6%....................        -16.7        -33.2        -43.9        -55.9
----------------------------------------------------------------------------------------------------------------

                          Table III.F.1-5--Model Year Impacts of Alternative Scenarios
----------------------------------------------------------------------------------------------------------------
                                                                       Model year lifetime
                                   Scenario    -----------------------------------------------------------------
                                                 MY 2012    MY 2013    MY 2014    MY 2015    MY 2016     Total
----------------------------------------------------------------------------------------------------------------
Total GHG Reductions (MMT CO2  Primary........      -88.8     -130.2     -174.2     -244.2     -324.6     -962.0
 eq).
                               4%.............      -39.9      -96.6     -155.4     -226.5     -303.6     -822.0
                               6%.............      -61.7     -146.5     -237.0     -332.2     -427.6   -1,204.9
Fuel Savings (Billion Gallons  Primary........       -7.3      -10.5      -13.9      -19.5      -26.5      -77.7
 Gasoline Equivalent).
                               4%.............       -2.9       -7.1      -12.2      -18.0      -24.6      -64.8
                               6%.............       -4.9      -12.0      -19.4      -27.3      -35.6      -99.1
----------------------------------------------------------------------------------------------------------------

2. Overview of Climate Change Impacts From GHG Emissions
    Once emitted, GHGs that are the subject of this regulation can
remain in the atmosphere for decades to centuries, meaning that (1)
their concentrations become well-mixed throughout the global atmosphere
regardless of emission origin, and (2) their effects on climate are
long lasting. GHG emissions come mainly from the combustion of fossil
fuels (coal, oil, and gas), with additional contributions from the
clearing of forests and agricultural activities. The transportation
sector represents a significant portion, 28%, of U.S. GHG
emissions.\297\
---------------------------------------------------------------------------

    \297\ U.S. EPA (2009) Inventory of U.S. Greenhouse Gas Emissions
and Sinks: 1990-2007. EPA-430-R-09-004, Washington, DC.
---------------------------------------------------------------------------

    This section provides a summary of observed and projected changes
in GHG emissions and associated climate change impacts. The source
document for the section below is the Technical Support Document (TSD)
\298\ for EPA's Endangerment and Cause or Contribute Findings Under the
Clean Air Act.\299\ Below is the Executive Summary of the TSD which
provides technical support for the endangerment and cause or contribute
analyses concerning GHG emissions under section 202(a) of the Clean Air
Act. The TSD reviews observed and projected changes in climate based on
current and projected atmospheric GHG concentrations and emissions, as
well as the related impacts and risks from climate change that are
projected in the absence of GHG mitigation actions, including this
action and other U.S. and global actions. The TSD was updated and
revised based on expert technical review and public comment as part of
EPA's rulemaking process for the final Endangerment Findings. The key
findings synthesized here and the information throughout the TSD are
primarily drawn from the assessment reports of the Intergovernmental
Panel on Climate Change (IPCC), the U.S. Climate Change Science Program
(CCSP), the U.S. Global Change Research Program (USGCRP), and the
National Research Council (NRC).\300\
---------------------------------------------------------------------------

    \298\ ``Technical Support Document for Endangerment and Cause or
Contribute Findings for Greenhouse Gases Under Section 202(a) of the
Clean Air Act.'' Docket: EPA-HQ-OAR-2009-0472-11292.
    \299\ See 74 FR 66496 (Dec. 15, 2009).
    \300\ For a complete list of core references from IPCC, USGCRP/
CCSP, NRC and others relied upon for development of the TSD for
EPA's Endangerment and Cause or Contribute Findings see section
1(b), specifically, Table 1.1 of the TSD.
---------------------------------------------------------------------------

a. Observed Trends in Greenhouse Gas Emissions and Concentrations
    The primary long-lived GHGs directly emitted by human activities
include carbon dioxide (CO2), methane (CH4),
nitrous oxide (N2O), hydrofluorocarbons (HFCs),
perfluorocarbons (PFCs), and sulfur hexafluoride (SF6).
Greenhouse gases have a warming effect by trapping heat in the
atmosphere that would otherwise escape to space. In 2007, U.S. GHG
emissions were 7,150 teragrams \301\ of CO2 equivalent \302\
(TgCO2eq). The dominant gas emitted is CO2,
mostly from fossil fuel combustion. Methane is the second largest
component of U.S. emissions, followed by N2O and the
fluorinated gases (HFCs, PFCs, and SF6). Electricity
generation is the largest emitting sector (34% of total U.S. GHG
emissions), followed by transportation (28%) and industry (19%).
---------------------------------------------------------------------------

    \301\ One teragram (Tg) = 1 million metric tons. 1 metric ton =
1,000 kilograms = 1.102 short tons = 2,205 pounds.
    \302\ Long-lived GHGs are compared and summed together on a
CO2-equivalent basis by multiplying each gas by its
global warming potential (GWP), as estimated by IPCC. In accordance
with United Nations Framework Convention on Climate Change (UNFCCC)
reporting procedures, the U.S. quantifies GHG emissions using the
100-year timeframe values for GWPs established in the IPCC Second
Assessment Report.
---------------------------------------------------------------------------

    Transportation sources under Section 202(a) \303\ of the Clean Air
Act (passenger cars, light duty trucks, other trucks and buses,
motorcycles, and passenger cooling) emitted 1,649 TgCO2eq in
2007, representing 23% of total U.S. GHG emissions. U.S. transportation
sources under Section 202(a) made up 4.3% of total global GHG emissions
in 2005,\304\ which, in addition to the United States as a whole,
ranked only behind total GHG emissions from China, Russia, and India
but ahead of Japan, Brazil, Germany, and the rest of the world's
countries. In 2005, total U.S. GHG emissions were responsible for 18%
of global emissions, ranking only behind China, which was responsible
for 19% of global GHG emissions. The scope of this action focuses on
GHG emissions under Section 202(a) from passenger cars and light duty
trucks source categories (see Section III.F.1).
---------------------------------------------------------------------------

    \303\ Source categories under Section 202(a) of the Clean Air
Act are a subset of source categories considered in the
transportation sector and do not include emissions from non-highway
sources such as boats, rail, aircraft, agricultural equipment,
construction/mining equipment, and other off-road equipment.
    \304\ More recent emission data are available for the United
States and other individual countries, but 2005 is the most recent
year for which data for all countries and all gases are available.
---------------------------------------------------------------------------

    The global atmospheric CO2 concentration has increased
about 38% from pre-industrial levels to 2009, and almost all of the
increase is due to anthropogenic emissions. The global atmospheric
concentration of CH4 has increased by 149% since pre-
industrial levels (through 2007); and the N2O concentration
has increased by 23% (through 2007). The observed concentration
increase in these gases can also be attributed primarily to
anthropogenic emissions. The industrial fluorinated gases, HFCs, PFCs,
and SF6, have relatively low atmospheric concentrations but
the total radiative forcing due to these gases is increasing rapidly;
these gases are almost entirely anthropogenic in origin.
    Historic data show that current atmospheric concentrations of the
two most important directly emitted, long-lived GHGs (CO2
and CH4) are well above the natural range of atmospheric
concentrations compared to at least the last 650,000 years. Atmospheric
GHG concentrations have been increasing because anthropogenic emissions
have been outpacing the rate at which GHGs are removed from the
atmosphere by

natural processes over timescales of decades to centuries.
b. Observed Effects Associated With Global Elevated Concentrations of
GHGs
    Current ambient air concentrations of CO2 and other GHGs
remain well below published exposure thresholds for any direct adverse
health effects, such as respiratory or toxic effects.
    The global average net effect of the increase in atmospheric GHG
concentrations, plus other human activities (e.g., land-use change and
aerosol emissions), on the global energy balance since 1750 has been
one of warming. This total net heating effect, referred to as forcing,
is estimated to be +1.6 (+0.6 to +2.4) watts per square meter (W/m\2\),
with much of the range surrounding this estimate due to uncertainties
about the cooling and warming effects of aerosols. However, as aerosol
forcing has more regional variability than the well-mixed, long-lived
GHGs, the global average might not capture some regional effects. The
combined radiative forcing due to the cumulative (i.e., 1750 to 2005)
increase in atmospheric concentrations of CO2,
CH4, and N2O is estimated to be +2.30 (+2.07 to
+2.53) W/m\2\. The rate of increase in positive radiative forcing due
to these three GHGs during the industrial era is very likely to have
been unprecedented in more than 10,000 years.
    Warming of the climate system is unequivocal, as is now evident
from observations of increases in global average air and ocean
temperatures, widespread melting of snow and ice, and rising global
average sea level. Global mean surface temperatures have risen by 1.3
 0.32 [deg]F (0.74 [deg]C  0.18 [deg]C) over
the last 100 years. Eight of the 10 warmest years on record have
occurred since 2001. Global mean surface temperature was higher during
the last few decades of the 20th century than during any comparable
period during the preceding four centuries.
    Most of the observed increase in global average temperatures since
the mid-20th century is very likely due to the observed increase in
anthropogenic GHG concentrations. Climate model simulations suggest
natural forcing alone (i.e., changes in solar irradiance) cannot
explain the observed warming.
    U.S. temperatures also warmed during the 20th and into the 21st
century; temperatures are now approximately 1.3 [deg]F (0.7 [deg]C)
warmer than at the start of the 20th century, with an increased rate of
warming over the past 30 years. Both the IPCC \305\ and the CCSP
reports attributed recent North American warming to elevated GHG
concentrations. In the CCSP (2008) report,\306\ the authors find that
for North America, ``more than half of this warming [for the period
1951-2006] is likely the result of human-caused greenhouse gas forcing
of climate change.''
---------------------------------------------------------------------------

    \305\ Hegerl, G.C. et al. (2007) Understanding and Attributing
Climate Change. In: Climate Change 2007: The Physical Science Basis.
Contribution of Working Group I to the Fourth Assessment Report of
the Intergovernmental Panel on Climate Change [Solomon, S., D. Qin,
M. Manning, Z. Chen, M. Marquis, K.B. Averyt, M. Tignor, and H.L.
Miller (eds.)]. Cambridge University Press, Cambridge, United
Kingdom and New York, NY, USA.
    \306\ CCSP (2008) Reanalysis of Historical Climate Data for Key
Atmospheric Features: Implications for Attribution of Causes of
Observed Change. A Report by the U.S. Climate Change Science Program
and the Subcommittee on Global Change Research [Randall Dole, Martin
Hoerling, and Siegfried Schubert (eds.)]. National Oceanic and
Atmospheric Administration, National Climatic Data Center,
Asheville, NC, 156 pp.
---------------------------------------------------------------------------

