(i.e., model years 2021-2025). These technology improvements are the
very technologies EPA and NHTSA describe in detail in Chapter 3 of the
draft Joint Technical Support Document and which we forecasted
penetration rates earlier in this section III.D, and they include for
example: gasoline direct injection fuel systems; downsized and
turbocharged gasoline engines (including in some cases with the
application of cooled exhaust gas recirculation); continued
improvements in engine friction reduction and low friction lubricants;
transmissions with an increased number of forward gears (e.g., 8
speeds); improvements in transmission shifting logic; improvements in
transmission gear box efficiency; vehicle mass reduction; lower rolling
resistance tires, and improved vehicle aerodynamics. In many (though
not all) cases these technologies are beginning to penetrate the U.S.
light-duty vehicle market.
    In general, these technologies must go through the automotive
product development cycle in order to be introduced into a vehicle. In
some cases additional research is needed before the technologies'
CO2 benefits can be fully realized and large-scale
manufacturing can be achieved. The subject of technology penetration
phase-in rates is discussed in more detail in Chapter 3.5 of the draft
Joint Technical Support Document. In that Chapter, we explain that why
many CO2 reducing technologies should be able to penetrate
the new vehicle market at high levels between now and MY 2016. There
are also many of the key technologies we project as being needed to
achieve the proposed 2017-2025 standards which will only be able to
penetrate the market at relatively low levels (e.g., a maximum level of
30% or less) by MY 2016, and even by MY 2021. These include important
powertrain technologies such as 8-speed transmissions and second or
third generation downsized engines with turbocharging,
    The majority of these technologies must be integrated into vehicles
during the product redesign schedule, which is typically on a 5-year
cycle. EPA discussed in the MY 2012-2016 rule the significant costs and
potential risks associated with requiring major technologies to be
added in-between the typical 5-year vehicle redesign schedule (see 75
FR at 25467-68, May 7, 2010). In addition, engines and transmissions
generally have longer lifetimes then 5 years, typically on the order of
10 years. Thus major powertrain technologies generally take longer to
penetrate the new vehicle fleet then can be done in a 5-year redesign
cycle. As detailed in Chapter 3.5 of the draft Joint TSD, EPA projects
that 8-speed transmissions could increase their maximum penetration in
the fleet from 30% in MY 2016 to 80% in 2021 and to 100% in MY 2025.
Similarly, we project that second generation downsized and turbocharged
engines (represented in our assessment as engines with a brake-mean
effective pressure of 24 bars) could penetrate the new vehicle fleet at
a maximum level of 15% in MY 2016, 30% in MY 2021, and 75% in MY 2025.
When coupled with the typical 5-year vehicle redesign schedule, EPA
projects that it is not possible for all of the advanced gasoline
vehicle technologies we have assessed to penetrate the fleet in a
single 5-year vehicle redesign schedule.
    Given the status of the technologies we project to be used to
achieve the proposed MY2017-2025 standards and the product development
and introduction process which is fairly standard in the automotive
industry today, our assessment of the MY2011 and MY2012 vehicles in
comparison to the proposed standards supports our overall feasibility
assessment, and reinforces our assessment of the lead time needed for
the industry to achieve the proposed standards.

E. Certification, Compliance, and Enforcement

1. Compliance Program Overview
    This section summarizes EPA's comprehensive program to ensure
compliance with emission standards for carbon dioxide (CO2),
nitrous oxide (N2O), and methane (CH4), as
described in Section III.B. An effective compliance program is
essential to achieving the environmental and public health benefits
promised by these mobile source GHG standards. EPA's GHG compliance
program is designed around two overarching priorities: (1) to address
Clean Air Act (CAA) requirements and policy objectives; and (2) to
streamline the compliance process for both manufacturers and EPA by
building on existing practice wherever possible, and by structuring the
program such that manufacturers can use a single data set to satisfy
both GHG and Corporate Average Fuel Economy (CAFE) testing and
reporting requirements. The EPA and NHTSA programs replicate the
compliance protocols established in the MY 2012-2016 rule.\364\ The
certification, testing, reporting, and associated compliance activities
track current practices and are thus familiar to manufacturers. As is
the case under the 2012-2016 program, EPA and NHTSA have designed a
coordinated compliance approach for 2017-2025 such that the compliance
mechanisms for both GHG and CAFE standards are consistent and non-
duplicative. Readers are encouraged to review the MY 2012-2016 final
rule for background and a detailed description of these certification,
compliance, and enforcement requirements.
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    \364\ 75 FR 25468.
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    Vehicle emission standards established under the CAA apply
throughout a vehicle's full useful life. Today's rule establishes fleet
average greenhouse gas standards where compliance with the fleet
average is determined based on the testing performed at time of
production, as with the current CAFE fleet average. EPA is also
establishing in-use standards that apply throughout a vehicle's useful
life, with the in-use standard determined by adding an adjustment
factor to the emission results used to calculate the fleet average.
EPA's program will thus not only assess compliance with the fleet
average standards described in Section III.B, but will also assess
compliance with the in-use standards. As it does now, EPA will use a
variety of compliance mechanisms to conduct these assessments,
including pre-production certification and post-production, in-use
monitoring once vehicles enter customer service. Under this compliance
program manufacturers will also be afforded numerous flexibilities to
help achieve compliance, both stemming from the program design itself
in the form of a manufacturer-specific CO2 fleet average
standard, as well as in various credit banking and trading
opportunities, as described in

Section III.C. The compliance program is summarized in further detail
below.
2. Compliance With Fleet-Average CO2 Standards
    Fleet average emission levels can only be determined when a
complete fleet profile becomes available at the close of the model
year. Therefore, EPA will determine compliance with the fleet average
CO2 standards when the model year closes out, based on
actual production figures for each model and on model-level emissions
data collected through testing over the course of the model year.
Manufacturers will submit this information to EPA in an end-of-year
report which is discussed in detail in Section III.E.5.h of the MY
2012-2016 final rule preamble (see 75 FR 25481).
a. Compliance Determinations
    As described in Section III.B above, the fleet average standards
will be determined on a manufacturer by manufacturer basis, separately
for cars and trucks, using the footprint attribute curves. EPA will
calculate the fleet average emission level using actual production
figures and, for each model type, CO2 emission test values
generated at the time of a manufacturer's CAFE testing. EPA will then
compare the actual fleet average to the manufacturer's footprint
standard to determine compliance, taking into consideration use of
averaging and credits.
    Final determination of compliance with fleet average CO2
standards may not occur until several years after the close of the
model year due to the flexibilities of carry-forward and carry-back
credits and the remediation of deficits (see Section III.B). A failure
to meet the fleet average standard after credit opportunities have been
exhausted could ultimately result in penalties and injunctive orders
under the CAA as described in Section III.E.6 below.
b. Required Minimum Testing For Fleet Average CO2
    EPA will require and use the same test data to determine a
manufacturer's compliance with both the CAFE standard and the fleet
average CO2 emissions standard. Please see Section III.E.2.b
of the MY 2012-2016 final rule preamble (75 FR 25469) for details.
3. Vehicle Certification
    CAA section 203(a)(1) prohibits manufacturers from introducing a
new motor vehicle into commerce unless the vehicle is covered by an
EPA-issued certificate of conformity. Section 206(a)(1) of the CAA
describes the requirements for EPA issuance of a certificate of
conformity, based on a demonstration of compliance with the emission
standards established by EPA under section 202 of the Act. The
certification demonstration requires emission testing, and must be done
for each model year.\365\
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    \365\ CAA section 206(a)(1).
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    Since compliance with a fleet average standard depends on actual
production volumes, it is not possible to determine compliance with the
fleet average at the time the manufacturer applies for and receives a
certificate of conformity for a test group. Instead, EPA will continue
to condition each certificate of conformity for the GHG program upon a
manufacturer's demonstration of compliance with the manufacturer's
fleet-wide average CO2 standard. Please see Section III.E.3
of the MY 2012-2016 final rule preamble (75 FR 25470) for a discussion
of how EPA will certify vehicles under the GHG standards.
4. Useful Life Compliance
    Section 202(a)(1) of the CAA requires emission standards to apply
to vehicles throughout their statutory useful life, as further
described in Section III.A. The in-use CO2 standard under
the greenhouse gas program would apply to individual vehicles and is
separate from the fleet-average standard. The in-use CO2
standard for each model would be the model specific CO2
level used in calculating the fleet average, adjusted to be 10% higher
to account for test-to-test and production variability that might
affect in-use test results. Please see Section III.E.4 of the MY 2012-
2016 final rule preamble (75 FR 25473 for a detailed discussion of the
in-use standard, in-use testing requirements, and deterioration factors
for CO2, N2O, and CH4.
5. Credit Program Implementation
    As described in Section III.C, several credit programs are
available under this rulemaking. Please see Section III.E.5 of the MY
2012-2016 final rule preamble (75 FR 25477) for a detailed explanation
of credit program implementation, sample credit and deficit
calculations, and end-of-year reporting requirements.
6. Enforcement
    The enforcement structure EPA promulgated under the MY 2012-2016
rulemaking remains in place. Please see Section III.E.6 of the MY 2012-
2016 final rule preamble (75 FR 25482) for a discussion of these
provisions.
Prohibited Acts in the CAA
    Section 203 of the Clean Air Act describes acts that are prohibited
by law. This section and associated regulations apply equally to the
greenhouse gas standards as to any other regulated emission. Acts that
are prohibited by section 203 of the Clean Air Act include the
introduction into commerce or the sale of a vehicle without a
certificate of conformity, removing or otherwise defeating emission
control equipment, the sale or installation of devices designed to
defeat emission controls, and other actions. This proposal includes a
section that details these prohibited acts, as did the 2012 greenhouse
gas regulations.
7. Other Certification Issues
a. Carryover/Carry Across Certification Test Data
    EPA's certification program for vehicles allows manufacturers to
carry certification test data over and across certification testing
from one model year to the next, when no significant changes to models
are made. EPA would continue to apply this policy to CO2,
N2O and CH4 certification test data and would
allow manufacturers to use carryover and carry across data to
demonstrate CO2 fleet average compliance if they have done
so for CAFE purposes.
b. Compliance Fees
    The CAA allows EPA to collect fees to cover the costs of issuing
certificates of conformity for the classes of vehicles covered by this
rule.
    At this time the extent of any added costs to EPA as a result of
this rule is not known. EPA will assess its compliance testing and
other activities associated with the rule and may amend its fees
regulations in the future to include any warranted new costs.
c. Small Entity Exemption
    EPA would exempt small entities, and these entities (necessarily)
would not be subject to the certification requirements of this rule.
    As discussed in Section III.B.7, businesses meeting the Small
Business Administration (SBA) criterion of a small business as
described in 13 CFR 121.201 would not be subject to the GHG
requirements, pending future regulatory action. Small entities are
currently covered by a number of EPA motor vehicle emission
regulations, and they routinely submit information and data on an
annual basis as part of their compliance responsibilities.

