fat, or corn oil.
                                                                --Dedicated facility     Biomass-based diesel.
                                                                 that processes only
                                                                 renewable biomass.
Non-ester renewable diesel...........  Waste grease, waste      --Hydrotreating........  Advanced biofuel.
                                        oils, tallow, chicken
                                        fat, or non-food grade
                                        corn oil.
                                                                --Coprocessing facility
                                                                 that also processes
                                                                 petroleum feedstocks.
Non-ester renewable diesel...........  Soybean oil and other    --Hydrotreating........  Renewable fuel.
                                        virgin plant oils.
Cellulosic gasoline..................  Cellulose and            --Thermochemical         Cellulosic biofuel.
                                        hemicellulose from       gasification of
                                        corn stover,             biomass.
                                        switchgrass,
                                        miscanthus, wheat
                                        straw, rice straw,
                                        sugarcane bagasse,
                                        forest waste, yard
                                        waste, or planted
                                        trees.
                                                                --Fischer-Tropsch
                                                                 process.
                                                                --Catalytic
                                                                 depolymerization.
----------------------------------------------------------------------------------------------------------------
\a\ Under our assumed 100-year timeframe and 2% discount rate.

    As stated earlier, there may be other potential pathways that could
lead to qualifying renewable fuel. While we do not have sufficient
information at this time to evaluate the likely lifecycle GHG impact
and thus assign those pathways to one of the four renewable fuel
categories, we do plan on doing these evaluations for the final rule.
Pathways that we intend to subject to lifecycle analysis include
butanol from starches or oils and renewable diesel from biomass using
pyrolysis or catalytic reforming. We request comment on the inputs
necessary to apply lifecycle analysis to these pathways. We also
request comment on other pathways that should be analyzed and the data
that would be necessary for those analyses.
    For pathways that are not included in the lookup table in the final
rule, we are also proposing a regulatory mechanism whereby a producer
could temporarily assign their renewable fuel to one of the four
renewable fuel categories under certain conditions. For further
discussion of this issue, see Section III.D.5.

F. Total GHG Emission Reductions

    Our analysis of the overall GHG emission impacts of this proposed
rulemaking was performed in parallel with the lifecycle analysis
performed to develop the individual fuel thresholds described in
previous sections. The same system boundaries apply such that this
analysis includes the effects of three main areas: (a) emissions
related to the production of biofuels, including the growing of
feedstock (corn, soybeans, etc.) with associated domestic and
international land use change impacts, transport of feedstock to fuel
production plants, fuel production, and distribution of finished fuel;
(b) emissions related to the extraction, production and distribution of
petroleum gasoline and diesel fuel that is replaced by use of biofuels;
and (c) difference in tailpipe combustion of the renewable and
petroleum based fuels. As discussed in the previous sections we will be
updating our lifecycle approach for the final rule and there are some
areas that we were not able to quantify at this time, such as secondary
impacts in the energy sector. We are working to include this for our
final rule analysis.
    Consistent with the fuel volume feasibility analysis and criteria
pollutant emissions, our analysis of the GHG impacts of increased
renewable fuel use was conducted by comparing the impacts of the 2022
36 Bgal of renewable fuel volumes required by EISA to a projected 2022
reference case of approximately 14 Bgal of renewable fuel volumes.
Similar to what was done to calculate lifecycle thresholds for
individual fuels we considered the change in 2022 of these two volume
scenarios of renewable fuels to determine overall GHG impacts of the
rule. The reference case for the GHG emission comparisons was taken
from the AEO 2007 projected renewable fuel production levels for 2022
prior to enactment of EISA. This scenario provided a point of
comparison for assessing the impacts of the RFS2 standard volumes on
GHG emissions. We ran these multi-fuel scenarios through our FASOM and
FAPRI models and applied the Winrock land use change assumptions to
determine to overall GHG impacts. We were only able to analyze 2022
reference and control cases. However, in reality the impacts of corn
ethanol and soybean biodiesel will be experienced beginning in 2009,
with the impacts of cellulosic ethanol and sugarcane ethanol growing in
later years as their volumes increase.
    The main difference between this overall impacts analysis and the
analysis conducted to develop the threshold values for the individual
fuels is that we analyzed the total change in renewable fuels in one
scenario as opposed to looking at individual fuel impacts. When
analyzing the impact of the total 36 billion gallons of renewable fuel,
we also took into account the agricultural sector interactions
necessary to produce the full complement of feedstock. We also

considered a mix of plant types and configurations for the 2022
renewable fuel production representing the mix of plants we project to
be in operation in 2022. This is based on the same analysis used in the
plant location and fuel feasibility analysis described in Section V.B.
    For this overall impacts analysis we used a different petroleum
baseline fuel that is offset from renewable fuel use. The lifecycle
threshold values are required by EISA to be based on a 2005 petroleum
fuel baseline. For this inventory analysis of the overall impacts of
the rule we considered the crude oil and finished product that would be
replaced in 2022. Displaced petroleum product analysis was consistent
with work performed for the energy security analysis described in
Section IX.B. For this analysis we consider that 25% of displaced
gasoline will be imported gasoline. For the domestic production we
assumed replacement of the 2022 crude mix which is projected to include
7.6% tar sands and 3.8% Venezuelan heavy crude which is higher then the
projected mix in 2005 which includes 5% tar sands and 1% Venezuelan
heavy crude.
    Given these many differences, simply adding up the individual
lifecycle results determined in Section VI.C. multiplied by their
respective volumes would yield a different assessment of the overall
rule impacts. The two analyses are separate in that the overall rule
impacts capture interactions between the different fuels that can not
be broken out into per fuels impacts, while the threshold values
represent impacts of specific fuels but do not account for all the
interactions.
    For example, when we consider the combined impact of the different
fuel volumes when analyzed separately, the overall land use change is
9.0 million acres. However, when we analyze the volume changes all
together, the overall land use change is approximately 10% higher.
    The primary reason for the difference in acre change between the
sum of the individual fuel scenarios and the combined fuel scenarios is
that when looking at individual fuels there is some interaction between
different crops (e.g., corn replacing soybeans), but with combined
volume scenario when all mandates need to be met there is less
opportunity for crop replacement (e.g., both corn and soybean acres
needed) and therefore more land is required.
    Important findings of our analysis include:
     As with the threshold lifecycle calculations, assumptions
about timing to consider impacts over and discount rates will have a
significant impact on results.
     We estimate the largest overall agricultural sector impact
is an increase in land use change impacts, reflecting the shift of crop
production internationally to meet the biofuel demand in the U.S.
Increased crop production internationally resulted in land use change
emissions associated with converting land into crop production.
     Our analysis indicates that overall domestic agriculture
emissions would increase. There is a relatively small increase in total
domestic crop acres however, there are additional inputs required due
to the removal of crop residues. The assumption is that removal will
require more inputs to make up for lost residue nutrients. These
additional inputs result in GHG emissions from production and from
N2O releases from application. This effect is somewhat
offset by reductions due to lower livestock production. These results
are dependent on our agricultural sector input and emission assumptions
that are being updated for the final rule (e.g., N2O
emission factor work).
     In particular due to this international impact, the
potential overall GHG emission reductions of biofuels produced from
food crops such as corn ethanol and soy biodiesel are significantly
impacted. Large near term emission increases due to land use change
require a number of years before the emission reductions due to corn
ethanol and soy biodiesel use will offset the near term emission
increase as discussed in the threshold calculation section.
     Cellulosic biofuels contribute by far the most to the
total emission reductions due to both their superior per gallon
emission reductions and the large volume of these fuels anticipated to
be used by 2022.
    The timing of the impact of land use change and ongoing renewable
fuels benefits were discussed in the previous lifecycle fuel threshold
section. The issue is slightly different for this analysis since we are
considering absolute tons of emissions and not determining a threshold
comparison to petroleum fuels. However the results can be presented in
a similar manner to our individual fuels analysis in that we can
determine net benefits over time with different discount rates and over
a different time frame for consideration.
    As discussed in previous sections on lifecycle GHG thresholds there
is an initial one time release from land conversion and smaller ongoing
releases but there are also ongoing benefits of using renewable fuels
over time replacing petroleum fuel use. Based on the volume scenario
considered, the one time land use change impacts result in 448 million
metric tons of CO2-eq. emissions increase. There are, however, based on
the biofuel use replacing petroleum fuels, GHG reductions in each year.
When modeling the program as if all fuel volume changes occur in 2022,
and considering 100 years of emission impacts that are discounted by 2%
per year, we get an estimated total discounted NPV reduction in GHG
emissions of 6.8 billion tons over 100 years. Totaling the emissions
impacts over 30 years but assuming a 0% discount rate over this 30 year
period would result in an estimated total NPV reduction in GHG
emissions of 4.5 billion tons over 30 years.
    This total NPV reduction can be converted into annual average GHG
reductions, which can be used for the calculations of the monetized GHG
benefits as shown in Section IX.C.4. This annualized value is based on
converting the lump sum present values described above into their
annualized equivalents. For this analysis we convert the NPV results
for the 100 year 2% discount rate into an annualized average such that
the NPV of the annualized average emissions will equal the NPV of the
actual emission stream over 100 years with a 2% discount rate. This
results in an annualized average emission reduction of approximately160
million metric tons of CO2-eq. emissions. A comparable value assuming
30 years of GHG emissions changes but not applying a discount rate to
those emissions results in an estimated annualized average emission
reduction of approximately 150 million metrics tons of CO2-eq.
emissions.

G. Effects of GHG Emission Reductions and Changes in Global Temperature
and Sea Level

1. Introduction
    The reductions in CO2 and other GHGs associated with the
proposal will affect climate change projections. Because GHGs mix well
in the atmosphere and have long atmospheric lifetimes, changes in GHG
emissions will affect future climate for decades to centuries. One
common indicator of climate change is global mean surface temperature
and sea level rise. This section estimates the response in global mean
surface temperature projections to the estimated net global GHG
emissions reductions associated with the proposed rulemaking (See
Section VI.F for the estimated net reductions in global emissions over
time by GHG).

