***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

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## Chapter 6: **Health and Envir onmental Impacts**  6.1 **Health and Environmental Effects o f**  **Non -**  **GHG Pollutants** 6.1.1 Health Effects Associated with Exposure to Non - GHG Pollutants In this section we will discuss the health effects associated with non - GHG pollutants, specificall y: particulate matter, ozone, nitrogen oxides (NO X ), sulfur oxides (SO X ), carbon monoxide and air toxics. These pollutants will not be directl y regulated b y the standards, but the standards wi ll affect emissions of these pollutants and precursors. 

### 6.1.1.1 Particulate Matter 6.1.1.1.1 Background on Particulate Matter Particulate matter (PM) is a highl y complex mixture of solid particles and liquid droplets distributed among numerous atmospheric gases which int eract with solid and liquid phases. Particles range in size from those smaller than 1 nanometer (10 - 9 meter) to over 100 micrometer (μm, or 10 - 6 meter) in diameter (for reference, a typical strand of human hair is 70 μm in diameter and a grain of salt is a bout 100 μm). Atmospheric particles can be grouped into several classes according to their aerodynamic and ph ys ical sizes . Generall y, the three broad classes of particles considered b y EPA includ e ultrafine particles (UFP, aerodyn amic diameter <0.1 μm), “ fine ” particles ( PM 2.5 ; particles with a nominal mean aerodynamic diam e ter less than or equal to 2.5 μm), and “thoracic” particles ( PM 10 ; particles with a nominal mean aerody namic diam e ter less than or equal to 10 μm ). Particles that fall within the size range between PM 2.5 and PM 10 , are referred to as “thoracic coarse particles” (PM 10 - 2.5, particles with a nominal mean aerodynamic diameter less than or equal to 10 μm and greater than 2.5 μm ) . EPA currentl y has standards that regulate PM 2.5 and PM 10 . A P articles span man y sizes and shapes and may consist of hundreds of different chemicals . Particles are emitted directly from sources and are also formed through atmospheric chemical reactions; the former are often referred to as “primary” particles, and th e latter as “secondary” particles. Particle concentration and composition varies b y time of ye ar and location , and in addition to differences in source emissions, is affected by several weather - related factors, such as temperature, clouds, humidity , and w ind. A further layer of complexity comes from particles ’ ability to shift between solid/liquid and gaseous phases, which is influenced by concentration and meteorology , especially temperature. Fine particles are produced primaril y b y combustion processes and b y transformations of gaseous emissions (e.g., sulfur oxides ( SO X ) , nitrogen oxides (NO X ) and volatile organic compounds ( VOCs ) ) in the atmosphere. The chemical and physical properties of P M 2.5 may A Regulatory definitions of PM size fractions, and information on reference and equivalent methods for measuring PM in ambient air, are provided in 40 CFR Parts 50, 53, and 58. With regard to national ambient air quality standards (NAAQS) which provide protection against health and welfare effects, the 24 - hour PM 10 standard provides protection against effects associated with short - term exposure to thoracic coarse particles (i.e., PM 10 - 2.5 ).***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 2 vary greatly with time, region, meteorology , and source category . Thus, PM 2.5 may include a complex mixture of different components including sulfates, nitrates, organic compounds, elemental carbon and metal compounds. These particles can remain in the atmosphere for day s to weeks and travel through the atmosphere hundreds to thousands of kilometers. 1 

### 6.1.1.1.2 Health Effects o f Particulate Matter Scientific studies show ambient PM is associated with a broad range of health effects. These health effect s are discussed in detail in the December 2009 Integrated Science Assessment for Particulate Matter (PM I SA) . 2 The PM IS A summarizes health effects evidence associated with both short - and long - term exposures to PM 2.5 , PM 10 - 2.5 , and ultrafine particles. The PM I SA concludes that human exposures to ambient PM 2.5 concentrations are associated with a number of adverse health effects and characterizes the weight of evidence for these health outcomes. B The discussion below highlights the PM I SA’s conclusion s pertaining to health effects associated with both short - and long - term PM exposures. Further discussion of health effects associated with PM 2.5 can also be found in the rulemaking documents for the most recent review of the PM NAAQS completed in 2012 . 3 , 4 EPA has concluded that a causal relationship exists between both long - and short - term exposures to PM 2.5 and premature mortality and cardiovascular effects and a likely causal relationship exists between long - and short - term PM 2.5 exposures and respirato ry effects. Further, there is evidence suggestive of a causal relationship between long - term PM 2.5 exposures and other health effects, including developmental and reproductive effects (e.g., low birth weight, infant mortality) and carcinogenic, mutagenic, and genotoxic effects (e.g., lung cancer mortality). C As summarized in the Final PM NAAQS rule, and discussed extensively in the 2009 PM ISA, the available scientific evidence significantl y strengthens the link between long - and short term exposure to PM 2 .5 and premature mortality, while providing indications that the magnitude of the PM 2.5 - mortality

association with long - term exposures may be larger than previously estimated. 5 , 6 The strongest evidence comes from recent studies investigating long - term exposure to PM 2.5 and cardiovascular - related mortalit y. The evidence supporting a causal relationship between long - term PM 2.5 exposure and mortality also includes consideration of new studies that demonstrated an improvement in community health following reductions in ambient fine particles. 7

B The causal framework draws upon the assessment and integration of evidence from across epidemiological, controlled human exposure, and toxicological studies, and the related uncertainties that ultimately influence our understanding of the evidence. This framework employs a five - level hierarchy that classifies the overall weight of evidence and causality using the following categorizations: causal relationship, likely to be causal relationship, suggestive of a causal relationship, inadequate to infer a cau sal relationship, and not likely to be a causal relationship (U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F, Table 1

– 3). C These causal inferences are based not only on the more expansive epidemiological evidence available in this review of the PM NAAQS but also reflect consideration of important progress that has been made to advance understanding of a number of potential bi ologic modes of action or pathways for PM - related cardiovascular and respiratory effects (U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F, Chapt er 5).***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 3 Several studies evaluated in the 2009 PM I SA have examined the association between card iovascular effects and long - term PM 2.5 exposures in multi - city studies conducted in the U.S. and Europe. Thes e studies have provided new evidence linking long - term exposure to PM 2.5 with an array

of cardiovascular effects such as heart attacks, congestive heart failure, stroke, and mortality . This evidence is coherent with studies of short - term exposure to PM 2.5 that have observed associations with a continuum of effects ranging from subtle changes in indicators of cardiovascular health to serious clinical events, such as increased hospitalizations and emergency department visits due to cardiovascular disease and cardiovascular mortality. 8 As detailed in the 2009 PM I SA, extended anal ys es of seminal epidemiological studies , as well as more recent epidemiol ogical studies conducted in the U.S. and abroad , provide strong evidence of respiratory - related morbidity effects associated with long - term PM 2.5 exposure. The strongest evidence for respiratory - related effects is from studies that evaluated decrements in lung function growth (in children), increased respiratory s ymptoms, and asthma development. The strongest evidence from short - term PM 2.5 exposure studies has been observed for increased respiratory - related emergency department visits and hospital admissi ons for chronic obstructive pulmonary

disease (COPD) and respiratory infections. 9 The body of scientific evidence detailed in the 2009 PM I SA is still limited with respect to associations between long - term PM 2.5 exposures and developmental and reproductive effects as well as cancer, mutagenic, and genotoxic effects . The strongest evidence for an association between PM 2.5 and developmental and reproductive effects comes from epidemiological studies of low birth weight and infant mortality , especially due to respiratory

causes during the post neonatal period (i.e., 1 month to 12 months of age). With regard to cancer effects, ‘‘[m]ultiple epidemiologic studies have shown a consistent positive association between PM 2.5 and lung cancer mortality , but studies have generall y not reported associations between PM 2.5 and lung cancer incidence.’’ 10 , 11 Specific groups within the general population are at increased risk for experiencing adverse health effects related to PM exposures. 12 , 13 , 14 , 15 The evidence detailed in the 2009 PM ISA expands our understanding of previousl y identified at - risk populations and lifestages (i.e., children, older adults, and individuals with pre - existing heart and lung disease) and supports the identification of add itional at - risk populations (e.g., persons with lower socioeconomic status, genetic differences). Additionally , there is emerging, though still limited, evidence for additional potentially

at - risk populations and lifestages , such as those with diabetes, p eople who are obese, pregnant women, and the developing fetus. 16 For PM 10 - 2.5 , the 2009 PM I SA conclude d that available evidence was suggestive of a causal relationship between short - term exposures to PM 10 - 2.5 and cardiovascular effects (e.g., hospital admissions and ED visits, changes in cardiovascular function), respiratory effects ( e.g. , ED visits and hospital admissions, increase in markers of pulmonary inflammation), and premature mortality . Data we re ina dequate to draw conclusions regarding the relationships between long - term exposure to PM 10 - 2. 5 and various health effects. 17 , 18 , 19 For ultrafine particles, the 2009 PM I SA conclude d that the evidence wa s suggestive of a causal relationship between short - term exposures and cardiovascular effects, including changes in heart rh ythm and vasomotor function (the ability of blood vessels to expand and contract) . It***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 4 also conclude d that there wa s evidence suggestive of a causal relationship between short - term exposur e to ultrafine particles and respiratory effects , including lung function and pulmonary inflammation, with limited and inconsistent evidence for increases in ED visits and hospital admissions . Data we re inadequate to draw conclusions regarding the relatio nship between short term exposure to ultrafine particle and additional health effects including premature mortality as well as long - term exposure to ultrafine particles and all health outcomes evaluated . 20 , 21 