    As discussed in detail in Section III.B.5, small volume
manufacturers with annual sales volumes of less than 5,000 vehicles
would be required to meet primary GHG standards or to petition the
Agency for alternative standards.
d. Onboard Diagnostics (OBD) and CO2 Regulations
    As under the current program, EPA would not require CO2,
N2O, and CH4 emissions as one of the applicable
standards required for the OBD monitoring threshold.
e. Applicability of Current High Altitude Provisions to Greenhouse
Gases
    As under the current program, vehicles covered by this rule would
be required to meet the CO2, N2O and
CH4 standard at altitude but would not normally be required
to submit vehicle CO2 test data for high altitude. Instead,
they would submit an engineering evaluation indicating that common
calibration approaches will be utilized at high altitude.
f. Applicability of Standards to Aftermarket Conversions
    With the exception of the small entity and small business
exemptions, EPA's emission standards, including greenhouse gas
standards, will continue to apply as stated in the applicability
sections of the relevant regulations. EPA expects that some aftermarket
conversion companies will qualify for and seek the small entity and/or
small business exemption, but those that do not qualify will be
required to meet the applicable emission standards, including the
greenhouse gas standards to qualify for a tampering exemption under 40
CFR subpart F. Fleet average standards are not generally appropriate
for fuel conversion manufacturers because the ``fleet'' of vehicles to
which a conversion system may be applied has already been accounted for
under the OEM's fleet average standard. Therefore, EPA is proposing to
retain the process promulgated in 40 CFR subpart F anti-tampering
regulations whereby conversion manufacturers demonstrate compliance at
the vehicle rather than the fleet level. Fuel converters will continue
to show compliance with greenhouse gas standards by submitting data to
demonstrate that the conversion EDV N2O, CH4 and
CREE results are less than or equal to the OEM's in-use standard for
that subconfiguration.. EPA is also proposing to continue to allow
conversion manufacturers, on a test group basis, to convert
CO2 overcompliance into CO2 equivalents of
N2O and/or CH4 that can be subtracted from the
CH4 and N2O measured values to demonstrate
compliance with CH4 and/or N2O standards.
g. Geographical Location of Greenhouse Gas Fleet Vehicles
    EPA emission certification regulations require emission compliance
\366\ in the 50 states, the District of Columbia, the Puerto Rico, the
Virgin Islands, Guam, American Samoa and the Commonwealth of the
Northern Mariana Islands.
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    \366\ Section 216 of the Clean Air Act defines the term commerce
to mean ``(A) commerce between any place in any State and any place
outside thereof; and (B) commerce wholly within the District of
Columbia.''
    Section 302(d) of the Clean Air Act reads ``The term ``State''
means a State, the District of Columbia, the Commonwealth of Puerto
Rico, the Virgin Islands, Guam, and American Samoa and includes the
Commonwealth of the Northern Mariana Islands.'' In addition, 40 CFR
85.1502 (14) regarding the importation of motor vehicles and motor
vehicle engines defines the United States to include ``the States,
the District of Columbia, the Commonwealth of Puerto Rico, the
Commonwealth of the Northern Mariana Islands, Guam, American Samoa,
and the U.S. Virgin Islands.''
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8. Warranty, Defect Reporting, and Other Emission-Related Components
Provisions
    This rulemaking would retain warranty, defect reporting, and other
emission-related component provisions promulgated in the MY 2012-2016
rulemaking. Please see Section III.E.10 of the MY 2012-2016 final rule
preamble (75 FR 25486) for a discussion of these provisions.
9. Miscellaneous Technical Amendments and Corrections
    EPA is proposing a number of noncontroversial amendments and
corrections to the existing regulations. Because the regulatory
provisions for the EPA greenhouse gas program, NHTSA's CAFE program,
and the joint fuel economy and environment labeling program are all
intertwined in 40 CFR Part 600, this proposed rule presents an
opportunity to make corrections and clarifications to all or any of
these programs. Consequently, a number of minor and non-substantive
corrections are being proposed to the regulations that implement these
programs.
    Amendments include the following:
     In section 86.135-12, we have removed references to the
model year applicability of N2O measurement. This
applicability is covered elsewhere in the regulations, and we believe
that--where possible--testing regulations should be limited to the
specifics of testing and measurement.
     The definition of ``Footprint'' in 86.1803-01 is revised
to clarify measurement and rounding. The previous definition stated
that track width is ``measured in inches,'' which may inadvertently
imply measuring and recording to the nearest inch. The revised
definition clarifies that measurements should be to the nearest one
tenth of an inch, and average track width should be rounded to the
nearest tenth of an inch.
    We are also proposing a solution to a situation in which a
manufacturer of a clean alternative fuel conversion is attempting to
comply with the fuel conversion regulations (see 40 CFR part 85 subpart
F) at a point in time before which certain data is available from the
original manufacturer of the vehicle. Clean alternative fuel
conversions are subject to greenhouse gas standards if the vehicle as
originally manufactured was subject to greenhouse gas standards, unless
the conversion manufacturer qualifies for exemption as a small
business. Compliance with light-duty vehicle greenhouse gas emission
standards is demonstrated by complying with the N2O and
CH4 standards and the in-use CO2 exhaust emission
standard set forth in 40 CFR 86.1818-12(d) as determined by the
original manufacturer for the subconfiguration that is identical to the
fuel conversion emission data vehicle (EDV). However, the
subconfiguration data may not be available to the fuel conversion
manufacturer at the time they are seeking EPA certification. Several
compliance options are currently provided to fuel conversion
manufacturers that are consistent with the compliance options for the
original equipment manufacturers. EPA is proposing to add another
option that would be applicable starting with the 2012 model year. The
new option would allow clean alternative fuel conversion manufacturers
to satisfy the greenhouse gas standards if the sum of CH4
plus N2O plus CREE emissions from the vehicle pre-conversion
is less than the sum post-conversion, adjusting for the global warming
potential of the constituents.
10. Base Tire Definition
    One of the factors in a manufacturer's calculation of vehicle
footprint is the base tire. Footprint is based on a vehicle's wheel
base and track width, and track width in turn is ``the lateral distance
between the centerlines of the base tires at ground, including the
camber angle.'' \367\ EPA's current definition of base tire is the
``tire specified as standard equipment by the

manufacturer.'' \368\ EPA understands that some manufacturers may be
applying this base tire definition in different ways, which could lead
to differences across manufacturers in how they are ultimately
calculating footprints. EPA invites public comment on whether the base
tire definition should be clarified to ensure a more uniform
application across manufacturers. For example, NHTSA is proposing a
specific change to the base tire definition for the CAFE program (see
Section IV.I.5.g, and proposed 49 CFR 523.2). Because the calculation
of footprint is a fundamental aspect of both the greenhouse gas
standards and the CAFE standards, EPA welcomes comments on whether the
existing base tire definition should be clarified, and specific changes
to the definition that would address this issue.
---------------------------------------------------------------------------

    \367\ See 40 CFR 86.1803-01.
    \368\ See 40 CFR 86.1803-01, and 40 CFR 600.002. Standard
equipment means those features or equipment which are marketed on a
vehicle over which the purchaser can exercise no choice.
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11. Treatment of Driver-Selectable Modes and Conditions
    EPA is requesting comments on whether there is a need to clarify in
the regulations how EPA treats driver-selectable modes (such as multi-
mode transmissions and other user-selectable buttons or switches) that
may impact fuel economy and GHG emissions. New technologies continue to
arrive on the market, with increasing complexity and an increasing
array of ways a driver can make choices that affect the fuel economy
and greenhouse gas emissions. For example, some start-stop systems may
offer the driver the option of choosing whether or not the system is
enabled. Similarly, vehicles with ride height adjustment or grill
shutters may allow drivers to override those features.
    Under the current regulations, EPA draws a distinction between
vehicles tested for purposes of CO2 emissions performance
and fuel economy and vehicles tested for non-CO2 emissions
performance. When testing emission data vehicles for certification
under Part 86 for non-CO2 emissions standards, a vehicle
that has multiple operating modes must meet the applicable emission
standards in all modes, and on all fuels. Sometimes testing may occur
in all modes, but more frequently the worst-case mode is selected for
testing to represent the emission test group. For example, a vehicle
that allows the user to disengage the start-stop capability must meet
the standards with and without the start-stop system operating (in some
cases EPA has determined that the operation of start-stop is the worst
case for emissions controlled by the catalyst because of the spike in
emissions associated with each start). Similarly, a plug-in hybrid
electric vehicle is tested in charge-sustaining (i.e., gasoline-only)
operation. Current regulations require the reporting of CO2
emissions from certification tests conducted under Part 86, but EPA
regulations also recognize that these values, from emission data
vehicles that represent a test group, are ultimately not the values
that are used to establish in-use CO2 standards (which are
established on much more detailed sub-configuration-specific level) or
the model type CO2 and fuel economy values used for fleet
averaging under Part 600.
    When EPA tests vehicles for fuel economy and CO2
emissions performance, user-selectable modes are treated somewhat
differently, where the goals are different and where worst-case
operation may not be the appropriate method. For example, EPA does not
believe that the fuel economy and CO2 emissions value for a
PHEV should ignore the use of grid electricity, or that other dual fuel
vehicles should ignore the real-world use of alternative fuels that
reduce GHG emissions. The regulations address the use of utility
factors to properly weight the CO2 performance on the
conventional fuel and the alternative fuel. Similarly, non-
CO2 emission certification testing may be done in a
transmission mode that is not likely to be the predominant mode used by
consumers. Testing under Part 600 must determine a single fuel economy
value for each model type for the CAFE program and a single
CO2 value for each model type for EPA's program. With
respect to transmissions, Part 600 refers to 86.128, which states the
following:

    All test conditions, except as noted, shall be run according to
the manufacturer's recommendations to the ultimate purchaser,
Provided, That: Such recommendations are representative of what may
reasonably be expected to be followed by the ultimate purchaser
under in-use conditions.