2. Estimated Projected Reductions in Global Mean Surface Temperatures
    EPA estimated changes in projected global mean surface temperatures
to 2100 using the MiniCAM (Mini Climate Assessment Model) integrated
assessment model \320\ coupled with the MAGICC (Model for the
Assessment of Greenhouse-gas Induced Climate Change) simple climate
model.\321\ MiniCAM 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 change in the global mean
surface temperature over time. Given the magnitude of the estimated
emissions reductions associated with the proposed rule, a simple
climate model such as MAGICC is reasonable for estimating the climate
response.
---------------------------------------------------------------------------

    \320\ MiniCAM 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 greenhouse gases (GHG's), emitted
in 14 globally disaggregated global regions (i.e., U.S., Western
Europe, China), the fate of emissions to the atmosphere, and the
consequences of changing concentrations of greenhouse related gases
for climate change. MiniCAM 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. For a recent report and
detailed description and discussion of MiniCAM, see Clarke, L., J.
Edmonds, H. Jacoby, H. Pitcher, J. Reilly, R. Richels, 2007.
Scenarios of Greenhouse Gas Emissions and Atmospheric
Concentrations. Sub-report 2.1A of Synthesis and Assessment Product
2.1 by the U.S. Climate Change Science Program and the Subcommittee
on Global Change Research. Department of Energy, Office of
Biological & Environmental Research, Washington, DC., USA, 154 pp.
    \321\ MAGICC consists of a suite of coupled gas-cycle, climate
and ice-melt models integrated into a single framework. The
framework allows the user to determine changes in GHG
concentrations, global-mean surface air temperature and sea-level
resulting from anthropogenic emissions of carbon dioxide (CO2),
methane (CH4), nitrous oxide (N2O), reactive gases (e.g., CO,
NOX, VOCs), the halocarbons (e.g. HCFCs, HFCs, PFCs) and
sulfur dioxide (SO2). MAGICC emulates the global-mean temperature
responses of more sophisticated coupled Atmosphere/Ocean General
Circulation Models (AOGCMs) with high accuracy. Wigley, T.M.L. and
Raper, S.C.B. 1992. Implications for Climate and Sea-Level of
Revised IPCC Emissions Scenarios Nature 357, 293-300. Raper, S.C.B.,
Wigley T.M.L. and Warrick R.A. 1996. in Sea-Level Rise and Coastal
Subsidence: Causes, Consequences and Strategies J.D. Milliman, B.U.
Haq, Eds., Kluwer Academic Publishers, Dordrecht, The Netherlands,
pp. 11-45. Wigley, T.M.L. and Raper, S.C.B. 2002. Reasons for larger
warming projections in the IPCC Third Assessment Report J. Climate
15, 2945-2952.
---------------------------------------------------------------------------

    EPA applied the estimated annual GHG emissions changes for the
proposal to the MiniCAM U.S. Climate Change Science Program (CCSP)
Synthesis and Assessment Product baseline emissions.\322\ Specifically,
the CO2, N2O, and CH4 annual emission
changes from 2022-2121 from Section VI.F were applied as net reductions
to the MiniCAM CCSP global baseline net emissions for each GHG. Post-
2121, we assumed no change in emissions from the baseline. This
assumption is more conservative than allowing the emissions reductions
to continue.
---------------------------------------------------------------------------

    \322\ Clarke et al., 2007.
---------------------------------------------------------------------------

    Table VI.G.2 provides our estimated reductions in projected global
mean surface temperatures and sea level associated with the proposed
increase in renewable fuels in 2022. To capture some of the uncertainty
in the climate system, we estimated the changes in projected
temperatures and sea level across the most current Intergovernmental
Panel on Climate Change (IPCC) range of climate sensitivities, 1.5
[deg]C to 6.0 [deg]C.\323\ To illustrate the time profile of the
estimated reductions in projected global mean surface temperatures and
sea level, we have also provided Figures VI.G.2-1 and VI.G.2-2.
---------------------------------------------------------------------------

    \323\ 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 and
described 3 [deg]C as a ``best estimate.'' The IPCC goes on to note
that climate sensitivity is ``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/

Table VI.G.2-1--Estimated Reductions in Projected Global Mean Surface Temperature and Global Mean Sea Level From
                    Baseline in 2030, 2050, 2100, and 2200 for the Proposed Standard in 2022
----------------------------------------------------------------------------------------------------------------
                                                                       Climate sensitivity
                                                ----------------------------------------------------------------
                                                     1.5           2            3           4.5           6
----------------------------------------------------------------------------------------------------------------
                          Change in global mean surface temperatures (degrees Celsius)
----------------------------------------------------------------------------------------------------------------
2030...........................................        0.000        0.000       -0.001       -0.001       -0.001
2050...........................................       -0.001       -0.002       -0.002       -0.002       -0.003
2100...........................................       -0.003       -0.004       -0.005       -0.006       -0.007
2200...........................................       -0.003       -0.004       -0.006       -0.008       -0.009
----------------------------------------------------------------------------------------------------------------
                               Change in global mean sea level rise (centimeters)
----------------------------------------------------------------------------------------------------------------
2030...........................................       -0.002       -0.002       -0.003       -0.003       -0.003
2050...........................................       -0.012       -0.014       -0.017       -0.020       -0.022
2100...........................................       -0.045       -0.052       -0.063       -0.074       -0.082
2200...........................................       -0.077       -0.091       -0.114       -0.143       -0.172
----------------------------------------------------------------------------------------------------------------

    The results in Table VI.G.2-1 and Figures VI.G.2-1 and VI.G.2-2
show small, but detectable, reductions in the global mean surface
temperature and sea level rise projections across all climate
sensitivities. Overall, the reductions are small relative to the IPCC's
``best estimate'' temperature increases by 2100 of 1.8 [deg]C to 4.0
[deg]C.\324\ Although IPCC does not issue ``best estimate'' sea level
rise projections, the model-based range across SRES scenarios is 18 to
59 cm by 2099.\325\ Both figures illustrate that the overall emissions
reductions can decrease projected annual temperature and sea level for
all climate sensitivities. This means that the distribution of
potential temperatures in any particular year is shifting down.
However, the shift is not uniform. The magnitude of the decrease is
larger for higher climate

sensitivities. Thus, the probability of a higher temperature or sea
level in any year is lowered more than the probability of a lower
temperature or sea level. For instance, in 2100, the reduction in
projected temperature for climate sensitivities of 3 and 6 is
approximately 65% and 140% greater than the reduction for a climate
sensitivity of 1.5. This difference grows over time, to approximately
80% and 185% by 2200. The same pattern appears in the reductions in the
sea level rise projections.\326\ Also noteworthy in Figures VI.G.2-1
and VI.G.2-2 is that the size of the decreases grows over time due to
the cumulative effect of a lower stock of GHGs in the atmosphere (i.e.,
concentrations).\327\
---------------------------------------------------------------------------

    \324\ IPCC WGI, 2007. The baseline increases by 2100 from our
MiniCAM-MAGICC runs are 2 [deg]C to 5 [deg]C for global mean surface
temperature and 35 to 74 centimeters for global mean sea level.
    \325\ ``Because understanding of some important effects driving
sea level rise is too limited, this report does not assess the
likelihood, nor provide a best estimate or an upper bound for sea
level rise.'' IPCC Synthesis Report, p. 45
    \326\ In 2100, the reduction in projected sea level rise for
climate sensitivities of 3 and 6 is approximately 40% and 80%
greater than the reduction for a climate sensitivity of 1.5. This
difference grows over time, to approximately 50% and 120% by 2200.
    \327\ For global average temperature after 2100, the growth in
the size of the decrease noticeable slows. This is because the
emissions changes associated with the policy were only estimated for
100 years. Note that even with emissions reductions stopping after
100 years, there continues to be a decrease in projected
temperatures due to reduced inertia in the climate system from the
earlier emissions reductions. However, unlike temperature, after
2100, the size of the decrease in sea level rise increases as the
projected reduction in warming has a continued effect on ice melt
and ocean thermal expansion.
---------------------------------------------------------------------------

    The bottom line is that the risk of climate change is being
lowered, as the probabilities of any level of temperature increase and
sea level rise are reduced and the probabilities of the largest
temperature increases and sea level rise are reduced even more. For the
Final Rulemaking, we hope to more explicitly estimate the shapes of the
distributions and the estimated shifts in the shapes in response to the
Rulemakings.
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VII. How Would the Proposal Impact Criteria and Toxic Pollutant
Emissions and Their Associated Effects?

A. Overview of Impacts

    Today's proposal would influence the emissions of ``criteria''
pollutants (those pollutants for which a National Ambient Air Quality
Standard has been established), criteria pollutant precursors,\328\ and
air toxics, which may affect overall air quality and health. Emissions
would be affected by the processes required to produce and distribute
large volumes of biofuels proposed in today's action and the direct
effects of these fuels on vehicle and equipment emissions. As detailed
in Chapter 3 of the Draft Regulatory Impact Analysis (DRIA), we have
estimated emissions impacts of production and distribution-related
emissions using the life cycle analysis methodology described in
Section VI with emission factors for criteria and toxic emissions for
each stage of the life cycle, including agriculture, feedstock
transportation, and the production and distribution of biofuel;
included in this analysis are the impacts of reduced gasoline and
diesel refining as these fuels are displaced by biofuels. Emission
impacts of tailpipe and evaporative emissions for on and off road
sources have been estimated by incorporating ``per vehicle'' fuel
effects from recent research into mobile source emission inventory
estimation methods.
---------------------------------------------------------------------------

    \328\ NOX and VOC are precursors to the criteria
pollutant ozone; we group them with criteria pollutants in this
chapter for ease of discussion.
---------------------------------------------------------------------------

    For today's proposal we are presenting two sets of emission impacts
meant to present a range of the possible effects of ethanol blends on
light-duty vehicle emissions. This approach is carried forward from
analysis supporting the first RFS rule, which presented ``primary'' and
``sensitivity'' fuel effects cases differentiated by E10 effects on
cars and trucks. For this analysis we also analyze two fuel effects
scenarios, now termed ``less sensitive'' and ``more sensitive,''
referring to the sensitivity of car and truck exhaust emissions to both
E10 and E85 blends. As detailed in Section VII.C, the ``less
sensitive'' case does not apply any E10 effects to NOx or HC emissions
for later model year vehicles, or E85 effects for any pollutant, while
the ``more sensitive'' case assumes that later model year vehicles have
lower fuel sensitivity than earlier model vehicles. EPA and other
parties are in the midst of gathering additional data to help clarify
emissions impacts of ethanol on light-duty vehicles, and should be able
to reflect the new data for the final rule.
    Analysis of criteria and toxic emission impacts was performed for
calendar year 2022, since this year reflects the full implementation of
today's proposal. Our 2022 projections account for projected growth in
vehicle travel and the effects of applicable emission and fuel economy
standards, including Tier 2 and Mobile Source Air Toxics (MSAT) rules
for cars and light trucks and recently finalized controls on spark-
ignited off-road engines. The impacts were analyzed relative to three
different reference case ethanol volumes, ranging from 3.64 to 13.2
billion gallons per year, in order to understand the impacts of today's
proposal in different contexts. To assess the total impact of the RFS
program, emissions were analyzed relative to the RFS1 rule base case of
3.64 billion gallons in 2004. To assess the impact of today's proposal
relative to the current mandated volumes, we analyzed impacts relative
to RFS1 mandate of 7.5 billion gallons of renewable fuel use by 2012,
which was estimated to include 6.7 billion gallons of ethanol.\329\ In
order to assess the impact of today's proposal relative to the level of
ethanol projected to already be in place by 2022, the AEO2007
projection of 13.2 billion gallons of

ethanol in 2022 was analyzed. For this analysis our modeling was based
on the differences between the AEO2007 reference case and the control
case; to generate impacts for the RFS1 base and mandated volumes we
simply scaled the modeled AEO2007-based impacts up according to the
larger increases in renewable fuel volumes relative to the other
reference cases. For the final rule we plan to directly model the RFS1
mandate reference case as well as the AEO2007 case.
---------------------------------------------------------------------------

    \329\ For this analysis these RFS1 base and mandated ethanol
levels were assumed constant to 2022.
---------------------------------------------------------------------------

    For the proposal we have only estimated the change in national
emission totals that would result from today's proposal. These totals
may not be a good indication of local or regional air quality and
health impacts. These results are aggregated across highly localized
sources, such as emissions from ethanol plants and evaporative
emissions from cars, and reflect offsets such as decreased emissions
from gasoline refineries. The location and composition of emissions
from these disparate sources may strongly influence the air quality and
health impacts of today's proposed action, and full-scale photochemical
air quality modeling is necessary to accurately assess this. These
localized impacts will be assessed in the final rule as discussed in
Section VII.D.
    Our projected emission impacts for the ``less sensitive'' and
``more sensitive'' cases are shown in Table VII.A-1 and VII.A-2 for
2022. Shown relative to each reference case are the expected emission
changes for the U.S. in that year, and the percent contribution of this
impact relative to the total U.S. inventory. Overall we project the
proposed program will result in significant increases in ethanol and
acetaldehyde emissions--increasing the total U.S. inventories of these
pollutants by 30-40% in 2022 relative to the RFS1 mandate case. We
project more modest increases in NOx, HC, PM,
SO2, formaldehyde, and acrolein relative to the RFS1 mandate
case. We project a decrease in ammonia (NH3) emissions due
to reductions in livestock agricultural activity, CO (due to impacts of
ethanol on exhaust emissions from vehicles and nonroad equipment), and
benzene (due to displacement of gasoline with ethanol in the fuel
pool). As shown, the direction of changes for 1,3-butadiene and
naphthalene depends on whether it is the ``less sensitive'' or ``more
sensitive'' case.