    Observations show that changes are occurring in the amount,
intensity, frequency and type of precipitation. Over the contiguous
United States, total annual precipitation increased by 6.1% from 1901
to 2008. It is likely that there have been increases in the number of
heavy precipitation events within many land regions, even in those
where there has been a reduction in total precipitation amount,
consistent with a warming climate.
    There is strong evidence that global sea level gradually rose in
the 20th century and is currently rising at an increased rate. It is
not clear whether the increasing rate of sea level rise is a reflection
of short-term variability or an increase in the longer-term trend.
Nearly all of the Atlantic Ocean shows sea level rise during the last
50 years with the rate of rise reaching a maximum (over 2 millimeters
[mm] per year) in a band along the U.S. east coast running east-
northeast.
    Satellite data since 1979 show that annual average Arctic sea ice
extent has shrunk by 4.1% per decade. The size and speed of recent
Arctic summer sea ice loss is highly anomalous relative to the previous
few thousands of years.
    Widespread changes in extreme temperatures have been observed in
the last 50 years across all world regions, including the United
States. Cold days, cold nights, and frost have become less frequent,
while hot days, hot nights, and heat waves have become more frequent.
    Observational evidence from all continents and most oceans shows
that many natural systems are being affected by regional climate
changes, particularly temperature increases. However, directly
attributing specific regional changes in climate to emissions of GHGs
from human activities is difficult, especially for precipitation.
    Ocean CO2 uptake has lowered the average ocean pH
(increased acidity) level by approximately 0.1 since 1750. Consequences
for marine ecosystems can include reduced calcification by shell-
forming organisms, and in the longer term, the dissolution of carbonate
sediments.
    Observations show that climate change is currently affecting U.S.
physical and biological systems in significant ways. The consistency of
these observed changes in physical and biological systems and the
observed significant warming likely cannot be explained entirely due to
natural variability or other confounding non-climate factors.
c. Projections of Future Climate Change With Continued Increases in
Elevated GHG Concentrations
    Most future scenarios that assume no explicit GHG mitigation
actions (beyond those already enacted) project increasing global GHG
emissions over the century, with climbing GHG concentrations. Carbon
dioxide is expected to remain the dominant anthropogenic GHG over the
course of the 21st century. The radiative forcing associated with the
non-CO2 GHGs is still significant and increasing over time.
    Future warming over the course of the 21st century, even under
scenarios of low-emission growth, is very likely to be greater than
observed warming over the past century. According to climate model
simulations summarized by the IPCC,\307\ through about 2030, the global
warming rate is affected little by the choice of different future
emissions scenarios. By the end of the 21st century, projected average
global warming (compared to average temperature around 1990) varies
significantly depending on the emission scenario and climate
sensitivity assumptions, ranging from 3.2 to 7.2 [deg]F (1.8 to 4.0
[deg]C), with an uncertainty range of 2.0 to 11.5 [deg]F (1.1 to 6.4
[deg]C).
---------------------------------------------------------------------------

    \307\ Meehl, G.A. et al. (2007) Global Climate Projections. In:
Climate Change 2007: The Physical Science Basis. Contribution of
Working Group I to the Fourth Assessment Report of the
Intergovernmental Panel on Climate Change [Solomon, S., D. Qin, M.
Manning, Z. Chen, M. Marquis, K.B. Averyt, M. Tignor and H.L. Miller
(eds.)]. Cambridge University Press, Cambridge, United Kingdom and
New York, NY, USA.
---------------------------------------------------------------------------

    All of the United States is very likely to warm during this
century, and most areas of the United States are expected to warm by
more than the global

average. The largest warming is projected to occur in winter over
northern parts of Alaska. In western, central and eastern regions of
North America, the projected warming has less seasonal variation and is
not as large, especially near the coast, consistent with less warming
over the oceans.
    It is very likely that heat waves will become more intense, more
frequent, and longer lasting in a future warm climate, whereas cold
episodes are projected to decrease significantly.
    Increases in the amount of precipitation are very likely in higher
latitudes, while decreases are likely in most subtropical latitudes and
the southwestern United States, continuing observed patterns. The mid-
continental area is expected to experience drying during summer,
indicating a greater risk of drought.
    Intensity of precipitation events is projected to increase in the
United States and other regions of the world. More intense
precipitation is expected to increase the risk of flooding and result
in greater runoff and erosion that has the potential for adverse water
quality effects.
    It is likely that hurricanes will become more intense, with
stronger peak winds and more heavy precipitation associated with
ongoing increases of tropical sea surface temperatures. Frequency
changes in hurricanes are currently too uncertain for confident
projections.
    By the end of the century, global average sea level is projected by
IPCC \308\ to rise between 7.1 and 23 inches (18 and 59 centimeter
[cm]), relative to around 1990, in the absence of increased dynamic ice
sheet loss. Recent rapid changes at the edges of the Greenland and West
Antarctic ice sheets show acceleration of flow and thinning. While an
understanding of these ice sheet processes is incomplete, their
inclusion in models would likely lead to increased sea level
projections for the end of the 21st century.
---------------------------------------------------------------------------

    \308\ IPCC (2007) Summary for Policymakers. In: Climate Change
2007: The Physical Science Basis. Contribution of Working Group I to
the Fourth Assessment Report of the Intergovernmental Panel on
Climate Change [Solomon, S., D. Qin, M. Manning, Z. Chen, M.
Marquis, K.B. Averyt, M. Tignor and H.L. Miller (eds.)]. Cambridge
University Press, Cambridge, United Kingdom and New York, NY, USA.
---------------------------------------------------------------------------

    Sea ice extent is projected to shrink in the Arctic under all IPCC
emissions scenarios.
d. Projected Risks and Impacts Associated With Future Climate Change
    Risk to society, ecosystems, and many natural Earth processes
increase with increases in both the rate and magnitude of climate
change. Climate warming may increase the possibility of large, abrupt
regional or global climatic events (e.g., disintegration of the
Greenland Ice Sheet or collapse of the West Antarctic Ice Sheet). The
partial deglaciation of Greenland (and possibly West Antarctica) could
be triggered by a sustained temperature increase of 2 to 7 [deg]F (1 to
4 [deg]C) above 1990 levels. Such warming would cause a 13 to 20 feet
(4 to 6 meter) rise in sea level, which would occur over a time period
of centuries to millennia.
    The CCSP \309\ reports that climate change has the potential to
accentuate the disparities already evident in the American health care
system, as many of the expected health effects are likely to fall
disproportionately on the poor, the elderly, the disabled, and the
uninsured. The IPCC \310\ states with very high confidence that climate
change impacts on human health in U.S. cities will be compounded by
population growth and an aging population.
---------------------------------------------------------------------------

    \309\ Ebi, K.L., J. Balbus, P.L. Kinney, E. Lipp, D. Mills, M.S.
O'Neill, and M. Wilson (2008) Effects of Global Change on Human
Health. In: Analyses of the effects of global change on human health
and welfare and human systems. A Report by the U.S. Climate Change
Science Program and the Subcommittee on Global Change Research.
[Gamble, J.L. (ed.), K.L. Ebi, F.G. Sussman, T.J. Wilbanks,
(Authors)]. U.S. Environmental Protection Agency, Washington, DC,
USA, pp. 2-1 to 2-78.
    \310\ Field, C.B. et al. (2007) North America. In: Climate
Change 2007: Impacts, Adaptation and Vulnerability. Contribution of
Working Group II to the Fourth Assessment Report of the
Intergovernmental Panel on Climate Change [M.L. Parry, O.F.
Canziani, J.P. Palutikof, P.J. van der Linden and C.E. Hanson
(eds.)]. Cambridge University Press, Cambridge, United Kingdom and
New York, NY, USA.
---------------------------------------------------------------------------

    Severe heat waves are projected to intensify in magnitude and
duration over the portions of the United States where these events
already occur, with potential increases in mortality and morbidity,
especially among the elderly, young, and frail.
    Some reduction in the risk of death related to extreme cold is
expected. It is not clear whether reduced mortality from cold will be
greater or less than increased heat-related mortality in the United
States due to climate change.
    Increases in regional ozone pollution relative to ozone levels
without climate change are expected due to higher temperatures and
weaker circulation in the United States and other world cities relative
to air quality levels without climate change. Climate change is
expected to increase regional ozone pollution, with associated risks in
respiratory illnesses and premature death. In addition to human health
effects, tropospheric ozone has significant adverse effects on crop
yields, pasture and forest growth, and species composition. The
directional effect of climate change on ambient particulate matter
levels remains uncertain.
    Within settlements experiencing climate change, certain parts of
the population may be especially vulnerable; these include the poor,
the elderly, those already in poor health, the disabled, those living
alone, and/or indigenous populations dependent on one or a few
resources. Thus, the potential impacts of climate change raise
environmental justice issues.
    The CCSP \311\ concludes that, with increased CO2 and
temperature, the life cycle of grain and oilseed crops will likely
progress more rapidly. But, as temperature rises, these crops will
increasingly begin to experience failure, especially if climate
variability increases and precipitation lessens or becomes more
variable. Furthermore, the marketable yield of many horticultural crops
(e.g., tomatoes, onions, fruits) is very likely to be more sensitive to
climate change than grain and oilseed crops.
---------------------------------------------------------------------------

    \311\ Backlund, P., A. Janetos, D.S. Schimel, J. Hatfield, M.G.
Ryan, S.R. Archer, and D. Lettenmaier (2008) Executive Summary. In:
The Effects of Climate Change on Agriculture, Land Resources, Water
Resources, and Biodiversity in the United States. A Report by the
U.S. Climate Change Science Program and the Subcommittee on Global
Change Research. Washington, DC., USA, 362 pp.
---------------------------------------------------------------------------

    Higher temperatures will very likely reduce livestock production
during the summer season in some areas, but these losses will very
likely be partially offset by warmer temperatures during the winter
season.
    Cold-water fisheries will likely be negatively affected; warm-water
fisheries will generally benefit; and the results for cool-water
fisheries will be mixed, with gains in the northern and losses in the
southern portions of ranges.
    Climate change has very likely increased the size and number of
forest fires, insect outbreaks, and tree mortality in the interior
West, the Southwest, and Alaska, and will continue to do so. Over North
America, forest growth and productivity have been observed to increase
since the middle of the 20th century, in part due to observed climate
change. Rising CO2 will very likely increase photosynthesis
for forests, but the increased photosynthesis will likely only increase
wood production in young forests on fertile soils. The combined effects
of expected increased temperature, CO2, nitrogen deposition,
ozone, and forest

disturbance on soil processes and soil carbon storage remain unclear.
    Coastal communities and habitats will be increasingly stressed by
climate change impacts interacting with development and pollution. Sea
level is rising along much of the U.S. coast, and the rate of change
will very likely increase in the future, exacerbating the impacts of
progressive inundation, storm-surge flooding, and shoreline erosion.
Storm impacts are likely to be more severe, especially along the Gulf
and Atlantic coasts. Salt marshes, other coastal habitats, and
dependent species are threatened by sea level rise, fixed structures
blocking landward migration, and changes in vegetation. Population
growth and rising value of infrastructure in coastal areas increases
vulnerability to climate variability and future climate change.
    Climate change will likely further constrain already overallocated
water resources in some regions of the United States, increasing
competition among agricultural, municipal, industrial, and ecological
uses. Although water management practices in the United States are
generally advanced, particularly in the West, the reliance on past
conditions as the basis for current and future planning may no longer
be appropriate, as climate change increasingly creates conditions well
outside of historical observations. Rising temperatures will diminish
snowpack and increase evaporation, affecting seasonal availability of
water. In the Great Lakes and major river systems, lower water levels
are likely to exacerbate challenges relating to water quality,
navigation, recreation, hydropower generation, water transfers, and
binational relationships. Decreased water supply and lower water levels
are likely to exacerbate challenges relating to aquatic navigation in
the United States.
    Higher water temperatures, increased precipitation intensity, and
longer periods of low flows will exacerbate many forms of water
pollution, potentially making attainment of water quality goals more
difficult. As waters become warmer, the aquatic life they now support
will be replaced by other species better adapted to warmer water. In
the long term, warmer water and changing flow may result in
deterioration of aquatic ecosystems.
    Ocean acidification is projected to continue, resulting in the
reduced biological production of marine calcifiers, including corals.
    Climate change is likely to affect U.S. energy use and energy
production and physical and institutional infrastructures. It will also
likely interact with and possibly exacerbate ongoing environmental
change and environmental pressures in settlements, particularly in
Alaska where indigenous communities are facing major environmental and
cultural impacts. The U.S. energy sector, which relies heavily on water
for hydropower and cooling capacity, may be adversely impacted by
changes to water supply and quality in reservoirs and other water
bodies. Water infrastructure, including drinking water and wastewater
treatment plants, and sewer and stormwater management systems, will be
at greater risk of flooding, sea level rise and storm surge, low flows,
and other factors that could impair performance.
    Disturbances such as wildfires and insect outbreaks are increasing
in the United States and are likely to intensify in a warmer future
with warmer winters, drier soils, and longer growing seasons. Although
recent climate trends have increased vegetation growth, continuing
increases in disturbances are likely to limit carbon storage,
facilitate invasive species, and disrupt ecosystem services.
    Over the 21st century, changes in climate will cause species to
shift north and to higher elevations and fundamentally rearrange U.S.
ecosystems. Differential capacities for range shifts and constraints
from development, habitat fragmentation, invasive species, and broken
ecological connections will alter ecosystem structure, function, and
services.
    Climate change impacts will vary in nature and magnitude across
different regions of the United States.
     Sustained high summer temperatures, heat waves, and
declining air quality are projected in the Northeast,\312\
Southeast,\313\ Southwest,\314\ and Midwest.\315\ Projected climate
change would continue to cause loss of sea ice, glacier retreat,
permafrost thawing, and coastal erosion in Alaska.
---------------------------------------------------------------------------