    For multi-mode transmissions EPA relies on guidance letter CISD-09-
19 (December 3, 2009) to guide the determination of what is
``representative of what may reasonably be expected to be followed by
the ultimate purchaser under in-use conditions.'' If EPA can make a
determination that one mode is the ``predominant'' mode (meaning nearly
total usage), then testing may be done in that mode. However, if EPA
cannot be convinced that a single mode is predominant, then fuel
economy and GHG results from each mode are typically averaged with
equal weighting. There are also detailed provisions that explain how a
manufacturer may conduct surveys to support a statement that a given
mode is predominant. However, CISD-09-19 only addresses transmissions,
and states the following regarding other technologies:

    ``Please contact EPA in advance to request guidance for vehicles
equipped with future technologies not covered by this document,
unusual default strategies or driver selectable features, e.g.,
hybrid electric vehicles where the multimode button or switch
disables or modifies any fuel saving features of the vehicle (such
as the stop-start feature, air conditioning compressor operation,
electric-only operation, etc.).''

    The unique operating characteristics of these technologies
essentially often requires that EPA determine fuel economy and
CO2 testing and calculations on a case-by-case basis.
Because the CAFE and CO2 programs require a single value to
represent a model type, EPA must make a decision regarding how to
account for multiple modes of operation. When a manufacturer brings
such a technology to us for consideration, we will evaluate the
technology (including possibly requiring that the manufacturer give us
a vehicle to test) and provide the manufacturer with instructions on
how to determine fuel economy and CO2 emissions. In general
we will evaluate these technologies in the same way and following the
same principles we use to evaluate transmissions under CISD-09-19,
making a determination as to whether a given operating mode is
predominant or not (using the criteria for predominance described in
CISD-09-19). These instructions are provided to the manufacturer under
the authority for special test procedures described in 40 CFR 600.111-
08. EPA would apply the same approach to testing for compliance with
the in-use CO2 standard, so testing for the CO2
fleet average and testing for compliance with the in-use CO2
standard would be consistent. EPA requests comment on whether the
current approach and regulatory provisions are sufficient, or whether
additional regulations or guidance should be developed to describe
EPA's process. EPA recognizes that ultimately no regulation can
anticipate all options, devices, and operator controls that may arrive
in the future, and adequate flexibility to address future situations is
an important attribute for fuel economy and CO2 emissions
testing.

F. How would this proposal reduce GHG emissions and their associated
effects?

    This action is an important step towards curbing growth of GHG
emissions from cars and light trucks. In the absence of control, GHG
emissions worldwide and in the U.S. are projected to continue steady
growth. Table III-54 shows emissions of CO2, methane
(CH4), nitrous oxide (N2O) and air conditioning
refrigerant (HFC-134a) on a CO2-equivalent basis for
calendar years 2010, 2020, 2030, 2040 and 2050. As shown below, U.S.
GHGs are estimated to make up roughly 15 percent of total worldwide
emissions in 2010. Further, the contribution of direct emissions from
cars and light-trucks to this U.S. share reaches an estimated 17
percent of U.S. emissions by 2030 in the absence of control. As
discussed later in this section, this steady rise in GHG emissions is
associated with numerous adverse impacts on human health, food and
agriculture, air quality, and water and forestry resources.
[GRAPHIC] [TIFF OMITTED] TP01DE11.119

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    \369\ ADAGE and GCAM model projections of worldwide and U.S. GHG
emissions are provided for context only. The baseline data in these
models differ in certain assumptions from the baseline used in this
proposal. For example, the ADAGE baseline is calibrated to AEO 2010,
which includes the EISA 35 MPG by 2020 provision, but does not
explicitly include the MYs 2012-2016 rule. All emissions data were
rounded to two significant digits.
    \a\GCAM model.
    \370\ Based on the Representative Concentration Pathway scenario
in GCAM available at http://www.globalchange.umd.edu/gcamrcp. See
section III.F.3 and DRIA Chapter 6.4 for additional information on
GCAM.
    \b\ ADAGE model.
    \371\ Based on the ADAGE reference case used in U.S. EPA (2010).
``EPA Analysis of the American Power Act of 2010'' U.S.
Environmental Protection Agency, Washington, DC, USA
(http:www.epagov/climatechange/economics/economicanalyses.html).
    \c\ OMEGA model, Tailpipe CO2 and HFC134a only
(includes impacts of MYs 2012-2016 rule).
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    This rule will result in significant reductions as newer, cleaner
vehicles come into the fleet. As discussed in Section I, this GHG rule
is part of a joint National Program such that a large part of the
projected benefits, but by no means all, would be achieved jointly with
NHTSA's CAFE standards, which are described in detail in Section IV.
EPA estimates the reductions attributable to the GHG program over time
assuming the model year 2025 standards continue indefinitely post-2025,
compared to a reference scenario in which the 2016 model year GHG
standards continue indefinitely beyond 2016.
    EPA estimated greenhouse impacts from several sources including:
(a) The impact of the standards on tailpipe CO2 emissions,
(b) projected improvements in the efficiency of vehicle air
conditioning systems, \372\ (c) reductions in direct emissions of the
refrigerant and potent greenhouse gas HFC-134a from air conditioning
systems, (d) ``upstream'' emission reductions from gasoline extraction,
production and distribution processes as a result of reduced gasoline
demand associated with this rule, and (e) ``upstream'' emission
increases from power plants as electric powertrain vehicles increase in
prevalence as a result of this rule. EPA additionally accounted for the
greenhouse gas impacts of additional vehicle miles travelled (VMT) due
to the ``rebound'' effect discussed in Section III.H.
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    \372\ While EPA anticipates that the majority of mobile air
conditioning systems will be improved in response to the MY 2012-
2016 rulemaking, the agency expects that the remainder will be
improved as a result of this action.
---------------------------------------------------------------------------

    Using this approach EPA estimates the proposed standards would cut
annual fleetwide car and light truck tailpipe CO2 emissions
by approximately 230 MMT or 18 percent by 2030, when 85 percent of car
and light truck miles will be travelled by vehicles meeting the MY 2017
or later standards. An additional 65 MMTCO2eq of reduced
emissions are attributable to reductions in gasoline production,
distribution and transport. 15 MMTCO2eq of additional
emissions will be attributable to increased electricity production. In
total, EPA estimates that compared to a baseline of indefinite 2016
model year standards, net GHG emission reductions from the program
would be approximately 300 million metric tons CO2-
equivalent (MMTCO2eq) annually by 2030, which represents a
reduction of 4% of total U.S. GHG emissions and 0.5% of total worldwide
GHG emissions projected in that year. These GHG savings would result in
savings of approximately 26 billion gallons of petroleum-based
gasoline.\373\
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    \373\ All estimates of fuel savings presented here assume that
manufacturers use air conditioning leakage credits as part of their
compliance strategy. If these credits were not used, the fuel
savings would be larger.
---------------------------------------------------------------------------

    EPA projects the total reduction of the program over the full life
of model year 2017-2025 vehicles to be about 1,970 MMTCO2eq,
with fuel savings of 170 billion gallons (3.9 billion barrels) of
gasoline over the life of these vehicles.
    The impacts on atmospheric CO2 concentrations, global
mean surface temperature, sea level rise, and ocean pH resulting from
these emission reductions are discussed in Section III.F.3.

1. Impact on GHG Emissions
    The modeling of fuel savings and greenhouse gas emissions is
substantially similar to that which was conducted in the 2012-2016
Final Rulemaking and the MY 2017-2025 Interim Joint Technical
Assessment Report (TAR). As detailed in Draft RIA chapter 4, EPA
estimated calendar year tailpipe CO2 reductions based on
pre- and post-control CO2 gram per mile levels from EPA's
OMEGA model, coupled with VMT projections derived from AEO 2011 Final
Release. These estimates reflect the real-world CO2
emissions reductions projected for the entire U.S. vehicle fleet in a
specified calendar year. EPA also estimated full lifetime reductions
for model years 2017-2025 using pre- and post-control CO2
levels projected by the OMEGA model, coupled with projected vehicle
sales and lifetime mileage estimates. These estimates reflect the real-
world CO2 emissions reductions projected for model years
2017 through 2025 vehicles over their entire life. Upstream impacts
from power plant emissions came from OMEGA estimates of EV/penetration
into the fleet (approximately 3%). For both calendar year and model
year assessments, EPA estimated the environmental impact of the
advanced technology multiplier, pickup truck hybrid electric vehicle
(HEV) and performance based incentives and air conditioning credits.
The impact of the off-cycle credits were not explicitly estimated, as
these credits are assumed to be inherently environmentally neutral
(Section III.B). EPA also did not assess the impact of the credit
banking carry-forward programs.
    As in the MY 2012-2016 rulemaking, this proposal allows
manufacturers to earn credits for improvements to controls for both
direct and indirect AC emissions. Since these improvements are
relatively low cost, EPA again projects that manufacturers will take
advantage of this flexibility, leading to reductions from emissions
associated with vehicle air conditioning systems. As explained above,
these reductions will come from both direct emissions of air
conditioning refrigerant over the life of the vehicle and tailpipe
CO2 emissions produced by the increased load of the A/C
system on the engine. In particular, EPA estimates that direct
emissions of HFC-134a, one of the most potent greenhouse gases, would
be fully removed from light-duty vehicles through the phase-in of
alternative refrigerants. More efficient air conditioning systems would
also lead to fuel savings and additional reductions in upstream
emissions from fuel production and distribution. Our estimated
reductions from the A/C credit program assume that manufacturers will
fully utilize the program by MY 2021.
    Upstream greenhouse gas emission reductions associated with the
production and distribution of fuel were estimated using emission
factors from DOE's GREET1.8 model, with modifications as detailed in
Chapter 5 of the DRIA. These estimates include both international and
domestic emission reductions, since reductions in foreign exports of
finished gasoline and/or crude would make up a significant share of the
fuel savings resulting from the GHG standards. Thus, significant
portions of the upstream GHG emission reductions will occur outside of
the U.S.; a breakdown of projected international versus domestic
reductions is included in the DRIA.
    Electricity emission factors were derived from EPA's Integrated
Planning Model (IPM). EPA uses IPM to analyze the projected impact of
environmental policies on the electric power sector in the 48
contiguous states and the District of Columbia. IPM is a multi-
regional, dynamic, deterministic linear programming model of the U.S.
electric power sector. It provides forecasts of least-cost capacity
expansion, electricity dispatch, and emission control strategies for
meeting energy demand and environmental, transmission, dispatch, and
reliability constraints. EPA derived average national CO2
emission factors from the IPM version 4.10 base case run for the
``Proposed Transport Rule.'' \374\ As discussed in Draft TSD Chapter 4,
for the Final Rulemaking, EPA may consider emission factors other than
national power generation, such as marginal power emission factors, or
regional emission factors.
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    \374\ EPA. IPM. http://www.epa.gov/airmarkt/progsregs/epa-ipm/BaseCasev410.html. ``Proposed Transport Rule/NODA version'' of IPM.
TR--SB--Limited Trading v.4.10.
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a. Calendar Year Reductions for Future Years
    Table III-55 shows reductions estimated from these GHG standards
assuming a pre-control case of 2016 MY standards continuing
indefinitely beyond 2016, and a post-control case in which 2025 MY GHG
standards continue indefinitely beyond 2025. These reductions are
broken down by upstream and downstream components, including air
conditioning improvements, and also account for the offset from a 10
percent VMT ``rebound'' effect as discussed in Section III.H. Including
the reductions from upstream emissions, total reductions are estimated
to reach 297 MMTCO2eq annually by 2030, and grow to over 540
MMTCO2eq in 2050 as cleaner vehicles continue to come into
the fleet.