                          Table VII.A-1--RFS2 ``Less Sensitive'' Case Emission Impacts in 2022 Relative to Each Reference Case
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                     RFS1 base                     RFS1 mandate                       AEO2007
                                                         -----------------------------------------------------------------------------------------------
                        Pollutant                                           Percent of                      Percent of                      Percent of
                                                           Annual short     total U.S.     Annual short     total U.S.     Annual short     total U.S.
                                                               tons          inventory         tons          inventory         tons          inventory
--------------------------------------------------------------------------------------------------------------------------------------------------------
NOx.....................................................         312,400             2.8         274,982             2.5         195,735             1.7
HC......................................................         112,401             1.0          72,362             0.6          -8,193           -0.07
PM10....................................................          50,305             1.4          37,147             1.0           9,276             0.3
PM2.5...................................................          14,321             0.4          11,452             0.3           5,376            0.16
CO......................................................      -2,344,646            -4.4      -1,669,872            -3.1        -240,943            -0.4
Benzene.................................................          -2,791            -1.7          -2,507            -1.5          -1,894            -1.1
Ethanol.................................................         210,680            36.5         169,929            29.4          83,761            14.5
1,3-Butadiene...........................................             344             2.9             255             2.1              65             0.5
Acetaldehyde............................................          12,516            33.7          10,369            27.9           5,822            15.7
Formaldehyde............................................           1,647             2.3           1,348             1.9             714             1.0
Naphthalene.............................................               5            0.03               3            0.02              -1           -0.01
Acrolein................................................             290             5.0             252             4.4             174             3.0
SO2.....................................................          28,770             0.3           4,461            0.05         -47,030            -0.5
NH3.....................................................         -27,161            -0.6         -27,161            -0.6         -27,161            -0.6
--------------------------------------------------------------------------------------------------------------------------------------------------------

                          Table VII.A-2--RFS2 ``More Sensitive'' Case Emission Impacts in 2022 Relative to Each Reference Case
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                     RFS1 base                     RFS1 Mandate                       AEO2007
                                                         -----------------------------------------------------------------------------------------------
                        Pollutant                                           Percent of                      Percent of                      Percent of
                                                           Annual short     total U.S.     Annual short     total U.S.     Annual short     total U.S.
                                                               tons          inventory         tons          inventory         tons          inventory
--------------------------------------------------------------------------------------------------------------------------------------------------------
NOx.....................................................         402,795             3.6         341,028             3.0         210,217             1.9
HC......................................................         100,313             0.9          63,530             0.6         -15,948           -0.14
PM10....................................................          46,193             1.3          33,035             0.9           5,164            0.15
PM2.5...................................................          10,535             0.3           7,666             0.2           1,589            0.05
CO......................................................      -3,779,572            -7.0      -3,104,798            -5.8      -1,675,869            -3.1
Benzene.................................................          -5,962            -3.5          -5,494            -3.3          -4,489            -2.7
Ethanol.................................................         228,563            39.6         187,926            32.5         105,264            18.2
1,3-Butadiene...........................................            -212            -1.8            -282            -2.4            -430            -3.6
Acetaldehyde............................................          16,375            44.0          14,278            38.4           9,839            26.5
Formaldehyde............................................           3,373             4.7           3,124             4.3           2,596             3.6
Naphthalene.............................................            -175            -1.2            -178            -1.3            -187            -1.3
Acrolein................................................             253             4.4             218             3.8             143             2.5
SO2.....................................................          28,770             0.3           4,461            0.05         -47,030            -0.5
NH3.....................................................         -27,161            -0.6         -27,161            -0.6         -27,161            -0.6
--------------------------------------------------------------------------------------------------------------------------------------------------------

    The breakdown of these results by the fuel production/distribution
(``well-to-pump'' emissions) and vehicle and equipment (``pump-to-
wheel'') emissions is discussed in the following sections.

B. Fuel Production & Distribution Impacts of the Proposed Program

    Fuel production and distribution emission impacts of the proposed
program were estimated in conjunction with the development of life
cycle GHG emission impacts and the GHG emission inventories discussed
in Section VI. These emissions are calculated according to the
breakdowns of agriculture, feedstock transport, fuel production, and
fuel distribution; the basic calculation is a function of fuel volumes
in the analysis year and the emission factors associated with each
process or subprocess. Additionally, the emission impact of displaced
petroleum is estimated, using the same domestic/import shares discussed
in Section VI above.
    In general the basis for this life cycle evaluation was the
analysis conducted as part of the Renewable Fuel Standard (RFS1)
rulemaking, but enhanced significantly. While our approach for the RFS1
was to rely heavily on the ``Greenhouse Gases, Regulated Emissions, and
Energy Use in Transportation'' (GREET) model, developed by the
Department of Energy's Argonne National Laboratory (ANL), we are now
able to take advantage of additional information and models to
significantly strengthen and expand our analysis for this proposed
rule. In particular, the modeling of the agriculture sector was greatly
expanded beyond the RFS1 analysis, employing economic and agriculture
models to consider factors such as land-use impact, agricultural
burning, fertilizer, pesticide use, livestock, crop allocation, and
crop exports.
    Other updates and enhancements to the GREET model assumptions
include updated feedstock energy requirements and estimates of excess
electricity available for sale from new cellulosic ethanol plants,
based on modeling by the National Renewable Energy Laboratory (NREL).
EPA also updated the fuel and feedstock transport emission factors to
account for recent EPA emission standards and modeling, such as the
diesel truck standards published in 2001 and the locomotive and
commercial marine standards finalized in 2008. Emission factors for new
corn ethanol plants continue to use the values developed for the RFS1
rule, which were based on data submitted by states for dry mill plants.
There are no new standards planned at this time that would offer any
additional control of emissions from corn or cellulosic ethanol plants.
In addition, GREET does not include air toxics or ethanol. Thus
emission factors for ethanol and the following air toxics were added:
benzene, 1,3-butadiene, formaldehyde, acetaldehyde, acrolein and
naphthalene.
    Results of these calculations relative to each of the reference
cases for 2022 are shown in Table VII.B-1 for the criteria pollutants,
ammonia, ethanol and individual air toxic pollutants. It should be
noted that the impacts relative to the two RFS1 reference cases (3.64
and 6.7 billion gallons) rely on applying ethanol volume proportions to
the modeling results of the AEO2007 reference case (13.2 billion
gallons). Due to the complex interactions involved in projections in
the agricultural modeling, we did not attempt to adjust the
agricultural inputs of the AEO reference case for the other two
reference cases. So the fertilizer and pesticide quantities, livestock
counts, and total agricultural acres were the same for all three
reference cases. The agricultural modeling that had been done for the
RFS1 rule itself was much simpler and inconsistent with the new
modeling, so it would be inappropriate to use those estimates. Thus, we
plan to conduct additional agricultural modeling specifically for the
RFS1 mandate case prior to finalizing this rule.
    The fuel production and distribution impacts of the proposed
program on VOC are mainly due to increases in emissions connected with
biofuel production, countered by decreases in emissions associated with
gasoline production and distribution as ethanol displaces some of the
gasoline. Increases in NOX, PM2.5, and
SOX are driven by combustion emissions from the substantial
increase in corn and cellulosic ethanol production. Ethanol plants
(corn and cellulosic) tend to have greater combustion emissions
relative to petroleum refineries on a per-BTU of fuel produced basis.
Increases in SOX emissions are primarily due to corn ethanol
production. Ammonia emissions are expected to decrease substantially
due to lower livestock counts, which more than offsets increased
ammonia from fertilizer use.
    Ethanol vapor and most air toxic emissions associated with fuel
production and distribution are projected to increase. Relative to the
U.S. total reference case emissions with RFS1 mandate ethanol volumes,
increases of 10-20% for acetaldehyde and ethanol vapor are especially
significant because they are driven directly by the increased ethanol
production and distribution. Formaldehyde and acrolein increases are
smaller, on the order of 1-5%. Benzene emissions are estimated to
decrease by 1% due to decreased gasoline production. There are also
very small increases in 1,3-butadiene and decreases in naphthalene
relative to the U.S. total emissions.

         Table VII.B-1--Fuel Production and Distribution Impacts in 2022 Relative to Each Reference Case
----------------------------------------------------------------------------------------------------------------
                                         RFS1 base                 RFS1 mandate                 AEO2007
                                --------------------------------------------------------------------------------
           Pollutant                           Percent of                 Percent of                 Percent of
                                    Annual     total U.S.      Annual     total U.S.      Annual     total U.S.
                                  short tons    inventory    short tons    inventory    short tons    inventory
----------------------------------------------------------------------------------------------------------------
NOX............................      241,041          2.1       222,732          2.0       183,951          1.6
HC.............................       77,295          0.7        46,702          0.4       -17,501         -0.2
PM10...........................       50,482          1.4        37,324          1.1         9,453          0.3
PM2.5..........................       14,419          0.4        11,550          0.3         5,473          0.16
CO.............................      186,559          0.3       179,855          0.3       165,656         -0.5
Benzene........................       -1,670         -1.0        -1,686         -1.0        -1,719         -1.0
Ethanol........................      115,187         19.9       100,134         17.3        68,379         11.8
1,3-Butadiene..................           16          0.13           16          0.14           17          0.14
Acetaldehyde...................        7,460         20.1         6,680         18.0         5,029         13.5
Formaldehyde...................          877          1.2           800          1.1           638          0.9
Naphthalene....................           -6         -0.04           -5         -0.04           -4         -0.03
Acrolein.......................          278          4.8           244          4.2           174          3.0

SO2............................       28,770          0.3         4,461          0.05      -47,030         -0.5
NH3............................      -27,161         -0.6       -27,161         -0.6       -27,161         -0.6
----------------------------------------------------------------------------------------------------------------

C. Vehicle and Equipment Emission Impacts of Fuel Program

    The effects of the fuel program on vehicle and equipment emissions
are a direct function of the effects of these fuels on exhaust and
evaporative emissions from vehicles and off-road equipment, and
evaporation of fuel from portable containers. To assess these impacts
we conducted separate analyses to quantify the emission impacts of
additional E10 due to today's proposal on gasoline vehicles, nonroad
spark-ignited engines and portable fuel containers; E85 on cars and
light trucks; biodiesel on diesel vehicles; and increased refueling
events due to lower energy density of biofuels.\330\
---------------------------------------------------------------------------

    \330\ The impact of renewable diesel was not estimated for the
proposal; we expect little overall impact on criteria and toxic
emissions due to the relatively small volume change, and because
emission effects relative to conventional diesel are presumed to be
negligible.
---------------------------------------------------------------------------