### 6.1.1.2 Ozone 6.1.1.2.1 Background on Ozone Ground - level ozone pollution is ty pically formed through reaction s involving VOCs and NO X in the lower atmosphere in the presence of sunlight. These pollutants, often referred to as ozone precursors, are emitted by man y t ypes of pollution sources such as highway and nonroad motor vehicles and engines, power plants, chemical plants, refineries, makers of consumer and commercial products, industrial facilities, and smaller area sources. The science of ozone formation, transport, and accumulation is complex. Ground - level ozone is produced and destroyed in a cyclical set of chemical reactions, many of which are sensitive to temperature and sunlight. When ambient temperatures and sunlight levels remain high for several day s and the air is relativel y stagnant, ozone and its precursors can build up and result in more ozone than ty picall y occurs on a single high - temperature day. Ozone and its precursors can be transported hundreds of miles downwind of precursor emissions, resulting in elevated ozone levels even in areas with low VOC or NO X emissions. The highest levels of ozone are produced when both VOC and NO X emissions are present in significant quantities on clear summer day s. Relatively small amounts of NO X enable ozone to form rapidly

when VOC levels are relativel y high, but ozone production is quickly limited by removal of the NO X . Under these conditions NO X reductions are highl y effective in reducing ozone while VOC reductions have little effect. Such conditions are called “NO X - limited.” Because the c ontribution of VOC emissions from biogenic (natural) sources to local ambient ozone concentrations can be significant, even some areas where man - made VOC emissions are relativel y low can be NO X - limited. Ozone concentrations in an area also can be lowered b y the reaction of nitric oxide (NO) with ozone, forming nitrogen dioxide (NO 2 ) . A s the air moves downwind and the cycle continues, the NO 2 forms additional ozone. The importance of this reaction depends, in part, on the relative concentrations of NO X , VO C, and ozone, all of which change with time and location. When NO X levels are relatively high and VOC levels relativel y low, NO X forms inorganic nitrates (i.e., particles) but relatively little ozone. Such conditions are called “VOC - limited . ” Under thes e conditions, VOC reductions are effective in reducing ozone, but NO X reductions can actuall y increase local ozone under certain circumstances. Even in VOC - limited urban areas, NO X reductions are not expected to increase ozone levels if the NO X reductions are sufficientl y large. Rural areas are usually NO X - limited, due to the relativel y large amounts of biogenic VOC emissions in such areas. Urban areas can be either VOC - or NO X - limited, or a mixture of both, in which ozone levels exhibit moderate sensiti vity to changes in either pollutant.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

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### 6.1.1.2.2 Health Effects o f Ozone This section provides a summary of the health effects associated with exposure to ambient concentrations of ozone . D The information in this section is based on the information and conclusions in the February 2013 Integrated Science Assessment for Ozone (Ozone I SA) . 22 The Ozone I SA concludes that human exposures to ambient concentrations of ozone are associated with a number of adverse health effects and characterizes the weight of evidence for these health effects. E The discussion below highlights the Ozone I SA’s conclusions pertaining to health effects associated with both short - term and long - term periods of exposure to ozone. For short - term exposure to ozone, the Ozone I SA c oncludes that respiratory effects, including lung function decrements, pulmonary inflammation, exacerbation of asthma, respiratory - related hospital admissions, and mortality , are causally associated with ozone exposure. It also concludes that cardiovascul ar effects, including decreased cardiac function and increased vascular disease, and total mortality are likely to be causall y associated with short - term exposure to ozone and that evidence is suggestive of a causal relationship between central nervous s ys tem effects and short - term exposure to ozone. For long - term exposure to ozone, the Ozone I SA concludes that respiratory effects, including new onset asthma, pulmonary inflammation and injury , are likel y to be causall y related with ozone exposure. The Oz one I SA characterizes the evidence as suggestive of a causal relationship for associations between long - term ozone exposure and cardiovascular effects, reproductive and developmental effects, central nervous sy stem effects and total mortality . The evidenc e is inadequate to infer a causal relationship between chronic ozone exposure and increased risk of lung cancer. Finally , interindividual variation in human responses to ozone exposure can result in some groups being at increased risk for detrimental effec ts in response to exposure. The Ozone ISA identified several groups that are at increased risk for ozone - related health effects. These groups are people with asthma, children and older adults, individuals with reduced intake of certain nutrients (i.e., V itamins C and E), outdoor workers, and individuals having certain genetic variants related to oxidative metabolism or inflammation. Ozone exposure during childhood can have lasting effects through adulthood. Such effects include altered function of the r espiratory

and immune sy stems. Children absorb higher doses (normalized to lung surface area) of ambient ozone, compared to adults, due to their increased time spent outdoors, higher ventilation rates relative to body size, and a tendency

to breathe a gre ater fraction of air through the mouth. Children also have a higher asthma prevalence compared to adults. Additional children’s vulnerability

and susceptibility

factors are listed in Section XIV of the preamble.

D Human exposure to ozone varies over time due to changes in ambient ozone concentration and because people mo ve between locations which have notable different ozone concentrations. Also, the amount of ozone delivered to the lung is not only influe nced by the ambient concentrations but also by the breathing route and rate. E The ISA evaluates evidence and draw s conclusions on the causal relationship between relevant pollutant exposures and health effects, assigning one of five “weight of evidence” d eterminations: causal relationship, likely to be a causal relationship, suggestive of a causal relationship, inadequate to infer a causal relationship, and not likely to be a causal relationship. For more information on these levels of evidence, please r efer to Table II in the Preamble of the ISA.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

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### 6.1.1.3 Nitrogen Oxides 6.1.1.3.1 Background on Nitrogen Ox ides Nitrogen dioxide (NO 2 ) is a member of the nitrogen oxide (NO X ) famil y of gases. Most NO 2 is formed in the air through the oxidation of nitric oxide (NO) emitted when fuel is burned at a high temperature. NO 2 and its gas phase oxidation products can dissolve in water droplets and further oxidize to form nitric acid which react s with ammonia to form nitrates, which are important components of ambient PM. The health effects of ambient PM are discussed in Chapter 6.1.1.1.2 . NO X along with VOCs are the two major precursors of ozone. The health effects of ozone are covered in Chapter 6.1.1.2.2 . 

