-OAR-
2011-0135.
---------------------------------------------------------------------------

    States with PM2.5 nonattainment areas will be required
to take action to bring those areas into attainment in the future.
Designated nonattainment areas not currently attaining the 1997 annual
PM2.5 NAAQS are required to attain the NAAQS by 2015 and
will be required to maintain the 1997 annual PM2.5 NAAQS
thereafter. The 2006 24-hour PM2.5 nonattainment areas are
required to attain the 2006 24-hour PM2.5 NAAQS in the 2015
to 2019 time frame and will be required to maintain the 2006 24-hour
PM2.5 NAAQS thereafter. Areas to be designated nonattainment
for the 2012 primary annual PM2.5 NAAQS will likely be
required to attain the 2012 NAAQS in the 2021 to 2025 time frame. The
Tier 3 standards finalized here begin taking effect in 2017.
    The EPA has already adopted many mobile source emission control
programs that are expected to reduce ambient PM concentrations. As a
result of these and other federal, state and local programs, the number
of areas that fail to meet the PM2.5 NAAQS in the future is
expected to decrease. However, even with the implementation of all
current state and federal regulations, there are projected to be
counties violating the PM2.5 NAAQS well into the future.
Thus additional federal control programs, such as Tier 3, can assist
areas with attainment dates in 2017 and beyond in attaining the NAAQS
as expeditiously as practicable and may relieve areas with already
stringent local regulations from some of the burden associated with
adopting additional local controls.
d. Current Concentrations of PM10
    In the December 2012 action in which the EPA promulgated the
revised primary annual PM2.5 NAAQS, the EPA also retained
the existing primary and secondary 24-hour PM10 standards at
150 [micro]g/m\3\. As of December 5, 2013, over 11 million people live
in the 40 areas that are designated as nonattainment for the
PM10 NAAQS. There are 33 full or partial counties that make
up the PM10 nonattainment areas.
3. Oxides of Nitrogen and Sulfur
a. Background
    Nitrogen dioxide (NO2) is a member of the NOX
family of gases. Most NO2 is formed in the air through the
oxidation of nitric oxide (NO) emitted when fuel is burned at a high
temperature. Sulfur dioxide (SO2), a member of the sulfur
oxide (SOX) family of gases, is formed from burning fuels
containing sulfur (e.g., coal or oil derived), extracting gasoline from
oil, or extracting metals from ore.
    SO2 and NO2 and their gas phase oxidation
products can dissolve in water droplets and further oxidize to form
sulfuric and nitric acid which react with ammonia to form sulfates and
nitrates, both of which are important components of ambient PM. The
health effects of ambient PM are discussed in Section II.B.2.b of this
preamble. NOX and VOC are the two major precursors of ozone.
The health effects of ozone are covered in Section II.B.2.1.b.
b. Health Effects of NO2
    The most recent review of the health effects of oxides of nitrogen
completed by the EPA can be found in the 2008 Integrated Science
Assessment for Nitrogen Oxides (NOX ISA).\67\ The EPA
concluded that the findings of epidemiologic, controlled human
exposure, and animal toxicological studies provide evidence that is
sufficient to infer a likely causal relationship between respiratory
effects and short-term NO2 exposure. The 2008 NOX
ISA concluded that the strongest evidence for such a relationship comes
from epidemiologic studies of respiratory effects including increased
respiratory symptoms, emergency department visits, and hospital
admissions. Based on both short- and long-term exposure studies, the
2008 NOX ISA concluded that individuals with preexisting
pulmonary conditions (e.g., asthma or COPD), children, and older adults
are potentially at greater risk of NO2-related respiratory
effects. Based on findings from controlled human exposure studies, the
2008 NOX ISA also drew two broad conclusions regarding
airway responsiveness following NO2 exposure. First, the
NOX

ISA concluded that NO2 exposure may enhance the sensitivity
to allergen-induced decrements in lung function and increase the
allergen-induced airway inflammatory response following 30-minute
exposures of asthmatic adults to NO2 concentrations as low
as 260 ppb. Second, exposure to NO2 has been found to
enhance the inherent responsiveness of the airway to subsequent
nonspecific challenges in controlled human exposure studies of healthy
and asthmatic adults. Small but statistically significant increases in
nonspecific airway hyperresponsiveness were reported for asthmatic
adults following 30-minute exposures to 200-300 ppb NO2 and
following 1-hour exposures of asthmatics to 100 ppb NO2.
Enhanced airway responsiveness could have important clinical
implications for asthmatics since transient increases in airway
responsiveness following NO2 exposure have the potential to
increase symptoms and worsen asthma control. Together, the
epidemiologic and experimental data sets form a plausible, consistent,
and coherent description of a relationship between NO2
exposures and an array of adverse health effects that range from the
onset of respiratory symptoms to hospital admission.
---------------------------------------------------------------------------

    \67\ U.S. EPA (2008). Integrated Science Assessment for Oxides
of Nitrogen--Health Criteria (Final Report). EPA/600/R-08/071.
Washington, DC: U.S.EPA.
---------------------------------------------------------------------------

    In evaluating a broader range of health effects, the 2008
NOX ISA concluded evidence was ``suggestive but not
sufficient to infer a causal relationship'' between short-term
NO2 exposure and premature mortality and between long-term
NO2 exposure and respiratory effects. The latter was based
largely on associations observed between long-term NO2
exposure and decreases in lung function growth in children.
Furthermore, the 2008 NOX ISA concluded that evidence was
``inadequate to infer the presence or absence of a causal
relationship'' between short-term NO2 exposure and
cardiovascular effects as well as between long-term NO2
exposure and cardiovascular effects, reproductive and developmental
effects, premature mortality, and cancer.\68\ The conclusions for these
health effect categories were informed by uncertainties in the evidence
base such as the independent effects of NO2 exposure within
the broader mixture of traffic-related pollutants, limited evidence
from experimental studies, and/or an overall limited literature base.
---------------------------------------------------------------------------