    \312\ Northeast includes West Virginia, Maryland, Delaware,
Pennsylvania, New Jersey, New York, Connecticut, Rhode Island,
Massachusetts, Vermont, New Hampshire, and Maine.
    \313\ Southeast includes Kentucky, Virginia, Arkansas,
Tennessee, North Carolina, South Carolina, southeast Texas,
Louisiana, Mississippi, Alabama, Georgia, and Florida.
    \314\ Southwest includes California, Nevada, Utah, western
Colorado, Arizona, New Mexico (except the extreme eastern section),
and southwest Texas.
    \315\ The Midwest includes Minnesota, Wisconsin, Michigan, Iowa,
Illinois, Indiana, Ohio, and Missouri.
---------------------------------------------------------------------------

     Reduced snowpack, earlier spring snowmelt, and increased
likelihood of seasonal summer droughts are projected in the Northeast,
Northwest,\316\ and Alaska. More severe, sustained droughts and water
scarcity are projected in the Southeast, Great Plains,\317\ and
Southwest.
---------------------------------------------------------------------------

    \316\ The Northwest includes Washington, Idaho, western Montana,
and Oregon.
    \317\ The Great Plains includes central and eastern Montana,
North Dakota, South Dakota, Wyoming, Nebraska, eastern Colorado,
Nebraska, Kansas, extreme eastern New Mexico, central Texas, and
Oklahoma.
---------------------------------------------------------------------------

     The Southeast, Midwest, and Northwest in particular are
expected to be impacted by an increased frequency of heavy downpours
and greater flood risk.
     Ecosystems of the Southeast, Midwest, Great Plains,
Southwest, Northwest, and Alaska are expected to experience altered
distribution of native species (including local extinctions), more
frequent and intense wildfires, and an increase in insect pest
outbreaks and invasive species.
     Sea level rise is expected to increase storm surge height
and strength, flooding, erosion, and wetland loss along the coasts,
particularly in the Northeast, Southeast, and islands.
     Warmer water temperatures and ocean acidification are
expected to degrade important aquatic resources of islands and coasts
such as coral reefs and fisheries.
     A longer growing season, low levels of warming, and
fertilization effects of carbon dioxide may benefit certain crop
species and forests, particularly in the Northeast and Alaska.
Projected summer rainfall increases in the Pacific islands may augment
limited freshwater supplies. Cold-related mortality is projected to
decrease, especially in the Southeast. In the Midwest in particular,
heating oil demand and snow-related traffic accidents are expected to
decrease.
    Climate change impacts in certain regions of the world may
exacerbate problems that raise humanitarian, trade, and national
security issues for the United States. The IPCC \318\ identifies the
most vulnerable world regions as the Arctic, because of the effects of
high rates of projected warming on natural systems; Africa, especially
the sub-Saharan region, because of current low adaptive capacity as
well as climate change; small islands, due to high exposure of
population and infrastructure to risk of sea level rise

and increased storm surge; and Asian mega-deltas, such as the Ganges-
Brahmaputra and the Zhujiang, due to large populations and high
exposure to sea level rise, storm surge and river flooding. Climate
change has been described as a potential threat multiplier with regard
to national security issues.
---------------------------------------------------------------------------

    \318\ Parry, M.L. et al. (2007) Technical Summary. In: Climate
Change 2007: Impacts, Adaptation and Vulnerability. Contribution of
Working Group II to the Fourth Assessment Report of the
Intergovernmental Panel on Climate Change [M.L. Parry, O.F.
Canziani, J.P. Palutikof, P.J. van der Linden, and C.E. Hanson
(eds.)], Cambridge University Press, Cambridge, United Kingdom, pp.
23-78.
---------------------------------------------------------------------------

3. Changes in Global Climate Indicators Associated With the Rule's GHG
Emissions Reductions
    EPA examined \319\ the reductions in CO2 and other GHGs
associated with this action and analyzed the projected effects on
global mean surface temperature and sea level, two common indicators of
climate change. The analysis projects that this action will reduce
climate warming and sea level rise. Although the projected reductions
are small in overall magnitude by themselves, they are quantifiable and
would contribute to reducing climate change risks. A commenter agreed
that the modeling results showed small, but quantifiable, reductions in
the global atmospheric CO2 concentration, as well as a
reduction in projected global mean surface temperature and sea level
rise, from implementation of this action, across all climate
sensitivities. As such, the commenter encourages the agencies to move
forward with this action while continuing to develop additional, more
stringent vehicle standards beyond 2016.
---------------------------------------------------------------------------

    \319\ Using the Model for the Assessment of Greenhouse Gas
Induced Climate Change (MAGICC, http://www.cgd.ucar.edu/cas/wigley/
magicc/), EPA estimated the effects of this action's greenhouse gas
emissions reductions on global mean temperature and sea level.
Please refer to Chapter 7.4 of the RIA for additional information.
---------------------------------------------------------------------------

    Another commenter indicated that the projected changes in climate
impacts resulting from this action are small and therefore not
meaningful. EPA disagrees with this view as the reductions may be small
in overall magnitude, but in the global climate change context, they
are quantifiable showing a clear directional signal across a range of
climate sensitivities.320 321 EPA therefore determines that
the projected reductions in atmospheric CO2, global mean
temperature and sea level rise are meaningful in the context of this
rule. EPA addresses this point further in the Response to Comments
document. For the final rule, EPA provides an additional climate change
impact analysis for projected changes in ocean pH in the context of
this action. In addition, EPA updated the modeling analysis based on
the revised GHG emission reductions provided in Section III.F.1;
however, the change in modeling results was very small in magnitude.
Based on the reanalysis the results for projected atmospheric
CO2 concentrations are estimated to be reduced by an average
of 2.9 ppm (previously 3.0 ppm), global mean temperature is estimated
to be reduced by 0.006 to 0.015 [deg]C by 2100 (previously 0.007 to
0.016 [deg]C) and sea-level rise is projected to be reduced by
approximately 0.06-0.14cm by 2100 (previously 0.06-0.15cm).
---------------------------------------------------------------------------

    \320\ The National Research Council (NRC) 2001 study, Climate
Change Science: An Analysis of Some Key Questions, defines climate
sensitivity as the sensitivity of the climate system to a forcing is
commonly expressed in terms of the global mean temperature change
that would be expected after a time sufficiently long enough for
both the atmosphere and ocean to come to equilibrium with the change
in climate forcing.
    \321\ To capture some of the uncertainty in the climate system,
the changes in atmospheric CO2, projected temperatures
and sea level were estimated across the most current
Intergovernmental Panel on Climate Change (IPCC) range of climate
sensitivities, 1.5 [deg]C to 6.0 [deg]C.
---------------------------------------------------------------------------

a. Estimated Projected Reductions in Atmospheric CO2
Concentration, Global Mean Surface Temperatures Sea Level Rise and
Ocean pH
    EPA estimated changes in the atmospheric CO2
concentration, global mean surface temperature and sea level to 2100
resulting from the emissions reductions in this action using the Model
for the Assessment of Greenhouse Gas Induced Climate Change (MAGICC,
version 5.3). This widely-used, peer reviewed modeling tool was also
used to project temperature and sea level rise under different
emissions scenarios in the Third and Fourth Assessments of the
Intergovernmental Panel on Climate Change (IPCC).
    GHG emissions reductions from Section III.F.1 were applied as net
reductions to a peer reviewed global reference case (or baseline)
emissions scenario to generate an emissions scenario specific to this
action. For the scenario related to this action, all emissions
reductions were assumed to begin in 2012, with zero emissions change in
2011 (from the reference case) followed by emissions linearly
increasing to equal the value supplied in Section III.F.1 for 2020 and
then continuing to 2100. Details about the reference case scenario and
how the emissions reductions were applied to generate the scenario can
be found in the RIA Chapter 7.
    Changes in atmospheric CO2 concentration, temperature,
and sea-level for both the reference case and the emissions scenarios
associated with this action were computed using MAGICC. To compute the
reductions in the atmospheric CO2 concentrations as well as
in temperature and sea level resulting from this action, the output
from the scenario associated with this final rule was subtracted from
an existing Global Change Assessment Model (GCAM, formerly MiniCAM)
reference emission scenario. To capture some key uncertainties in the
climate system with the MAGICC model, changes in temperature and sea-
level rise were projected across the most current IPCC range for
climate sensitivities which ranges from 1.5 [deg]C to 6.0 [deg]C
(representing the 90% confidence interval).\322\ This wide range
reflects the uncertainty in this measure of how much the global mean
temperature would rise if the concentration of carbon dioxide in the
atmosphere were to double. Details about this modeling analysis can be
found in the RIA Chapter 7.4.
---------------------------------------------------------------------------

    \322\ In IPCC reports, equilibrium climate sensitivity refers to
the equilibrium change in the annual mean global surface temperature
following a doubling of the atmospheric equivalent carbon dioxide
concentration. The IPCC states that climate sensitivity is
``likely'' to be in the range of 2 [deg]C to 4.5 [deg]C, ``very
unlikely'' to be less than 1.5 [deg]C, and ``values substantially
higher than 4.5 [deg]C cannot be excluded.'' IPCC WGI, 2007, Climate
Change 2007--The Physical Science Basis, Contribution of Working
Group I to the Fourth Assessment Report of the IPCC, http://
www.ipcc.ch/.
---------------------------------------------------------------------------

    The results of this modeling, summarized in Table III.F.3-1, show
small, but quantifiable, reductions in atmospheric CO2
concentrations, projected global mean surface temperature and sea level
resulting from this action, across all climate sensitivities. As a
result of the emission reductions from this action, the atmospheric
CO2 concentration is projected to be reduced by an average
of 2.9 parts per million (ppm), the global mean temperature is
projected to be reduced by approximately 0.006-0.015[deg]C by 2100, and
global mean sea level rise is projected to be reduced by approximately
0.06-0.14cm by 2100. The reductions are small relative to the IPCC's
2100 ``best estimates'' for global mean temperature increases (1.8-4.0
[deg]C) and sea level rise (0.20-0.59m) for all global GHG emissions
sources for a range of emissions scenarios. EPA used a peer reviewed
model, the MAGICC model, to do this analysis. This analysis is specific
to this rule and therefore does not come from previously published
work. Further discussion of EPA's modeling analysis is found in the
final RIA.