[GRAPHIC] [TIFF OMITTED] TP01DE11.120

    The total program emission reductions yield significant emission
decreases relative to worldwide and national total emissions.
[GRAPHIC] [TIFF OMITTED] TP01DE11.121

b. Lifetime Reductions for 2017-2025 Model Years
    EPA also analyzed the emission reductions over the full life of the
2017-2025 model year cars and light trucks that would be affected by
this program.\375\ These results, including both upstream and
downstream GHG contributions, are presented in Table III-57, showing
lifetime reductions of about 2,065 MMTCO2eq.
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    \375\ As detailed in DRIA Chapter 4 and TSD Chapter 4, for this
analysis the full life of the vehicle is represented by average
lifetime mileages for cars (197,000 miles [MY 2017] and 211,000
miles [MY 2025]) and trucks (235,000 miles [MY 2017] and 249,000
miles [MY 2025]). These estimates are a function of how far vehicles
are driven per year and scrappage rates.
[GRAPHIC] [TIFF OMITTED] TP01DE11.122

c. Impacts of VMT Rebound Effect
    As noted above and discussed more fully in Section III.H., the
effect of a decrease in fuel cost per mile on vehicle use (VMT
``rebound'') was accounted for in our assessment of economic and
environmental impacts of this proposed 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 decrease in fuel
cost per mile; i.e., a 10 percent decrease in fuel cost per mile from
our proposed standards would result in a 1 percent increase in VMT.
Results are shown in Table III-58. This increase is accounted for in
the reductions presented in Table III-55 and Table III-56). The table
below compares the reductions under two different scenarios; one in
which the VMT estimate is entirely insensitive to the cost of travel,
and one in which both control and reference scenario VMT are affected
by the rebound effect. This topic is further discussed in DRIA chapter
4.
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    \376\ This assessment assumes that owners of grid-electric
powered vehicles react similarly to changes int eh cost of driving s
owners of conventional gasoline vehicles. We seek comment on this
approach in Section III.H.4c.

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[GRAPHIC] [TIFF OMITTED] TP01DE11.123

d. Analysis of Alternatives
    EPA analyzed four alternative scenarios for this proposal (Table
III-59). EPA assumed that manufacturers would use air conditioning
improvements and the HEV and performance based pickup incentives in
identical penetrations as in the primary scenario. EPA re-estimated the
impact of the electric vehicle multiplier under each alternative. Under
these assumptions, EPA expects achieved fleetwide average emission
levels of 150 g/mile CO2 to 177 g/mile CO2eq (6%)
in 2025. As in the primary scenario, EPA assumed that the fleet
complied with the standards. For full details on modeling assumptions,
please refer to DRIA Chapter 4. EPA's assessment of these alternative
standards is discussed in Section III.D.6

[GRAPHIC] [TIFF OMITTED] TP01DE11.124

[GRAPHIC] [TIFF OMITTED] TP01DE11.125

2. Climate Change Impacts From GHG Emissions
    The impact of GHG emissions on the climate has been reviewed in the
2012-2016 light-duty rulemaking and recent heavy-duty GHG rulemaking.
See 75 FR at 25491; 76 FR at 57294. This section briefly discusses
again some of the climate impact context for transportation emissions.
These previous discussions noted that once emitted, GHGs that are the
subject of this regulation can remain in the atmosphere for decades to
millennia, 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, agricultural
activities, cement production, and some industrial activities.
Transportation activities, in aggregate, were the second largest
contributor to total U.S. GHG emissions in 2009 (27 percent of total
emissions).\377\
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    \377\ U.S. EPA (2011) Inventory of U.S. Greenhouse Gas Emissions
and Sinks: 1990-2009. EPA 430-R-11-005. (Docket EPA-HQ-OAR-2010-
0799).
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    The Administrator relied on thorough and peer-reviewed assessments
of climate change science prepared by the Intergovernmental Panel on
Climate Change (``IPCC''), the United States Global Change Research
Program (``USGCRP''), and the National Research Council of the National
Academies (``NRC'') \378\ as the primary scientific and technical basis
for the Endangerment and Cause or Contribute Findings for Greenhouse
Gases Under Section 202(a) of the Clean Air Act (74 FR 66496, December
15, 2009). These assessments comprehensively address the scientific
issues the Administrator had to examine, providing her both data and
information on a wide range of issues pertinent to the Endangerment
Finding. These assessments have been rigorously reviewed by the expert
community, and also by United States government agencies and
scientists, including by EPA itself.
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    \378\ 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. (Docket EPA-HQ-OAR-2010-
0799).
---------------------------------------------------------------------------

    Based on these assessments, the Administrator determined, in
essence, that greenhouse gases cause warming; that levels of greenhouse
gases are increasing in the atmosphere due to human activity; the
climate is warming; recent warming has been attributed to the increase
in greenhouse gases; and that warming of the climate threatens human
health and welfare. The Administrator further found that emissions of
well-mixed greenhouse gases from new motor vehicles and engines
contribute to the air pollution for which the endangerment finding was
made. Specifically, the Administrator found under section 202(a) of the
Act that six greenhouse gases (carbon dioxide, methane, nitrous oxide,
hydrofluorocarbons, perfluorocarbons, and sulfur hexafluoride) taken in
combination endanger both the public health and the public welfare of
current and future generations, and further found that the combined
emissions of these greenhouse gases from new motor vehicles and engines
contribute to the greenhouse gas air pollution that endangers public
health and welfare.
    More recent assessments have produced similar conclusions to those
of the assessments upon which the Administrator relied. In May 2010,
the NRC published its comprehensive assessment, ``Advancing the Science
of Climate Change.'' \379\ It concluded that ``climate change is
occurring, is caused largely by human activities, and poses significant
risks for--and in many cases is already affecting--a broad range of
human and natural systems.'' Furthermore, the NRC stated that this
conclusion is based on findings that are ``consistent with the
conclusions of recent assessments by the U.S. Global Change Research
Program, the Intergovernmental Panel on Climate Change's Fourth
Assessment Report, and other assessments of the state of scientific
knowledge on climate change.'' These are the same assessments that
served as the primary scientific references underlying the
Administrator's Endangerment Finding. Another NRC assessment, ``Climate
Stabilization Targets: Emissions, Concentrations, and Impacts over
Decades to Millennia,'' was published

in 2011. This report found that climate change due to carbon dioxide
emissions will persist for many centuries. The report also estimates a
number of specific climate change impacts, finding that every degree
Celsius (C) of warming could lead to increases in the heaviest 15% of
daily rainfalls of 3 to 10%, decreases of 5 to 15% in yields for a
number of crops (absent adaptation measures that do not presently
exist), decreases of Arctic sea ice extent of 25% in September and 15%
annually averaged, along with changes in precipitation and streamflow
of 5 to 10% in many regions and river basins (increases in some
regions, decreases in others). The assessment also found that for an
increase of 4 degrees C nearly all land areas would experience summers
warmer than all but 5% of summers in the 20th century, that for an
increase of 1 to 2 degrees C the area burnt by wildfires in western
North America will likely more than double, that coral bleaching and
erosion will increase due both to warming and ocean acidification, and
that sea level will rise 1.6 to 3.3 feet by 2100 in a 3 degree C
scenario. The assessment notes that many important aspects of climate
change are difficult to quantify but that the risk of adverse impacts
is likely to increase with increasing temperature, and that the risk of
abrupt climate changes can be expected to increase with the duration
and magnitude of the warming.
---------------------------------------------------------------------------

    \379\ National Research Council (NRC) (2010). Advancing the
Science of Climate Change. National Academy Press. Washington, DC.
(Docket EPA-HQ-OAR-2010-0799).
---------------------------------------------------------------------------