### 6.1.1.3.2 Health Effects o f Nitrogen Oxides The most recent review of the health effects of oxides of nitrogen completed by EPA can be found in the 2008 Integrated Science Assessment for Oxides of Nitrogen

– Health Criteria ( Oxides of Nitrogen IS A) . 23 EPA concluded that the findings of epidemiologic al , controlled human exposure, and animal toxicological studies provide d evidence that wa s sufficient to infer a likely causal relationship between respiratory effects and short - term NO 2 expo sure. The 2008 ISA for Oxides of Nitrogen conclude d that the strongest evidence for such a relationship comes from epidemiologic al studies of respiratory effects including increased respiratory sy mptoms, emergency

department visits, and hospital admission s. Based on both short - and long - term exposure studies, the 2008 I SA for Oxides of Nitrogen concluded that individuals with preexisting pulmonary

conditions (e.g., asthma or COPD), children, and older adults are potentially

at greater risk of NO 2 - related respiratory effects. Based on findings from controlled human exposure studies , the 2008 IS A for Oxides of Nitrogen also dr e w two broad conclusions regarding airway

responsiveness following NO 2 exposure. First, the NO X ISA conclude d that NO 2 exposure may

enhance the sensitivity

to allergen - induced decrements in lung function and increase the allergen - induced airway inflammatory

response following 30 - minute exposures of asthmatic adult s to NO 2 concentrations as low as 26 0 pp b . 24 Second, exposure to NO 2 was found to enhance the inherent responsiveness of the airway to subsequent nonspecific challenges in controlled human exposure s tudies of healthy and asthmatic adults. S tatistically significant increases in nonspecific airway responsiveness we re reported for asthmatic adults following 30 - minute exposures to 200 - 300 ppb NO 2 and following 1 - hour exposures to 1 00 pp b NO 2 . 25 Enhanced airway

responsiveness could have important clinical implications for asthmatics since transient increases in airway responsiveness following NO 2 exposure have the potential to increase sy

mptoms and worsen asthma control. Together, the epidemiol ogic al and experimental data sets form ed a plausible, consistent, and coherent description of a relationship between NO 2 exposures and an array

of adverse health effects that range from the onset of respiratory sy mptoms to hospital admission s and emergency department visits for respiratory causes, especiall y asthma . 26 In evaluating a broader range of health effects, the 2008 I SA for Oxides of Nitrogen concluded evidence was “suggestive but not sufficient to infer a causal relationship” between short - term N O 2 exposure and premature mortality and between long - term NO 2 exposure and respiratory

effects. The latter was based largel y on associations observed between long - term NO 2 exposure and decreases in lung function growth in children. Furthermore, the 2008 ISA for***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 7 Oxides of Nitrogen concluded that evidence was “inadequate to infer the presence or absence of a causal relationship” between short - term NO 2 exposure and cardiovascular effects as well as between long - term NO 2 exposure and cardiovascular effects, r eproductive and developmental effects, premature mortality , and cancer. 27 The conclusions for these health effect categories were informed b y uncertainties in the evidence base such as the independent effects of NO 2 exposure within the broader mixture of traffic - related pollutants, limited evidence from experimental studies, and/or an overall limited literature base. 

### 6.1.1.4 Sulfur Oxides 6.1.1.4.1 Background Sulfur dioxide (SO 2 ), a member of the sulfur oxide (SO X ) family of gases, is formed from burning fuels containing sulfur (e.g., coal or oil), extracting gasoline from oil, or extracting metals from ore. SO 2 and its gas phase oxidation products can dissolve in water droplets and further oxidize to form sulfuric acid which react s with ammonia to form sulfates, which ar e important components of ambient PM. The health effects of ambient PM are discussed in Chapter 6.1.1.1.2 . 

### 6.1.1.4.2 Health Effects o f Sulfur Oxides This section provides an overview of the health effects associated with SO 2 . Additional information on the health effects of SO 2 can be found in the 2008 Integrated Science Assessment for Sulfur Oxides

– Health Criteria (SO X ISA) . 28 Following an extensive evaluation of health evidence from epidemiologic and laboratory studies, EPA has concluded that there is a causal relationship between respiratory health effects and short - term exposure to SO 2 . The immediate effect of SO 2 on the re spiratory s ys tem in humans is bronchoconstriction. Asthmatics are more sensitive to the effects of SO 2 likely resulting from preexisting inflammation associated with this disease. In addition to those with asthma (both children and adults), potentially s ensitive groups include all children and the elderl y. In free - breathing laboratory studies involving controlled human exposures to SO 2 , respiratory effects have consistently been observed following 5 - 10 min exposures at SO 2 concentrations ≥ 400 pp b in asthmatics engaged in moderate to heav y levels of exercise , with respiratory effects occurring at concentrations as low as 200 ppb in some asthmatics . A clear concentration - response relationship has been demonstrated in these studies following exposures to S O 2 at concentrations between 2 00 and 10 00 pp b , both in terms of increasing severit y of respiratory s ymptoms and decrements in lung function, as well as the percentage of asthmatics adversel y affected. In epidemiologic studies, respiratory effects have bee n observed in areas where the mean 24 - hour SO 2 levels range from 1 to 30 ppb, with maximum 1 to 24 - hour average SO 2 values ranging from 12 to 75 ppb. Important new multicity studies and several other studies have found an association between 24 - hour avera ge ambient SO 2 concentrations and respiratory s ymptoms in children, particularly

those with asthma. Generally consistent associations also have been observed between ambient SO 2 concentrations and emergency department visits and hospitalizations for all r espiratory causes, particularly

among children and older adults ( ≥ 65 ye ars), and for asthma. A limited subset of epidemiologic studies ha s examined potential confounding b y copollutants using multipollutant regression models. These anal ys es indicate***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 8 that although copollutant adjustment has varying degrees of influence on the SO 2 effect estimates, the effect of SO 2 on respiratory health outcomes appears to be generall y robust and independent of the effects of gaseous and particulate copollutants, suggesti ng that the observed effects of SO 2 on respiratory endpoints occur independent of the effects of other ambient air pollutants. Consistent associations between short - term exposure to SO 2 and mortality have been observed in epidemiologic studies, with large r effect estimates reported for respiratory mortalit y than for cardiovascular mortality . While this finding is consistent with the demonstrated effects of SO 2 on respiratory

morbidity , uncertaint y remains with respect to the interpretation of these observ ed mortalit y associations due to potential confounding b y various copollutants. Therefore, EPA has concluded that the overall evidence is suggestive of a causal relationship between short term exposure to SO 2 and mortality . Significant associations between short - term exposure to SO 2 and emergency department visits and hospital admissions for cardiovascular diseases have also been reported. However, these findings have been inconsistent across studies and do not provide adequate evidence to infer a c ausal relationship between SO 2 exposure and cardiovascular morbidity. 

### 6.1.1.5 Carbon Monoxide 6.1.1.5.1 Background Carbon monoxide (CO) is a colorless, odorless gas emitted from combustion processes. Nationally

and, particularly

in urban areas, the majority of CO emissions to ambient air come from mobile sources. 

### 6.1.1.5.2 Health Effects of Carbon Monoxide In formation on the health effects of carbon monoxide (C O ) can be found in the January 2010 Integrated Science Assessment for Carbon Monoxide (CO I SA) . 29 The CO I SA concludes that ambient concentrations of CO are associated with a number of adverse health effects. F This section provides a summary of the health effects associated with exposure to ambient concentrations of CO . G Controlled human exposure studies of subjects with coro nary artery disease show a decrease in the time to onset of exercise - induced angina (chest pain) and electrocardiogram changes following CO exposure. In addition, epidemiologic studies show associations between short - term CO exposure and cardiovascular mo rbidity , particularl y increased emergency room visits and hospital admissions for coronary heart disease (including ischemic heart disease,

F The ISA evaluates the health evidence associated with different health effects, assigning one of five “weight of evidence” determinations: causal relationship, likely to be a causal relationship, suggestive of a causal relationship, inadequate to infer a causal relationship, and not likely to be a causal relationship. For definitions of these levels of evidence, please refer to Section 1.6 of the ISA. G Personal exposure includes contributions from many s ources, and in many different environments. Total personal exposure to CO includes both ambient and non - ambient components; and both components may contribute to adverse health effects.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 9 myocardial infarction, and angina). Some epidemiologic evidence is also available for increased hospital admissions and emergency room visits for congestive heart failure and cardiovascular disease as a whole. The CO I SA concludes that a causal relationship is likely to exist between short - term exposures to CO and cardiovascular morbidity . It also concludes that avai lable data are inadequate to conclude that a causal relationship exists between long - term exposures to CO and cardiovascular morbidity . Animal studies show various neurological effects with in - utero CO exposure. Controlled human exposure studies report central nervous s ys tem and behavioral effects following low - level CO exposures, although the findings have not been consistent across all studies. The CO I SA concludes the evidence is suggestive of a causal relationship with both short - and long - term expo sure to CO and central nervous s ys tem effects. A number of studies cited in the CO I SA have evaluated the role of CO exposure in birth outcomes such as preterm birth or cardiac birth defects. The epidemiologic studies provide limited evidence of a CO - indu ced effect on preterm births and birth defects, with weak evidence for a decrease in birth weight. Animal toxicological studies have found perinatal CO exposure to affect birth weight, as well as other developmental outcomes. The CO ISA concludes the evi dence is suggestive of a causal relationship between long - term exposures to CO and developmental effects and birth outcomes. Epidemiologic studies provide evidence of associations between ambient CO concentrations and respiratory morbidity