    For the proposal we have analyzed inventory impacts for two fuel
effects scenarios to attempt to bound the potential impacts on ethanol
on gasoline-fueled vehicle exhaust emissions:
    (1) ``Less Sensitive'': No exhaust VOC or NOX emission
impact on Tier 1 and later vehicles due to E10, and no impact due to
E85. This was termed the ``primary'' case in the RFS1 rule.
    (2) ``More Sensitive'': VOC and NOX emission impacts due
to E10 based on limited test data from newer technology vehicles that
were analyzed as part of the RFS1 rule. This data showed a 7% reduction
in exhaust VOC emissions and an 8% increase in per-vehicle
NOX emissions for Tier 1 and later vehicles using E10
relative to E0. The E10 effects are consistent with the ``sensitivity''
case from the RFS1 rule. For RFS2 this case also includes E85 effects
reflecting significant increases in acetaldehyde, formaldehyde and
ethanol emissions, and reductions in PM and CO.
    EPA and other parties are in the midst of gathering additional data
on the emission impacts of ethanol fuels on later model vehicles, which
we plan to consider in updating our final rule analysis.
    We have also estimated the E10 effects on permeation emissions from
light-duty vehicles based on testing previously completed by the
Coordinating Research Council (CRC). Nonroad spark ignition (SI)
emission impacts of E10 were based on EPA's NONROAD model and show
trends similar to light duty vehicles. Biodiesel effects for this
analysis were based on a new analysis of recent biodiesel testing,
detailed in the DRIA, showing a 2% increase in NOX with a
20% biodiesel blend, a 16% decrease in PM, and a 14% decrease in HC.
These results essentially confirm the results of an earlier EPA
analysis.
    Summarized vehicle and equipment emission impacts in 2022 are shown
in Table VII.C-1 and VII.C-2 for the ``less sensitive'' and ``more
sensitive'' cases. Table VII.C-3 shows the biodiesel contribution to
these impacts, which are comparatively small. While the two fuel effect
scenarios only differ with respect to exhaust emissions from cars and
trucks, the totals shown below reflect the net impacts from all mobile
sources, including car and truck evaporative emissions, off road
emissions, and portable fuel containers, using the same emissions
impacts for these sources in both cases. Additional breakdowns by
mobile source category can be found in Chapter 3 of the DRIA.
    As shown in Tables VII.C-1 and VII.C-2, the vehicle and equipment
ethanol impacts vary widely between the two fuel effects cases. Under
the ``less sensitive'' case, CO and benzene are projected to decrease
in 2022 under today's proposal, while NOX, HC and the other
air toxics (except acrolein) are projected to increase due to the
impacts of E10. For the ``more sensitive'' case, NOX impacts
are higher and HC impacts lower due to the E10 effects on cars and
trucks, and the inclusion of E85 effects leads to larger reductions in
CO, benzene and 1,3-butadiene but more significant increases in
ethanol, acetaldehyde and formaldehyde. The impacts on acrolein
emissions in both cases, and on naphthalene in the ``more sensitive''
case depend on which reference case is considered, with small increases
relative to the RFS1 base and mandate cases and a decrease relative to
the AEO reference case.

             Table VII.C-1--2022 Vehicle and Equipment ``Less Sensitive'' Case Emission Impacts by Fuel Type Relative to Each Reference Case
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                     RFS1 base                     RFS1 mandate                       AEO2007
                                                         -----------------------------------------------------------------------------------------------
                        Pollutant                                           Percent of                      Percent of                      Percent of
                                                           Annual short     total U.S.     Annual short     total U.S.     Annual short     total U.S.
                                                               tons          inventory         tons          inventory         tons          inventory
--------------------------------------------------------------------------------------------------------------------------------------------------------
NOX.....................................................          71,359             0.6          52,250             0.5          11,784            0.11
HC......................................................          35,106             0.3          25,659             0.2           9,308            0.08
PM10....................................................            -177            0.00            -177            0.00            -177            0.00
PM2.5...................................................             -98            0.00             -98            0.00             -98            0.00
CO......................................................      -2,531,205            -4.7      -1,849,728            -3.4        -406,599            -0.8
Benzene.................................................          -1,122            -0.7            -821            -0.5            -174            -0.1
Ethanol.................................................          95,493            16.5          69,795            12.1          15,383             2.7
1,3-Butadiene...........................................             328             2.7             238             2.0              48             0.4
Acetaldehyde............................................           5,057            13.6           3,689             9.9             793             2.1

Formaldehyde............................................             771             1.1             548             0.8              76            0.11
Naphthalene.............................................              10            0.07               8            0.05               3            0.02
Acrolein................................................              12             0.2               8            0.14            -0.4           -0.01
SO2.....................................................               0             0.0               0             0.0               0             0.0
NH3.....................................................               0             0.0               0             0.0               0             0.0
--------------------------------------------------------------------------------------------------------------------------------------------------------

             Table VII.C-2--2022 Vehicle and Equipment ``More Sensitive'' Case Emission Impacts by Fuel Type Relative to Each Reference Case
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                     RFS1 base                     RFS1 mandate                       AEO2007
                                                         -----------------------------------------------------------------------------------------------
                        Pollutant                                           Percent of                      Percent of                      Percent of
                                                           Annual short     total U.S.     Annual short     total U.S.     Annual short     total U.S.
                                                               tons          inventory         tons          inventory         tons          inventory
--------------------------------------------------------------------------------------------------------------------------------------------------------
NOX.....................................................         161,754             1.4         118,295             1.1          26,266             0.2
HC......................................................          23,018             0.2          16,828            0.15           1,553            0.01
PM10....................................................          -4,289           -0.12          -4,289           -0.12          -4,289           -0.12
PM2.5...................................................          -3,884           -0.12          -3,884           -0.12          -3,884           -0.12
CO......................................................      -3,966,131            -7.4      -3,284,654            -6.1      -1,841,524            -3.4
Benzene.................................................          -4,293            -2.6          -3,808            -2.3          -2,770            -1.6
Ethanol.................................................         113,376            19.6          87,792            15.2          36,886             6.4
1,3-Butadiene...........................................            -228            -1.9            -298            -2.5            -446            -3.7
Acetaldehyde............................................           8,915            24.0           7,598            20.4           4,809            12.9
Formaldehyde............................................           2,497             3.5           2,324             3.2           1,958             2.7
Naphthalene.............................................            -170            -1.2            -172            -1.2            -182            -1.3
Acrolein................................................             -25            -0.4             -27            -0.5             -31            -0.5
SO2.....................................................               0             0.0               0             0.0               0             0.0
NH3.....................................................               0             0.0               0             0.0               0             0.0
--------------------------------------------------------------------------------------------------------------------------------------------------------

  Table VII.C-3--2022 Vehicle and Equipment Biodiesel Emission Impacts
                     Relative to All Reference Cases
       [these impacts are included in Tables VII.C-1 and VII.C-2]
------------------------------------------------------------------------
                                                              Biodiesel
                                                               impacts
                         Pollutant                          ------------
                                                                Annual
                                                              short tons
------------------------------------------------------------------------
NOX........................................................          418
HC.........................................................         -753
PM10.......................................................         -177
PM2.5......................................................          -98
CO.........................................................       -1,275
Benzene....................................................         -9.4
Ethanol....................................................          0.0
1,3-Butadiene..............................................         -5.1
Acetaldehyde...............................................          -21
Formaldehyde...............................................          -57
Naphthalene................................................        -0.12
Acrolein...................................................         -2.7
SO2........................................................          0.0
NH3........................................................          0.0
------------------------------------------------------------------------

D. Air Quality Impacts

    Although the purpose of this proposal is to implement the renewable
fuel requirements established by the Energy Independence and Security
Act (EISA) of 2007, this proposed rule would also impact emissions of
criteria and air toxic pollutants. We first present current levels of
PM2.5, ozone and air toxics and then discuss the national-
scale air quality modeling analysis that will be performed for the
final rule.
1. Current Levels of PM2.5, Ozone and Air Toxics
    This proposal may have impacts on levels of PM2.5, ozone
and air toxics.\331\ Nationally, levels of PM2.5, ozone and
air toxics are declining.332 333 However, as of December 16,
2008, approximately 88 million people live in the 39 areas that are
designated as nonattainment for the 1997 PM2.5 National
Ambient Air Quality Standard (NAAQS) and approximately 132 million
people live in the 57 areas that are designated as nonattainment for
the 1997 8-hour ozone NAAQS. The 1997 PM2.5 NAAQS was
recently revised and the 2006 24-hour PM2.5 NAAQS became
effective on December 18, 2006. Area designations for the 2006 24-hour
PM2.5 NAAQS are expected to be promulgated in 2009 and
become effective 90 days after publication in the Federal Register. In
addition, the majority of Americans continue to be exposed to ambient
concentrations of air toxics at levels which have the potential to
cause adverse health effects.\334\ The levels of air toxics to which
people are exposed vary depending on where people live and work and the
kinds of activities in which they engage, as discussed in

detail in U.S. EPA's recent Mobile Source Air Toxics Rule.\335\
---------------------------------------------------------------------------

    \331\ The proposed standards may also impact levels of ambient
CO, a criteria pollutant (see Table VII.A-1 above for co-pollutant
emission impacts). For this analysis, however, we focus on the
proposal's impacts on ambient PM2.5 and ozone formation,
since CO is a relatively minor problem in comparison to some of the
other criteria pollutants. For example, as of August 15, 2008 there
are approximately 675,000 people living in 3 areas (which include 4
counties) that are designated as nonattainment for CO.
    \332\ \\ U.S. EPA (2003) National Air Quality and Trends Report,
2003 Special Studies Edition. Office of Air Quality Planning and
Standards, Research Triangle Park, NC. Publication No. EPA 454/R-03-
005. http://www.epa.gov/air/airtrends/aqtrnd03/http://www.epa.gov/air/airtrends/aqtrnd03/.
    \333\ \\ U.S. EPA (2007) Final Regulatory Impact Analysis:
Control of Hazardous Air Pollutants from Mobile Sources, Office of
Transportation and Air Quality, Ann Arbor, MI, Publication No.
EPA420-R-07-002. http://www.epa.gov/otaq/toxics.htm
    \334\ U.S. Environmental Protection Agency (2007). Control of
Hazardous Air Pollutants from Mobile Sources; Final Rule. 72 FR
8434, February 26, 2007.
    \335\ U.S. Environmental Protection Agency (2007). Control of
Hazardous Air Pollutants from Mobile Sources; Final Rule. 72 FR
8434, February 26, 2007.
---------------------------------------------------------------------------