    In the 2010 report cited above, the NRC stated that some of the
largest potential risks associated with future climate change may come
not from relatively smooth changes that are reasonably well understood,
but from extreme events, abrupt changes, and surprises that might occur
when climate or environmental system thresholds are crossed. Examples
cited as warranting more research include the release of large
quantities of GHGs stored in permafrost (frozen soils) across the
Arctic, rapid disintegration of the major ice sheets, irreversible
drying and desertification in the subtropics, changes in ocean
circulation, and the rapid release of destabilized methane hydrates in
the oceans.
    On ocean acidification, the same report noted the potential for
broad, ``catastrophic'' impacts on marine ecosystems. Ocean acidity has
increased 25 percent since pre-industrial times, and is projected to
continue increasing. By the time atmospheric CO2 content
doubles over its preindustrial value, there would be virtually no place
left in the ocean that can sustain coral reef growth. Ocean
acidification could have dramatic consequences for polar food webs
including salmon, the report said.
    Importantly, these recent NRC assessments represent another
independent and critical inquiry of the state of climate change
science, separate and apart from the previous IPCC and USGCRP
assessments.
3. Changes in Global Climate Indicators Associated With the Proposal's
GHG Emissions Reductions
    EPA examined \380\ the reductions in CO2 and other GHGs
associated with this rulemaking and analyzed the projected effects on
atmospheric CO2 concentrations, global mean surface
temperature, sea level rise, and ocean pH which are common variables
used as indicators of climate change.\381\ The analysis projects that
the proposed rule, if adopted, will reduce atmospheric concentrations
of CO2, global climate warming, ocean acidification, and sea
level rise relative to the reference case. Although the projected
reductions and improvements are small in comparison to the total
projected climate change, they are quantifiable, directionally
consistent, and will contribute to reducing the risks associated with
climate change. Climate change is a global phenomenon and EPA
recognizes that this one national action alone will not prevent it: EPA
notes this would be true for any given GHG mitigation action when taken
alone or when considered in isolation. EPA also notes that a
substantial portion of CO2 emitted into the atmosphere is
not removed by natural processes for millennia, and therefore each unit
of CO2 not emitted into the atmosphere due to this rule
avoids essentially permanent climate change on centennial time scales.
---------------------------------------------------------------------------

    \380\ Using the Model for the Assessment of Greenhouse Gas
Induced Climate Change (MAGICC) 5.3v2, http://www.cgd.ucar.edu/cas/wigley/magicc/ magicc/), EPA estimated the effects of this rulemaking's
greenhouse gas emissions reductions on global mean temperature and
sea level. Please refer to Chapter 6.4 of the DRIA for additional
information.
    \381\ Due to timing constraints, this analysis was conducted
with preliminary estimates of the emissions reductions projected
from this proposal, which were similar to the final estimates.
---------------------------------------------------------------------------

    EPA determines that the projected reductions in atmospheric
CO2, global mean temperature and sea level rise are
meaningful in the context of this proposed action. In addition, EPA has
conducted an analysis to evaluate the projected changes in ocean pH in
the context of the changes in emissions from this rulemaking. The
results of the analysis demonstrate that relative to the reference
case, projected atmospheric CO2 concentrations are estimated
by 2100 to be reduced by 3.29 to 3.68 part per million by volume
(ppmv), global mean temperature is estimated to be reduced by 0.0076 to
0.0184 [deg]C, and sea-level rise is projected to be reduced by
approximately 0.074-0.166 cm, based on a range of climate
sensitivities. The analysis also demonstrates that ocean pH will
increase by 0.0018 pH units by 2100 relative to the reference case.
a. Estimated 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 temperature, and sea level rise out to 2100
resulting from the emissions reductions in this rulemaking using the
Global Change Assessment Model (GCAM, formerly MiniCAM), integrated
assessment model \382\ coupled with the Model for the Assessment of
Greenhouse Gas Induced Climate Change (MAGICC, version 5.3v2).\383\
GCAM was used to create the globally and temporally consistent set of
climate relevant variables required for running MAGICC. MAGICC was then
used to estimate the projected change in these variables over time.
Given the magnitude of the estimated emissions reductions associated
with this action, a simple climate model such as MAGICC is reasonable
for estimating the atmospheric and climate response. 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 IPCC.
---------------------------------------------------------------------------

    \382\ GCAM is a long-term, global integrated assessment model of
energy, economy, agriculture and land use, that considers the
sources of emissions of a suite of GHGs, emitted in 14 globally
disaggregated regions, the fate of emissions to the atmosphere, and
the consequences of changing concentrations of greenhouse related
gases for climate change. GCAM begins with a representation of
demographic and economic developments in each region and combines
these with assumptions about technology development to describe an
internally consistent representation of energy, agriculture, land-
use, and economic developments that in turn shape global emissions.
Brenkert A, S. Smith, S. Kim, and H. Pitcher, 2003: Model
Documentation for the MiniCAM. PNNL-14337, Pacific Northwest
National Laboratory, Richland, Washington. (Docket EPA-HQ-OAR-2010-
0799).
    \383\ Wigley, T.M.L. 2008. MAGICC 5.3.v2 User Manual. UCAR--
Climate and Global Dynamics Division, Boulder, Colorado. http://www.cgd.ucar.edu/cas/wigley/magicc/ (Docket EPA-HQ-OAR-2010-0799).
---------------------------------------------------------------------------

    The integrated impact of the following pollutant and greenhouse gas
emissions changes are considered: CO2, CH4,
N2O, HFC-134a, NOX, CO, SO2, and
volatile organic compounds (VOC). For these pollutants an annual time-
series of (upstream + downstream) emissions

reductions estimated from the rulemaking were applied as net reductions
to a global reference case (or baseline) emissions scenario in GCAM to
generate an emissions scenario specific to this proposed rule.\384\ The
emissions reductions past 2050 for all gases were scaled with total
U.S. road transportation fuel consumption from the GCAM reference
scenario. Road transport fuel consumption past 2050 does not change
significantly and thus emissions reductions remain relatively constant
from 2050 through 2100. Specific details about the GCAM reference case
scenario can be found in Chapter 6.4 of the DRIA that accompanies this
proposal.
---------------------------------------------------------------------------

    \384\ Due to timing constraints, this analysis was conducted
with preliminary estimates of the emissions reductions projected
from this proposal, which were similar to the final estimates.
---------------------------------------------------------------------------

    MAGICC calculates the forcing response at the global scale from
changes in atmospheric concentrations of CO2,
CH4, N2O, HFCs, and tropospheric ozone
(O3). It also includes the effects of temperature changes on
stratospheric ozone and the effects of CH4 emissions on
stratospheric water vapor. Changes in CH4, NOX,
VOC, and CO emissions affect both O3 concentrations and
CH4 concentrations. MAGICC includes the relative climate
forcing effects of changes in sulfate concentrations due to changing
SO2 emissions, including both the direct effect of sulfate
particles and the indirect effects related to cloud interactions.
However, MAGICC does not calculate the effect of changes in
concentrations of other aerosols such as nitrates, black carbon, or
organic carbon, making the assumption that the sulfate cooling effect
is a proxy for the sum of all the aerosol effects. Therefore, the
climate effects of changes in PM2.5 emissions and precursors
(besides SO2) which are presented in the DRIA Chapter 6 were
not included in the calculations in this chapter. MAGICC also
calculates all climate effects at the global scale. This global scale
captures the climate effects of the long-lived, well-mixed greenhouse
gases, but does not address the fact that short-lived climate forcers
such as aerosols and ozone can have effects that vary with location and
timing of emissions. Black carbon in particular is known to cause a
positive forcing or warming effect by absorbing incoming solar
radiation, but there are uncertainties about the magnitude of that
warming effect and the interaction of black carbon (and other co-
emitted aerosol species) with clouds. While black carbon is likely to
be an important contributor to climate change, it would be premature to
include quantification of black carbon climate impacts in an analysis
of these proposed standards. See generally, EPA, Response to Comments
to the Endangerment Finding Vol. 9 section <IP_ADDRESS> and the discussion
of black carbon in the endangerment finding at 74 FR at 66520.
Additionally, the magnitude of PM2.5 emissions changes (and
therefore, black carbon emission changes) related to these proposed
standards are small in comparison to the changes in the pollutants
which have been included in the MAGICC model simulations.
    Changes in atmospheric CO2 concentration, global mean
temperature, and sea level rise for both the reference case and the
emissions scenarios associated with this action were computed using
MAGICC. To calculate the reductions in the atmospheric CO2
concentrations as well as in temperature and sea level resulting from
this proposal, the output from the policy scenario associated with
EPA's proposed standards 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 atmospheric CO2, global mean temperature
and sea level rise were projected across the most current IPCC range of
climate sensitivities, from 1.5 [deg]C to 6.0 [deg]C.\385\ This range
reflects the uncertainty for equilibrium climate sensitivity for how
much global mean temperature would rise if the concentration of carbon
dioxide in the atmosphere were to double. The information for this
range come from constraints from past climate change on various time
scales, and the spread of results for climate sensitivity from
ensembles of models.\386\ Details about this modeling analysis can be
found in the DRIA Chapter 6.4.
---------------------------------------------------------------------------

    \385\ 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/ (Docket EPA-HQ-OAR-2010-0799).
    \386\ 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. (Docket EPA-HQ-OAR-2010-0799).
---------------------------------------------------------------------------

    The results of this modeling, summarized in Table III-62, show
small, but quantifiable, reductions in atmospheric CO2
concentrations, projected global mean temperature and sea level
resulting from this action, across all climate sensitivities. As a
result of the emission reductions from the proposed standards, relative
to the reference case the atmospheric CO2 concentration is
projected to be reduced by 3.29-3.68 ppmv by 2100, the global mean
temperature is projected to be reduced by approximately 0.0076-0.0184
[deg]C by 2100, and global mean sea level rise is projected to be
reduced by approximately 0.074-0.166 cm by 2100. The range of
reductions in global mean temperature and sea level rise is larger than
that for CO2 concentrations because CO2
concentrations are only weakly coupled to climate sensitivity through
the dependence on temperature of the rate of ocean absorption of
CO2, whereas the magnitude of temperature change response to
CO2 changes (and therefore sea level rise) is more tightly
coupled to climate sensitivity in the MAGICC model.