such as changes in pulmonary function, respiratory sy mptoms, and hospital admissions. A limited number of epidemiologic studies considered copollutants such as ozone, SO 2 , and PM in two - pollutant models and found that CO risk estimates were generall y robust, although thi s limited evidence makes it difficult to disentangle effects attributed to CO itself from those of the larger complex air pollution mixture. Controlled human exposure studies have not extensively evaluated the effect of CO on respiratory morbidity . Anima l studies at levels of 50 - 100 ppm CO show preliminary evidence of altered pulmonary

vascular remodeling and oxidative injury . The CO ISA concludes that the evidence is suggestive of a causal relationship between short - term CO exposure and respiratory morb idit y, and inadequate to conclude that a causal relationship exists between long - term exposure and respiratory

morbidit y. Finally , the CO I SA concludes that the epidemiologic evidence is suggestive of a causal relationship between short - term concentratio ns of CO and mortality . Epidemiologic studies provide evidence of an association between short - term exposure to CO and mortality , but limited evidence is available to evaluate cause - specific mortality outcomes associated with CO exposure. In addition, th e attenuation of CO risk estimates which was often observed in copollutant models contributes to the uncertainty as to whether CO is acting alone or as an indicator for other combustion - related pollutants. The CO I SA also concludes that there is not likel y to be a causal relationship between relevant long - term exposures to CO and mortality .***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

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### 6.1.1.6 Diesel Exhaust 6.1.1.6.1 Background on Diesel Exhaust Diesel exhaust consists of a complex mixture composed of carbon dioxide, oxygen, nitrogen, water vapor, carbon monoxide, nitrogen compounds, sulfur compounds and numerous low - molecular - weight h ydrocarbons. A number of these gaseous h ydrocarbon components are individually

known to be toxic, including aldehydes, benzene and 1,3 - butadiene. The diesel particulate matter present in diesel exhaust consists mostly of fine particles (< 2.5 μm), of which a significant fraction is ultrafine particles (< 0.1 μm). T hese particles have a large surface area which makes them an excellent medium for adsorbing organics and their small size makes them highl y respirable. Man y of the organic compounds present in the gases and on the particles, such as polycyclic organic matter, are individuall y known to have mutagenic and carcinogenic properties. Diesel exhaust varies significantly in chemical composition and particle sizes between different engine t ypes (heav y - dut y, light - duty), engine operating conditions (idle, accelerate, decelerate), and fuel formulations (high/low sulfur fuel). Also, there are emissions differences between on - road and nonroad engines because the nonroad engines are generally of older technology . After being emitted in the engine exhaust, diesel exhaust undergoes dilution as well as chemical and ph ys ical changes in the atmosphere. The lifetime for some of the compounds present in diesel exhaust ranges from hours to days. 

### 6.1.1.6.2 Health Effects of Diesel Exhaust In EPA’s 2002 Diesel Health Assessment Document (Diesel HAD), exposure to diesel exhaust was classified as likely to be carcinogenic to humans by inhalation from environmental exposures, in accordance with the revised draft 1996/1999 EPA cancer guidelines. 30 , 31 A number of other agencies (National Insti tute for Occupational Safet y and Health, the International Agency for Research on Cancer, the World Health Organization, California EPA, and the U.S. Department of Health and Human Services) had made similar hazard classifications prior to 2002. EPA also concluded in the 2002 Diesel HAD that it was not possible to calculate a cancer unit risk for diesel exhaust due to limitations in the exposure data for the occupational groups or the absence of a dose - response relationship. In the absence of a cancer uni t risk, the Diesel HAD sought to provide additional insight into the significance of the diesel exhaust cancer hazard by estimating possible ranges of risk that might be present in the population. An exploratory analysis was used to characterize a range o f possible lung cancer risk. The outcome was that environmental risks of cancer from long - term diesel exhaust exposure s could plausibly range from a s low as 10 - 5 to as high as 10 - 3 . Because of uncertainties, the anal ys is acknowledged that the risks could be lower than 10 - 5 , and a zero risk from diesel exh aust exposure could not be ruled out. Noncancer health effects of acute and chronic exposure to diesel exhaust emissions are also of concern to EPA. EPA derived a diesel exhaust reference concentration ( RfC) from consideration of four well - conducted chronic rat inhalation studies showing adverse pulmonary effects. The RfC is 5 μg/m 3 for diesel exhaust measured as diesel particulate matter. This RfC***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 11 does not consider allergenic effects such as those asso ciated with asthma or immunologic or the potential for cardiac effects. There was emerging evidence in 2002, discussed in the Diesel HAD, that exposure to diesel exhaust can exacerbate these effects, but the exposure - response data were lacking at that tim e to derive an RfC based on these then emerging considerations. The Diesel HAD states, “With [diesel particulate matter] being a ubiquitous component of ambient PM, there is an uncertainty about the adequacy of the existing [diesel exhaust] noncancer data

base to identify

all of the pertinent [diesel exhaust] - caused noncancer health hazards.” The Diesel HAD also notes “that acute exposure to [diesel exhaust] has been associated with irritation of the eye, nose, and throat, respiratory s ymptoms (cough and p hlegm), and neuroph ys iological sy mptoms such as headache, lightheadedness, nausea, vomiting, and numbness or tingling of the extremities.” The Diesel HAD noted that the cancer and noncancer hazard conclusions applied to the general use of diesel engines t hen on the market and as cleaner engines replace a substantial number of existing ones, the applicability of the conclusions would need to be reevaluated. It is important to note that the Diesel HAD also briefly summarizes health effects associated with ambient PM and discusses EPA’s then - annual PM 2.5 NAAQS of 15 μg/m 3

. In 2012, EPA revised the annual PM 2.5 NAAQS to 12 μg/m 3

. There is a large and extensive body of human data showing a wide spectrum of adverse health effects associated with exposure to ambient PM, of which diesel exhaust is an important component. The PM 2.5 NAAQS is designed to provide protection from the noncancer health effects and premature mortality attributed to exposure to PM 2.5 . The contribution of diesel PM to total ambient PM varies in different regions of the country and also, within a region, from one area to another. The contribution can be high in near - roadway environments , for example , or in other location s where diesel engine use is concentrated. Since 2002, several new studies have been published which continue to report increased lung cancer risk with occupational exposure to diesel exhaust from older engine s . Of particular note since 2011 are three new epidemiology studies which have examined lung cancer in occupation al populations, for example, truck drivers, underground nonmetal miners and other diesel motor related occupations. These studies reported increased ris k of lung cancer with exposure to diesel exhaust with evidence of positive exposure - response relationships to varying degrees. 32 , 33 , 34 These newer studies (along with others that have appeared in the scientific literature) add to the evidence EPA evaluated in the 2002 Diesel HAD and further reinforce s the concern that diesel exhaust exposure likely poses a lung cancer hazard. The findings from these newer studies do not necessarily appl y to newer technology diesel engines since the newer engines have large reductions in the emission constituents compared to older technology diesel engines . In light of the growing body of scientific literature evaluating the health effects of exposure to diesel exhaust, i n June 2012 the World Health Organization’s International Agency for Research on Cance r (IARC) , a recognized international authority on the carcinogenic potential of chemicals and other agents , evaluated the full range of cancer related health effects data for diesel engine exhaust . IARC concluded that diesel exhaust should be regarded as “carcinogenic to humans.” 35 This designation was an update from its 1988 evaluation that considered the evidence to be indicative of a “probable human carcinogen.”***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 12 