    \68\ U.S. EPA (2008). Integrated Science Assessment for Oxides
of Nitrogen--Health Criteria (Final Report). EPA/600/R-08/071.
Washington, DC: U.S.EPA.
---------------------------------------------------------------------------

c. Health Effects of SO2
    Information on the health effects of SO2 can be found in
the 2008 Integrated Science Assessment for Sulfur Oxides
(SO2 ISA).\69\ Short-term peaks of SO2 have long
been known to cause adverse respiratory health effects, particularly
among individuals with asthma. In addition to those with asthma (both
children and adults), potentially sensitive groups include all children
and the elderly. During periods of elevated ventilation, asthmatics may
experience symptomatic bronchoconstriction within minutes of exposure.
Following an extensive evaluation of health evidence from epidemiologic
and laboratory studies, the EPA concluded that there is a causal
relationship between respiratory health effects and short-term exposure
to SO2. Separately, based on an evaluation of the
epidemiologic evidence of associations between short-term exposure to
SO2 and mortality, the EPA concluded that the overall
evidence is suggestive of a causal relationship between short-term
exposure to SO2 and mortality.
---------------------------------------------------------------------------

    \69\ 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.
---------------------------------------------------------------------------

d. Current Concentrations of NO2
    The EPA most recently completed a review of the primary NAAQS for
NO2 in January 2010. There are two primary NAAQS for
NO2: an annual standard (53 ppb) and a 1-hour standard (100
ppb). The EPA promulgated area designations in the Federal Register on
February 17, 2012. In this initial round of designations, all areas of
the country were designated as ``unclassifiable/attainment'' for the
2010 NO2 NAAQS based on data from the existing air quality
monitoring network. The EPA and state agencies are working to establish
an expanded network of NO2 monitors, expected to be deployed
in the 2014-2017 time frame. Once three years of air quality data have
been collected from the expanded network, the EPA will be able to
evaluate NO2 air quality in additional
locations.70 71
---------------------------------------------------------------------------

    \70\ 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.
    \71\ 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.
---------------------------------------------------------------------------

e. Current Concentrations of SO2
    The EPA most recently completed a review of the primary
SO2 NAAQS in June 2010. The current primary NAAQS for
SO2 is a 1-hour standard of 75 ppb. The EPA finalized the
initial area designations for 29 nonattainment areas in 16 states in a
notice published in the Federal Register on August 5, 2013. In this
first round of designations, EPA only designated nonattainment areas
that were violating the standard based on existing air quality
monitoring data provided by the states. The Agency did not have
sufficient information to designate any area as ``attainment'' or make
final decisions about areas for which additional modeling or monitoring
is needed (78 FR 47191, August 5, 2013). EPA anticipates designating
areas for the revised SO2 standard in multiple rounds.
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 January
2010 Integrated Science Assessment for Carbon Monoxide (CO ISA).\72\
The CO ISA concludes that ambient concentrations of CO are associated
with a number of adverse health effects.\73\ This section provides a
summary of the health effects associated with exposure to ambient
concentrations of CO.\74\
---------------------------------------------------------------------------

    \72\ 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.
    \73\ 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.
    \74\ 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.
---------------------------------------------------------------------------

    Controlled human exposure studies of subjects with coronary artery
disease show a decrease in the time to onset of exercise-induced angina
(chest pain) and electrocardiogram changes following CO exposure. In
addition, epidemiologic studies 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 CO ISA concludes
that a causal relationship is likely to exist between short-term
exposures to CO and cardiovascular morbidity. It also concludes that
available data are inadequate to conclude that a causal relationship
exists between long-term exposures to CO and cardiovascular morbidity.
    Animal studies show various neurological effects with in-utero CO
exposure. Controlled human exposure studies report central nervous
system and behavioral effects following low-level CO exposures,
although the findings have not been consistent across all studies. The
CO ISA concludes the evidence is suggestive of a causal relationship
with both short- and long-term exposure to CO and central nervous
system effects.
    A number of studies cited in the CO ISA have evaluated the role of
CO exposure in birth outcomes such as preterm birth or cardiac birth
defects. 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
perinatal CO exposure to affect birth weight, as well as other
developmental outcomes. The CO ISA concludes the evidence is suggestive
of a causal relationship between long-term exposures to CO and
developmental effects and birth outcomes.
    Epidemiologic studies provide evidence of associations between
ambient CO concentrations and respiratory morbidity such as changes in
pulmonary function, respiratory symptoms, and hospital admissions. A
limited number of epidemiologic studies considered copollutants such as
ozone, SO2, and PM in two-pollutant models and found that CO
risk estimates were generally robust, although this limited evidence
makes it difficult to disentangle effects attributed to CO itself from
those of the larger complex air pollution mixture. Controlled human
exposure studies have not extensively evaluated the effect of CO on
respiratory morbidity. Animal studies at levels of 50-100 ppm CO show
preliminary evidence of altered pulmonary vascular remodeling and
oxidative injury. The CO ISA concludes that the evidence is suggestive
of a causal relationship between short-term CO exposure and respiratory
morbidity, and inadequate to conclude that a causal relationship exists
between long-term exposure and respiratory morbidity.
    Finally, the CO ISA concludes that the epidemiologic evidence is
suggestive of a causal relationship between short-term concentrations
of CO and mortality. Epidemiologic 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 CO ISA also
concludes that there is not likely to be a causal relationship between
relevant long-term exposures to CO and mortality.
b. Current Concentrations of CO
    There are two NAAQS for CO: an 8-hour standard (9 ppm) and a 1-hour
standard (35 ppm). The primary NAAQS for CO were retained in August
2011. There are currently no CO nonattainment areas; as of September
27, 2010, all CO nonattainment areas were redesignated to maintenance
areas. The designations were based on the existing community-wide
monitoring network. EPA is making changes to the ambient air monitoring
requirements for CO. The new requirements are expected to result in
approximately 52 CO monitors operating near roads within 52 urban areas
by January 2015 (76 FR 54294, August 31, 2011).
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.'' \75\ 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.\76\
---------------------------------------------------------------------------

    \75\ U.S. EPA. (2011) Summary of Results for the 2005 National-
Scale Assessment. www.epa.gov/ttn/atw/nata2005/05pdf/sum_results.pdf.
    \76\ U.S. EPA (2011) 2005 National-Scale Air Toxics Assessment.
http://www.epa.gov/ttn/atw/nata2005.
---------------------------------------------------------------------------

a. Health Effects of Air Toxics
i. Benzene
    The EPA's Integrated Risk Information System (IRIS) database lists
benzene as a known human carcinogen (causing leukemia) by all routes of
exposure, and concludes that exposure is associated with additional
health effects, including genetic changes in both humans and animals
and increased proliferation of bone marrow cells in
mice.77 78 79 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.80 81 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.82 83
---------------------------------------------------------------------------