[GRAPHIC] [TIFF OMITTED] TP01DE11.126

    The projected reductions are small relative to the change in
temperature (1.8-4.8 [deg]C), sea level rise (23-55 cm), and ocean
acidity (-0.30 pH units) from 1990 to 2100 from the MAGICC simulations
for the GCAM reference case. However, this is to be expected given the
magnitude of emissions reductions expected from the program in the
context of global emissions. This uncertainty range does not include
the effects of uncertainty in future emissions. It should also be noted
that the calculations in MAGICC do not include the possible effects of
accelerated ice flow in Greenland and/or Antarctica: the recent NRC
report estimated a likely sea level increase for a business-as-usual
scenario of 0.5 to 1.0 meters.\387\ Further discussion of EPA's
modeling analysis is found in the DRIA, Chapter 6.
---------------------------------------------------------------------------

    \387\ National Research Council (NRC), 2011. Climate
Stabilization Targets: Emissions, Concentrations, and Impacts over
Decades to Millennia. Washington, DC: National Academies Press.
(Docket EPA-HQ-OAR-2010-0799).
---------------------------------------------------------------------------

    EPA used the computer program CO2SYS,\388\ version 1.05, to
estimate projected changes in ocean pH for tropical waters based on the
atmospheric CO2 concentration change (reduction) resulting
from this proposal. The program performs calculations relating
parameters of the CO2 system in seawater. EPA used the
program to calculate ocean pH as a function of atmospheric
CO2 concentrations, among other specified input conditions.
Based on the projected atmospheric CO2 concentration
reductions resulting from this proposal, the program calculates an
increase in ocean pH of 0.0018 pH units in 2100 relative to the
reference case (compared to a decrease of 0.3 pH units from 1990 to
2100 in the reference case). Thus, this analysis indicates the
projected decrease in atmospheric CO2 concentrations from
the program will result in an increase in ocean pH. For additional
validation, results were generated using different known constants from
the literature. A comprehensive discussion of the modeling analysis
associated with ocean pH is provided in the DRIA, Chapter 6.
---------------------------------------------------------------------------

    \388\ 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. (Docket EPA-HQ-OAR-
2010-0799).
---------------------------------------------------------------------------

    As discussed in III.F.2, the 2011 NRC assessment on ``Climate
Stabilization Targets: Emissions, Concentrations, and Impacts over
Decades to Millennia'' determined how a number of climate impacts--such
as heaviest daily rainfalls, crop yields, and Arctic sea ice extent--
would change with a temperature change of 1 degree Celsius (C) of
warming. These relationships of impacts with temperature change could
be combined with the calculated reductions in warming in Table III-56
to estimate changes in these impacts associated with this rulemaking.
b. Program's Effect on Climate
    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. Reductions in
emissions in the near-term are important in determining long-term
climate stabilization and associated impacts experienced not just over
the next decades but in the coming centuries and millennia.\389\ Though
the magnitude of the avoided climate change projected here is small in
comparison to the total projected changes, these reductions represent a
reduction in the adverse risks associated with climate change (though
these risks were not formally estimated for this action) across a range
of equilibrium climate sensitivities.
---------------------------------------------------------------------------

    \389\ National Research Council (NRC) (2011). Climate
Stabilization Targets: Emissions, Concentrations, and Impacts over
Decades to Millennia. National Academy Press. Washington, DC.
(Docket EPA-HQ-OAR-2010-0799).
---------------------------------------------------------------------------

    EPA's analysis of the program's impact on global climate conditions
is intended to quantify these potential reductions using the best
available science. EPA's modeling results show repeatable, consistent
reductions relative to the reference case in changes of CO2
concentration, temperature, sea-level rise, and ocean pH over the next
century.

G. How would the proposal impact non-GHG emissions and their associated
effects?

    Although this rule focuses on GHGs, it will also have an impact on
non-GHG pollutants. Sections G.1 of this preamble details the criteria
pollutant and air toxic inventory changes of this proposed rule. The
following sections, G.2 and G.3, discuss the health and environmental
effects associated with

the criteria and toxic air pollutants that are being impacted by this
proposed rule. In Section G.4 we discuss the potential impact of this
proposal on concentrations of criteria and air toxic pollutants in the
ambient air. The tools and methodologies used in this analysis are
substantially similar to those used in the MYs 2012-2016 light duty
rulemaking.
1. Inventory
a. Impacts
    In addition to reducing the emissions of greenhouse gases, this
rule would influence ``non-GHG'' pollutants, i.e., ``criteria'' air
pollutants and their precursors, and air toxics. The proposal would
affect emissions of carbon monoxide (CO), fine particulate matter
(PM2.5), sulfur dioxide (SOX), volatile organic
compounds (VOC), nitrogen oxides (NOX), 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 both in total and broken
down by the three drivers of these changes: a) ``downstream'' emission
changes, reflecting the estimated effects of VMT rebound (discussed in
Sections III.F and III.H) and decreased consumption of fuel; b)
``upstream'' emission reductions due to decreased extraction,
production and distribution of motor vehicle gasoline; c) ``upstream''
emission increases from power plants as electric powertrain vehicles
increase in prevalence as a result of this rule. Program impacts on
criteria and toxics emissions are discussed below, followed by
individual discussions of the methodology used to calculate each of
these three sources of impacts.
    As shown in Table III-63, EPA estimates that the proposed light
duty vehicle program would result in reductions of NOX, VOC,
PM2.5 and SOX, but would increase CO
emissions.\390\ For NOX, VOC, and PM2.5, we
estimate net reductions because the net emissions reductions from
reduced fuel refining, distribution and transport is larger than the
emission increases due to increased VMT and increased electricity
production. In the case of CO, we estimate slight emission increases,
because there are relatively small reductions in upstream emissions,
and thus the projected emission increases due to VMT rebound and
electricity production 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 downstream and fuel refining
sources.
---------------------------------------------------------------------------

    \390\ While estimates for CY 2020 and 2030 are shown here,
estimates through 2050 are shown in RIA Ch. 4.
---------------------------------------------------------------------------

    For all criteria pollutants the overall impact of the proposed
program would be small compared to total U.S. inventories across all
sectors. In 2030, EPA estimates that the program would reduce total
NOX, PM and SOX inventories by 0.1 to 0.8 percent
and reduce the VOC inventory by 1.1 percent, while increasing the total
national CO inventory by 0.5 percent.
    As shown in Table III-64, EPA estimates that the proposed program
would result in similarly small changes for air toxic emissions
compared to total U.S. inventories across all sectors. In 2030, EPA
estimates the proposed program would increase total 1,3 butadiene and
acetaldehyde emissions by 0.1 to 0.4 percent. Total acrolein, benzene
and formaldehyde emissions would decrease by similarly small amounts.

[GRAPHIC] [TIFF OMITTED] TP01DE11.127

[GRAPHIC] [TIFF OMITTED] TP01DE11.128

b. Methodology
    As in the MYs 2012-2016 rulemaking, for the downstream analysis,
the current version of the EPA motor vehicle emission simulator
(MOVES2010a) was used to estimate base VOC, CO, NOX, PM and
air toxics emission rates. Additional emissions from light duty cars
and trucks attributable to the rebound effect were then calculated
using the OMEGA model post-processor. A more complete discussion of the
inputs, methodology, and results is contained in RIA Chapter 4.
    This proposal assumes that MY 2017 and later vehicles are compliant
with the agency's Tier 2 emission standards. This proposal does not
model any future Tier 3 emission standards, because these standards
have not yet been proposed (see Section III.A). We intend for the
analysis assessing the impacts of both the final Tier 3 emission
standards and the final 2017-2025 LD GHG to be included in the final
Tier 3 rule. For the proposals, we are taking care to coordinate the
modeling of each rule to

properly assess the air quality impact of each action independently
without double counting.
    As in the MYs 2012-2016 GHG rulemaking, for this analysis we
attribute decreased fuel consumption from this program to petroleum-
based fuels only, while assuming no effect on volumes of ethanol and
other renewable fuels because they are mandated under the Renewable
Fuel Standard (RFS2). For the purposes of this emission analysis, we
assume that all gasoline in the timeframe of the analysis is blended
with 10 percent ethanol (E10). However, as a consequence of the fixed
volume of renewable fuels mandated in the RFS2 rulemaking and the
decreasing petroleum consumption predicted here, we anticipate that
this proposal would in fact increase the fraction of the U.S. fuel
supply that is made up by renewable fuels. Although we are not modeling
this effect in our analysis of this proposal, the Tier 3 rulemaking
will make more refined assumptions about future fuel properties,
including (in a final Tier 3 rule) accounting for the impacts of the LD
GHG rule. In this rulemaking EPA modeled the three impacts on criteria
pollutant emissions (rebound driving, changes in fuel production, and
changes in electricity production) discussed above.
    While electric vehicles have zero tailpipe emissions, EPA assumes
that manufacturers will plan for these vehicles in their regulatory
compliance strategy for non-GHG emissions standards, and will not over-
comply with those standards. Since the Tier 2 emissions standards are
fleet-average standards, we assume that if a manufacturer introduces
EVs into its fleet, that it would correspondingly compensate through
changes to vehicles elsewhere in its fleet, rather than meet an overall
lower fleet-average emissions level.\391\ Consequently, EPA assumes
neither tailpipe pollutant benefit (other than CO2) nor an
evaporative emission benefit from the introduction of electric vehicles
into the fleet. Other factors which may impact downstream non-GHG
emissions, but are not estimated in this analysis, include: The
potential for decreased criteria pollutant emissions due to increased
air conditioner efficiency; reduced refueling emissions due to less
frequent refueling events and reduced annual refueling volumes
resulting from the GHG standards; and increased hot soak evaporative
emissions due to the likely increase in number of trips associated with
VMT rebound modeled in this proposal. In all, these additional analyses
would likely result in small changes relative to the national
inventory.
---------------------------------------------------------------------------

    \391\ Historically, manufacturers have reduced precious metal
loading in catalysts in order to reduce costs. See http://www.platinum.matthey.com/media-room/our-view-on-.-.-./thrifting-of-precious-metals-in-autocatalysts/ Accessed 11/08/2011.
Alternatively, manufacturers could also modify vehicle calibration.
---------------------------------------------------------------------------

    To determine the upstream fuel production 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,\392\ but in some cases the GREET values
were modified or updated by EPA to be consistent with the National
Emission Inventory (NEI).\393\ 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 a memo to the docket. These emission
factors were incorporated into the OMEGA post-processor.
---------------------------------------------------------------------------

    \392\ 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/.
    \393\ U.S. EPA. 2002 National Emissions Inventory (NEI) Data and
Documentation, http://www.epa.gov/ttn/chief/net/2002inventory.html.
---------------------------------------------------------------------------

    As with the GHG emission analysis discussed in section III.F,
electricity emission factors were derived from EPA's Integrated
Planning Model (IPM). EPA uses IPM to analyze the projected impact of
environmental policies on the electric power sector in the 48
contiguous states and the District of Columbia. IPM is a multi-
regional, dynamic, deterministic linear programming model of the U.S.
electric power sector. It provides forecasts of least-cost capacity
expansion, electricity dispatch, and emission control strategies for
meeting energy demand and environmental, transmission, dispatch, and
reliability constraints. EPA derived average national CO2
emission factors from the IPM version 4.10 run for the ``Proposed
Transport Rule.'' \394\ As discussed in Draft TSD Chapter 4, for the
Final Rulemaking, EPA may consider emission factors other than national
power generation, such as marginal power emission factors, or regional
emission factors.
---------------------------------------------------------------------------