### 6.1.1.7 Air Toxics Heav y - dut y vehicle emissions contribute to ambient levels of air toxics known or suspected as human or animal carcinogens, or that have noncancer health effects. The population experiences an elevated risk of cancer and other noncancer health effects from exposure to the class of pollutants known collectively as “air toxics.” 36 The se compounds include, but are not limited to, benzene, 1,3 - butadiene, formaldehyde, acetaldehyde, acrolein, polycyclic organic matter, and naphthalene. These compounds were identified as national or regional risk drivers or contributors in the 2005 Nation al - scale Air Toxics Assessment and have significant inventory

contributions from mobile sources. 37 

### 6.1.1.7.1 Health Effects of Benzene EPA’s IRI S database lists benzene as a known human carcinogen (causing leukemia) by all routes of exposure, and concludes that exp osure is associated with additional health effects, including genetic changes in both humans and animals and increased proliferation of bone marrow cells in mice. 38 , 39 , 40 EPA states in its IRI S database that data indicate a causal relationship between benzene exposure and acute ly mphocy tic leukemia and suggest a relationship between benzene exposure and chronic non - ly mphocy tic leukemia and chronic ly mphocy tic leukemia. E PA’s IRI S documentation for benzene also lists a range of 2.2 x 10 - 6 to 7.8 x 10 - 6 as the unit risk estimate (URE) for benzene. H , 41 The International Agency for Research on Carcinogens (IARC) has determined that benzene is a human carcinogen and the U.S. D epartment of Health and Human Services (DHHS) has characterized benzene as a known human carcinogen. 42 , 43 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. 44 , 45 The most sensitive noncancer effect observed in humans, based on current data, is the depression of the absolute ly mphocy te count in blood. 46 , 47 EPA’s inhalation reference concentration (RfC) for benzene is 30 μg/m 3 . The RfC is based on suppressed absolute ly mphocy te counts seen in humans under occupational exposure conditions. In addition, recent work, including studies sponsored b y the Health Effects Institute (HE I), provides evidence that biochemical responses are occurrin g at lower levels of benzene exposure than previousl y known. 48 , 49 , 50 , 51 EPA’s IRI S program has not yet evaluated these new data. EPA does not currentl y have an acute reference concentration for benzene. The Agency for Toxic Substances and Disease Registry

( ATSDR) Minimal Risk L evel (MRL) for acute exposure to benzene is 29 μg/m 3 for 1 - 14 day s exposure. 52 , I 

### 6.1.1.7.2 Health Effects of 1,3 -Butadiene EPA has characterized 1,3 - butadiene as carcinogenic to humans by inhalation. 53 , 54 The IARC has determined that 1,3 - butadiene is a human carcinogen and the U.S. DHHS has H A unit risk estimate is defined as the increase in the lifetime ris k of an individual who is exposed for a lifetime to 1 μg/m3 benzene in air. I A minimal risk level (MRL) is defined as an estimate of the daily human exposure to a hazardous substance that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration of exposure.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 13 characterized 1,3 - butadiene as a known human carcinogen. 55 , 56 , 57 There are numerous studies consistently

demonstrating that 1,3 - butadiene is metabolized into genotoxic m etabolites 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 b y genotoxic metabolites. Animal dat a suggest that females may be more sensitive than males for cancer effects associated with 1,3 - butadiene exposure; there are insufficient data in humans from which to draw conclusions about sensitive subpopulations. The URE for 1,3 - butadiene is 3 × 10 - 5 p er μg/m 3

. 58 1, 3 - butadiene also causes a variet y 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. 59 Based on this critical effect and the benchmark concentration methodology , an RfC for chronic health effects was calculated at 0.9 ppb (approximately 2 μg/m 3 ). 

### 6.1.1.7.3 Health Effects of Formaldehyde In 1991, EPA concluded that formaldeh yde is a carcinogen based on nasal tumors in animal bioassays. 60 An Inhalation URE for cancer and a Reference Dose for oral noncancer effects were developed by the a genc y and posted on the Integrated Risk Information Sy stem (IRI S) database. Since that time, the National Toxicology Program (NTP) an d International Agency for Research on Cancer (IARC) have concluded that formaldehyde is a known human carcinogen. 61 , 62 , 63 The conclusions b y IAR C and NTP reflect the results of epidemiologic research published since 1991 in combination with previous animal, human and mechanistic evidence. Research conducted b y the National Cancer Institute reported an increased risk of nasophary

ngeal cancer and specific l ymphohematopoietic malignancies among workers exposed to formaldeh yde. 64 , 65 , 66 A National Institute of Occu pational Safety

and Health study

of garment workers also reported increased risk of death due to leukemia among workers exposed to formaldeh yde. 67 Extended follow - up of a cohort of British chemical workers did not report evidence of an increase in nasopharyn geal or l ymphohematopoietic cancers, but a continuing statistically

significant excess in lung cancers was reported. 68 Finall y, a study of embalmers reported formaldeh yd e exposures to be associated with an increased risk of myeloid leukemia but not brain cancer. 69 Health effects of formaldehyde in addition to cancer were reviewed b y the Agency for Toxics Substances and D isease Registry in 1999 70 and supplemented in 2010 , 71 and by the World Health Organization. 72 These organizations reviewed the scientific literature concerning health effects linked to formaldehyde exposure to evaluate hazards and dose response relationships and define d exposure concentrations for minimal risk levels (MRL s). The health endpoints reviewed included sensory

irritation of eyes and respiratory tract, pulmonary

function, nasal histopathology , and immune sy stem effects. In addition, research on reproductive and developmental effects and neurological effects were discussed along with several studies that suggest that formaldeh yd e may increase the risk of asthma

– particularl y in the young. EPA released a draft Toxicological Review of Formaldehyde

– Inhalation Assessment through the IR IS program for peer review by the National Research Council (NRC) and public comment in June 2010. 73 The draft assessment reviewed more recent research from animal and***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 14 human studies on cancer and other health effects. The NRC released their review report in April 2011 74 (http://www.nap.edu/catalog.php?record_id=13142). EPA is currently developing a new draft assessment in response to this review. 

### 6.1.1.7.4 Health Effects ofAcetaldehyde Acetaldeh yd e is classified in EPA’s IRI S database as a probable human carcinogen, based on nasal tumors in rats, and is considered toxic by the inhalation, oral, and intravenous routes. 75 The URE in IRIS for acetaldeh yd e is 2.2 × 10 - 6 per μg/m 3

. 76 Acetaldehyde is reasonabl y anticipated to be a human carcinogen by the U.S. DHHS in the 1 3 th Report on Carcinogens and is classified as possibly carcinogenic to humans (Group 2B) b y the IARC. 77 , 78 EPA is currentl y conducting a reassessment of cancer risk from inhalation exposure to acetaldeh yde. The primary noncancer effects of exposure to acetaldehyde vapors include irritation of the eyes, skin, and respiratory tract. 79 Inshort - term (4 week) rat studies, degeneration of olfactory epithelium was observed at various concentration levels of acetaldehyde expos ure. 80 , 81 Data from these studies were used b y EPA to develop an inhalation reference concentration of 9 μg/m 3 . Some asthmatics have been shown to be a sensitive subpopulation to decrements in functional expiratory

volume (FEV1 test) and bronchoconstriction upon acetaldeh yde inhalation. 82 The agency is currentl y conducting a reassessment of the health hazards from inhalation exposure to acetaldeh yde. 

### 6.1.1.7.5 Health Effects ofAcrolein EPA most recently

evaluated the toxicological and health effe cts literature related to acrolein in 2003 and concluded that the human carcinogenic potential of acrolein could not be determined because the available data were inadequate. No information was available on the carcinogenic effects of acrolein in humans and the animal data provided inadequate evidence of carcinogenicity . 83 The IARC determined in 1995 that acrolein was not classifiable as to its carcinogenicity

in humans. 84 Lesions to the lungs and upper respiratory tract of rats, rabbits, and hamsters hav e been observed after subchronic exposure to acrolein. 85 The a gency has developed an RfC for acrolein of 0.02 μg/m 3 and an RfD of 0.5 μg/kg - day . 86 EPA is considering updating the acrolein assessment with data that have become available since the 2003 asses sment was completed. Acrolein is extremely

acrid and irritating to humans when inhaled, with acute exposure resulting in upper respiratory tract irritation, mucus hy persecretion and congestion. The intense irritancy of this carbonyl has been demonstrated during controlled tests in human subjects, who suffer intolerable eye and nasal mucosal sensory reactions within minutes of exposure. 87 These data and additional studies regarding acute effects of human exposure to acrolein are summarized in EPA’s 2003 IR I S Human Health Assessment for acrolein. 88 Studies in humans indicate that levels as low as 0.09 ppm (0.21 mg/m 3 ) for five minutes may elicit subjective complaints of eye irritation with increasing concentrations leading to more extensive eye, nose and resp iratory

s ymptoms. Acute exposures in animal studies report bronchial hy per responsiveness. Based on animal data ( more pronounced respiratory irritancy in mice with***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 1 5 allergic airway

disease in comparison to non - diseased mice 89 ) and demonstration of similar effects in humans (e.g., reduction in respiratory rate), individuals with compromised respiratory function (e.g., emph ys ema, asthma) are expected to be at increased risk of developing adverse responses to strong respiratory irritants such as acrolein. EP A does not currently have an acute reference concentration for acrolein. The available health effect reference values for acrolein have been summarized by EPA and include an ATSDR MRLfor acute exposure to acrolein of 7 μg/m 3 for 1 - 14 day s exposure; and R eference Exposure L evel ( REL ) values from the California Office of Environmental Health Hazard Assessment ( OEHHA ) for one - hour and 8 - hour exposures of 2.5 μg/m 3 and 0.7 μg/m 3 , respectively. 90 