    Table III.F.3-1--Effect of GHG Emissions Reductions on Projected Changes in Global Climate for the Final
                                               Vehicles Rulemaking
                              [For climate sensitivities ranging from 1.5-6 [deg]C]
----------------------------------------------------------------------------------------------------------------
                    Measure                                   Units                    Year     Projected change
----------------------------------------------------------------------------------------------------------------
Atmospheric CO2 Concentration.................  ppm..............................         2100          -2.7-3.1
Global Mean Surface Temperature...............  [deg]C...........................         2100      -0.006-0.015
Sea Level Rise................................  Cm...............................         2100        -0.06-0.14
Ocean pH......................................  pH units.........................         2100            0.0014
----------------------------------------------------------------------------------------------------------------

    As a substantial portion of CO2 emitted into the
atmosphere is not removed by natural processes for millennia, each unit
of CO2 not emitted into the atmosphere avoids essentially
permanent climate change on centennial time scales. Though the
magnitude of the avoided climate change projected here is small, these
reductions would represent a reduction in the adverse risks associated
with climate change (though these risks were not formally estimated for
this action) across all climate sensitivities.
    The IPCC \323\ has noted that ocean acidification due to the direct
effects of elevated CO2 concentrations will impair a wide
range of planktonic and other marine organisms that use aragonite to
make their shells or skeletons. EPA used the Program CO2SYS,\324\
version 1.05 to estimate projected changes in tropical ocean pH based
on the atmospheric CO2 concentration reductions resulting
from this action and other specified input conditions (e.g., sea
surface temperature characteristic of tropical waters). The program
performs calculations relating parameters of the carbon dioxide
(CO2) system in seawater. EPA used the program to calculate
ocean pH as a function of atmospheric CO2, among other
specified input conditions. Based on the projected atmospheric
CO2 concentration reductions (average of 2.9 ppm by 2100)
that would result from this rule, the program calculates an increase in
ocean pH of about 0.0014 pH units in 2100. Thus, this analysis
indicates the projected decrease in atmospheric CO2
concentrations from today's rule would result in an increase in ocean
pH.
---------------------------------------------------------------------------

    \323\ Fischlin, A. et al. (2007) Ecosystems, their Properties,
Goods, and Services. In: Climate Change 2007: Impacts, Adaptation
and Vulnerability. Contribution of Working Group II to the Fourth
Assessment Report of the Intergovernmental Panel on Climate Change
[M.L. Parry, O.F. Canziani, J.P. Palutikof, P.J. van der Linden and
C.E. Hanson (eds.)]. Cambridge University Press, Cambridge, United
Kingdom and New York, NY, USA.
    \324\ Lewis, E., and D. W. R. Wallace. 1998. Program Developed
for CO2 System Calculations. ORNL/CDIAC-105. Carbon
Dioxide Information Analysis Center, Oak Ridge National Laboratory,
U.S. Department of Energy, Oak Ridge, Tennessee.
---------------------------------------------------------------------------

    EPA's analysis of the rule's effect on global climate conditions is
intended to quantify these potential reductions using the best
available science. While EPA's modeling results of the effect of this
rule alone show small differences in climate effects (CO2
concentration, temperature, sea-level rise, ocean pH), when expressed
in terms of global climate endpoints and global GHG emissions, they
yield results that are repeatable and consistent within the modeling
frameworks used.

G. How will the standards impact non-GHG emissions and their associated
effects?

    In addition to reducing the emissions of greenhouse gases, this
rule will influence the emissions of ``criteria'' air pollutants and
air toxics (i.e., hazardous air pollutants). The criteria air
pollutants include carbon monoxide (CO), fine particulate matter
(PM2.5), sulfur dioxide (SOX) and the ozone precursors
hydrocarbons (VOC) and oxides of nitrogen (NOX); the air
toxics include benzene, 1,3-butadiene, formaldehyde, acetaldehyde, and
acrolein. Our estimates of these non-GHG emission impacts from the GHG
program are shown by pollutant in Table III.G-1 and Table III.G-2 in
total, and broken down by the two drivers of these changes: (a)
``Upstream'' emission reductions due to decreased extraction,
production and distribution of motor gasoline; and (b) ``downstream''
emission increases, reflecting the effects of VMT rebound (discussed in
Sections III.F and III.H) and the effects of our assumptions about
ethanol-blended fuel (E10), as discussed below. Total program impacts
on criteria and toxics emissions are discussed below, followed by
individual discussions of the upstream and downstream impacts. Those
are followed by discussions of the effects on air quality, health, and
other environmental concerns.
    As in the proposal, for this analysis we attribute decreased fuel
consumption from this program to gasoline only, while assuming no
effect on volumes of ethanol and other renewable fuels because they are
mandated under the Renewable Fuel Standard (RFS2). However, because
this rule does not assume RFS2 volumes of ethanol in the baseline, the
result is a greater projected market share of E10 in the control
case.\325\ In fact, the GHG standards will not be affecting the market
share of E10, because EPA's analysis for the RFS2 rule predicts 100%
E10 penetration by 2014.\326\
---------------------------------------------------------------------------

    \325\ When this rule's analysis was initiated, the RFS2 rule was
not yet final. Therefore, it assumes the ethanol volumes in Annual
Energy Outlook 2007 (U.S. Energy Information Administration, Annual
Energy Outlook 2007, Transportation Demand Sector Supplemental
Table. http://www.eia.doe.gov/oiaf/archive/aeo07/supplement/
index.html)
    \326\ EPA 2010, Renewable Fuel Standard Program (RFS2)
Regulatory Impact Analysis. EPA-420-R-10-006. February 2010. Docket
EPA-HQ-OAR-2009-0472-11332. See also 75 FR 14670, March 26, 2010.
---------------------------------------------------------------------------

    The amount of E10 affects downstream non-GHG emissions. In the
proposal, EPA stated these same fuel assumptions and qualitatively
noted that there were likely unquantified impacts on non-GHG emissions
between the two cases. In DRIA Chapter 5, EPA indicated its plans to
quantify these impacts in the air quality modeling and in the final
rule inventories. Upstream emission impacts depend only on fuel
volumes, so the impacts presented here reflect only the reduced
gasoline consumption.
    The inventories presented in this rulemaking include an analysis of
these fuel effects which was conducted using EPA's Motor Vehicle
Emission Simulator (MOVES2010). The most notable impact, although still
relatively slight, is a 2.2 percent increase in 2030 in national
acetaldehyde emissions over the baseline scenario. It should be noted
that these emission impacts are not due to the new GHG vehicle
standards. These impacts are instead a consequence of the assumed
ethanol volumes. This program does not mandate an increase in E10, nor
any particular fuel blend. The emission impact of this shift was also
modeled in the RFS2 rule.
    As shown in Table III.G-1, EPA estimates that this program would
result in reductions of NOX, VOC, PM and

SOX, but would increase CO emissions. For NOX,
VOC, and PM we estimate net reductions because the emissions reductions
from upstream sources are larger than the emission increases due to
downstream sources. In the case of CO, we estimate slight emission
increases, because there are relatively small reductions in upstream
emissions, and thus the projected downstream emission increases are
greater than the projected emission decreases due to reduced fuel
production. For SOX, downstream emissions are roughly
proportional to fuel consumption, therefore a decrease is seen in both
upstream and downstream sources.
    For all criteria pollutants the overall impact of the program would
be relatively small compared to total U.S. inventories across all
sectors. In 2030, EPA estimates the program would reduce total
NOX, PM and SOX inventories by 0.1 to 0.8 percent
and reduce the VOC inventory by 1.0 percent, while increasing the total
national CO inventory by 0.6 percent.
    As shown in Table III.G-2, EPA estimates that the GHG program would
result in small changes for air toxic emissions compared to total U.S.
inventories across all sectors. In 2030, EPA estimates the program
would reduce total benzene and 1,3 butadiene emissions by 0.1 to 0.3
percent. Total acrolein and formaldehyde emissions would increase by
0.1 percent. Acetaldehyde emissions would increase by 2.2 percent.
    One commenter requested that EPA present emission inventories for
additional air toxics. EPA is presenting inventories for certain air
toxic emissions which were identified as key national and regional-
scale cancer and noncancer risk drivers in past National Air Toxics
Assessments (NATA). For additional details, please refer to the
Response to Comments document.\327\
---------------------------------------------------------------------------

    \327\ U.S. EPA. National Air Toxics Assessment. 2002, 1999, and
1996. Available at: http://www.epa.gov/nata/.
---------------------------------------------------------------------------

    Other factors which may impact non-GHG emissions, but are not
estimated in this analysis, include:
     Vehicle technologies used to reduce tailpipe
CO2 emissions; because the regulatory standards for non-GHG
emissions are the primary driver for these emissions, EPA expects the
impact of this program to be negligible on non-GHG emission rates per
mile.
     The potential for increased market penetration of diesel
vehicles; because these vehicles would be held to the same
certification and in-use standards for criteria pollutants as their
gasoline counterparts, EPA expects their impact to be negligible on
criteria pollutants and other non-GHG emissions. EPA does not project
increased penetration of diesels as necessary to meet the GHG
standards.
     Early introduction of electric vehicles and plug-in hybrid
electric vehicles, which would reduce criteria emissions in cases where
those vehicles are able to be certified to lower certification
standards. This would also likely reduce gaseous air toxics.
     Reduced refueling emissions due to less frequent refueling
events and reduced annual refueling volumes resulting from the GHG
standards.
     Increased hot soak evaporative emissions due to the likely
increase in number of trips associated with VMT rebound modeled in this
rule.

                           Table III.G-1--Annual Criteria Emission Impacts of Program
                                                  [Short tons]
----------------------------------------------------------------------------------------------------------------
                                          Total impacts           Upstream impacts         Downstream impacts
                                   -----------------------------------------------------------------------------
                                        2020         2030         2020         2030         2020         2030
----------------------------------------------------------------------------------------------------------------
VOC...............................      -60,187     -115,542      -64,506     -126,749        4,318       11,207
    % of total inventory..........       -0.51%       -1.01%       -0.55%       -1.11%        0.04%        0.01%
CO................................        3,992      170,675       -6,165      -12,113       10,156      182,788
    % of total inventory..........        0.01%        0.56%       -0.02%       -0.04%        0.01%         0.6%
NOX...............................       -5,881      -21,763      -19,291      -37,905       13,410       16,143
    % of total inventory..........        -0.02       -0.07%       -0.06%       -0.12%        0.04%        0.05%
PM2.5.............................       -2,398       -4,564       -2,629       -5,165        231.0        602.3
    % of total inventory..........       -0.03%       -0.05%       -0.03%       -0.06%        0.00%        0.01%
SOX...............................      -13,832      -27,443      -11,804      -23,194       -2,027       -4,249
    % of total inventory..........       -0.41%       -0.82%       -0.35%       -0.69%       -0.06%       -0.13%
----------------------------------------------------------------------------------------------------------------

                           Table III.G-2--Annual Air Toxic Emission Impacts of Program
                                                  [Short tons]
----------------------------------------------------------------------------------------------------------------
                                          Total impacts           Upstream impacts         Downstream impacts
                                   -----------------------------------------------------------------------------
                                        2020         2030         2020         2030         2020         2030
----------------------------------------------------------------------------------------------------------------
1,3[dash]Butadiene................          -95          -21         -1.5         -3.0        -93.6        -18.1
    % of total inventory..........       -0.38%       -0.10%       -0.01%       -0.01%       -0.37%       -0.09%
Acetaldehyde......................          760          668         -6.8        -13.4        766.9        681.5
    % of total inventory..........        2.26%        2.18%       -0.02%       -0.04%        2.28%        2.22%
Acrolein..........................            1            5         -0.9         -1.8          1.7          6.5
    % of total inventory..........        0.01%        0.07%       -0.01%       -0.03%        0.03%        0.10%
Benzene...........................         -890         -523       -139.6       -274.3       -750.0       -248.3
    % of total inventory..........       -0.48%       -0.29%       -0.08%       -0.15%       -0.40%       -0.14%
Formaldehyde......................          -49           15        -51.4       -101.0          2.1        116.3
    % of total inventory..........       -0.06%        0.02%       -0.06%       -0.12%        0.00%        0.14%
----------------------------------------------------------------------------------------------------------------