    EPA has already adopted many emission control programs that are
expected to reduce ambient PM2.5, ozone and air toxics
levels. These control programs include the Small SI and Marine SI
Engine Rule (73 FR 59034, October 8, 2008), Locomotive and Commercial
Marine Rule (73 FR 25098, May 6, 2008), Mobile Source Air Toxics Rule
(72 FR 8428, February 26, 2007), Clean Air Interstate Rule (70 FR
25162, May 12, 2005), Clean Air Nonroad Diesel Rule (69 FR 38957, June
29, 2004), Heavy Duty Engine and Vehicle Standards and Highway Diesel
Fuel Sulfur Control Requirements (66 FR 5002, Jan. 18, 2001) and the
Tier 2 Motor Vehicle Emissions Standards and Gasoline Sulfur Control
Requirements (65 FR 6698, Feb. 10, 2000). As a result of these
programs, the ambient concentration of air toxics, PM2.5 and
ozone in the future is expected to decrease.
2. Impacts of Proposed Standards on Future Ambient Concentrations of
PM2.5, Ozone and Air Toxics
    The atmospheric chemistry related to ambient concentrations of
PM2.5, ozone and air toxics is very complex, making
predictions based solely on emissions changes extremely difficult. For
the final rule, a national-scale air quality modeling analysis will be
performed to analyze the impacts of the proposed standards on ambient
concentrations of PM2.5, ozone, and selected air toxics
(i.e., benzene, formaldehyde, acetaldehyde, ethanol, acrolein and 1,3-
butadiene). The length of time needed to prepare necessary inventory
and model updates has precluded us from performing air quality modeling
for this proposal.
    The air quality modeling we plan to perform (described more
specifically below), will allow us to account for changes in the
spatial distribution of PM and PM precursors, and changes in VOC
speciation which could impact secondary PM formation. For example,
reductions in aromatics in gasoline may reduce ambient PM
concentrations by reducing secondary PM formation. Section 3.3 of the
Draft Regulatory Impact Analysis (DRIA) for this proposal contains more
information on aromatics and secondary aerosol formation.
    In addition, air quality modeling will account for changes in fuel
type and spatial distribution of fuels that would change emissions of
ozone precursor species and thus could affect ozone concentrations.
Section 3.3 of the DRIA for this proposed rule provides more detail on
the atmospheric chemistry and potential changes in ozone formation due
to increased usage of ethanol fuels.
    Section VII.A above presents projections of the changes in air
toxics emissions due to the proposed standards. The substantial
increase in emissions of ethanol and acetaldehyde suggests a likely
increase in ambient levels of acetaldehyde from both direct emissions
and secondary formation as ethanol breaks down in the atmosphere.
Formaldehyde and acrolein emissions would also increase somewhat, while
emissions of benzene and 1,3-butadiene would decrease as a result of
the proposed standards. Full-scale photochemical modeling is necessary
to provide the needed spatial and temporal detail to more completely
and accurately estimate the changes in ambient levels of these
pollutants.
    For the final rule, EPA intends to use a 2005-based Community
Multi-scale Air Quality (CMAQ) modeling platform as the tool for the
air quality modeling. The CMAQ modeling system is a comprehensive
three-dimensional grid-based Eulerian air quality model designed to
estimate the formation and fate of oxidant precursors, primary and
secondary PM concentrations and deposition, and air toxics, over
regional and urban spatial scales (e.g., over the contiguous
U.S.).336 337 338 The CMAQ model is a well-known and well-
established tool and is commonly used by EPA for regulatory analyses,
for instance the recent ozone NAAQS proposal, and by States in
developing attainment demonstrations for their State Implementation
Plans.\339\ The CMAQ model (version 4.6) was peer-reviewed in February
of 2007 for EPA as reported in ``Third Peer Review of CMAQ Model,'' and
the peer review report for version 4.7 (described below) is currently
being finalized.\340\
---------------------------------------------------------------------------

    \336\ U.S. Environmental Protection Agency, Byun, D.W., and
Ching, J.K.S., Eds, 1999. Science algorithms of EPA Models-3
Community Multiscale Air Quality (CMAQ modeling system, EPA/600/R-
99/030, Office of Research and Development).
    \337\ Byun, D.W., and Schere, K.L., 2006. Review of the
Governing Equations, Computational Algorithms, and Other Components
of the Models-3 Community Multiscale Air Quality (CMAQ) Modeling
System, J. Applied Mechanics Reviews, 59 (2), 51-77.
    \338\ Dennis, R.L., Byun, D.W., Novak, J.H., Galluppi, K.J.,
Coats, C.J., and Vouk, M.A., 1996. The next generation of integrated
air quality modeling: EPA's Models-3, Atmospheric Environment, 30,
1925-1938.
    \339\ U.S. EPA (2007). Regulatory Impact Analysis of the
Proposed Revisions to the National Ambient Air Quality Standards for
Ground-Level Ozone. EPA document number 442/R-07-008, July 2007.
    \340\ Aiyyer, A., Cohan, D., Russell, A., Stockwell, W.,
Tanrikulu, S., Vizuete, W., Wilczak, J., 2007. Final Report: Third
Peer Review of the CMAQ Model. p. 23.
---------------------------------------------------------------------------

    CMAQ includes many science modules that simulate the emission,
production, decay, deposition and transport of organic and inorganic
gas-phase and particle-phase pollutants in the atmosphere. We intend to
use the most recent CMAQ version (version 4.7) which was officially
released by EPA's Office of Research and Development (ORD) in December
2008, and reflects updates to earlier versions in a number of areas to
improve the underlying science. These include (1) enhanced secondary
organic aerosol (SOA) mechanism to include chemistry of isoprene,
sesquiterpene, and aged in-cloud biogenic SOA in addition to terpene;
(2) improved vertical convective mixing; (3) improved heterogeneous
reaction involving nitrate formation; and (4) an updated gas-phase
chemistry mechanism, Carbon Bond 05 (CB05), with extensions to model
explicit concentrations of air toxic species as well as chlorine and
mercury. This mechanism, CB05-toxics, also computes concentrations of
species that are involved in aqueous chemistry and that are precursors
to aerosols. Section 3.3.3 of the DRIA for this proposal discusses SOA
formation and details about the improvements made to the SOA mechanism
within this recent release of CMAQ.

E. Health Effects of Criteria and Air Toxic Pollutants

1. Particulate Matter
a. Background
    Particulate matter (PM) represents 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. PM is further described
by breaking it down into size fractions. PM10 refers to
particles generally less than or equal to 10 micrometers ([mu]m) in
aerodynamic diameter. PM2.5 refers to fine particles,
generally less than or equal to 2.5 [mu]m in aerodynamic diameter.
Inhalable (or ``thoracic'') coarse particles refer to those particles
generally greater than 2.5 [mu]m but less than or equal to 10 [mu]m in
aerodynamic diameter. Ultrafine PM refers to particles less than 100
nanometers (0.1 [mu]m) in aerodynamic diameter. Larger particles tend
to be removed by the respiratory clearance mechanisms (e.g., coughing),
whereas

smaller particles are deposited deeper in the lungs.
    Fine particles are produced primarily by combustion processes and
by transformations of gaseous emissions (e.g., SOX,
NOX and VOC) in the atmosphere. The chemical and physical
properties of PM2.5 may vary greatly with time, region,
meteorology and source category. Thus, PM2.5 may include a
complex mixture of different pollutants including sulfates, nitrates,
organic compounds, elemental carbon and metal compounds. These
particles can remain in the atmosphere for days to weeks and travel
hundreds to thousands of kilometers.
b. Health Effects of PM
    Scientific studies show ambient PM is associated with a series of
adverse health effects. These health effects are discussed in detail in
the 2004 EPA Particulate Matter Air Quality Criteria Document (PM
AQCD), and the 2005 PM Staff Paper.341 342 Further
discussion of health effects associated with PM can also be found in
the DRIA for this rule.
---------------------------------------------------------------------------

    \341\ U.S. EPA (2004) Air Quality Criteria for Particulate
Matter (Oct. 2004), Volume I Document No. EPA600/P-99/002aF and
Volume II Document No. EPA600/P-99/002bF. This document is available
in Docket EPA-HQ-OAR-2005-0161.
    \342\ U.S. EPA (2005) Review of the National Ambient Air Quality
Standard for Particulate Matter: Policy Assessment of Scientific and
Technical Information, OAQPS Staff Paper. EPA-452/R-05-005. This
document is available in Docket EPA-HQ-OAR-2005-0161.
---------------------------------------------------------------------------

    Health effects associated with short-term exposures (hours to days)
to ambient PM include premature mortality, increased hospital
admissions, heart and lung diseases, increased cough, adverse lower-
respiratory symptoms, decrements in lung function and changes in heart
rate rhythm and other cardiac effects. Studies examining populations
exposed to different levels of air pollution over a number of years,
including the Harvard Six Cities Study and the American Cancer Society
Study, show associations between long-term exposure to ambient
PM2.5 and both total and cardiovascular and respiratory
mortality.\343\ In addition, a reanalysis of the American Cancer
Society Study shows an association between fine particle and sulfate
concentrations and lung cancer mortality.\344\
---------------------------------------------------------------------------

    \343\ Dockery, D.W.; Pope, C.A. III: Xu, X.; et al. 1993. An
association between air pollution and mortality in six U.S. cities.
N Engl J Med 329:1753-1759.
    \344\ Pope, C.A., III; Burnett, R.T.; Thun, M.J.; Calle, E.E.;
Krewski, D.; Ito, K.; Thurston, G.D. (2002) Lung cancer,
cardiopulmonary mortality, and long-term exposure to fine
particulate air pollution. J. Am. Med. Assoc. 287:1132-1141.
---------------------------------------------------------------------------

2. Ozone
a. Background
    Ground-level ozone pollution is typically formed by the reaction of
volatile organic compounds (VOC) and nitrogen oxides (NOX)
in the lower atmosphere in the presence of heat and sunlight. These
pollutants, often referred to as ozone precursors, are emitted by many
types of pollution sources, such as highway and nonroad motor vehicles
and engines, power plants, chemical plants, refineries, makers of
consumer and commercial products, industrial facilities, and smaller
area sources.
    The science of ozone formation, transport, and accumulation is
complex.\345\ 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.
---------------------------------------------------------------------------

    \345\ U.S. EPA Air Quality Criteria for Ozone and Related
Photochemical Oxidants (Final). U.S. Environmental Protection
Agency, Washington, D.C., EPA 600/R-05/004aF-cF, 2006. This document
is available in Docket EPA-HQ-OAR-2005-0161. This document may be
accessed electronically at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_cd.html.
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b. Health Effects of Ozone
    The health and welfare effects of ozone are well documented and are
assessed in EPA's 2006 Ozone Air Quality Criteria Document (ozone AQCD)
and 2007 Staff Paper.346 347 Ozone can irritate the
respiratory system, causing coughing, throat irritation, and/or
uncomfortable sensation in the chest. Ozone can reduce lung function
and make it more difficult to breathe deeply; breathing may also become
more rapid and shallow than normal, thereby limiting a person's
activity. Ozone can also aggravate asthma, leading to more asthma
attacks that require medical attention and/or the use of additional
medication. In addition, there is suggestive evidence of a contribution
of ozone to cardiovascular-related morbidity and highly suggestive
evidence that short-term ozone exposure directly or indirectly
contributes to non-accidental and cardiopulmonary-related mortality,
but additional research is needed to clarify the underlying mechanisms
causing these effects. In a recent report on the estimation of ozone-
related premature mortality published by the National Research Council
(NRC), a panel of experts and reviewers concluded that short-term
exposure to ambient ozone is likely to contribute to premature deaths
and that ozone-related mortality should be included in estimates of the
health benefits of reducing ozone exposure.\348\ Animal toxicological
evidence indicates that with repeated exposure, ozone can inflame and
damage the lining of the lungs, which may lead to permanent changes in
lung tissue and irreversible reductions in lung function. People who
are more susceptible to effects associated with exposure to ozone can
include children, the elderly, and individuals with respiratory disease
such as asthma. Those with greater exposures to ozone, for instance due
to time spent outdoors (e.g., children and outdoor workers), are also
of particular concern.
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    \346\ U.S. EPA Air Quality Criteria for Ozone and Related
Photochemical Oxidants (Final). U.S. Environmental Protection
Agency, Washington, DC, EPA 600/R-05/004aF-cF, 2006. This document
is available in Docket EPA-HQ-OAR-2005-0161. This document may be
accessed electronically at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_cd.html.
    \347\ 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. This document is
available in Docket EPA-HQ-OAR-2005-0161. This document is available
electronically at: http:www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html..
    \348\ National Research Council (NRC), 2008. Estimating
Mortality Risk Reduction and Economic Benefits from Controlling
Ozone Air Pollution. The National Academies Press: Washington, DC.
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    The 2006 ozone AQCD also examined relevant new scientific
information that has emerged in the past decade, including the impact
of ozone exposure on such health effects as changes in lung structure
and biochemistry, inflammation of the lungs, exacerbation and causation
of asthma, respiratory illness-related school absence, hospital
admissions and premature mortality. Animal toxicological studies have
suggested potential interactions between ozone and PM, with increased
responses observed to mixtures of the two pollutants compared to either
ozone or PM alone. The respiratory morbidity observed in animal studies
along with the evidence from epidemiologic studies supports a causal
relationship between acute ambient ozone exposures and increased
respiratory-related emergency room visits and hospitalizations in the
warm season. In addition, there is