### 6.1.1.7.6 Health Effects of Polycyclic Organic Matter (POM) The term pol yc yclic organic matter (POM) defines a broad class of compounds that includes the polycyclic aromatic hydrocarbon compounds (PAHs). One of these compounds, naphthalene, is discussed separately below. POM compounds are formed primarily from combustion and are present in the atmosphere in gas and particulate form. Cancer is the major concern from exposure to POM. Epidemiologic studies have reported an increase in lung cancer in humans exposed to diesel exhaust, coke oven emissions, roofing tar emission s, and cigarette smoke; all of these mixtures contain POM compounds. 91 92 Animal studies have reported respiratory

tract tumors from inhalation exposure to benzo[a]py rene and alimentary

tract and liver tumors from oral exposure to benzo[a]py rene. 93 In1997 E PA classified seven PAHs (benzo[a]py

rene, benz[a]anthracene, chry sene, benzo[b]fluoranthene, benzo[k]fluoranthene, dibenz[a,h]anthracene, and indeno[1,2,3 - cd]py rene) as Group B2, probable human carcinogens. 94 Since that time, studies have found that matern al exposures to PAHs in a population of pregnant women were associated with several adverse birth outcomes, including low birth weight and reduced length at birth, as well as impaired cognitive development in preschool children (3 years of age). 95 , 96 These and similar studies are being evaluated as a part of the ongoing IRIS assessment of health effects associated with exposure to benzo[a]py rene. 

### 6.1.1.7.7 Health Effects of 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 primaril y a product of combustion. Acute (short - term) exposure of humans to naphthalene b y inhalation, ingestion, or dermal contact is associated with hemoly tic anemia and damage to the liver and the nervous sy stem. 97 Chronic (long term) exposure of workers and rodents to naphthalene has been reported to cause cataracts and retinal damage. 98 EPA released an external review draft of a reassessment of the inhalation carcinogenicity of naphthalene based on a number of recent animal carcinogenicity

studies. 99 The draft re assessment completed external peer review. 100 Based on external peer review comments received, a revised draft assessment that considers all routes of exposure, as well as cancer and noncancer effects, is under development. The external review draft does n ot represent official agency opinion and was released solel y for the purposes of external peer review and public comment. The National Toxicology Program listed naphthalene as "reasonably

anticipated to be a human carcinogen" in 2004 on the basis of bioas say s reporting clear evidence of carcinogenicity in rats and some evidence of carcinogenicity in mice. 101***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 16 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. 102 Naphthalene also causes a number of chronic non - cancer effects in animals, including abnormal cell changes and growth in respiratory and nasal tissues. 103 The current EPA IRI S assessment includes noncancer data on h yperplasia and metaplasia in nasal tissue that form the basis of the inhalation RfC of 3 μg/m 3

. 104 The ATSDR MRLfor acute exposure to naphthalene is 0.6 mg/kg/day . 

### 6.1.1.7.8 Health Effects of Other Air Toxics In addition to the compounds described above, other compounds in gaseous hydrocarbon and PM emissions from vehicles w ill be affected by this proposal . Mobile source air toxic compounds that would potentially be impacted include eth ylbenzene, propionaldehyde, toluene, and x yl ene. Information regarding the health effects of th ese compounds can be found in EPA’s IR IS database. 105 

### 6.1.1.8 Exposure and Health Effects Associated with Traffic In addition to health concerns resulting from specific air pollutants, a large number of studies have examined the health status of populations near maj or roadways. These studies frequentl y have emplo ye d exposure metrics that are not specific to individual pollutants, but rather reflect the large number of different pollutants found in elevation near major roads. In this section of the RIA, information o n health effects associated with air quality near major roads or traffic in general is summarized. Generally , the section makes use of publications that sy stematically

review literature on a given health topic. In particular, this section makes frequent reference of a report of by the Health Effects Institute (HEI) Panel on the Health Effects of Traffic - Related Air Pollution, published in 2010 as a review of relevant studies. J , 106 Other sy stematic reviews of relevant literature are cited were appropriate. 

### 6.1.1.8.1 Populations near Major Roads Numerous studies have estimated the size and demographics of populations that live near major roads. Other studies have estimated the number of schools near major roads, and the populations of students in such schools. Every two ye ars, the U.S. Census Bureau’s American Housing Survey (AHS) has reported whether housing units are within 300 feet of an “airport, railroad, or highway with four or more lanes.” The 2009 survey reports that over 22 million homes, or 17 percent of all housing

J It should be noted that there are no peer reviewed EPA - authored review s of traffic - related health studies. The HEI panel primarily used epidemiology studies for inferring whether there was sufficient evid ence of a causal association exists between a particular health effect and traffic - related air pollution. In its weight - of - evidence determinations, the panel also placed “considerable weight” on controlled human exposure studies. However, it restricted co nsideration of other toxicological studies to whether or not the studies provided “general mechanistic support” for the inferences of causality made on the basis of epidemiology.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 17 units in the U.S., were located in such areas. Assuming that populations and housing units are in the same locations, this corresponds to a population of more than 50 million U.S. residents in close proximity

to high - traffic roadway s or other transportation sources. According to the Central Intelligence Agency ’s World Factbook, in 2010, the United States had 6,506,204 km or roadway s, 224,792 km of railway s, and 15,079 airports. As such, highways represent the overwhelming majorit y of transportat ion facilities described b y this factor in the AHS. The AHS reports are published every two years, and until 2011 recorded whether homes were located near highway s with four or more lanes, railroads, or airports. As such, trends in the AHS can be reported to describe whether a greater or lesser proportion of homes are located near major roads over time. Figure 6 - 1 depicts trends in the number and proportion of homes located near major transportation sources, which generally indicate large roadway s. As the figure indicates, since 2005, there has been a substantial increase in the number and percentage of homes located near major transportation sources. As such, the population in close proximity to these sources, which may be affected b y near - road air quality and health concerns, appears to have increas ed over time.

**Figure 6**  **- 1**  **T rends**  **in Populations**  **Near Large Highways, Railroads, and Airports** Furthermore, according to data from the 2008 American Time Use Survey (ATUS), conducted b y the Bureau of Labor St atistics (BTS), Americans spend more than an hour traveling each day , on average. 107 Although the ATUS does not indicate their mode of travel, the majority of trips undertaken nationally is by motor vehicle. 108 As such, daily travel activit y brings nearl y al l residents into a high - exposure microenvironment for part of the day . 0. 0% 2. 0% 4. 0% 6. 0% 8. 0% 10. 0% 12. 0% 14. 0% 16. 0% 18. 0%

10 12 14 16 18 20 22 24

1997 1999 2001 2003 2005 2007 2009PercentNearInfrastructureMillionHomes

Ye ar o f Amer ic an Housi ng S ur vey Mi llion H ousi ng Un its Near 4 + L an e High wa y, Railroad, or Airport***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 18 

### 6.1.1.8.2 Premature M ortality The HEI panel report concluded that evidence linking traffic - associated air pollution with premature mortality

from all causes was “suggestive but not sufficient” t o infer a causal relationship. This conclusion was based largel y on several long - term studies that “qualitativel y” examined whether or not someone was exposed to traffic - associated air pollution. In addition, based on several short - term studies of exposure, the panel concluded that there was “suggestive but not sufficient” evidence to infer a causal relation between traffic - related exposure and cardiovascular mortality. 