    \77\ 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.
    \78\ 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.
    \79\ 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.
    \80\ A unit risk estimate is defined as the increase in the
lifetime risk of an individual who is exposed for a lifetime to 1
[mu]g/m3 benzene in air.
    \81\ 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.
    \82\ 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.
    \83\ 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.
---------------------------------------------------------------------------

    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.84 85 The most sensitive
noncancer effect observed in humans, based on current data, is the
depression of the absolute lymphocyte count in blood.86 87
EPA's inhalation reference concentration (RfC) for benzene is 30 [mu]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,
provides evidence that biochemical responses are occurring at lower
levels of benzene exposure than previously known.88 89 90 91
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 [mu]g/m\3\ for 1-14 days
exposure.92 93
---------------------------------------------------------------------------

    \84\ Aksoy, M. (1989). Hematotoxicity and carcinogenicity of
benzene. Environ. Health Perspect. 82: 193-197.
    \85\ Goldstein, B.D. (1988). Benzene toxicity. Occupational
medicine. State of the Art Reviews. 3: 541-554.
    \86\ 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.
    \87\ 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.
    \88\ 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.
    \89\ 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.
    \90\ Lan, Qing, Zhang, L., Li, G., Vermeulen, R., et al. (2004).
Hematotoxically in Workers Exposed to Low Levels of Benzene. Science
306: 1774-1776.
    \91\ 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.
    \92\ 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.
    \93\ 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.
---------------------------------------------------------------------------

ii. Formaldehyde
    In 1991, EPA concluded that formaldehyde is a carcinogen based on
nasal tumors in animal bioassays.\94\ An Inhalation Unit Risk for
cancer and a Reference Dose for oral noncancer effects were developed
by the Agency and posted on the IRIS database. Since that time, the
National Toxicology Program (NTP) and International Agency for Research
on Cancer (IARC) have concluded that formaldehyde is a known human
carcinogen.95 96 97
---------------------------------------------------------------------------

    \94\ EPA. Integrated Risk Information System. Formaldehyde
(CASRN 50-00-0) http://www.epa.gov/iris/subst/0419/htm.
    \95\ National Toxicology Program, U.S. Department of Health and
Human Services (HHS), 12th Report on Carcinogens, June 10, 2011.
    \96\ IARC Monographs on the Evaluation of Carcinogenic Risks to
Humans Volume 88 (2006): Formaldehyde, 2-Butoxyethanol and 1-tert-
Butoxypropan-2-ol.
    \97\ IARC Mongraphs on the Evaluation of Carcinogenic Risks to
Humans Volume 100F (2012): Formaldehyde.
---------------------------------------------------------------------------

    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.98 99 100 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.\101\ 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.\102\
Finally, a study of embalmers reported formaldehyde exposures to be
associated with an increased risk of myeloid leukemia but not brain
cancer.\103\
---------------------------------------------------------------------------

    \98\ 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.
    \99\ 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.
    \100\ 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.
    \101\ Pinkerton, L. E. 2004. Mortality among a cohort of garment
workers exposed to formaldehyde: an update. Occup. Environ. Med. 61:
193-200.
    \102\ 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.
    \103\ 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.
---------------------------------------------------------------------------

    Health effects of formaldehyde in addition to cancer were reviewed
by the Agency for Toxics Substances and Disease Registry in 1999 \104\
and supplemented in 2010,\105\ and by the World Health
Organization.\106\ 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.
---------------------------------------------------------------------------

    \104\ ATSDR. 1999. Toxicological Profile for Formaldehyde, U.S.
Department of Health and Human Services (HHS), July 1999.
    \105\ ATSDR. 2010. Addendum to theToxicological Profile for
Formaldehyde. U.S. Department of Health and Human Services (HHS),
October 2010.
    \106\ IPCS. 2002. Concise International Chemical Assessment
Document 40. Formaldehyde. World Health Organization.
---------------------------------------------------------------------------

    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.\107\
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.\108\ The EPA is currently revising
the draft assessment in response to this review.
---------------------------------------------------------------------------

    \107\ 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.
    \108\ 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.
---------------------------------------------------------------------------

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.\109\ The URE in
IRIS for

acetaldehyde is 2.2 x 10-6 per [mu]g/m\3\.\110\ 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.111 112 EPA is
currently conducting a reassessment of cancer risk from inhalation
exposure to acetaldehyde.
---------------------------------------------------------------------------

    \109\ 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.
    \110\ 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.
    \111\ 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.
    \112\ International Agency for Research on Cancer (IARC).
(1999). Re-evaluation of some organic chemicals, hydrazine, and
hydrogen peroxide. IARC Monographs on the Evaluation of Carcinogenic
Risk of Chemical to Humans, Vol 71. Lyon, France.
---------------------------------------------------------------------------

    The primary noncancer effects of exposure to acetaldehyde vapors
include irritation of the eyes, skin, and respiratory tract.\113\ In
short-term (4 week) rat studies, degeneration of olfactory epithelium
was observed at various concentration levels of acetaldehyde
exposure.114 115 Data from these studies were used by EPA to
develop an inhalation reference concentration of 9 [mu]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.\116\ The agency is
currently conducting a reassessment of the health hazards from
inhalation exposure to acetaldehyde.
---------------------------------------------------------------------------

    \113\ 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.
    \114\ 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.
    \115\ 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.
    \116\ 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.
---------------------------------------------------------------------------

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.\117\ The IARC determined in
1995 that acrolein was not classifiable as to its carcinogenicity in
humans.\118\
---------------------------------------------------------------------------

    \117\ 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.
    \118\ 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.
---------------------------------------------------------------------------

    Lesions to the lungs and upper respiratory tract of rats, rabbits,
and hamsters have been observed after subchronic exposure to
acrolein.\119\ The Agency has developed an RfC for acrolein of 0.02
[mu]g/m\3\ and an RfD of 0.5 [mu]g/kg-day.\120\ EPA is considering
updating the acrolein assessment with data that have become available
since the 2003 assessment was completed.
---------------------------------------------------------------------------