    \394\ EPA. IPM. http://www.epa.gov/airmarkt/progsregs/epa-ipm/BaseCasev410.html. ``Proposed Transport Rule/NODA version'' of IPM.
TR--SB--Limited Trading v.4.10.
---------------------------------------------------------------------------

2. Health Effects of Non-GHG Pollutants
    In this section we discuss health effects associated with exposure
to some of the criteria and air toxic pollutants impacted by the
proposed vehicle standards.
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).\395\ Current National Ambient Air
Quality Standards (NAAQS) use PM2.5 as the indicator for
fine particles (with PM2.5 generally referring to particles
with a nominal mean aerodynamic diameter less than or equal to 2.5
micrometers ([micro]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 [micro]m and less than or equal to 10 [micro]m, or
PM10-2.5). Ultrafine particles are a subset of fine
particles, generally less than 100 nanometers (0.1 [mu]m) in diameter.
---------------------------------------------------------------------------

    \395\ Regulatory definitions of PM size fractions, and
information on reference and equivalent methods for measuring PM in
ambient air, are provided in 40 CFR parts 50, 53, and 58.
---------------------------------------------------------------------------

    Fine particles are produced primarily by combustion processes and
by transformations of gaseous emissions (e.g., sulfur oxides
(SOX), nitrogen oxides (NOX), and volatile
organic compounds (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 components 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 Particulate Matter
    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 (ISA) for Particulate Matter.\396\
Further discussion of health effects associated with PM can also be
found in the draft RIA. The ISA summarizes health effects evidence
associated with both short-term and long-term exposures to
PM2.5, PM10-2.5, and ultrafine particles.
---------------------------------------------------------------------------

    \396\ U.S. EPA (2009) Integrated Science Assessment for
Particulate Matter (Final Report). U.S. Environmental Protection
Agency, Washington, DC, EPA/600/R-08/139F, Docket EPA-HQ-OAR-2010-
0799.
---------------------------------------------------------------------------

    The ISA concludes that health effects associated with short-term
exposures (hours to days) to ambient PM2.5 include
mortality, cardiovascular effects, such as altered vasomotor function
and hospital admissions and emergency department visits for ischemic
heart disease and congestive heart failure, and respiratory effects,
such as exacerbation of asthma symptoms in children and hospital
admissions and emergency department visits for chronic obstructive
pulmonary disease and respiratory infections.\397\ The ISA notes that
long-term exposure (months to years) to PM2.5 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.\398\
The ISA concludes that the currently available scientific evidence from
epidemiologic, controlled human exposure, and toxicological studies
supports a causal association 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 scientific
evidence is suggestive of a causal association for reproductive and
developmental effects and cancer, mutagenicity, and genotoxicity and
long-term exposure to PM2.5.\399\
---------------------------------------------------------------------------

    \397\ See U.S. EPA, 2009 Final PM ISA, Note 396, at Section
<IP_ADDRESS>.
    \398\ See U.S. EPA 2009 Final PM ISA, Note 396, at page 2-12,
Sections <IP_ADDRESS> and <IP_ADDRESS>.
    \399\ See U.S. EPA 2009 Final PM ISA, Note 396, at 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. 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.\400\
---------------------------------------------------------------------------

    \400\ See U.S. EPA 2009 Final PM ISA, Note 396, at Section
2.3.4, Table 2-6.
---------------------------------------------------------------------------

    For ultrafine particles, 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 ultrafine particles and
respiratory effects. Data are inadequate to draw conclusions regarding
the health effects associated with long-term exposure to ultrafine
particles.\401\
---------------------------------------------------------------------------

    \401\ See U.S. EPA 2009 Final PM ISA, Note 396, at 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
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. 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.
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 and 2007 Staff
Paper.402 403 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. Ozone
can irritate the respiratory system, causing coughing, throat
irritation, and breathing discomfort. Ozone can reduce lung function
and cause pulmonary inflammation in healthy individuals. Ozone can also
aggravate asthma, leading to more asthma attacks that require medical
attention and/or the use of additional medication. Thus, ambient ozone
may cause both healthy and asthmatic individuals to limit their outdoor
activities. 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 report on the estimation of ozone-related
premature mortality published by 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.\404\ 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. The respiratory effects
observed in controlled human exposure studies and animal studies are
coherent with the evidence from epidemiologic studies supporting 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.
---------------------------------------------------------------------------

    \402\ 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-2010-0799.
    \403\ 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-2010-0799.
    \404\ 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-2010-0799.
---------------------------------------------------------------------------

c. Nitrogen Oxides and Sulfur Oxides
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. Sulfur Dioxide (SO2) a member of the sulfur
oxide (SOX) family of gases, is formed from burning fuels
containing sulfur (e.g., coal or oil derived), extracting gasoline from
oil, or extracting metals from ore.
    SO2 and NO2 can dissolve in water droplets
and further oxidize to form sulfuric and nitric acid which react with
ammonia to form sulfates and nitrates, both of which are important
components of ambient PM. The health effects of ambient PM are
discussed in Section III.G.3.a.ii of this preamble. NOX and
NMHC are the two major precursors of ozone. The health effects of ozone
are covered in Section III.G.3.b.ii.
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.\405\
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. 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. Small but significant increases in non-specific
airway hyperresponsiveness were reported following 1-hour exposures of
asthmatics to 0.1 ppm NO2. Enhanced airway responsiveness
could have important clinical implications for asthmatics since
transient increases in airway responsiveness following NO2
exposure have the potential to increase symptoms and worsen asthma
control. Together, the epidemiologic and experimental data sets form a
plausible, consistent, and coherent description of a relationship
between NO2 exposures and an array of adverse health effects
that range from the onset of respiratory symptoms to hospital
admission.
---------------------------------------------------------------------------

    \405\ 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-2010-0799.
---------------------------------------------------------------------------

    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.\406\
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.
---------------------------------------------------------------------------

    \406\ 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-2010-0799.
---------------------------------------------------------------------------

d. Carbon Monoxide
    Information on the health effects of CO can be found in the EPA
Integrated Science Assessment (ISA) for Carbon Monoxide.\407\ The ISA
concludes that ambient concentrations of CO are associated with a
number of adverse health effects.\408\ This section provides a summary
of the health effects associated with exposure to ambient
concentrations of CO.\409\
---------------------------------------------------------------------------

    \407\ U.S. EPA, 2010. Integrated Science Assessment for Carbon
Monoxide (Final Report). U.S. Environmental Protection Agency,
Washington, DC, EPA/600/R-09/019F, 2010. Available at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=218686. Docket EPA-HQ-
OAR-2010-0799.
    \408\ The ISA evaluates the health evidence associated with
different health effects, assigning one of five ``weight of
evidence'' determinations: causal relationship, likely to be a
causal relationship, suggestive of a causal relationship, inadequate
to infer a causal relationship, and not likely to be a causal
relationship. For definitions of these levels of evidence, please
refer to Section 1.6 of the ISA.
    \409\ 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 to exist between short-term exposures to CO and
cardiovascular morbidity. It also concludes that available data are
inadequate to conclude that a causal relationship exists between long-
term exposures to CO and cardiovascular morbidity.
    Animal studies show various neurological effects with in-utero CO
exposure. Controlled human exposure studies report inconsistent neural
and behavioral effects following low-level CO exposures. The ISA
concludes the evidence is suggestive of a causal relationship with both
short- and long-term exposure to CO and central nervous system effects.
    A number of epidemiologic and animal toxicological studies cited in
the ISA have evaluated associations between CO exposure and birth
outcomes such as preterm birth or cardiac birth defects. The
epidemiologic studies provide limited evidence of a CO-induced effect
on preterm births and birth defects, with weak evidence for a decrease
in birth weight. Animal

toxicological studies have found associations between perinatal CO
exposure and decrements in birth weight, as well as other developmental
outcomes. The ISA concludes these studies are suggestive of a causal
relationship between long-term exposures to CO and developmental
effects and birth outcomes.
    Epidemiologic studies provide evidence of effects on respiratory
morbidity such as changes in pulmonary function, respiratory symptoms,
and hospital admissions associated with ambient CO concentrations. A
limited number of epidemiologic studies considered copollutants such as
ozone, SO2, and PM in two-pollutant models and found that CO
risk estimates were generally robust, although this limited evidence
makes it difficult to disentangle effects attributed to CO itself from
those of the larger complex air pollution mixture. Controlled human
exposure studies have not extensively evaluated the effect of CO on
respiratory morbidity. Animal studies at levels of 50-100 ppm CO show
preliminary evidence of altered pulmonary vascular remodeling and
oxidative injury. The ISA concludes that the evidence is suggestive of
a causal relationship between short-term CO exposure and respiratory
morbidity, and inadequate to conclude that a causal relationship exists
between long-term exposure and respiratory morbidity.
    Finally, the ISA concludes that the epidemiologic evidence is
suggestive of a causal relationship between short-term exposures to CO
and mortality. Epidemiologic studies provide evidence of an association
between short-term exposure to CO and mortality, but limited evidence
is available to evaluate cause-specific mortality outcomes associated
with CO exposure. In addition, the attenuation of CO risk estimates
which was often observed in copollutant models contributes to the
uncertainty as to whether CO is acting alone or as an indicator for
other combustion-related pollutants. The ISA also concludes that there
is not likely to be a causal relationship between relevant long-term
exposures to CO and mortality.
e. Air Toxics
    Light-duty vehicle emissions contribute to ambient levels of air
toxics known or suspected as human or animal carcinogens, or that have
noncancer health effects. The population experiences an elevated risk
of cancer and other noncancer health effects from exposure to the class
of pollutants known collectively as ``air toxics.'' \410\ These
compounds include, but are not limited to, benzene, 1,3-butadiene,
formaldehyde, acetaldehyde, acrolein, polycyclic organic matter, and
naphthalene. These compounds were identified as national or regional
risk drivers or contributors in the 2005 National-Scale Air Toxics
Assessment and have significant inventory contributions from mobile
sources.\411\
---------------------------------------------------------------------------