### 6.1.1.8.3 Cardiovascular E ffects **6.1.1.8.3.1 Cardiac**  **P**

**hysiology** Exposure to traffic - associated pollutants has been associated with changes in cardiac phy siology , including cardiac function. One common measure of cardiac function is heart rate variability

(HRV), an indicator of the heart’s ability to respond to variations in stress, reflecting the nervous s ys t em’s ability to regulate the heart. K Reduced HRV is associated with adverse cardiovascular events, such as myocardial infarction, in heart disease patients. The HEI panel concluded that available evidence provides evidence for a causal association between exposure to traffic - related pollutants and reduced control of HRV by the nervous s ys tem. Overall, the panel concluded that the evidence was “suggestive but not sufficient” to infer a causal relation between traffic - related pollutants and cardiac functio n. Studies suggest that the HRV changes from traffic - related air pollution result in changes to heart rh ythms, which can lead to arrh ythmia. 109 , 110 **6.1.1.8.3.2 Heart**  **Attack and Atherosclerosis** The HEI panel concluded that epidemiologic evidence of the association between traffic related pollutants and heart attacks and atherosclerosis was “suggestive but not sufficient” to infer a causal association. In addition, the panel concluded that the toxicology studies they reviewed provided “suggestive evidence that exposure to traffic emissions, including ambient and laboratory - generated [PM] and diesel - and gasoline - engine exhaust, alters cardiovascular function.” The panel noted there are few studies of human volunteers exposed to real - world traffic mixture, which were not entirel y consistent. The panel notes that the studies provide consistent evidence for exposure to PM and impaired cardiovascular responses. In addition to the HEI study, several other reviews of available evidence conclude that there is evidence supporting a causal association between traffic - related air pollution and cardiovascular disease. 111 A number of mechanisms for cardiovascular disease are highlighted in the HEI and AHA report, including modified blood vessel endothelial function ( e.g. , the ability to dilate), atherosclerosis, and oxidative stress. The HEI review cites “two well executed studies” in which

K The autonomic nervous system (ANS) consists of sympathetic and parasympathe tic components. The sympathetic ANS signals body systems to “fight or flight.” The parasympathetic ANS signals the body to “rest and digest.” In general, HRV is indicative of parasympathetic control of the heart.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 19 hospitalization for acute myocardial infarction (i.e., heart attack) were associated with traffic exposures and a prospective study finding higher r ates of arterial hardening and coronary heart disease near traffic. 

### 6.1.1.8.4 Respiratory E ffects **6.1.1.8.4.1 Asthma**  Pediatric asthma and asthma sy mptoms are the effects that have been evaluated by the largest number of studies in the epidemiologic literature on the topic. In general, studies consistently

show effects of residential or school exposure to traffic and asthma sy mptoms, and the effects are frequentl y statistically significant. Studies have employed both short - term and long - term exposure metrics, and a range of dif ferent respiratory

measures. HEI Special Report 17 (HEI Panel on the Health Effects of Traffic - Related Air Pollution, 2010) concluded that there is sufficient evidence for a causal association between exposure to traffic - related air pollution and exacerbation of asthma sy mptoms in children. While there is general consistency in studies examining asthma incidence in children, the available studies emplo y different definitions of asthma (e.g., self - reported vs. hospital records), methods of exposure assess ment, and population age ranges. As such, the overall evidence, while supportive of an association between traffic exposure and new onset asthma, are less consistent than for asthma sy mptoms. The HE I report determined that evidence is between “sufficient ” and “suggestive” of a causal relationship between exposure to traffic - related air pollution and incident (new onset) asthma in children (HEI Panel on the Health Effects of Traffic - Related Air Pollution, 2010). A recent meta - anal ys is of studies on incide nt asthma and air pollution in general, based on studies dominated by traffic - linked exposure metrics, also concluded that available evidence is consistent with HEI’s conclusion (Anderson et al., 2011). The study reported excess main risk estimates for di fferent pollutants ranging from 7 - 16 percent per 10  g/m 3 of long - term exposure (random effects models). Other qualitative reviews (Salam et al., 2008; Braback and Forsberg, 2009) conclude that available evidence is consistent with the hy pothesis that tra ffic - associated air pollutants are associated with incident asthma. **6.1.1.8.4.2 Chronic**  **Obstructive Pulmonary Disease (COPD)**  The HEI panel reviewed available studies examining COPD in the context of traffic associated air pollution. Because of how the panel selected studies for inclusion in review, there were onl y two studies that they used to review the available evidence. Both studies reported some positive associations, but not for all traffic metrics. The small number of studies and lack of consistency

across tr affic metrics led the panel to conclude that there is insufficient evidence for traffic - associated air pollution causing COPD. **6.1.1.8.4.3 Allergy**  There are numerous human and animal experimental studies that provides strongl y suggestive evidence that traffic - related air pollutants can enhance allergic responses to common allergens. 112 , 113 , 114 However, in its review of 16 epidemiologic studies that address traffic - related air pollution’s effect on allergies, the HEI expert panel (HEI, 2010) reported that only two such studi es showed consistently positive associations. As a result, despite the strong ly suggestive***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 20 experimental evidence, the panel concluded that there is “inadequate/insufficient” evidence of an association between allergy and traffic - associated air pollution. As noted above, the HEI panel considered toxicological studies only based on whether or not they provide mechanistic support for observations and inferences derived from epidemiology . **6.1.1.8.4.4 Lung**  **F**

**unction** There are numerous measurements of breathing (spirometry) that indicate the presence or degree of airway

disease, such as asthma and chronic obstructive pulmonary disease (COPD). Forced vital capacity (FVC) is measured when a patient maximally fills their lungs and then blows their hardest in completely exhalin g. The peak expiratory flow (PEF) is the maximum air flow achievable during exhalation. The forced expiratory volume in the first second of exhalation is referred to as FEV 1 . FEV 1 and PEF reflect the function of the large airway s. FVC and FEV 1 , along w ith their ratio (FVC/FEV 1 ) are used to classify airway obstruction in asthma and COPD. Measurements of air flow at various times during forced exhalation, such as 25 percent, 50 percent, and 75 percent, are also used. The flow at 75 percent of forced exh alation (FEF 75 ) reflects the status of small airway s, which asthma and COPD affect. The HEI panel concluded that the available literature suggests that long - term exposure to traffic - related air pollution is associated with reduced lung function in adolescents and young adults and that lung function is lower in populations in areas with hi gh traffic - related air pollutant levels. However, the panel noted the difficulty of disentangling traffic - specific exposures from urban air pollution in general. The studies reviewed that were more specifically oriented toward traffic were not consistent in their findings. As a result, the panel found that the evidence linking lung function and traffic exposure is “inadequate and insufficient” to infer a causal relationship. 

### 6.1.1.8.5 Reproductive and Developmental Effects Several studies have reported associatio ns between traffic - related air pollution and adverse birth outcomes, such as preterm birth and low birth weight. At the time of the HEI review, the panel concluded that evidence for adverse birth outcomes being causall y associated with traffic - related exp osures was “inadequate and insufficient.” Onl y four studies met the panel’s inclusion criteria, and had limited geographic coverage. One study provided evidence of small but consistently

increased risks using multiple exposure metrics. No studies were at the time available that examined traffic - specific exposures and congenital abnormalities. Since then, several studies investigating birth outcomes have been published, but no new s ys tematic reviews. One new meta - analy sis of air pollution and congenital abnormalities has been published, though none of the reviewed studies includes traffic - specific exposure information. The HEI panel also reviewed toxicological studies of traffic - related air pollutants and fertility . While numerous studies examining anim al or human exposure and sperm count have been published, the panel concluded that the generally high exposure concentrations employed in the studies limited the applicability to ty pical ambient concentrations. Because there was no overlap in the effects studied by epidemiology

and toxicology

studies, no sy

nthesis review of the combined literature was undertaken.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 21 Since the HEI panel’s publication, a sy stematic review and meta - anal ys is of air pollution and congenital abnormalities was published. 115 In that r eview, onl y one study directly included nearb y traffic in its exposure anal ys is. As such, there are no sy stematic reviews that specifically address traffic’s impact on congenital abnormalities. 

### 6.1.1.8.6 Cancer **6.1.1.8.6.1 Childhood**  **C ancer**  Earlier this year, Boothe et al. (201 4) published a sy stematic review and meta - analy sis of studies of childhood leukemia risks associated for populations near major roads. 116 The study concluded that childhood leukemia was positivel y associated with residential exposure during childhood, but n ot during the prenatal period. Other literature reviews have not concluded that available evidence supports an association between childhood leukemia and traffic exposure. 117 , 118 For example, the HEI panel concluded that the available epidemiologic evidence w as “inadequate and insufficient” to infer a causal relationship between traffic - related air pollution and childhood cancer. **6.1.1.8.6.2 Adult**  **C**

**ancer** Several studies have examined the risk of adult lung cancers in relation to exposure to traffic - related air pollutants. The HEI panel evaluated four such studies, and rated the available evidence as “inadequate and insufficient” to infer a causal relation for non - occupational lung cancer. 