    \119\ 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.
    \120\ 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.
---------------------------------------------------------------------------

    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.\121\ 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.\122\ 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 \123\) 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 [mu]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 [mu]g/m\3\ and 0.7 [mu]g/m\3\,
respectively.\124\
---------------------------------------------------------------------------

    \121\ 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.
    \122\ 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.
    \123\ 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.
    \124\ 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.
---------------------------------------------------------------------------

v. 1,3-Butadiene
    EPA has characterized 1,3-butadiene as carcinogenic to humans by
inhalation.125 126 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.127 128 129

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 [mu]g/m\3\.\130\ 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.\131\
Based on this critical effect and the benchmark concentration
methodology, an RfC for chronic health effects was calculated at 0.9
ppb (approximately 2 [mu]g/m\3\).
---------------------------------------------------------------------------

    \125\ 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.
    \126\ 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.
    \127\ 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.
    \128\ 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.
    \129\ 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.
    \130\ 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.
    \131\ 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.
---------------------------------------------------------------------------

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.132 133 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.\134\ 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.\135\ 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).136 137 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.
---------------------------------------------------------------------------

    \132\ 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.
    \133\ 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.
    \134\ 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.
    \135\ 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.
    \136\ 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.
    \137\ 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.
---------------------------------------------------------------------------

viii. 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.\138\ Chronic
(long term) exposure of workers and rodents to naphthalene has been
reported to cause cataracts and retinal damage.\139\ EPA released an
external review draft of a reassessment of the inhalation
carcinogenicity of naphthalene based on a number of recent animal
carcinogenicity studies.\140\ The draft reassessment completed external
peer review.\141\ 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.\142\ 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.\143\
---------------------------------------------------------------------------

    \138\ 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.
    \139\ 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.
    \140\ 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.
    \141\ 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.
    \142\ 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.
    \143\ International Agency for Research on Cancer (IARC).
(2002). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans. Vol. 82. Lyon, France.
---------------------------------------------------------------------------

    Naphthalene also causes a number of chronic non-cancer effects in
animals,

including abnormal cell changes and growth in respiratory and nasal
tissues.\144\ 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 [mu]g/m\3\.\145\ The ATSDR MRL for acute
exposure to naphthalene is 0.6 mg/kg/day.
---------------------------------------------------------------------------

    \144\ 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.
    \145\ 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.
---------------------------------------------------------------------------

ix. Other Air Toxics
    In addition to the compounds described above, other compounds in
gaseous hydrocarbon and PM emissions from motor vehicles will be
affected by this action. Mobile source air toxic compounds that will
potentially be impacted include ethylbenzene, propionaldehyde, toluene,
and xylene. Information regarding the health effects of these compounds
can be found in EPA's IRIS database.\146\
---------------------------------------------------------------------------

    \146\ U.S. EPA Integrated Risk Information System (IRIS)
database is available at: www.epa.gov/iris.
---------------------------------------------------------------------------

b. Current Concentrations of Air Toxics
    The most recent available data indicate that 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.\147\ 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.\148\ According to the National Air Toxic
Assessment (NATA) for 2005,\149\ 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.
---------------------------------------------------------------------------

    \147\ U.S. EPA. (2011) Summary of Results for the 2005 National-
Scale Assessment. www.epa.gov/ttn/atw/nata2005/05pdf/sum_results.pdf.
    \148\ U.S. Environmental Protection Agency (2007). Control of
Hazardous Air Pollutants from Mobile Sources; Final Rule. 72 FR
8434, February 26, 2007.
    \149\ U.S. EPA. (2011). 2005 National-Scale Air Toxics
Assessment. http://www.epa.gov/ttn/atw/nata2005/.
---------------------------------------------------------------------------

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.\150\ 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.
---------------------------------------------------------------------------

    \150\ 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.
---------------------------------------------------------------------------

    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.\151, 152\ These findings suggest a substantial roadway
source of these carbonyls.
---------------------------------------------------------------------------

    \151\ 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.
    \152\ 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.
---------------------------------------------------------------------------

    In the past 15 years, many studies have been published with results
reporting that populations who live, work, or go to school near high-
traffic roadways experience higher rates of numerous adverse health
effects, compared to populations far away from major roads.\153\ In
addition, numerous studies have found adverse health effects associated
with spending time in traffic, such as commuting or walking along high-
traffic roadways.\154\ \155\ \156\ \157\ The health outcomes with the
strongest evidence linking them with traffic-associated air pollutants
are respiratory effects, particularly in asthmatic children, and
cardiovascular effects.
---------------------------------------------------------------------------

    \153\ 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.
    \154\ Laden, F.; Hart, J.E.; Smith, T.J.; Davis, M.E.; Garshick,
E. (2007) Cause-specific mortality in the unionized U.S. trucking
industry. Environmental Health Perspect 115:1192-1196.
    \155\ Peters, A.; von Klot, S.; Heier, M.; Trentinaglia, I.;
H[ouml]rmann, A.; Wichmann, H.E.; L[ouml]wel, H. (2004) Exposure to
traffic and the onset of myocardial infarction. New England J Med
351: 1721-1730.
    \156\ Zanobetti, A.; Stone, P.H.; Spelzer, F.E.; Schwartz, J.D.;
Coull, B.A.; Suh, H.H.; Nearling, B.D.; Mittleman, M.A.; Verrier,
R.L.; Gold, D.R. (2009) T-wave alternans, air pollution and traffic
in high-risk subjects. Am J Cardiol 104: 665-670.
    \157\ Dubowsky Adar, S.; Adamkiewicz, G.; Gold, D.R.; Schwartz,
J.; Coull, B.A.; Suh, H. (2007) Ambient and microenvironmental
particles and exhaled nitric oxide before and after a group bus
trip. Environ Health Perspect 115: 507-512.
---------------------------------------------------------------------------

    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.\158\ 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.\159\ \160\ \161\ 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).\162\ \163\ \164\
\165\
---------------------------------------------------------------------------