1. Upstream Impacts of Program
    No substantive comments were received on the upstream inventory
modeling used in the proposal. The rulemaking inventories were updated
with the revised estimates of fuel savings as detailed in Section
III.F.
    Reducing tailpipe CO2 emissions from light-duty cars and
trucks through tailpipe standards and improved A/C efficiency will
result in reduced fuel demand and reductions in the emissions
associated with all of the processes involved in getting petroleum to
the pump. These upstream emission impacts on criteria pollutants are
summarized in Table III.G-1. The upstream reductions grow over time as
the fleet turns over to cleaner CO2 vehicles, so that by
2030 VOC would decrease by 127,000 tons, NOX by 38,000 tons,
and PM2.5 by 5,000 tons. Table III.G-2 shows the
corresponding impacts on upstream air toxic emissions in 2030.
Formaldehyde decreases by 101 tons, benzene by 274 tons, acetaldehyde
by 13 tons, acrolein by 2 tons, and 1,3-butadiene by 3 tons.
    To determine these impacts, EPA estimated the impact of reduced
petroleum volumes on the extraction and transportation of crude oil as
well as the production and distribution of finished gasoline. For the
purpose of assessing domestic-only emission reductions it was necessary
to estimate the fraction of fuel savings attributable to domestic
finished gasoline, and of this gasoline what fraction is produced from
domestic crude. For this analysis EPA estimated that 50 percent of fuel
savings is attributable to domestic finished gasoline and that 90
percent of this gasoline originated from imported crude. Emission
factors for most upstream emission sources are based on the GREET1.8
model, developed by DOE's Argonne National Laboratory,\328\ but in some
cases the GREET values were modified or updated by EPA to be consistent
with the National Emission Inventory (NEI).\329\ The primary updates
for this analysis were to incorporate newer information on gasoline
distribution emissions for VOC from the NEI, which were significantly
higher than GREET estimates; and the incorporation of upstream emission
factors for the air toxics estimated in this analysis: benzene, 1,3-
butadiene, acetaldehyde, acrolein, and formaldehyde. The development of
these emission factors is detailed in RIA Chapter 5.
---------------------------------------------------------------------------

    \328\ Greenhouse Gas, Regulated Emissions, and Energy Use in
Transportation model (GREET), U.S. Department of Energy, Argonne
National Laboratory, http://www.transportation.anl.gov/modeling_
simulation/GREET/.
    \329\ U.S. EPA. 2002 National Emissions Inventory (NEI) Data and
Documentation, http://www.epa.gov/ttn/chief/net/2002inventory.html.
---------------------------------------------------------------------------

2. Downstream Impacts of Program
    No substantive comments were received on the emission modeling or
emission inventories presented in this section. However, two changes in
modeling differentiate the analysis presented here from that presented
in the proposal. Economic inputs such as fuel prices and vehicle sales
were updated from AEO 2009 to AEO 2010 Early Release, and as described
above, the effects of ethanol volume assumptions were explicitly
modeled. Thus, the primary differences in non-GHG emissions between the
proposed rule and final rule are attributed more to these changes in
analytic inputs, and less to changes in the GHG standards program.
    Downstream emission impacts attributable to this program are due to
the VMT rebound effect and the ethanol volume assumptions. As discussed
in more detail in Section III.H, the effect of fuel cost on VMT
(``rebound'') was accounted for in our assessment of economic and
environmental impacts of this rule. A 10 percent rebound case was used
for this analysis, meaning that VMT for affected model years is modeled
as increasing by 10 percent as much as the increase in fuel economy;
i.e., a 10 percent increase in fuel economy would yield approximately a
1 percent increase in VMT.
    As detailed in the introduction to this section, fuel composition
also has effects on vehicle emissions and particularly air toxics. The
relationship between fuel composition and emission impacts used in
MOVES2010 and applied in this analysis match those developed for the
recent Renewable Fuels Standard (RFS2) requirement, and are extensively
documented in the RFS2 RIA and supporting documents.\330\
---------------------------------------------------------------------------

    \330\ EPA 2010, Renewable Fuel Standard Program (RFS2)
Regulatory Impact Analysis. EPA-420-R-10-006. February 2010. Docket
EPA-HQ-OAR-2009-0472-11332. See also 75 FR 14670, March 26, 2010.
---------------------------------------------------------------------------

    Downstream emission impacts of the rebound effect are summarized in
Table III.G-1 for criteria pollutants and precursors and Table III.G-2
for air toxics. The emission impacts from the rebound effect and the
change in fuel supply grow over time as the fleet turns over to cleaner
CO2 vehicles, so that by 2030 VOC would increase by 11,000
tons, NOX by 16,000 tons, and PM2.5 by 600 tons.
Table III.G-2 shows the corresponding impacts on air toxic emissions.
These impacts in 2030 include 18 fewer tons of 1,3-butadiene, 668
additional tons of acetaldehyde, 248 fewer tons of benzene, 116
additional tons of formaldehyde, and 6.5 additional tons of acrolein.
    For this analysis, MOVES2010 was used to estimate base VOC, CO,
NOX, PM and air toxics emissions for both control and
reference cases. Rebound emissions from light duty cars and trucks were
then calculated using the OMEGA model post-processor and added to the
control case. A more complete discussion of the inputs, methodology,
and results is contained in RIA Chapter 5.
3. Health Effects of Non-GHG Pollutants
    In this section we discuss health effects associated with exposure
to some of the criteria and air toxics impacted by the vehicle
standards; PM, ozone, NOX and SOX, CO and air
toxics. No substantive comments were received on the health effects of
non-GHG pollutants.
a. Particulate Matter
i. Background
    Particulate matter is a generic term for a broad class of
chemically and physically diverse substances. It can be principally
characterized as discrete particles that exist in the condensed (liquid
or solid) phase spanning several orders of magnitude in size. Since
1987, EPA has delineated that subset of inhalable particles small
enough to penetrate to the thoracic region (including the
tracheobronchial and alveolar regions) of the respiratory tract
(referred to as thoracic particles). Current NAAQS use PM2.5
as the indicator for fine particles (with PM2.5 referring to
particles with a nominal mean aerodynamic diameter less than or equal
to 2.5 [mu]m), and use PM10 as the indicator for purposes of
regulating the coarse fraction of PM10 (referred to as
thoracic coarse particles or coarse-fraction particles; generally
including particles with a nominal mean aerodynamic diameter greater
than 2.5 [mu]m and less than or equal to 10 [mu]m, or
PM10-2.5). Ultrafine particles are a subset of fine
particles, generally less than 100 nanometers (0.1 [mu]m) in
aerodynamic diameter.
    Fine particles are produced primarily by combustion processes and
by transformations of gaseous emissions (e.g., SOX,
NOX and VOC) in the atmosphere. The chemical and physical
properties of PM2.5 may vary greatly with time, region,
meteorology, and source category. Thus, PM2.5 may include a
complex mixture of different pollutants including sulfates, nitrates,
organic compounds, elemental carbon

and metal compounds. These particles can remain in the atmosphere for
days to weeks and travel hundreds to thousands of kilometers.
ii. Health Effects of PM
    Scientific studies show ambient PM is associated with a series of
adverse health effects. These health effects are discussed in detail in
EPA's Integrated Science Assessment for Particulate Matter (ISA).\331\
Further discussion of health effects associated with PM can also be
found in the RIA for this rule. The ISA summarizes evidence associated
with PM2.5, PM10-2.5, and ultrafine particles
(UFPs).
---------------------------------------------------------------------------

    \331\ U.S. EPA (2009) Integrated Science Assessment for
Particulate Matter. EPA 600/R-08/139F, Docket EPA-HQ-OAR-2009-0472-
11295.
---------------------------------------------------------------------------

    The ISA concludes that health effects associated with short-term
exposures (hours to days) to ambient PM2.5 include non-fatal
cardiovascular effects, mortality, and respiratory effects, such as
exacerbation of asthma symptoms in children and hospital admissions and
emergency department visits for chronic obstructive pulmonary disease
(COPD) and respiratory infections.\332\ The ISA notes that long-term
exposure to PM2.5 (months to years) is associated with the
development/progression of cardiovascular disease, premature mortality,
and respiratory effects, including reduced lung function growth,
increased respiratory symptoms, and asthma development.\333\ The ISA
concludes that that the currently available scientific evidence from
epidemiologic, controlled human exposure studies, and toxicological
studies supports that a causal association exists between short- and
long-term exposures to PM2.5 and cardiovascular effects and
mortality. Furthermore, the ISA concludes that the collective evidence
supports likely causal associations between short- and long-term
PM2.5 exposures and respiratory effects. The ISA also
concludes that the evidence is suggestive of a causal association for
reproductive and developmental effects and cancer, mutagenicity, and
genotoxicity and long-term exposure to PM2.5.\334\
---------------------------------------------------------------------------

    \332\ U.S. EPA (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, 2009. Section <IP_ADDRESS>.
    \333\ U.S. EPA (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, 2009. page 2-12, Sections
<IP_ADDRESS> and <IP_ADDRESS>.
    \334\ U.S. EPA (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, 2009. Section 2.3.2.
---------------------------------------------------------------------------

    For PM10-2.5, the ISA concludes that the current
evidence is suggestive of a causal relationship between short-term
exposures and cardiovascular effects, such as hospitalization for
ischemic heart disease. There is also suggestive evidence of a causal
relationship between short-term PM10-2.5 exposure and
mortality and respiratory effects. Data are inadequate to draw
conclusions regarding the health effects associated with long-term
exposure to PM10-2.5.\335\
---------------------------------------------------------------------------

    \335\ U.S. EPA (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, 2009. Section 2.3.4,
Table 2-6.
---------------------------------------------------------------------------

    For UFPs, the ISA concludes that there is suggestive evidence of a
causal relationship between short-term exposures and cardiovascular
effects, such as changes in heart rhythm and blood vessel function. It
also concludes that there is suggestive evidence of association between
short-term exposure to UFPs and respiratory effects. Data are
inadequate to draw conclusions regarding the health effects associated
with long-term exposure to UFP's.\336\
---------------------------------------------------------------------------

    \336\ U.S. EPA (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, 2009. Section 2.3.5,
Table 2-6.
---------------------------------------------------------------------------

b. Ozone
i. Background
    Ground-level ozone pollution is typically formed by the reaction of
VOC and NOX in the lower atmosphere in the presence of heat
and sunlight. These pollutants, often referred to as ozone precursors,
are emitted by many types of pollution sources, such as highway and
nonroad motor vehicles and engines, power plants, chemical plants,
refineries, makers of consumer and commercial products, industrial
facilities, and smaller area sources.
    The science of ozone formation, transport, and accumulation is
complex.\337\ Ground-level ozone is produced and destroyed in a
cyclical set of chemical reactions, many of which are sensitive to
temperature and sunlight. When ambient temperatures and sunlight levels
remain high for several days and the air is relatively stagnant, ozone
and its precursors can build up and result in more ozone than typically
occurs on a single high-temperature day. Ozone can be transported
hundreds of miles downwind from precursor emissions, resulting in
elevated ozone levels even in areas with low local VOC or
NOX emissions.
---------------------------------------------------------------------------