suggestive evidence of a contribution of ozone to cardiovascular-
related morbidity and non-accidental and cardiopulmonary mortality.
3. Carbon Monoxide
    Carbon monoxide (CO) forms as a result of incomplete fuel
combustion. CO enters the bloodstream through the lungs, forming
carboxyhemoglobin and reducing the delivery of oxygen to the body's
organs and tissues. The health threat from CO is most serious for those
who suffer from cardiovascular disease, particularly those with angina
or peripheral vascular disease. Healthy individuals also are affected,
but only at higher CO levels. Exposure to elevated CO levels is
associated with impairment of visual perception, work capacity, manual
dexterity, learning ability and performance of complex tasks. Carbon
monoxide also contributes to ozone nonattainment since carbon monoxide
reacts photochemically in the atmosphere to form ozone.\349\ Additional
information on CO related health effects can be found in the Carbon
Monoxide Air Quality Criteria Document (CO AQCD).\350\
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    \349\ U.S. EPA (2000). Air Quality Criteria for Carbon Monoxide,
EPA/600/P-99/001F. This document is available in Docket EPA-HQ-OAR-
2005-0161.
    \350\ U.S. EPA (2000). Air Quality Criteria for Carbon Monoxide,
EPA/600/P-99/001F. This document is available in Docket EPA-HQ-OAR-
2005-0161.
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4. Air Toxics
    The population experiences an elevated risk of cancer and noncancer
health effects from exposure to the class of pollutants known
collectively as ``air toxics.''\351\ Fuel combustion contributes to
ambient levels of air toxics that can include, but are not limited to,
acetaldehyde, acrolein, benzene, 1,3-butadiene, formaldehyde, ethanol,
naphthalene and peroxyacetyl nitrate (PAN). Acrolein, benzene, 1,3-
butadiene, formaldehyde and naphthalene have significant contributions
from mobile sources and were identified as national or regional risk
drivers in the 1999 National-scale Air Toxics Assessment (NATA).\352\
PAN, which is formed from precursor compounds by atmospheric processes,
is not assessed in NATA. Emissions and ambient concentrations of
compounds are discussed in the DRIA chapter on emission inventories and
air quality (Chapter 3).
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    \351\ U. S. EPA. 1999 National-Scale Air Toxics Assessment.
http://www.epa.gov/ttn/atw/nata1999/risksum.html
    \352\ U.S. EPA. 2006. National-Scale Air Toxics Assessment for
1999. http://www.epa.gov/ttn/atw/nata1999
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a. Acetaldehyde
    Acetaldehyde is classified in EPA's IRIS database as a probable
human carcinogen, based on nasal tumors in rats, and is considered
toxic by the inhalation, oral, and intravenous routes.\353\
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.354 355 EPA is currently conducting a reassessment of
cancer risk from inhalation exposure to acetaldehyde.
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    \353\ U.S. EPA. 1991. Integrated Risk Information System File of
Acetaldehyde. Research and Development, National Center for
Environmental Assessment, Washington, DC. This material is available
electronically at.
    \354\ U.S. Department of Health and Human Services National
Toxicology Program 11th Report on Carcinogens available at:
ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-7FCE50709CB4C9322.
    \355\ International Agency for Research on Cancer (IARC). 1999.
Re-evaluation of some organic chemicals, hydrazine, and hydrogen
peroxide. IARC Monographs on the Evaluation of Carcinogenic Risk of
Chemical to Humans, Vol 71. Lyon, France.
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    The primary noncancer effects of exposure to acetaldehyde vapors
include irritation of the eyes, skin, and respiratory tract.\356\ In
short-term (4 week) rat studies, degeneration of olfactory epithelium
was observed at various concentration levels of acetaldehyde
exposure.357 358 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.\359\ The agency is currently conducting a reassessment of
the health hazards from inhalation exposure to acetaldehyde.
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    \356\ U.S. EPA. 1991. Integrated Risk Information System File of
Acetaldehyde. This material is available electronically at http://www.epa.gov/iris/subst/0290.htm.
    \357\ 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.
    \358\ 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.
    \359\ 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.
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b. Acrolein
    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.\360\ The IARC determined in 1995 that acrolein was not
classifiable as to its carcinogenicity in humans.\361\
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    \360\ 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.
    \361\ International Agency for Research on Cancer (IARC). 1995.
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 63, Dry cleaning, some chlorinated solvents and other
industrial chemicals, World Health Organization, Lyon, France.
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    Acrolein is extremely acrid and irritating to humans when inhaled,
with acute exposure resulting in upper respiratory tract irritation,
mucus hypersecretion and congestion. Levels considerably lower than 1
ppm (2.3 mg/m\3\) elicit subjective complaints of eye and nasal
irritation and a decrease in the respiratory rate.362 363
Lesions to the lungs and upper respiratory tract of rats, rabbits, and
hamsters have been observed after subchronic exposure to acrolein.
Based on animal data, 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. This was demonstrated in mice with allergic airway disease by
comparison to non-diseased mice in a study of the acute respiratory
irritant effects of acrolein.\364\
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    \362\ Weber-Tschopp, A.; Fischer, T.; Gierer, R.; et al. (1977)
Experimentelle reizwirkungen von Acrolein auf den Menschen. Int Arch
Occup Environ Hlth 40(2):117-130. In German.
    \363\ Sim, V.M.; Pattle, R.E. (1957) Effect of possible smog
irritants on human subjects. J Am Med Assoc 165(15):1908-1913.
    \364\ Morris J.B., Symanowicz P.T., Olsen J.E., 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.
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    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.\365\
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    \365\ Sim V.M., Pattle R.E. Effect of possible smog irritants on
human subjects. JAMA 165:1980-2010, 1957.
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c. Benzene
    The EPA's IRIS database lists benzene as a known human carcinogen
(causing leukemia) by all routes of exposure, and concludes that
exposure is associated with additional health effects, including

genetic changes in both humans and animals and increased proliferation
of bone marrow cells in mice.366 367 368 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.369 370
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    \366\ 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.
    \367\ International Agency for Research on Cancer (IARC). 1982.
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29, Some industrial chemicals and dyestuffs, World
Health Organization, Lyon, France, p. 345-389.
    \368\ 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.
    \369\ International Agency for Research on Cancer (IARC). 1987.
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 29, Supplement 7, Some industrial chemicals and
dyestuffs, World Health Organization, Lyon, France.
    \370\ U.S. Department of Health and Human Services National
Toxicology Program, 11th Report on Carcinogens, available at: http://ntp.niehs.nih.gov/go/16183.
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    A number of adverse noncancer health effects including blood
disorders, such as preleukemia and aplastic anemia, have also been
associated with long-term exposure to benzene.371 372 The
most sensitive noncancer effect observed in humans, based on current
data, is the depression of the absolute lymphocyte count in
blood.373 374 In addition, recent work, including studies
sponsored by the Health Effects Institute (HEI), provides evidence that
biochemical responses are occurring at lower levels of benzene exposure
than previously known.375 376 377 378 EPA's IRIS program has
not yet evaluated these new data.
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    \371\ Aksoy, M. (1989). Hematotoxicity and carcinogenicity of
benzene. Environ. Health Perspect. 82:193-197.
    \372\ Goldstein, B.D. (1988). Benzene toxicity. Occupational
medicine. State of the Art Reviews. 3:541-554.
    \373\ 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.
    \374\ U.S. EPA (2002) Toxicological Review of Benzene (Noncancer
Effects). Environmental Protection Agency, Integrated Risk
Information System (IRIS), Research and Development, National Center
for Environmental Assessment, Washington DC. This material is
available electronically at http://www.epa.gov/iris/subst/0276.htm.
    \375\ 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.
    \376\ 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.
    \377\ Lan, Qing, Zhang, L., Li, G., Vermeulen, R., et al. (2004)
Hematotoxicity in Workers Exposed to Low Levels of Benzene. Science
306:1774-1776.
    \378\ 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.
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d. 1,3-Butadiene
    EPA has characterized 1,3-butadiene as carcinogenic to humans by
inhalation.379 380 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.381 382 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.\383\
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    \379\ 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.
    \380\ 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.
    \381\ International Agency for Research on Cancer (IARC) (1999)
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 71, Re-evaluation of some organic chemicals,
hydrazine and hydrogen peroxide and Volume 97 (in preparation),
World Health Organization, Lyon, France.
    \382\ U.S. Department of Health and Human Services (2005)
National Toxicology Program, 11th Report on Carcinogens, available
at: http://ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932.
    \383\ Bevan, C.; Stadler, J.C.; Elliot, G.S.; et al. (1996)
Subchronic toxicity of 4-vinylcyclohexene in rats and mice by
inhalation. Fundam. Appl. Toxicol. 32:1-10.
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e. Ethanol
    EPA is conducting an assessment of the cancer and noncancer effects
of exposure to ethanol, a compound which is not currently listed in
EPA's IRIS. A description of these effects to the extent that
information is available will be presented, as required by Section 1505
of EPAct, in a report to Congress on public health, air quality and
water resource impacts of fuel additives. We expect to release that
report in 2009.
    Extensive data are available regarding adverse health effects
associated with the ingestion of ethanol while data on inhalation
exposure effects are sparse. As part of the IRIS assessment,
pharmacokinetic models are being evaluated as a means of extrapolating
across species (animal to human) and across exposure routes (oral to
inhalation) to better characterize the health hazards and dose-response
relationships for low levels of ethanol exposure in the environment.
    The IARC has classified ``alcoholic beverages'' as carcinogenic to
humans based on sufficient evidence that malignant tumors of the mouth,
pharynx, larynx, esophagus, and liver are causally related to the
consumption of alcoholic beverages.\384\ The U.S. DHHS in the 11th
Report on Carcinogens also identified ``alcoholic beverages'' as a
known human carcinogen (they have not evaluated the cancer risks
specifically from exposure to ethanol), with evidence for cancer of the
mouth, pharynx, larynx, esophagus, liver and breast.\385\ There are no
studies reporting carcinogenic effects from inhalation of ethanol. EPA
is currently evaluating the available human and animal cancer data to
identify which cancer type(s) are the most relevant to an assessment of
risk to humans from a low-level oral and inhalation exposure to
ethanol.
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    \384\ International Agency for Research on Cancer (IARC). 1988.
Monographs on the evaluation of carcinogenic risk of chemicals to
humans, Volume 44, Alcohol Drinking, World Health Organization,
Lyon, France.
    \385\ 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-7FCE50709CB4C9322.
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    Noncancer health effects data are available from animal studies as
well as epidemiologic studies. The epidemiologic data are obtained from
studies of alcoholic beverage