    \158\ 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.
    \159\ 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.
    \160\ 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.
    \161\ Raaschou-Nielsen, O.; Reynolds, P. (2006). Air pollution
and childhood cancer: a review of the epidemiological literature.
Int J Cancer 118: 2920-9.
    \162\ 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.
    \163\ 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]
    \164\ 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.
    \165\ Wu, J.; Wilhelm, M.; Chung, J.; et al. (2011). Comparing
exposure assessment methods for traffic-related air pollution in an
adverse pregnancy outcome study. Environ Res 111: 685-6692.
---------------------------------------------------------------------------

    In addition to health outcomes, particularly cardiopulmonary
effects, conclusions of numerous studies suggest mechanisms by which
traffic-related air pollution affects health. Numerous studies indicate
that near-roadway exposures may increase systemic inflammation,
affecting organ systems, including blood vessels and lungs.\166\ \167\
\168\ \169\ Long-term exposures in near-road environments have been
associated with inflammation-associated conditions, such as
atherosclerosis and asthma.\170\ \171\ \172\
---------------------------------------------------------------------------

    \166\ 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.
    \167\ Alexeef, SE.; Coull, B.A.; Gryparis, A.; et al. (2011).
Medium-term exposure to traffic-related air pollution and markers of
inflammation and endothelial function. Environ Health Perspect 119:
481-486. doi:10.1289/ehp.1002560 Available at http://dx.doi.org.
    \168\ 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.
    \169\ 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.]
    \170\ 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.
    \171\ 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.
    \172\ 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.
---------------------------------------------------------------------------

    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.\173\ \174\ \175\
---------------------------------------------------------------------------

    \173\ 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).
    \174\ 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.
    \175\ 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.
---------------------------------------------------------------------------

    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. Based on 2010 Census data, a 2013
publication estimated that 19 percent of the U.S. population (over 59
million people) lived within 500 meters of roads with at least 25,000
annual average daily traffic (AADT), while about 3.2 percent of the
population lived within 100 meters (about 300 feet) of such roads.\176\
Another 2013 study estimated that 3.7 percent of the U.S. population
(about 11.3 million people) lived within 150 meters (about 500 feet) of
interstate highways, or other freeways and expressways.\177\ As
discussed in Section III, on average, populations near major roads have
higher fractions of minority residents and lower socioeconomic status.
Furthermore, on average, Americans spend more than an hour traveling
each day, bringing nearly all residents into a high-exposure
microenvironment for part of the day.
---------------------------------------------------------------------------

    \176\ Rowangould, G.M. (2013) A census of the U.S. near-roadway
population: public health and environmental justice considerations.
Transportation Research Part D 25: 59-67.
    \177\ Boehmer, T.K.; Foster, S.L.; Henry, J.R.; Woghiren-
Akinnifesi, E.L.; Yip, F.Y. (2013) Residential proximity to major
highways--United States, 2010. Morbidity and Mortality Weekly Report
62(3);46-50.
---------------------------------------------------------------------------

    In light of these concerns, EPA has required and is working with
states to ensure that air quality monitors be placed near high-traffic
roadways for determining NAAQS compliance for CO, NO2, and
PM2.5 (in addition to those existing monitors located in
neighborhoods and other locations farther away from pollution sources).
Near-roadway monitors for NO2 begin operation between 2014
and 2017 in Core Based Statistical Areas (CBSAs) with population of at
least 500,000. Monitors for CO and PM2.5 begin operation
between 2015 and 2017. These monitors will further our understanding of
exposure in these locations.
    EPA 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
    The welfare effects of ozone can be observed across a variety of
scales, i.e. subcellular, cellular, leaf, whole plant, population and
ecosystem. Ozone effects that begin at small spatial scales, such as
the leaf of an individual plant, when they occur at sufficient

magnitudes (or to a sufficient degree) can result in effects being
propagated along a continuum to larger and larger spatial scales. For
example, effects at the individual plant level, such as altered rates
of leaf gas exchange, growth and reproduction can, when widespread,
result in broad changes in ecosystems, such as productivity, carbon
storage, water cycling, nutrient cycling, and community composition.
    Ozone can produce both acute and chronic injury in sensitive
species depending on the concentration level and the duration of the
exposure.\178\ In those sensitive species, \179\ effects from repeated
exposure to ozone throughout the growing season of the plant tend to
accumulate, so that even low concentrations experienced for a longer
duration have the potential to create chronic stress on
vegetation.\180\ Ozone damage to sensitive species includes impaired
photosynthesis and visible injury to leaves. The impairment of
photosynthesis, the process by which the plant makes carbohydrates (its
source of energy and food), can lead to reduced crop yields, timber
production, and plant productivity and growth. Impaired photosynthesis
can also lead to a reduction in root growth and carbohydrate storage
below ground, resulting in other, more subtle plant and ecosystems
impacts.\181\ These latter impacts include increased susceptibility of
plants to insect attack, disease, harsh weather, interspecies
competition and overall decreased plant vigor. The adverse effects of
ozone on areas with sensitive species could potentially lead to species
shifts and loss from the affected ecosystems,\182\ resulting in a loss
or reduction in associated ecosystem goods and services. Additionally,
visible ozone injury to leaves can result in a loss of aesthetic value
in areas of special scenic significance like national parks and
wilderness areas and reduced use of sensitive ornamentals in
landscaping.\183\
---------------------------------------------------------------------------

    \178\ 73 FR 16486 (March 27, 2008).
    \179\ 73 FR 16491 (March 27, 2008). Only a small percentage of
all the plant species growing within the U.S. (over 43,000 species
have been catalogued in the USDA PLANTS database) have been studied
with respect to ozone sensitivity.
    \180\ The concentration at which ozone levels overwhelm a
plant's ability to detoxify or compensate for oxidant exposure
varies. Thus, whether a plant is classified as sensitive or tolerant
depends in part on the exposure levels being considered. Chapter 9,
section 9.3.4 of U.S. EPA, 2013 Integrated Science Assessment for
Ozone and Related Photochemical Oxidants. Office of Research and
Development/National Center for Environmental Assessment. U.S.
Environmental Protection Agency. EPA 600/R-10/076F.
    \181\ 73 FR 16492 (March 27, 2008).
    \182\ 73 FR 16493/16494 (March 27, 2008), Per footnote 2 above,
ozone impacts could be occurring in areas where plant species
sensitive to ozone have not yet been studied or identified.
    \183\ 73 FR 16490/16497 (March 27, 2008).
---------------------------------------------------------------------------