    \337\ U.S. EPA (2006). Air Quality Criteria for Ozone and
Related Photochemical Oxidants (Final). EPA/600/R-05/004aF-cF.
Washington, DC: U.S. EPA. Docket EPA-HQ-OAR-2009-0472-0099 through -
0101.
---------------------------------------------------------------------------

ii. Health Effects of Ozone
    The health and welfare effects of ozone are well documented and are
assessed in EPA's 2006 Air Quality Criteria Document (ozone AQCD) and
2007 Staff Paper.338 339 Ozone can irritate the respiratory
system, causing coughing, throat irritation, and/or uncomfortable
sensation in the chest. Ozone can reduce lung function and make it more
difficult to breathe deeply; breathing may also become more rapid and
shallow than normal, thereby limiting a person's activity. Ozone can
also aggravate asthma, leading to more asthma attacks that require
medical attention and/or the use of additional medication. In addition,
there is suggestive evidence of a contribution of ozone to
cardiovascular-related morbidity and highly suggestive evidence that
short-term ozone exposure directly or indirectly contributes to non-
accidental and cardiopulmonary-related mortality, but additional
research is needed to clarify the underlying mechanisms causing these
effects. In a recent report on the estimation of ozone-related
premature mortality published by the National Research Council (NRC), a
panel of experts and reviewers concluded that short-term exposure to
ambient ozone is likely to contribute to premature deaths and that
ozone-related mortality should be included in estimates of the health
benefits of reducing ozone exposure.\340\ Animal toxicological evidence
indicates that with repeated exposure, ozone can inflame and damage the
lining of the lungs, which may lead to permanent changes in lung tissue
and irreversible reductions in lung function. People who are more
susceptible to effects associated with exposure to ozone can include
children, the elderly, and individuals with respiratory disease such as
asthma. Those with greater exposures to ozone, for instance due to

time spent outdoors (e.g., children and outdoor workers), are of
particular concern.
---------------------------------------------------------------------------

    \338\ U.S. EPA. (2006). Air Quality Criteria for Ozone and
Related Photochemical Oxidants (Final). EPA/600/R-05/004aF-cF.
Washington, DC: U.S. EPA.
    \339\ U.S. EPA (2007). Review of the National Ambient Air
Quality Standards for Ozone: Policy Assessment of Scientific and
Technical Information, OAQPS Staff Paper. EPA-452/R-07-003.
Washington, DC, U.S. EPA. Docket EPA-HQ-OAR-2009-0472-0105 through -
0106.
    \340\ National Research Council (NRC), 2008. Estimating
Mortality Risk Reduction and Economic Benefits from Controlling
Ozone Air Pollution. The National Academies Press: Washington, DC
Docket EPA-HQ-OAR-2009-0472-0322.
---------------------------------------------------------------------------

    The 2006 ozone AQCD also examined relevant new scientific
information that has emerged in the past decade, including the impact
of ozone exposure on such health effects as changes in lung structure
and biochemistry, inflammation of the lungs, exacerbation and causation
of asthma, respiratory illness-related school absence, hospital
admissions and premature mortality. Animal toxicological studies have
suggested potential interactions between ozone and PM with increased
responses observed to mixtures of the two pollutants compared to either
ozone or PM alone. The respiratory morbidity observed in animal studies
along with the evidence from epidemiologic studies supports a causal
relationship between acute ambient ozone exposures and increased
respiratory-related emergency room visits and hospitalizations in the
warm season. In addition, there is suggestive evidence of a
contribution of ozone to cardiovascular-related morbidity and non-
accidental and cardiopulmonary mortality.
c. NOX and SOX
i. 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. 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 can dissolve in water vapor 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 III.G.3.a of this preamble. NOX along
with non-methane hydrocarbon (NMHC) are the two major precursors of
ozone. The health effects of ozone are covered in Section III.G.3.b.
ii. Health Effects of NO2
    Information on the health effects of NO2 can be found in
the EPA Integrated Science Assessment (ISA) for Nitrogen Oxides.\341\
The EPA has 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 ISA concludes that
the strongest evidence for such a relationship comes from epidemiologic
studies of respiratory effects including symptoms, emergency department
visits, and hospital admissions. The ISA also draws two broad
conclusions regarding airway responsiveness following NO2
exposure. First, the ISA concludes 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 asthmatics to NO2
concentrations as low as 0.26 ppm. In addition, small but significant
increases in non-specific airway hyperresponsiveness were reported
following 1-hour exposures of asthmatics to 0.1 ppm NO2.
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 asthmatic subjects.
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.
---------------------------------------------------------------------------

    \341\ 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. Docket EPA-HQ-OAR-2009-0472-0350.
---------------------------------------------------------------------------

    Although the weight of evidence supporting a causal relationship is
somewhat less certain than that associated with respiratory morbidity,
NO2 has also been linked to other health endpoints. These
include all-cause (nonaccidental) mortality, hospital admissions or
emergency department visits for cardiovascular disease, and decrements
in lung function growth associated with chronic exposure.
iii. Health Effects of SO2
    Information on the health effects of SO2 can be found in
the EPA Integrated Science Assessment for Sulfur Oxides.\342\
SO2 has long been known to cause adverse respiratory health
effects, particularly among individuals with asthma. Other potentially
sensitive groups include 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 has 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 has concluded that the overall evidence is
suggestive of a causal relationship between short-term exposure to
SO2 and mortality.
---------------------------------------------------------------------------

    \342\ 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. Docket EPA-HQ-
OAR-2009-0472-0335.
---------------------------------------------------------------------------

d. Carbon Monoxide
    Information on the health effects of carbon monoxide (CO) can be
found in the EPA Integrated Science Assessment (ISA) for Carbon
Monoxide.\343\ The ISA concludes that ambient concentrations of CO are
associated with a number of adverse health effects.\344\ This section
provides a summary of the health effects associated with exposure to
ambient concentrations of CO.\345\
---------------------------------------------------------------------------

    \343\ U.S. EPA, 2010. Integrated Science Assessment for Carbon
Monoxide (Final Report). U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-09/019F, 2010. http://cfpub.epa.gov/ncea/
cfm/recordisplay.cfm?deid=218686.
    \344\ The ISA evaluates the health evidence associated with
different health effects, assigning one of five ``weight of
evidence'' determination: 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.
    \345\ 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.
---------------------------------------------------------------------------

    Human clinical studies of subjects with coronary artery disease
show a decrease in the time to onset of exercise-induced angina (chest
pain) and electrocardiogram changes following CO exposure. In addition,
epidemiologic studies show associations between short-term CO exposure
and cardiovascular morbidity, particularly increased emergency room
visits and hospital admissions for coronary heart disease (including
ischemic heart disease, myocardial infarction, and angina). Some
epidemiologic evidence is also available for increased hospital
admissions and emergency room visits for congestive heart failure and
cardiovascular disease as a whole. The ISA concludes that a causal
relationship is likely between short-term exposures to CO and
cardiovascular morbidity. It also concludes that available data are
inadequate to conclude that a causal

relationship exists between long-term exposures to CO and
cardiovascular morbidity.
    Animal studies show various neurological effects with in-utero CO
exposure. Controlled human exposure studies report inconsistent neural
and behavioral effects following low-level CO exposures. The ISA
concludes the evidence is suggestive of a causal relationship with both
short- and long-term exposure to CO and central nervous system effects.
    A number of epidemiologic and animal toxicological studies cited in
the ISA have evaluated associations between preterm birth and cardiac
birth defects and CO exposure. The epidemiologic studies provide
limited evidence of a CO-induced effect on pre-term births and birth
defects, with weak evidence for a decrease in birth weight. Animal
toxicological studies have found associations between perinatal CO
exposure and decrements in birth weight, as well as other developmental
outcomes. The ISA concludes these studies are suggestive of a causal
relationship between long-term exposures to CO and developmental
effects and birth outcomes.
    Epidemiologic studies provide evidence of effects on respiratory
morbidity such as changes in pulmonary function, respiratory symptoms,
and hospital admissions associated with ambient CO concentrations. A
limited number of epidemiologic studies considered copollutants such as
ozone, SO2, and PM in two-pollutant models and found that CO
risk estimates were generally robust, although this limited evidence
makes it difficult to disentangle effects attributed to CO itself from
those of the larger complex air pollution mixture. Controlled human
exposure studies have not extensively evaluated the effect of CO on
respiratory morbidity. Animal studies at levels of 50-100 ppm CO show
preliminary evidence of altered pulmonary vascular remodeling and
oxidative injury. The ISA concludes that the evidence is suggestive of
a causal relationship between short-term CO exposure and respiratory
morbidity, and inadequate to conclude that a causal relationship exists
between long-term exposure and respiratory morbidity.
    Finally, the ISA concludes that the epidemiologic evidence is
suggestive of a causal relationship between short-term exposures to CO
and mortality. Epidemiologic studies provide evidence of an association
between short-term exposure to CO and mortality, but limited evidence
is available to evaluate cause-specific mortality outcomes associated
with CO exposure. In addition, the attenuation of CO risk estimates
which was often observed in copollutant models contributes to the
uncertainty as to whether CO is acting alone or as an indicator for
other combustion-related pollutants. The ISA also concludes that there
is not likely to be a causal relationship between relevant long-term
exposures to CO and mortality.
e. Air Toxics
    Motor 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''.\346\ These
compounds include, but are not limited to, benzene, 1,3-butadiene,
formaldehyde, acetaldehyde, acrolein, polycyclic organic matter (POM),
and naphthalene. These compounds, except acetaldehyde, were identified
as national or regional risk drivers in the 2002 National-scale Air
Toxics Assessment (NATA) and have significant inventory contributions
from mobile sources.\347\ Emissions and ambient concentrations of
compounds are discussed in the RIA chapters on emission inventories and
air quality (Chapters 5 and 7, respectively).
---------------------------------------------------------------------------

    \346\ U.S. EPA. 2002 National-Scale Air Toxics Assessment.
http://www.epa.gov/ttn/atw/nata12002/risksum.html. Docket EPA-HQ-
OAR-2009-0472-11322.
    \347\ U.S. EPA. 2009. National-Scale Air Toxics Assessment for
2002. http://www.epa.gov/ttn/atw/nata2002/. Docket EPA-HQ-OAR-2009-
0472-11321.
---------------------------------------------------------------------------

i. Benzene
    The EPA's IRIS database lists benzene as a known human carcinogen
(causing leukemia) by all routes of exposure, and concludes that
exposure is associated with additional health effects, including
genetic changes in both humans and animals and increased proliferation
of bone marrow cells in mice.348 349 350 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. 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.351 352
---------------------------------------------------------------------------

    \348\ 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. Docket EPA-HQ-OAR-2009-0472-1659.
    \349\ International Agency for Research on Cancer (IARC). 1982.
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29. Some industrial chemicals and dyestuffs, World
Health Organization, Lyon, France, p. 345-389. Docket EPA-HQ-OAR-
2009-0472-0366.
    \350\ 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. Docket EPA-HQ-OAR-2009-0472-0370.
    \351\ International Agency for Research on Cancer (IARC). 1982.
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29. Some industrial chemicals and dyestuffs, World
Health Organization, Lyon, France. Docket EPA-HQ-OAR-2009-0472-0366.
    \352\ U.S. Department of Health and Human Services National
Toxicology Program 11th Report on Carcinogens available at: http://
ntp.niehs.nih.gov/go/16183.
---------------------------------------------------------------------------

    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.353 354 The
most sensitive noncancer effect observed in humans, based on current
data, is the depression of the absolute lymphocyte count in
blood.355 356 In addition, recent work, including studies
sponsored by the Health Effects Institute (HEI), provides evidence that
biochemical responses are occurring at lower levels of benzene exposure
than previously known.357 358 359 360 EPA's