consumption. Effects include neurological impairment, developmental
effects, cardiovascular effects, immune system depression, and effects
on the liver, pancreas and reproductive system.\386\ There is evidence
that children prenatally exposed via mothers' ingestion of alcoholic
beverages during pregnancy are at increased risk of hyperactivity and
attention deficits, impaired motor coordination, a lack of regulation
of social behavior or poor psychosocial functioning, and deficits in
cognition, mathematical ability, verbal fluency, and spatial
memory.387 388 389 390 391 392 393 394 In some people,
genetic factors influencing the metabolism of ethanol can lead to
differences in internal levels of ethanol and may render some
subpopulations more susceptible to risks from the effects of ethanol.
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    \386\ U.S. Department of Health and Human Services. 2000. 10th
Special Report to the U.S. Congress on Alcohol and Health. June
2000.
    \387\ Goodlett CR, KH Horn, F Zhou. 2005. Alcohol teratogenesis:
mechanisms of damage and strategies for intervention. Exp. Biol.
Med. 230:394-406.
    \388\ Riley EP, CL McGee. 2005. Fetal alcohol spectrum
disorders: an overview with emphasis on changes in brain and
behavior. Exp. Biol. Med. 230:357-365.
    \389\ Zhang X, JH Sliwowska, J Weinberg. 2005. Prenatal alcohol
exposure and fetal programming: effects on neuroendocrine and immune
function. Exp. Biol. Med. 230:376-388.
    \390\ Riley EP, CL McGee, ER Sowell. 2004. Teratogenic effects
of alcohol: a decade of brain imaging. Am. J. Med. Genet. Part C:
Semin. Med. Genet. 127:35-41.
    \391\ Gunzerath L, V Faden, S Zakhari, K Warren. 2004. National
Institute on Alcohol Abuse and Alcoholism report on moderate
drinking. Alcohol. Clin. Exp. Res. 28:829-847.
    \392\ World Health Organization (WHO). 2004. Global status
report on alcohol 2004. Geneva, Switzerland: Department of Mental
Health and Substance Abuse. Available: http://www.who.int/substance_abuse/publications/global_status_report_2004_overview.pdf.
    \393\ Chen W-JA, SE Maier, SE Parnell, FR West. 2003. Alcohol
and the developing brain: neuroanatomical studies. Alcohol Res.
Health 27:174-180.
    \394\ Driscoll CD, AP Streissguth, EP Riley. 1990. Prenatal
alcohol exposure comparability of effects in humans and animal
models. Neurotoxicol. Teratol. 12:231-238.
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f. Formaldehyde
    Since 1987, EPA has classified formaldehyde as a probable human
carcinogen based on evidence in humans and in rats, mice, hamsters, and
monkeys.\395\ EPA is currently reviewing recently published
epidemiological data. For instance, research conducted by the National
Cancer Institute (NCI) found an increased risk of nasopharyngeal cancer
and lymphohematopoietic malignancies such as leukemia among workers
exposed to formaldehyde.396 397 NCI is currently performing
an update of these studies. A recent National Institute of Occupational
Safety and Health (NIOSH) study of garment workers also found increased
risk of death due to leukemia among workers exposed to
formaldehyde.\398\ 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.\399\ Recently, the IARC re-
classified formaldehyde as a human carcinogen (Group 1).\400\
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    \395\ 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.
    \396\ Hauptmann, M.; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.;
Blair, A. 2003. Mortality from lymphohematopoietic malignancies
among workers in formaldehyde industries. Journal of the National
Cancer Institute 95: 1615-1623.
    \397\ 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.
    \398\ Pinkerton, L. E. 2004. Mortality among a cohort of garment
workers exposed to formaldehyde: an update. Occup. Environ. Med. 61:
193-200.
    \399\ 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.
    \400\ International Agency for Research on Cancer (IARC). 2006.
Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol. Volume
88. (in preparation), World Health Organization, Lyon, France.
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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.401 402
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    \401\ 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.
    \402\ 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.
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g. Naphthalene
    Naphthalene is found in small quantities in gasoline and diesel
fuels. Naphthalene emissions have been measured in larger quantities in
both gasoline and diesel exhaust compared with evaporative emissions
from mobile sources, indicating it is primarily a product of
combustion. EPA released an external review draft of a reassessment of
the inhalation carcinogenicity of naphthalene based on a number of
recent animal carcinogenicity studies.\403\ The draft reassessment
completed external peer review.\404\ 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. Once EPA evaluates public and peer reviewer comments, the
document will be revised. 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.\405\ 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.\406\ Naphthalene also
causes a number of chronic non-cancer effects in animals, including
abnormal cell changes and growth in respiratory and nasal tissues.\407\
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    \403\ 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.
    \404\ 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.
    \405\ 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.
    \406\ International Agency for Research on Cancer (IARC).
(2002). Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals for Humans. Vol. 82, Lyon, France.
    \407\ 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.
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h. Peroxyacetyl Nitrate (PAN)
    Peroxyacetyl nitrate (PAN) has not been evaluated by EPA's IRIS
program. Information regarding the potential carcinogenicity of PAN is
limited. As noted in the EPA air quality criteria

document for ozone and related photochemical oxidants, cytogenetic
studies indicate that PAN is not a potent mutagen, clastogen (a
compound that can cause breaks in chromosomes), or DNA-damaging agent
in mammalian cells either in vivo or in vitro. Some studies suggest
that PAN may be a weak bacterial mutagen at high concentrations much
higher than exist in present urban atmospheres.\408\
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    \408\ U.S. EPA. 2006. Air Quality Criteria for Ozone and Related
Photochemical Oxidants (Ozone CD). Research Triangle Park, NC:
National Center for Environmental Assessment; report no. EPA/600/R-
05/004aF-cF.3v. page 5-78. Available at http://cfpub.epa.gov/ncea/
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    Effects of ground-level smog causing intense eye irritation have
been attributed to photochemical oxidants, including PAN.\409\ Animal
toxicological information on the inhalation effects of the non-ozone
oxidants has been limited to a few studies on PAN. Acute exposure to
levels of PAN can cause changes in lung morphology, behavioral
modifications, weight loss, and susceptibility to pulmonary infections.
Human exposure studies indicate minor pulmonary function effects at
high PAN concentrations, but large inter-individual variability
precludes definitive conclusions.\410\
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    \409\ U.S. EPA. 2006. Air Quality Criteria for Ozone and Related
Photochemical Oxidants (Final). U.S. Environmental Protection
Agency, Washington, DC, EPA 600/R-05/004aF-cF. pages 5-63. This
document is available in Docket EPA-HQ-OAR-2005-0161. This document
may be accessed electronically at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_cd.html.
    \410\ U.S. EPA. 2006. Air Quality Criteria for Ozone and Related
Photochemical Oxidants (Final). U.S. Environmental Protection
Agency, Washington, DC, EPA 600/R-05/004aF-cF. pages 5-78. This
document is available in Docket EPA-HQ-OAR-2005-0161. This document
may be accessed electronically at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_cd.html.
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i. Other Air Toxics
    In addition to the compounds described above, other compounds in
gaseous hydrocarbon and PM emissions from vehicles will be affected by
today's proposed action. Mobile source air toxic compounds that will
potentially be impacted include ethylbenzene, polycyclic organic
matter, propionaldehyde, toluene, and xylene. Information regarding the
health effects of these compounds can be found in EPA's IRIS
database.\411\
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    \411\ U.S. EPA. Integrated Risk Information System (IRIS)
database is available at: www.epa.gov/iris.
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F. Environmental Effects of Criteria and Air Toxic Pollutants

    In this section we discuss some of the environmental effects of PM
and its precursors, such as visibility impairment, atmospheric
deposition, and materials damage and soiling, as well as environmental
effects associated with the presence of ozone in the ambient air, such
as impacts on plants, including trees, agronomic crops and urban
ornamentals, and environmental effects associated with air toxics.
1. Visibility
    Visibility can be defined as the degree to which the atmosphere is
transparent to visible light.\412\ Airborne particles degrade
visibility by scattering and absorbing light. Visibility is important
because it has direct significance to people's enjoyment of daily
activities in all parts of the country. Individuals value good
visibility for the well-being it provides them directly, where they
live and work, and in places where they enjoy recreational
opportunities. Visibility is also highly valued in natural areas such
as national parks and wilderness areas and special emphasis is given to
protecting visibility in these areas. For more information on
visibility see the final 2004 PM AQCD as well as the 2005 PM Staff
Paper.413 414
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    \412\ National Research Council, 1993. Protecting Visibility in
National Parks and Wilderness Areas. National Academy of Sciences
Committee on Haze in National Parks and Wilderness Areas. National
Academy Press, Washington, DC. This document is available in Docket
EPA-HQ-OAR-2005-0161. This book can be viewed on the National
Academy Press Web site at http://www.nap.edu/books/0309048443/html/.
    \413\ U.S. EPA (2004) Air Quality Criteria for Particulate
Matter (Oct 2004), Volume I Document No. EPA600/P-99/002aF and
Volume II Document No. EPA600/P-99/002bF. This document is available
in Docket EPA-HQ-OAR-2005-0161.
    \414\ U.S. EPA (2005) Review of the National Ambient Air Quality
Standard for Particulate Matter: Policy Assessment of Scientific and
Technical Information, OAQPS Staff Paper. EPA-452/R-05-005. This
document is available in Docket EPA-HQ-OAR-2005-0161.
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    EPA is pursuing a two-part strategy to address visibility. First,
to address the welfare effects of PM on visibility, EPA has set
secondary PM2.5 standards which act in conjunction with the
establishment of a regional haze program. In setting this secondary
standard EPA has concluded that PM2.5 causes adverse effects
on visibility in various locations, depending on PM concentrations and
factors such as chemical composition and average relative humidity.
Second, section 169 of the Clean Air Act provides additional authority
to address existing visibility impairment and prevent future visibility
impairment in the 156 national parks, forests and wilderness areas
categorized as mandatory class I federal areas (62 FR 38680-81, July
18, 1997).\415\ In July 1999 the regional haze rule (64 FR 35714) was
put in place to protect visibility in mandatory class I federal areas.
Visibility can be said to be impaired in both PM2.5
nonattainment areas and mandatory class I federal areas.
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    \415\ These areas are defined in CAA section 162 as those
national parks exceeding 6,000 acres, wilderness areas and memorial
parks exceeding 5,000 acres, and all international parks which were
in existence on August 7, 1977.
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2. Atmospheric Deposition
    Wet and dry deposition of ambient particulate matter delivers a
complex mixture of metals (e.g., mercury, zinc, lead, nickel, aluminum,
cadmium), organic compounds (e.g., POM, dioxins, furans) and inorganic
compounds (e.g., nitrate, sulfate) to terrestrial and aquatic
ecosystems. The chemical form of the compounds deposited depends on a
variety of factors including ambient conditions (e.g., temperature,
humidity, oxidant levels) and the sources of the material. Chemical and
physical transformations of the particulate compounds occur in the
atmosphere as well as the media onto which they deposit. These
transformations in turn influence the fate, bioavailability and
potential toxicity of these compounds. Atmospheric deposition has been
identified as a key component of the environmental and human health
hazard posed by several pollutants including mercury, dioxin and
PCBs.\416\
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    \416\ U.S. EPA (2000) Deposition of Air Pollutants to the Great
Waters: Third Report to Congress. Office of Air Quality Planning and
Standards. EPA-453/R-00-0005. This document is available in Docket
EPA-HQ-OAR-2005-0161.
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    Adverse impacts on water quality can occur when atmospheric
contaminants deposit to the water surface or when material deposited on
the land enters a waterbody through runoff. Potential impacts of
atmospheric deposition to waterbodies include those related to both
nutrient and toxic inputs. Adverse effects to human health and welfare
can occur from the addition of excess particulate nitrate nutrient
enrichment, which contributes to toxic algae blooms and zones of
depleted oxygen, which can lead to fish kills, frequently in coastal
waters. Particles contaminated with heavy metals or other toxins may
lead to the ingestion of contaminated fish, ingestion of contaminated
water, damage to the marine ecology, and limits to recreational uses.
Several studies have been conducted in U.S. coastal waters and in the
Great Lakes Region in which the role of ambient PM deposition and
runoff is