    The Integrated Science Assessment (ISA) for Ozone presents more
detailed information on how ozone affects vegetation and
ecosystems.\184\ The ISA concludes that ambient concentrations of ozone
are associated with a number of adverse welfare effects and
characterizes the weight of evidence for different effects associated
with ozone.\185\ The ISA concludes that visible foliar injury effects
on vegetation, reduced vegetation growth, reduced productivity in
terrestrial ecosystems, reduced yield and quality of agricultural
crops, and alteration of below-ground biogeochemical cycles are
causally associated with exposure to ozone. It also concludes that
reduced carbon sequestration in terrestrial ecosystems, alteration of
terrestrial ecosystem water cycling, and alteration of terrestrial
community composition are likely to be causally associated with
exposure to ozone.
---------------------------------------------------------------------------

    \184\ U.S. EPA. Integrated Science Assessment of Ozone and
Related Photochemical Oxidants (Final Report). U.S. Environmental
Protection Agency, Washington, DC, EPA/600/R-10/076F, 2013. The ISA
is available at http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492#Download.
    \185\ The Ozone ISA evaluates the evidence associated with
different ozone related health and welfare effects, assigning one of
five ``weight of evidence'' determinations: Causal relationship,
likely to be a causal relationship, suggestive of a causal
relationship, inadequate to infer a causal relationship, and not
likely to be a causal relationship. For more information on these
levels of evidence, please refer to Table II of the ISA.
---------------------------------------------------------------------------

b. Visibility
    Visibility can be defined as the degree to which the atmosphere is
transparent to visible light.\186\ Visibility impairment is caused by
light scattering and absorption by suspended particles and gases.
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.\187\
---------------------------------------------------------------------------

    \186\ National Research Council, (1993). Protecting Visibility
in National Parks and Wilderness Areas. National Academy of Sciences
Committee on Haze in National Parks and Wilderness Areas. National
Academy Press, Washington, DC. This book can be viewed on the
National Academy Press Web site at http://www.nap.edu/books/0309048443/html/.
    \187\ U.S. EPA. (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F.
---------------------------------------------------------------------------

    EPA is working to address visibility impairment. In 1999, EPA
finalized the regional haze program to protect the visibility in
Mandatory Class I Federal areas.\188\ There are 156 national parks,
forests and wilderness areas categorized as Mandatory Class I Federal
areas.\189\ 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. EPA has also 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.
---------------------------------------------------------------------------

    \188\ 64 FR 35714 (July 1, 1999).
    \189\ 62 FR 38680-38681 (July 18, 1997).
---------------------------------------------------------------------------

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.\190\
---------------------------------------------------------------------------

    \190\ 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.
---------------------------------------------------------------------------

    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.191 192 193 194 195
---------------------------------------------------------------------------

    \191\ U.S. EPA. (2004). National Coastal Condition Report II.
Office of Research and Development/Office of Water. EPA-620/R-03/
002.
    \192\ 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.
    \193\ 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.
    \194\ 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.
    \195\ 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 19
years.\196\ 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.\197\ 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.\198\
---------------------------------------------------------------------------

    \196\ U.S. EPA. (2013). U.S. EPA's Report on the Environment.
Data accessed online November 25, 2013 at: http://cfpub.epa.gov/eroe/index.cfm?fuseaction=detail.viewInd&lv=list.listBySubTopic&r=216610&subtop=341&ch=46.
    \197\ 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.
    \198\ 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.\199\ In laboratory experiments, a wide range of
tolerance to VOCs has been observed.\200\ 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.\201\
---------------------------------------------------------------------------

    \199\ U.S. EPA. (1991). Effects of organic chemicals in the
atmosphere on terrestrial plants. EPA/600/3-91/001.
    \200\ 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.
    \201\ 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.202 203 204
---------------------------------------------------------------------------

    \202\ Viskari E-L. (2000). Epicuticular wax of Norway spruce
needles as indicator of traffic pollutant deposition. Water, Air,
and Soil Pollut. 121:327-337.
    \203\ Ugrekhelidze D, F Korte, G Kvesitadze. (1997). Uptake and
transformation of benzene and toluene by plant leaves. Ecotox.
Environ. Safety 37:24-29.
    \204\ 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 rule reduce emissions and air pollution?

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

    The Tier 3 vehicle and fuel standards will significantly reduce the
tailpipe and evaporative emissions of light- and heavy-duty vehicles in
several ways, as described in this section. In addition, the gasoline
sulfur standard will reduce emissions of SO2 from existing
gasoline-powered vehicles and equipment. As described in Section II,
all of these emission reductions will 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 implementing closely-coordinated
requirements for both automakers and refiners in the same rulemaking
action. The Tier 3 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 action, we
have been able to integrate the provisions into a single, coordinated
program.
1. How do vehicles produce the emissions addressed in this action?
    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
    The pollutants 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 (as elemental carbon or soot)
and 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 gasoline.
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
elastomers in the fuel system, 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 will be improved under this action) 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 will the changes to gasoline sulfur content affect vehicle
emissions?
    Gasoline vehicles rely on highly efficient aftertreatment catalysts
to control tailpipe emissions of harmful pollutants like CO and
NOX, as well as VOCs that include air toxics and precursor
compounds to ozone and secondary PM in the atmosphere. These catalysts
utilize finely-dispersed precious metals that are susceptible to
deactivation by sulfur compounds in the exhaust. Studies have
repeatedly demonstrated that the presence of even a tiny amount of
sulfur in fuel has a measurable impact on the ability of the catalyst
to control emissions, and that emission levels of most pollutants,
especially NOX, are very sensitive to fuel
sulfur.205 206
---------------------------------------------------------------------------

    \205\ The Effects of Ultra-Low Sulfur Gasoline on Emissions from
Tier 2 Vehicles in the In-Use Fleet, EPA-420-R-14-002.
    \206\ Durbin, T., ``The Effect of Fuel Sulfur on NH3 and Other
Emissions from 2000-2001 Model Year Vehicles'', May 2003. Published
as Report E-60 by the Coordinating Research Council, Alpharetta, GA.