    \410\ U.S. EPA. (2011) Summary of Results for the 2005 National-
Scale Assessment. http://www.epa.gov/ttn/atw/nata2005/05pdf/sum_results.pdf. Docket EPA-HQ-OAR-2010-0799.
    \411\ U.S. EPA (2011) 2005 National-Scale Air Toxics Assessment.
http://www.epa.gov/ttn/atw/nata2005. Docket EPA-HQ-OAR-2010-0799.
---------------------------------------------------------------------------

i. Benzene
    The EPA's Integrated Risk Information System (IRIS) database lists
benzene as a known human carcinogen (causing leukemia) by all routes of
exposure, and concludes that exposure is associated with additional
health effects, including genetic changes in both humans and animals
and increased proliferation of bone marrow cells in
mice.412 413 414 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.415 416
---------------------------------------------------------------------------

    \412\ 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-2010-0799.
    \413\ International Agency for Research on Cancer. 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-
2010-0799.
    \414\ 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-2010-0799.
    \415\ See IARC, Note 413, above.
    \416\ U.S. Department of Health and Human Services National
Toxicology Program 11th Report on Carcinogens available at: http://ntp.niehs.nih.gov/go/16183. Docket EPA-HQ-OAR-2010-0799.
---------------------------------------------------------------------------

    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.417 418 The
most sensitive noncancer effect observed in humans, based on current
data, is the depression of the absolute lymphocyte count in
blood.419 420 In addition, published 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.421 422 423 424 EPA's IRIS program has
not yet evaluated these new data.
---------------------------------------------------------------------------

    \417\ Aksoy, M. (1989). Hematotoxicity and carcinogenicity of
benzene. Environ. Health Perspect. 82: 193-197. Docket EPA-HQ-OAR-
2010-0799.
    \418\ Goldstein, B.D. (1988). Benzene toxicity. Occupational
medicine. State of the Art Reviews. 3: 541-554. Docket EPA-HQ-OAR-
2010-0799.
    \419\ 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-2010-0799.
    \420\ U.S. EPA (2002) Toxicological Review of Benzene (Noncancer
Effects). 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/0276.htm. Docket
EPA-HQ-OAR-2010-0799.
    \421\ 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-2010-0799.
    \422\ 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-2010-0799.
    \423\ 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-2010-0799.
    \424\ 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-2010-
0799.
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ii. 1,3-Butadiene
    EPA has characterized 1,3-butadiene as carcinogenic to humans by
inhalation.425 426 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.427 428 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.429
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    \425\ 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-2010-0799.
    \426\ 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-2010-0799.
    \427\ International Agency for Research on Cancer (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-2010-
0799.
    \428\ 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. Docket EPA-HQ-OAR-2010-0799.
    \429\ 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-2010-
0799.
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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.\430\ EPA is currently reviewing epidemiological data published
since that time. For instance, research conducted by the National
Cancer Institute found an increased risk of nasopharyngeal cancer and
lymphohematopoietic malignancies such as leukemia among workers exposed
to formaldehyde.431, 432 In an analysis of the
lymphohematopoietic cancer mortality from an extended follow-up of
these workers, the National Cancer Institute confirmed an association
between lymphohematopoietic cancer risk and peak exposures.\433\ A
National Institute of Occupational Safety and Health study of garment
workers also found increased risk of death due to leukemia among
workers exposed to formaldehyde.\434\ 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.\435\ In
2006, the IARC re-classified formaldehyde as a human carcinogen (Group
1).\436\
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    \430\ 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-2010-0799.
    \431\ 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-2010-0799.
    \432\ 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-2010-0799.
    \433\ 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-2010-0799.
    \434\ 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-2010-0799.
    \435\ 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-2010-0799.
    \436\ International Agency for Research on Cancer. 2006.
Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol. Volume
88. (in preparation), World Health Organization, Lyon, France.
Docket EPA-HQ-OAR-2010-0799;
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    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.437 438
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    \437\ 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-
2010-0799.
    \438\ 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-2010-0799.
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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.\439\
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.440 441 EPA is currently conducting a reassessment of
cancer risk from inhalation exposure to acetaldehyde.
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    \439\ U.S. EPA. 1991. Integrated Risk Information System File of
Acetaldehyde. Research and Development, National Center for
Environmental Assessment, Washington, DC. Available at http://www.epa.gov/iris/subst/0290.htm. Docket EPA-HQ-OAR-2010-0799.
    \440\ U.S. Department of Health and Human Services National
Toxicology Program 11th Report on Carcinogens available at: http://ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. Docket EPA-HQ-OAR-2010-0799.
    \441\ International Agency for Research on Cancer. 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-2010-
0799.
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    The primary noncancer effects of exposure to acetaldehyde vapors
include irritation of the eyes, skin, and respiratory tract.\442\ In
short-term (4 week) rat studies, degeneration of olfactory epithelium
was observed at various concentration levels of acetaldehyde
exposure.443 444 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.\445\ The agency is currently conducting a reassessment of
the health hazards from inhalation exposure to acetaldehyde.
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    \442\ See Integrated Risk Information System File of
Acetaldehyde, Note 439, above.
    \443\ 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. Docket EPA-HQ-OAR-2010-0799.
    \444\ 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-2010-0799.
    \445\ 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-2010-0799.
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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.\446\ 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.\447\ 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.\448\
Lesions to the lungs and upper respiratory tract of rats, rabbits, and
hamsters have been observed after subchronic exposure to acrolein.\449\
Acute exposure effects in animal studies report bronchial hyper-
responsiveness.\450\ In one 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.\451\ 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.
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    \446\ 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. p. 10.
Available online at: http://www.epa.gov/ncea/iris/toxreviews/0364tr.pdf. Docket EPA-HQ-OAR-2010-0799.
    \447\ See U.S. EPA 2003 Toxicological review of acrolein, Note
446, above.
    \448\ See U.S. EPA 2003 Toxicological review of acrolein, Note
446, at p. 11.
    \449\ 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-2010-
0799.
    \450\ See U.S. 2003 Toxicological review of acrolein, Note 446,
at p. 15.
    \451\ 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-2010-0799.
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    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.\452\ The IARC determined in 1995 that acrolein was not
classifiable as to its carcinogenicity in humans.\453\
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    \452\ 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 Docket EPA-HQ-OAR-2010-
0799.
    \453\ International Agency for Research on Cancer. 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-2010-0799.
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vi. Polycyclic Organic Matter
    The term polycyclic organic matter (POM) defines a broad class of
compounds that includes the polycyclic aromatic hydrocarbon compounds
(PAHs). One of these compounds, naphthalene, is discussed separately
below. POM compounds are formed primarily from combustion and are
present in the atmosphere in gas and particulate form. Cancer is the
major concern from exposure to POM. Epidemiologic studies have reported
an increase in lung cancer in humans exposed to diesel exhaust, coke
oven emissions, roofing tar emissions, and cigarette smoke; all of
these mixtures contain POM compounds.454 455 Animal studies
have reported respiratory tract tumors from inhalation exposure to
benzo[a]pyrene and alimentary tract and liver tumors from oral exposure
to benzo[a]pyrene. In 1997 EPA classified seven PAHs (benzo[a]pyrene,
benz[a]anthracene, chrysene, benzo[b]fluoranthene,
benzo[k]fluoranthene, dibenz[a,h]anthracene, and indeno[1,2,3-
cd]pyrene) as Group B2, probable human carcinogens.\456\ Since that
time, studies have found that maternal exposures to PAHs in a
population of pregnant women were associated with several adverse birth
outcomes, including low birth weight and reduced length at birth, as
well as impaired cognitive development in preschool children (3 years
of age).457 458 EPA has not yet evaluated these studies.
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    \454\ Agency for Toxic Substances and Disease Registry (ATSDR).
1995. Toxicological profile for Polycyclic Aromatic Hydrocarbons
(PAHs). Atlanta, GA: U.S. Department of Health and Human Services,
Public Health Service. Available electronically at http://www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=122&tid=25.
    455 U.S. EPA (2002). Health Assessment Document for
Diesel Engine Exhaust. EPA/600/8-90/057F Office of Research and
Development, Washington, DC. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=29060. Docket EPA-HQ-OAR-2010-0799
    \456\ U.S. EPA (1997). Integrated Risk Information System File
of indeno(1,2,3-cd)pyrene. Research and Development, National Center
for Environmental Assessment, Washington, DC. This material is
available electronically at http://www.epa.gov/ncea/iris/subst/0457.htm.
    \457\ 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.
    458 Perera, F.P.; Rauh, V.; Whyatt, R.M.; Tsai, W.Y.;
Tang, D.; Diaz, D.; Hoepner, L.; Barr, D.; Tu, Y.H.; Camann, D.;
Kinney, P. (2006) Effect of prenatal exposure to airborne polycyclic
aromatic hydrocarbons on neurodevelopment in the first 3 years of
life among inner-city children. Environ Health Perspect 114: 1287-
1292.
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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.\459\ The draft reassessment
completed external peer review.\460\ 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.\461\ 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.\462\ Naphthalene also causes a number of
chronic non-cancer effects in animals, including abnormal cell changes
and growth in respiratory and nasal tissues.\463\
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    \459\ 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-2010-0799.
    \460\ 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-2010-0799.
    \461\ 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. Docket EPA-HQ-OAR-2010-0799.
    \462\ International Agency for Research on Cancer. (2002).
Monographs on the Evaluation of the Carcinogenic Risk of Chemicals
for Humans. Vol. 82. Lyon, France. Docket EPA-HQ-OAR-2010-0799.
    \463\ 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 Docket EPA-
HQ-OAR-2010-0799.

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viii. Other Air Toxics
    In addition to the compounds described above, other compounds in
gaseous hydrocarbon and PM emissions from light-duty vehicles will be
affected by this proposal. Mobile source air toxic compounds that would
potentially be impacted include ethylbenzene, propionaldehyde, toluene,
and xylene. Information regarding the health effects of these compounds
can be found in EPA's IRIS database.\464\
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    \464\ U.S. EPA Integrated Risk Information System (IRIS)
database is available at: http://www.epa.gov/iris.
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f. Exposure and Health Effects Associated With Traffic-Related Air
Pollution
    Populations who live, work, or attend school near major roads
experience elevated exposure 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,