IRIS program has not yet evaluated these new data.
---------------------------------------------------------------------------

    \353\ Aksoy, M. (1989). Hematotoxicity and carcinogenicity of
benzene. Environ. Health Perspect. 82: 193-197. Docket EPA-HQ-OAR-
2009-0472-0368.
    \354\ Goldstein, B.D. (1988). Benzene toxicity. Occupational
medicine. State of the Art Reviews. 3: 541-554. Docket EPA-HQ-OAR-
2009-0472-0325.
    \355\ 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. Docket EPA-HQ-OAR-2009-0472-0326.
    \356\ 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.
Docket EPA-HQ-OAR-2009-0472-0327.
    \357\ 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. Docket EPA-HQ-OAR-2009-0472-0328.
    \358\ 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. Docket
EPA-HQ-OAR-2009-0472-0329.
    \359\ Lan, Qing, Zhang, L., Li, G., Vermeulen, R., et al. (2004)
Hematotoxically in Workers Exposed to Low Levels of Benzene. Science
306: 1774-1776. Docket EPA-HQ-OAR-2009-0472-0330.
    \360\ 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. Docket EPA-HQ-OAR-2009-
0472-0385.
---------------------------------------------------------------------------

ii. 1,3-Butadiene
    EPA has characterized 1,3-butadiene as carcinogenic to humans by
inhalation.361 362 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.363 364 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. 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.\365\
---------------------------------------------------------------------------

    \361\ 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. Docket EPA-HQ-OAR-2009-0472-
0386.
    \362\ 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. Docket EPA-HQ-OAR-2009-0472-1660
    \363\ 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. Docket EPA-HQ-OAR-2009-
0472-0387.
    \364\ U.S. Department of Health and Human Services (2005)
National Toxicology Program 11th Report on Carcinogens available at:
ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-
7FCE50709CB4C932.
    \365\ 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. Docket EPA-HQ-OAR-2009-
0472-0388.
---------------------------------------------------------------------------

iii. Formaldehyde
    Since 1987, EPA has classified formaldehyde as a probable human
carcinogen based on evidence in humans and in rats, mice, hamsters, and
monkeys.\366\ EPA is currently reviewing recently published
epidemiological data. For instance, research conducted by the National
Cancer Institute (NCI) found an increased risk of nasopharyngeal cancer
and lymphohematopoietic malignancies such as leukemia among workers
exposed to formaldehyde.367 368 In an analysis of the
lymphohematopoietic cancer mortality from an extended follow-up of
these workers, NCI confirmed an association between lymphohematopoietic
cancer risk and peak exposures.\369\ A recent National Institute of
Occupational Safety and Health (NIOSH) study of garment workers also
found increased risk of death due to leukemia among workers exposed to
formaldehyde.\370\ Extended follow-up of a cohort of British chemical
workers did not find evidence of an increase in nasopharyngeal or
lymphohematopoietic cancers, but a continuing statistically significant
excess in lung cancers was reported.\371\ Recently, the IARC re-
classified formaldehyde as a human carcinogen (Group 1).\372\
---------------------------------------------------------------------------

    \366\ U.S. EPA (1987) Assessment of Health Risks to Garment
Workers and Certain Home Residents from Exposure to Formaldehyde,
Office of Pesticides and Toxic Substances, April 1987. Docket EPA-
HQ-OAR-2009-0472-0389.
    \367\ 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. Docket EPA-HQ-OAR-2009-0472-0336.
    \368\ 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. Docket EPA-HQ-OAR-2009-0472-0337.
    \369\ 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. Docket EPA-HQ-OAR-2009-0472-0338.
    \370\ Pinkerton, L.E. 2004. Mortality among a cohort of garment
workers exposed to formaldehyde: an update. Occup. Environ. Med. 61:
193-200. Docket EPA-HQ-OAR-2009-0472-0339.
    \371\ 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. Docket EPA-HQ-
OAR-2009-0472-0340.
    \372\ International Agency for Research on Cancer (IARC). 2006.
Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol. Volume
88. (in preparation), World Health Organization, Lyon, France.
Docket EPA-HQ-OAR-2009-0472-1164.
---------------------------------------------------------------------------

    Formaldehyde exposure also causes a range of noncancer health
effects, including irritation of the eyes (burning and watering of the
eyes), nose and throat. Effects from repeated exposure in humans
include respiratory tract irritation, chronic bronchitis and nasal
epithelial lesions such as metaplasia and loss of cilia. Animal studies
suggest that formaldehyde may also cause airway inflammation--including
eosinophil infiltration into the airways. There are several studies
that suggest that formaldehyde may increase the risk of asthma--
particularly in the young.373 374
---------------------------------------------------------------------------

    \373\ Agency for Toxic Substances and Disease Registry (ATSDR).
1999. Toxicological profile for Formaldehyde. Atlanta, GA: U.S.
Department of Health and Human Services, Public Health Service.
http://www.atsdr.cdc.gov/toxprofiles/tp111.html Docket EPA-HQ-OAR-
2009-0472-1191.
    \374\ WHO (2002) Concise International Chemical Assessment
Document 40: Formaldehyde. Published under the joint sponsorship of
the United Nations Environment Programme, the International Labour
Organization, and the World Health Organization, and produced within
the framework of the Inter-Organization Programme for the Sound
Management of Chemicals. Geneva. Docket EPA-HQ-OAR-2009-0472-1199.
---------------------------------------------------------------------------

iv. 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.\375\
Acetaldehyde is reasonably anticipated to be a human carcinogen by the
U.S. DHHS in the 11th Report on Carcinogens and is classified as
possibly carcinogenic to humans (Group 2B) by the
IARC.376 377 EPA is currently conducting a reassessment of
cancer risk from inhalation exposure to acetaldehyde.
---------------------------------------------------------------------------

    \375\ 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. Docket
EPA-HQ-OAR-2009-0472-0390.
    \376\ U.S. Department of Health and Human Services National
Toxicology Program 11th Report on Carcinogens available at:
ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-
7FCE50709CB4C932.
    \377\ 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. Docket EPA-HQ-OAR-2009-
0472-0387.
---------------------------------------------------------------------------

    The primary noncancer effects of exposure to acetaldehyde vapors
include irritation of the eyes, skin, and respiratory tract.\378\ In
short-term (4 week) rat studies, degeneration of olfactory epithelium
was observed at various concentration levels of

acetaldehyde exposure.379 380 Data from these studies were
used by EPA to develop an inhalation reference concentration. Some
asthmatics have been shown to be a sensitive subpopulation to
decrements in functional expiratory volume (FEV1 test) and
bronchoconstriction upon acetaldehyde inhalation.\381\ The agency is
currently conducting a reassessment of the health hazards from
inhalation exposure to acetaldehyde.
---------------------------------------------------------------------------

    \378\ 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.
    \379\ Appleman, L. M., R. A. Woutersen, V. J. Feron, R. N.
Hooftman, and W. R. F. Notten. 1986. Effects of the variable versus
fixed exposure levels on the toxicity of acetaldehyde in rats. J.
Appl. Toxicol. 6: 331-336.
    \380\ 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. Docket EPA-HQ-OAR-2009-0472-0392.
    \381\ 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):
940-3. Docket EPA-HQ-OAR-2009-0472-0408.
---------------------------------------------------------------------------

v. Acrolein
    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.\382\ 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.\383\ Evidence available from 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.\384\
Lesions to the lungs and upper respiratory tract of rats, rabbits, and
hamsters have been observed after subchronic exposure to acrolein.\385\
Acute exposure effects in animal studies report bronchial hyper-
responsiveness.\386\ In a recent study, the acute respiratory irritant
effects of exposure to 1.1 ppm acrolein were more pronounced in mice
with allergic airway disease by comparison to non-diseased mice which
also showed decreases in respiratory rate.\387\ Based on these animal
data 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.
---------------------------------------------------------------------------

    \382\ Sim VM, Pattle RE. Effect of possible smog irritants on
human subjects JAMA165: 1980-2010, 1957. Docket EPA-HQ-OAR-2009-
0472-0395.
    \383\ U.S. EPA (U.S. Environmental Protection Agency). (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.
    \384\ Weber-Tschopp, A; Fischer, T; Gierer, R; et al. (1977)
Experimentelle reizwirkungen von Acrolein auf den Menschen. Int Arch
Occup Environ Hlth 40(2):117-130. In German Docket EPA-HQ-OAR-2009-
0472-0394.
    \385\ 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. Docket EPA-HQ-OAR-2009-
0472-0391.
    \386\ U.S. EPA (U.S. Environmental Protection Agency). (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.
    \387\ 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.
Docket EPA-HQ-OAR-2009-0472-0396.
---------------------------------------------------------------------------

    EPA determined in 2003 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.\388\ The IARC determined in 1995 that acrolein was not
classifiable as to its carcinogenicity in humans.\389\
---------------------------------------------------------------------------

    \388\ 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.
    \389\ 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.
Docket EPA-HQ-OAR-2009-0472-0393.
---------------------------------------------------------------------------

vi. Polycyclic Organic Matter (POM)
    POM is generally defined as a large class of organic compounds
which have multiple benzene rings and a boiling point greater than 100
degrees Celsius. Many of the compounds included in the class of
compounds known as POM are classified by EPA as probable human
carcinogens based on animal data. One of these compounds, naphthalene,
is discussed separately below. Polycyclic aromatic hydrocarbons (PAHs)
are a subset of POM that contain only hydrogen and carbon atoms. A
number of PAHs are known or suspected carcinogens. Recent studies have
found that maternal exposures to PAHs (a subclass of POM) 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 at age three.390 391
EPA has not yet evaluated these recent studies.
---------------------------------------------------------------------------

    \390\ 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. Docket EPA-HQ-OAR-2009-0472-0372.
    \391\ 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. Docket EPA-HQ-OAR-2009-0472-0373.
---------------------------------------------------------------------------

vii. 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. EPA released an external review draft of a reassessment of
the inhalation carcinogenicity of naphthalene based on a number of
recent animal carcinogenicity studies.\392\ The draft reassessment
completed external peer review.\393\ Based on external peer review
comments received, additional analyses are being undertaken. This
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.\394\ 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.\395\ Naphthalene also causes a number
of chronic non-cancer effects in animals, including abnormal cell
changes and growth in respiratory and nasal tissues.\396\
---------------------------------------------------------------------------

    \392\ U.S. EPA 2004. 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. Docket EPA-HQ-OAR-2009-0472-0272.
    \393\ 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. Docket EPA-HQ-OAR-2009-0472-
0273.
    \394\ National Toxicology Program (NTP). (2004). 11th Report on
Carcinogens. Public Health Service, U.S. Department of Health and
Human Services, Research Triangle Park, NC. Available from: http://
ntp-server.niehs.nih.gov.
    \395\ International Agency for Research on Cancer (IARC).
(2002). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans. Vol. 82. Lyon, France. Docket EPA-HQ-OAR-2009-
0472-0274.
    \396\ 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.
---------------------------------------------------------------------------

viii. Other Air Toxics
    In addition to the compounds described above, other compounds in
gaseous hydrocarbon and PM emissions from vehicles will be affected by
this final rule. Mobile source air toxic compounds that would
potentially be impacted include ethylbenzene, propionaldehyde, toluene,
and xylene. Information regarding the health effects of these compounds
can be found in EPA's IRIS database.\397\
---------------------------------------------------------------------------