---------------------------------------------------------------------------

    Sulfur naturally occurs in crude oil and is carried through the
refining process into gasoline. EPA's Tier 2 rulemaking for light-duty
vehicles, published in 2000, required refiners to reduce sulfur levels
in gasoline to an average of 30 ppm, a reduction of about 90 percent
from the in-use baseline. At the time, there were indications that
sulfur reductions below 30 ppm may 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 below 30 ppm.\207\
---------------------------------------------------------------------------

    \207\ 65 FR 6698 (February 10, 2000).
---------------------------------------------------------------------------

    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 ultra-low
sulfur fuel.\208\ In particular, the study found a 32 percent decrease
in NOX when sulfur was reduced from 32 ppm to 6 ppm
(equivalent to a 25 percent decrease if sulfur levels were reduced from
30 to 10 ppm, assuming a linear effect). Another recent study by
Umicore showed reductions of 41 percent for NOX and 17
percent for hydrocarbons on a PZEV operating on fuel with 33 ppm and 3
ppm fuel (equivalent to reductions of 27 percent and 11 percent,
respectively, if sulfur levels were reduced from 30 to 10 ppm, assuming
a linear effect).\209\
---------------------------------------------------------------------------

    \208\ Regulatory Impact Analysis for the Control of Hazardous
Air Pollutants from Mobile Sources Final Rule, EPA 420-R-07-002,
Chapter 6.
    \209\ 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 of Tier 2 vehicles recently completed by EPA
confirmed these results, showing significant reductions in FTP-
composite NOX (14 percent), CO (10 percent) and total HC (15
percent) on the 5 ppm fuel, relative to 28 ppm fuel (equivalent to 12
percent, 9 percent, and 13 percent reduction, respectively, if sulfur
levels were reduced from 30 to 10 ppm, assuming a linear effect).\210\
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 52 percent reduction using 5 ppm fuel relative to 28 ppm fuel
(equivalent to 45 percent reduction if sulfur levels were reduced from
30 to 10 ppm, assuming a linear effect), consistent with the role of
sulfur in catalyst degradation discussed above. For additional details
regarding these results, please see Section IV.A.6.c.
---------------------------------------------------------------------------

    \210\ The Effects of Ultra-Low Sulfur Gasoline on Emissions from
Tier 2 Vehicles in the In-Use Fleet, EPA-420-R-14-002.
---------------------------------------------------------------------------

    Our application of these study results assumes a linear effect of
sulfur level on catalyst efficiency between the high and low sulfur
test fuels. This is reasonable given that the mass flow rate of sulfur
in exhaust gas changes in proportion to its concentration in the fuel,
and that the chemical kinetics of adsorption of sulfur to the precious
metal sites is approximately first order. Linearity of effect is also
supported by past studies with multiple fuel sulfur levels such as the
CRC E-60 and 2000 AAM/AIAM/Oil Industry emission test
programs.211 212
---------------------------------------------------------------------------

    \211\ Durbin, T., ``The Effect of Fuel Sulfur on NH3 and Other
Emissions from 2000-2001 Model Year Vehicles'', May 2003. Published
as Report E-60 by the Coordinating Research Council, Alpharetta, GA.
    \212\ ``AAM/AIAM/Oil Industry Low Sulfur & Oxygenate Test
Program'', 2000, last accessed on 01/15/14 at the following URL:
http://www.arb.ca.gov/fuels/gasoline/carfg3/aam_prstn.pdf.
---------------------------------------------------------------------------

    Based on these analyses, the benefits of the Tier 3 sulfur standard
are significant in two ways: They enable vehicles designed to the 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 will emissions be reduced?

    The Tier 3 standards will reduce emissions of VOC, NOX
(including NO2), direct PM2.5, CO,
SO2, and air toxics. The sulfur standards will reduce
emissions from the on-road fleet immediately upon implementation in
calendar year 2017. The vehicle standards will begin to reduce
emissions as the cleaner cars and trucks begin to enter the fleet in
model year 2017 and model year 2018, respectively. The magnitude of
reduction will grow as more Tier 3 vehicles enter the fleet. We present
emission reductions in calendar year 2018 to reflect the early
reductions expected from the Tier 3 standards, and in calendar year
2030, when 70 percent of the miles travelled are from vehicles that
meet the fully phased-in Tier 3 standards. Although 2030 is the
farthest year that is feasible for air quality modeling, the full
reduction of the vehicle program will be realized after 2030, when the
fleet has fully turned over to vehicles that meet the fully phased-in
Tier 3 standards; thus we present emission reductions projected in 2050
as well (see Chapter 7 of the RIA).
    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, RVP, and other fuel properties. We estimated emission
reductions compared to a reference case that assumed renewable fuel
volumes and ethanol blends based on the U.S. Energy Information
Administration's Annual Energy Outlook 2013 (AEO2013).\213\ As
described in Chapter 7 of the RIA, the reference and control scenarios
based on AEO2013 reflect a mix of E10, E15, and E85 in both 2018 and
2030. The reference case assumed an average sulfur level of 30 ppm (10
ppm in California) and continuation of the Tier 2 vehicle program
indefinitely, with the exception of California and Section 177 states
that have adopted the LEV III program.
---------------------------------------------------------------------------

    \213\ U.S. Energy Information Administration, Annual Energy
Outlook (April 15, 2013).
---------------------------------------------------------------------------

    The analysis described here accounts 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)
 Greenhouse Gas Emissions Standards and Fuel Efficiency
Standards for Medium- and Heavy-Duty Engines and Vehicles (76 FR 57106,
September 15, 2011)
 2017 and Later Model Year Light-Duty Vehicle Greenhouse Gas
Emissions and Corporate Average Fuel Economy

Standards (77 FR 62623, October 15, 2012)

The analysis also accounts for many other national rules and standards.
In addition, the modeling accounts for state and local rules including
California's most recent Low Emission Vehicle (LEV III) program adopted
in California and twelve other states (also referred to as Section 177
states),\214\ local fuel standards, Inspection/Maintenance programs,
Stage II refueling controls, the National Low Emission Vehicle Program
(NLEV), and the Section 177 states LEV and LEV II programs. See the
Tier 3 emissions modeling TSD for more detail.
---------------------------------------------------------------------------

    \214\ These states include Connecticut, Delaware, Maryland,
Maine, Massachusetts, New Jersey, New York, Oregon, Pennsylvania,
Rhode Island, Washington, and Vermont.
---------------------------------------------------------------------------

    A summary of emission reductions projected to result from Tier 3,
relative to the reference case, is shown in calendar years 2018 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 2018 are significant; for
example, combined NOX and VOC emissions will be reduced by
over 300,000 tons. By 2030, combined NOX and VOC emissions
will be reduced by roughly 500,000 tons, one quarter of the onroad
inventory. Many of the modeled air toxics will be significantly reduced
as well, including benzene, 1,3-butadiene, acetaldehyde, acrolein and
ethanol (ranging from 10 to nearly 30 percent of the national onroad
inventory by 2030). The relative reduction in overall emissions will
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 will have turned over to vehicles meeting the fully phased-in
Tier 3 standards, we estimate the Tier 3 program will reduce onroad
emissions of NOX and VOC nearly 31 percent from the level of
emissions projected without Tier 3 controls.