investigated.417 418 419 420 421 In addition, the process of
acidification affects both freshwater aquatic and terrestrial
ecosystems. Acid deposition causes acidification of sensitive surface
waters. The effects of acid deposition on aquatic systems depend
largely upon the ability of the ecosystem to neutralize the additional
acid. As acidity increases, aluminum leached from soils and sediments,
flows into lakes and streams and can be toxic to both terrestrial and
aquatic biota. The lower pH concentrations and higher aluminum levels
resulting from acidification make it difficult for some fish and other
aquatic organisms to survive, grow, and reproduce.
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    \417\ U.S. EPA (2004) National Coastal Condition Report II.
Office of Research and Development/Office of Water. EPA-620/R-03/
002. This document is available in Docket EPA-HQ-OAR-2005-0161.
    \418\ Gao, Y., E.D. Nelson, M.P. Field, et al. 2002.
Characterization of atmospheric trace elements on PM2.5
particulate matter over the New York-New Jersey harbor estuary.
Atmos. Environ. 36: 1077-1086.
    \419\ Kim, G., N. Hussain, J.R. Scudlark, and T.M. Church. 2000.
Factors influencing the atmospheric depositional fluxes of stable
Pb, 210Pb, and 7Be into Chesapeake Bay. J. Atmos. Chem. 36: 65-79.
    \420\ Lu, R., R.P. Turco, K. Stolzenbach, et al. 2003. Dry
deposition of airborne trace metals on the Los Angeles Basin and
adjacent coastal waters. J. Geophys. Res. 108(D2, 4074): AAC 11-1 to
11-24.
    \421\ \\ Marvin, C.H., M.N. Charlton, E.J. Reiner, et al. 2002.
Surficial sediment contamination in Lakes Erie and Ontario: A
comparative analysis. J. Great Lakes Res. 28(3): 437-450.
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    Adverse impacts on soil chemistry and plant life have been observed
for areas heavily influenced by atmospheric deposition of nutrients,
metals and acid species, resulting in species shifts, loss of
biodiversity, forest decline and damage to forest productivity.
Potential impacts also include adverse effects to human health through
ingestion of contaminated vegetation or livestock (as in the case for
dioxin deposition), reduction in crop yield, and limited use of land
due to contamination. Research on effects of acid deposition on forest
ecosystems has come to focus increasingly on the biogeochemical
processes that affect uptake, retention, and cycling of nutrients
within these ecosystems. Decreases in available base cations from soils
are at least partly attributable to acid deposition. Base cation
depletion is a cause for concern because of the role these ions play in
acid neutralization and because calcium, magnesium and potassium are
essential nutrients for plant growth and physiology. Changes in the
relative proportions of these nutrients, especially in comparison with
aluminum concentrations, have been associated with declining forest
health.
    The deposition of airborne particles can reduce the aesthetic
appeal of buildings and culturally important articles through soiling
and can contribute directly (or in conjunction with other pollutants)
to structural damage by means of corrosion or erosion.\422\ Particles
affect materials principally by promoting and accelerating the
corrosion of metals, by degrading paints, and by deteriorating building
materials such as concrete and limestone. Particles contribute to these
effects because of their electrolytic, hygroscopic, and acidic
properties and their ability to adsorb corrosive gases (principally
sulfur dioxide). The rate of metal corrosion depends on a number of
factors, including: The deposition rate and nature of the pollutant;
the influence of the metal protective corrosion film; the amount of
moisture present; variability in the electrochemical reactions; the
presence and concentration of other surface electrolytes; and the
orientation of the metal surface.
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    \422\ \\ U.S. EPA (2005). Review of the National Ambient Air
Quality Standards for Particulate Matter: Policy Assessment of
Scientific and Technical Information, OAQPS Staff Paper. This
document is available in Docket EPA-HQ-OAR-2005-0161.
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3. Plant and Ecosystem Effects of Ozone
    Ozone contributes to many environmental effects, with impacts to
plants and ecosystems being of most concern. Ozone can produce both
acute and chronic injury in sensitive species depending on the
concentration level and the duration of the exposure. Ozone effects
also tend to accumulate over the growing season of the plant, so that
even lower concentrations experienced for a longer duration have the
potential to create chronic stress on vegetation. Ozone damage to
plants includes visible injury to leaves and a reduction in food
production through impaired photosynthesis, both of which can lead to
reduced crop yields, forestry production, and use of sensitive
ornamentals in landscaping. In addition, the reduced food production in
plants and subsequent reduced root growth and storage below ground can
result in other, more subtle plant and ecosystems impacts. These
include increased susceptibility of plants to insect attack, disease,
harsh weather, interspecies competition and overall decreased plant
vigor. The adverse effects of ozone on forest and other natural
vegetation can potentially lead to species shifts and loss from the
affected ecosystems, resulting in a loss or reduction in associated
ecosystem goods and services. Last, visible ozone injury to leaves can
result in a loss of aesthetic value in areas of special scenic
significance like national parks and wilderness areas. The final 2006
Ozone Air Quality Criteria Document presents more detailed information
on ozone effects on vegetation and ecosystems.
4. Welfare Effects of Air Toxics
    Fuel combustion emissions contribute to ambient levels of
pollutants that contribute to adverse effects on vegetation. PAN is a
well-established phytotoxicant causing visible injury to leaves that
can appear as metallic glazing on the lower surface of leaves with some
leafy vegetables exhibiting particular sensitivity (e.g., spinach,
lettuce, chard).423 424 425 PAN has been demonstrated to
inhibit photosynthetic and non-photosynthetic processes in plants and
retard the growth of young navel orange trees.426 427 In
addition to its oxidizing capability, PAN contributes nitrogen to
forests and other vegetation via uptake as well as dry and wet
deposition to surfaces. As noted in Section X, nitrogen deposition can
lead to saturation of terrestrial ecosystems and research is needed to
understand the impacts of excess nitrogen deposition experienced in
some areas of the country on water quality and ecosystems.\428\
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    \423\ Nouchi I, S Toyama. 1998. Effects of ozone and
peroxyacetyl nitrate on polar lipids and fatty acids in leaves of
morning glory and kidney bean. Plant Physiol. 87:638-646.
    \424\ Oka E, Y Tagami, T Oohashi, N Kondo. 2004. A physiological
and morphological study on the injury caused by exposure to the air
pollutant, peroxyacetyl nitrate (PAN), based on the quantitative
assessment of the injury. J Plant Res. 117:27-36.
    \425\ Sun E-J, M-H Huang. 1995. Detection of peroxyacetyl
nitrate at phytotoxic level and its effects on vegetation in Taiwan.
Atmos. Env. 29:2899-2904.
    \426\ Koukol J, WM Dugger, Jr., RL Palmer. 1967. Inhibitory
effect of peroxyacetyl nitrate on cyclic photophosphorylation by
chloroplasts from black valentine bean leaves. Plant Physiol.
42:1419-1422.
    \427\ Thompson CR, G Kats. 1975. Effects of ambient
concentrations of peroxyacetyl nitrate on navel orange trees. Env.
Sci. Technol. 9:35-38.
    \428\ \\ Bytnerowicz A, ME Fenn. 1995. Nitrogen deposition in
California forests: A Review. Environ. Pollut. 92:127-146.
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    Volatile organic compounds (VOCs), some of which are considered air
toxics, have long been suspected to play a role in vegetation
damage.\429\ In laboratory experiments, a wide range of tolerance to
VOCs has been observed.\430\ Decreases in harvested seed pod weight

have been reported for the more sensitive plants, and some studies have
reported effects on seed germination, flowering and fruit ripening.
Effects of individual VOCs or their role in conjunction with other
stressors (e.g., acidification, drought, temperature extremes) have not
been well studied. In a recent study of a mixture of VOCs including
ethanol and toluene on herbaceous plants, significant effects on seed
production, leaf water content and photosynthetic efficiency were
reported for some plant species.\431\
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    \429\ U.S. EPA. 1991. Effects of organic chemicals in the
atmosphere on terrestrial plants. EPA/600/3-91/001.
    \430\ Cape JN, ID Leith, J Binnie, J Content, M Donkin, M
Skewes, DN Price, AR Brown, AD Sharpe. 2003. Effects of VOCs on
herbaceous plants in an open-top chamber experiment. Environ.
Pollut. 124:341-343.
    \431\ Cape JN, ID Leith, J Binnie, J Content, M Donkin, M
Skewes, DN Price, AR Brown, AD Sharpe. 2003. Effects of VOCs on
herbaceous plants in an open-top chamber experiment. Environ.
Pollut. 124:341-343.
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    Research suggests an adverse impact of vehicle exhaust on plants,
which has in some cases been attributed to aromatic compounds and in
other cases to nitrogen oxides.432 433 434 The impacts of
VOCs on plant reproduction may have long-term implications for
biodiversity and survival of native species near major roadways. Most
of the studies of the impacts of VOCs on vegetation have focused on
short-term exposure and few studies have focused on long-term effects
of VOCs on vegetation and the potential for metabolites of these
compounds to affect herbivores or insects.
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    \432\ Viskari E-L. 2000. Epicuticular wax of Norway spruce
needles as indicator of traffic pollutant deposition. Water, Air,
and Soil Pollut. 121:327-337.
    \433\ Ugrekhelidze D, F Korte, G Kvesitadze. 1997. Uptake and
transformation of benzene and toluene by plant leaves. Ecotox.
Environ. Safety 37:24-29.
    \434\ Kammerbauer H, H Selinger, R Rommelt, A Ziegler-Jons, D
Knoppik, B Hock. 1987. Toxic components of motor vehicle emissions
for the spruce Pciea abies. Environ. Pollut. 48:235-243.
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VIII. Impacts on Cost of Renewable Fuels, Gasoline, and Diesel

    We have assessed the impacts of the renewable fuel volumes required
by EISA on their costs and on the costs of the gasoline and diesel
fuels into which the renewable fuels will be blended. More details of
feedstock costs are addressed in Section X.A.

A. Renewable Fuel Production Costs

1. Ethanol Production Costs
a. Corn Ethanol
    A significant amount of work has been done in the last decade
surveying and modeling the costs involved in producing ethanol from
corn in order to serve business and investment purposes as well as to
try to educate energy policy decisions. Corn ethanol costs for our work
were estimated using models developed and maintained by USDA. Their
work has been described in a peer-reviewed journal paper on cost
modeling of the dry-grind corn ethanol process, and compares well with
cost information found in surveys of existing plants.435 436
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    \435\ Kwaitkowski, J.R., Macon, A., Taylor, F., Johnston, D.B.;