    \397\ U.S. EPA Integrated Risk Information System (IRIS)
database is available at: http://www.epa.gov/iris.
---------------------------------------------------------------------------

f. Exposure and Health Effects Associated With Traffic
    Populations who live, work, or attend school near major roads
experience elevated exposure concentrations to a wide range of air
pollutants, as well as higher risks for a number of adverse health
effects. While the previous sections of this preamble have focused on
the health effects associated with individual criteria pollutants or
air toxics, this section discusses the mixture of different exposures
near major roadways, rather than the effects of any single pollutant.
As such, this section emphasizes traffic-related air pollution, in
general, as the relevant indicator of exposure rather than any
particular pollutant.
    Concentrations of many traffic-generated air pollutants are
elevated for up to 300-500 meters downwind of roads with high traffic
volumes.\398\ Numerous sources on roads contribute to elevated roadside
concentrations, including exhaust and evaporative emissions, and
resuspension of road dust and tire and brake wear. Concentrations of
several criteria and hazardous air pollutants are elevated near major
roads. Furthermore, different semi-volatile organic compounds and
chemical components of particulate matter, including elemental carbon,
organic material, and trace metals, have been reported at higher
concentrations near major roads.
---------------------------------------------------------------------------

    \398\ Zhou, Y.; Levy, J.I. (2007) Factors influencing the
spatial extent of mobile source air pollution impacts: a meta-
analysis. BMC Public Health 7: 89. doi:10.1186/1471-2458-7-89.
---------------------------------------------------------------------------

    Populations near major roads experience greater risk of certain
adverse health effects. The Health Effects Institute published a report
on the health effects of traffic-related air pollution.\399\ It
concluded that evidence is ``sufficient to infer the presence of a
causal association'' between traffic exposure and exacerbation of
childhood asthma symptoms. The HEI report also concludes that the
evidence is either ``sufficient'' or ``suggestive but not sufficient''
for a causal association between traffic exposure and new childhood
asthma cases. A review of asthma studies by Salam et al. (2008) reaches
similar conclusions.\400\ The HEI report also concludes that there is
``suggestive'' evidence for pulmonary function deficits associated with
traffic exposure, but concluded that there is ``inadequate and
insufficient'' evidence for causal associations with respiratory health
care utilization, adult-onset asthma, COPD symptoms, and allergy. A
review by Holguin (2008) notes that the effects of traffic on asthma
may be modified by nutrition status, medication use, and genetic
factors.\401\
---------------------------------------------------------------------------

    \399\ HEI Panel on the Health Effects of Air Pollution. (2010)
Traffic-related air pollution: a critical review of the literature
on emissions, exposure, and health effects. [Online at http://
www.healtheffects.org].
    \400\ Salam, M.T.; Islam, T.; Gilliland, F.D. (2008) Recent
evidence for adverse effects of residential proximity to traffic
sources on asthma. Current Opin Pulm Med 14: 3-8.
    \401\ Holguin, F. (2008) Traffic, outdoor air pollution, and
asthma. Immunol Allergy Clinics North Am 28: 577-588.
---------------------------------------------------------------------------

    The HEI report also concludes that evidence is ``suggestive'' of a
causal association between traffic exposure and all-cause and
cardiovascular mortality. There is also evidence of an association
between traffic-related air pollutants and cardiovascular effects such
as changes in heart rhythm, heart attack, and cardiovascular disease.
The HEI report characterizes this evidence as ``suggestive'' of a
causal association, and an independent epidemiological literature
review by Adar and Kaufman (2007) concludes that there is ``consistent
evidence'' linking traffic-related pollution and adverse cardiovascular
health outcomes.\402\
---------------------------------------------------------------------------

    \402\ Adar, S.D.; Kaufman, J.D. (2007) Cardiovascular disease
and air pollutants: evaluating and improving epidemiological data
implicating traffic exposure. Inhal Toxicol 19: 135-149.
---------------------------------------------------------------------------

    Some studies have reported associations between traffic exposure
and other health effects, such as birth outcomes (e.g., low birth
weight) and childhood cancer. The HEI report concludes that there is
currently ``inadequate and insufficient'' evidence for a causal
association between these effects and traffic exposure. A review by
Raaschou-Nielsen and Reynolds (2006) concluded that evidence of an
association between childhood cancer and traffic-related air pollutants
is weak, but noted the inability to draw firm conclusions based on
limited evidence.\403\
---------------------------------------------------------------------------

    \403\ Raaschou-Nielsen, O.; Reynolds, P. (2006) Air pollution
and childhood cancer: A review of the epidemiological literature.
Int J Cancer 118: 2920-2929.
---------------------------------------------------------------------------

    There is a large population in the U.S. living in close proximity
of major roads. According to the Census Bureau's American Housing
Survey for 2007, approximately 20 million residences in the U.S., 15.6%
of all homes, are located within 300 feet (91 m) of a highway with 4+
lanes, a railroad, or an airport.\404\ Therefore, at current population
of approximately 309 million, assuming that population and housing
similarly distributed, there are over 48 million people in the U.S.
living near such sources. The HEI report also notes that in two North
American cities, Los Angeles and Toronto, over 40% of each city's
population live within 500 meters of a highway or 100 meters of a major
road. It also notes that about 33% of each city's population resides
within 50 meters of major roads. Together, the evidence suggests that a
large U.S. population lives in areas with elevated traffic-related air
pollution.
---------------------------------------------------------------------------

    \404\ U.S. Census Bureau (2008) American Housing Survey for the
United States in 2007. Series H-150 (National Data), Table 1A-6.
[Accessed at http://www.census.gov/hhes/www/housing/ahs/ahs07/
ahs07.html on January 22, 2009]
---------------------------------------------------------------------------

    People living near roads are often socioeconomically disadvantaged.
According to the 2007 American Housing Survey, a renter-occupied
property is over twice as likely as an owner-occupied property to be
located near a highway with 4+ lanes, railroad or airport. In the same
survey, the median household income of rental housing occupants was
less than half that of owner-occupants ($28,921/$59,886). Numerous
studies in individual urban areas report higher levels of traffic-
related air pollutants in areas with high minority or poor
populations.405 406 407
---------------------------------------------------------------------------

    \405\ Lena, T.S.; Ochieng, V.; Carter, M.; Holgu[iacute]n-Veras,
J.; Kinney, P.L. (2002) Elemental carbon and PM2.5 levels
in an urban community heavily impacted by truck traffic. Environ
Health Perspect 110: 1009-1015.
    \406\ Wier, M.; Sciammas, C.; Seto, E.; Bhatia, R.; Rivard, T.
(2009) Health, traffic, and environmental justice: collaborative
research and community action in San Francisco, California. Am J
Public Health 99: S499-S504.
    \407\ Forkenbrock, D.J. and L.A. Schweitzer, Environmental
Justice and Transportation Investment Policy. Iowa City: University
of Iowa, 1997.

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

    Students may also be exposed in situations where schools are
located near major roads. In a study of nine metropolitan areas across
the U.S., Appatova et al. (2008) found that on average greater than 33%
of schools were located within 400 m of an Interstate, U.S., or State
highway, while 12% were located within 100 m.\408\ The study also found
that among the metropolitan areas studied, schools in the Eastern U.S.
were more often sited near major roadways than schools in the Western
U.S.
---------------------------------------------------------------------------

    \408\ Appatova, A.S.; Ryan, P.H.; LeMasters, G.K.; Grinshpun,
S.A. (2008) Proximal exposure of public schools and students to
major roadways: a nationwide U.S. survey. J Environ Plan Mgmt
---------------------------------------------------------------------------

    Demographic studies of students in schools near major roadways
suggest that this population is more likely than the general student
population to be of non-white race or Hispanic ethnicity, and more
often live in low socioeconomic status locations.409 410 411
There is some inconsistency in the evidence, which may be due to
different local development patterns and measures of traffic and
geographic scale used in the studies.\408\
---------------------------------------------------------------------------

    \409\ Green, R.S.; Smorodinsky, S.; Kim, J.J.; McLaughlin, R.;
Ostro, B. (2004) Proximity of California public schools to busy
roads. Environ Health Perspect 112: 61-66.
    \410\ Houston, D.; Ong, P.; Wu, J.; Winer, A. (2006) Proximity
of licensed child care facilities to near-roadway vehicle pollution.
Am J Public Health 96: 1611-1617.
    \411\ Wu, Y.; Batterman, S. (2006) Proximity of schools in
Detroit, Michigan to automobile and truck traffic. J Exposure Sci
Environ Epidemiol 16: 457-470.
---------------------------------------------------------------------------

4. Environmental Effects of Non-GHG Pollutants
    In this section we discuss some of the environmental effects of PM
and its precursors such as visibility impairment, atmospheric
deposition, and materials damage and soiling, as well as environmental
effects associated with the presence of ozone in the ambient air, such
as impacts on plants, including trees, agronomic crops and urban
ornamentals, and environmental effects associated with air toxics. No
substantive comments were received on the environmental effects of non-
GHG pollutants.
a. Visibility
    Visibility can be defined as the degree to which the atmosphere is
transparent to visible light.\412\ 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.\413\
---------------------------------------------------------------------------

    \412\ 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. Docket EPA-HQ-OAR-2005-0161. This
book can be viewed on the National Academy Press Web site at http://
www.nap.edu/books/0309048443/html/.
    \413\ U.S. EPA (2009). Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, 2009. Docket EPA-HQ-OAR-
2009-0472-11295.
---------------------------------------------------------------------------

    EPA is pursuing a two-part strategy to address visibility. First,
EPA has concluded that PM2.5 causes adverse effects on
visibility in various locations, depending on PM concentrations and
factors such as chemical composition and average relative humidity, and
has set secondary PM2.5 standards.\414\ The secondary
PM2.5 standards act in conjunction with the regional haze
program. The regional haze rule (64 FR 35714) was put in place in July
1999 to protect the visibility in mandatory class I Federal areas.
There are 156 national parks, forests and wilderness areas categorized
as mandatory class I Federal areas (62 FR 38680-81, July 18,
1997).\415\ Visibility can be said to be impaired in both
PM2.5 nonattainment areas and mandatory class I Federal
areas.
---------------------------------------------------------------------------

    \414\ The existing annual primary and secondary PM2.5
standards have been remanded and are being addressed in the
currently ongoing PM NAAQS review.
    \415\ 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.
---------------------------------------------------------------------------

b. Plant and Ecosystem Effects of Ozone
    Elevated ozone levels contribute to environmental effects, with
impacts to plants and ecosystems being of most concern. Ozone can
produce both acute and chronic injury in sensitive species depending on
the concentration level and the duration of the exposure. Ozone effects
also tend to accumulate over the growing season of the plant, so that
even low concentrations experienced for a longer duration have the
potential to create chronic stress on vegetation. Ozone damage to
plants includes visible injury to leaves and impaired photosynthesis,
both of which can lead to reduced plant growth and reproduction,
resulting in reduced crop yields, forestry production, and use of
sensitive ornamentals in landscaping. In addition, the impairment of
photosynthesis, the process by which the plant makes carbohydrates (its
source of energy and food), can lead to a subsequent reduction in root
growth and carbohydrate storage below ground, resulting in other, more
subtle plant and ecosystems impacts.
    These latter impacts include increased susceptibility of plants to
insect attack, disease, harsh weather, interspecies competition and
overall decreased plant vigor. The adverse effects of ozone on forest
and other natural vegetation can potentially lead to species shifts and
loss from the affected ecosystems, resulting in a loss or reduction in
associated ecosystem goods and services. Lastly, visible ozone injury
to leaves can result in a loss of aesthetic value in areas of special
scenic significance like national parks and wilderness areas. The final
2006 Ozone Air Quality Criteria Document presents more detailed
information on ozone effects on vegetation and ecosystems.
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., POM, 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.\416\
---------------------------------------------------------------------------

    \416\ 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. Docket EPA-HQ-OAR-2009-0472-0091.
---------------------------------------------------------------------------

    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 the marine