                      Table III-1--Estimated Emission Reductions From the Tier 3 Standards
                                            [Annual U.S. short tons]
----------------------------------------------------------------------------------------------------------------
                                                               2018                            2030
                                                 ---------------------------------------------------------------
                                                                    % of Onroad                     % of Onroad
                                                       Tons          inventory         Tons          inventory
----------------------------------------------------------------------------------------------------------------
NOX.............................................         264,369              10         328,509              25
VOC.............................................          47,504               3         167,591              16
CO..............................................         278,879               2       3,458,041              24
Direct PM2.5....................................             130             0.1           7,892              10
Benzene.........................................           1,916               6           4,762              26
SO2.............................................          14,813              56          12,399              56
1,3-Butadiene...................................             257               5             677              29
Formaldehyde....................................             513               2           1,277              10
Acetaldehyde....................................             600               3           2,067              21
Acrolein........................................              40               3             127              15
Ethanol.........................................           2,704               2          19,950              16
----------------------------------------------------------------------------------------------------------------

    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 Tier 3 sulfur standards will 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 will also be expected to decrease from
the fleet of older (pre-Tier 2) light-duty vehicles as well as heavy-
duty gasoline vehicles,\215\ although to a lesser extent than for Tier
2 vehicles.
---------------------------------------------------------------------------

    \215\ Rao, V. (2001), Fuel Sulfur Effects on Exhaust Emissions:
Recommendations for MOBILE6, EPA-420-R-01-039.
---------------------------------------------------------------------------

    Table III-2 shows the reduction in NOX emissions, in
annual short tons, projected in calendar years 2018 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 Tier 3 sulfur standards, total onroad
NOX emissions are projected to drop 10 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 2018. The relative reduction grows as cleaner vehicles
turn over into the fleet. By 2030, we project that the reduction in
overall onroad NOX inventory will be 25 percent.

        Table III-2--Projected NOX Reductions From Tier 3 Program
                           [Annual U.S. tons]
------------------------------------------------------------------------
                                           2018               2030
------------------------------------------------------------------------
Total reduction...................            264,369            328,509
Reduction from pre-Tier 3 fleet               242,434             56,324
 due to sulfur standard...........
Reduction from Tier 3 fleet due to             21,934            272,185
 vehicle and sulfur standards.....
Percent reduction in onroad NOX                   10%                25%
 emissions........................
------------------------------------------------------------------------

2. VOC
    Table III-3 shows the reduction in VOC emissions, in annual short
tons, projected in calendar years 2018 and 2030 resulting from the Tier
3 standards. In 2018, as with NOX, we project reductions
from the pre-Tier 3 fleet with the fuel standards. By 2030, the
reduction in overall onroad VOC emissions will be 16 percent, the
majority of this from the vehicles meeting the fully phased-in Tier 3
standards. The evaporative standards are projected to account for
roughly one third of the overall vehicle program reduction in 2030.

        Table III-3--Projected VOC Reductions From Tier 3 Program
                           [Annual U.S. tons]
------------------------------------------------------------------------
                                           2018               2030
------------------------------------------------------------------------
Total reduction...................             47,504            167,591
Reduction from pre-Tier 3 fleet                38,786             11,249
 due to sulfur standard...........
Reduction from Tier 3 fleet due to              8,718            156,343
 vehicle and sulfur standards.....
Exhaust...........................             43,009            105,253
Evaporative.......................              4,495             62,339
Percent reduction in onroad VOC                    3%                16%
 emissions........................
------------------------------------------------------------------------

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.
In contrast to NOX and VOC, the immediate CO reductions in
the onroad fleet from sulfur control in 2018 are small, based on
research showing that fuel sulfur level has a minimal impact on CO
emissions from Tier 2 vehicles. The CO exhaust standards are projected
to reduce onroad CO emissions by 24 percent in 2030.

        Table III-4--Projected CO Reductions From Tier 3 Program
                           [Annual U.S. tons]
------------------------------------------------------------------------
                                           2018               2030
------------------------------------------------------------------------
Total reduction...................            278,879          3,458,041
Reduction from pre-Tier 3 fleet               122,171             17,734
 due to sulfur standard...........
Reduction from Tier 3 fleet due to            156,708          3,440,307
 vehicle and sulfur standards.....
Percent reduction in onroad CO                     2%                24%
 emissions........................
------------------------------------------------------------------------

4. Direct PM2.5
    Reductions in direct emissions of PM2.5 are projected to
result solely from the vehicle tailpipe standards, so meaningful
reductions are realized mainly as the fleet turns over. By 2030, we
project a reduction of about 7,900 tons annually, which represents
approximately 10 percent of the onroad direct PM2.5
inventory. The relative reduction in onroad emissions is projected to
grow to 28 percent in 2050, when nearly all of the fleet will have
turned over to vehicles meeting the fully phased-in Tier 3 standards.
Reductions in NOX and VOC emissions will 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 will be reduced by the 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, for most air toxics. 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]
----------------------------------------------------------------------------------------------------------------
                                                                  % Reduction in                  % Reduction in
                                                   Tons reduced       onroad       Tons reduced       onroad
                                                      in 2018        emissions        in 2030        emissions
----------------------------------------------------------------------------------------------------------------
Benzene.........................................           1,916               6           4,762              26
Acetaldehyde....................................             600               3           2,067              21
Formaldehyde....................................             513               2           1,277              10
1,3-Butadiene...................................             257               5             677              29
Acrolein........................................              40               3             127              15