### 6.1.1.8.7 Neurological E ffects The HEI panel found that current toxicologic and epidemiologic literature on the neurotoxicity

of traffic - related air pollution was inadequate for their evaluation. The panel noted that there were a number of toxicologic studies of traffic - associated pollutants, but found them to have diverse exposure protocols, anim al models, and endpoints, making them unsuitable for sy stematic evaluation. 

### 6.1.2 Environmental Effects Associated with Exposure to Non - GHG Pollutants In this section we will discuss the environmental effects associated with non - GHG pollutants, specifically : particulate matter, ozone, NO X , SO X and air toxics. 

### 6.1.2.1 Visibility

Degradation Visibility can be defined as the degree to which the atmosphere is transparent to visible light. 119 Visibility impairment is caused by light scattering and absorption by suspended particles and gases. Fine particles with significant light - extinction efficiencies include sulfates, nitrates, organic carbon, elemental carbon, and soil. 120 Visibility is important becaus e it has direct significance to people’s enjo ym ent of dail y 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 enjo y recreational oppor tunities. Visibility

is also highly

valued in significant natural areas, such as national parks and wilderness areas, and special emphasis is***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 22 given to protecting visibility in these areas. For more information on visibility see the final 2009 PM I SA. 121 T he extent to which any

amount of light extinction affects a person’s ability to view a scene depends on both scene and light characteristics. For example, the appearance of a nearb y object (e.g., a building) is generally less sensitive to a change in ligh t extinction than the appearance of a similar object at a greater distance. See Figure 6 - 2 for an illustration of the important factors affecting visibility .

**Figure 6**  **- 2**  **Im portant Factors Involved in Seeing a Scenic Vista (Malm**  **, 1999)** EPA is working to address visibility impairment. Reductions in air pollution from implementation of various programs associated with the Clean Air Act Amendments of 1990 (CAAA) provisions have resulted in substantial improvements in visibility, and will continue to do so in the future. Because trends in haze are closely associated with trends in particulate sulfate and nitrate due to the simple relationship between their concentration and light extinction, visibility trends have improved as emissions of SO 2 and NO X have decreased over time due to air pol lution regulations such as the Acid Rain Program. 122 In the Clean Air Act Amendments of 1977, Congress recognized visibility ’s value to society b y establishing a national goal to protect national parks and wilderness areas from visibility impairment caused by

manmade pollution. L In1999, EPA finalized the regional haze L See Section 169(a) of the Clean Air Act.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 23 program (64 FR 35714) to protect the visibility in Mandatory

Class I Federal areas. There are 156 national parks, forests and wilderness areas categorized as Mandatory Class IFederal areas (62 FR 38680 - 38681, July 18, 1997). These areas are defined in CAA S ection 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 . Figure 6 - 3 shows the location of the 156 Mandatory Class I Federal areas.

**Figure 6**  **- 3**  **Mandatory Class I Federal Areas in the U.S.**  EPA has also concluded that PM 2.5 causes adverse effects on visibility in other areas that are not protected b y the Regional Haze Rule, depending on PM 2.5 concentrations and other factors such as dry

chemical composition and relative humi dity (i.e., an indicator of the water composition of the particles) . EPA revised the PM 2.5 standards in December 2012 and established a target level of protection that is expected to be met through attainment of the existing secondary

standards for PM 2.5 . 

### 6.1.2.2 Visibility

Monitoring In conjunction with the U.S. National Park Service, the U.S. Forest Service, other Federal land managers, and State organizations in the U.S., EPA has supported visibility monitoring in national parks and wilderness areas since 198 8. The monitoring network was originally established at 20 sites, but it has now been expanded to 110 sites that represent all but one of the 156 M andatory

Federal Class Iareas across the country (see Figure 6 - 3 ). This long - term visibility monitoring network is known as IMPROVE (Interagency Monitoring of Protected Visual Environments). IMPROVE provides direct measurement of fine particles that contribute to visibility impairment. The IMPROVE network employ s aerosol measurements at all sites, and optical and***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 24 scene measurements at some of the sites. Aerosol measurements are taken for PM 10 and PM 2.5 mass, and for key

constituents of PM 2.5 , such as su lfate, nitrate, organic and elemental carbon OC and EC) , soil dust, and several other elements. Measurements for specific aerosol constituents are used to calculate "reconstructed" aerosol light extinction by multiplying the mass for each constituent b y i ts empirically - derived scattering and/or absorption efficiency , with adjustment for the relative humidity . The IMPROVE program utilizes both an “original” and a “revised” reconstruction formula for this purpose, with the latter explicitly accounting for s ea salt concentrations. Knowledge of the main constituents of a site's light extinction "budget" is critical for source apportionment and control strategy development. In addition to this indirect method of assessing light extinction, there are o ptical m easurements which directly measure light extinction or its components. Such measurements are made principall y with a nephelometer to measure light scattering, some sites also include an aethalometer for light absorption, or a few sites us e a transmissomet er, which measures total light extinction . Scene characteristics are ty picall y recorded usi ng digital or video photography and are used to determine the quality of visibility conditions (such as effects on color and contrast) associated with specific leve ls of light extinction as measured under both direct and aerosol - related methods. Directly measured light extinction is used under the IMPROVE protocol to cross check that the aerosol - derived light extinction levels are reasonable in establishing current visibility conditions. Aerosol - derived light extinction is used to document spatial and temporal trends and to determine how changes in atmospheric constituents would affect future visibility conditions. Annual average visibility conditions (reflecting li ght extinction due to both anthropogenic and non - anthropogenic sources) vary regionally

across the U.S. Visibility is ty picall y worse in the summer months, and the rural East generally has higher levels of impairment than remote sites in the West . Figure s 9 - 9 through 9 - 11 in the PM I SA detail the percent contributions to particulate light extinction for ammonium nitrate and sulfate, EC and OC, and coarse mass and fine soil, by

season. 123 

### 6.1.2.3 Plant and Ecosy stem Effects of Ozone The welfare effects of ozone can be observed across a variet y of scales, i.e. subcellular , c ellular, leaf, whole plant, population and ecos ys tem. Ozone effects that begin at small spatial scales, such as the leaf of an individual plant, when they occur at sufficient magnitudes (or t o a sufficient degree) can result in effects being propagated along a continuum to larger and larger spatial scales. For example, effects at the individual plant level, such as altered rates of leaf gas exchange, growth and reproduction can , when widespre ad, result in broad changes in ecos ys tems, such as productivity , carbon storage, water cycling, nutrient cycling, and community composition. Ozone can produce both acute and chronic injury in sensitive species depending on the concentration level and the d uration of the exposure. 124 Inthose sensitive species M , effects from repeated exposure to ozone throughout the growing season of the plant tend to accumulate, so

M 73 FR 16491 (March 27, 2008). Only a small percentage of all the plant species growing within the U.S. (over 43,000 species have been catalogued in the USDA PLANTS database) have been studied with respect to ozone sensitivity.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 25 that even low concentrations experienced for a longer duration have the potential to create chronic stress on vegetation. 125 , N Ozone damage to sensitive species includes impaired photosy nthesis and visible injury to leaves . T he impairment of photosy nthesis, the process by which the plant makes carbohydrates (its source of energy and food), can lead to reduced crop yi elds, timber production, and plant productivity and growth. Impaired photosy nthesis can also lead to a reduction in root growth and carbohydrate storage below ground, resulting in other, more subtle plant and ecosy stems impacts. 126 These latter impacts include increased susceptibility

of plants to insect attack, disease, harsh weather, interspecies competition and overall decreased plant vigor. The adverse effects of ozone on areas with sensitive species could potentially

lead to species shifts and loss from the affected ecos ys tems O , resulting in a loss or reduction in associated ecosy stem goods and services. 127 Additionall y, visible ozone injury to leaves can result in a loss of aesthetic value in areas of special scenic significance like national parks and wilderness areas and reduced use of sensitive ornamentals in landscaping . 128 T he Integrated Science Assessment (I SA) for Ozone presents more detailed information on how ozone effects vegetation and ecos ys tems. 129 The I SA concludes that ambient concentrations of ozone are associated with a number of adverse welfare effects and characterizes the weight of evidence for different effects associated with ozone. P The I SA concludes that visible foliar injury effects on vegetation, reduced veget ation growth, reduced productivity

in terrestrial ecos ys tems, reduced yi eld and quality of agricultural crops, and alteration of below - ground biogeochemical cycles are causall y associated with exposure to ozone. It also concludes that reduced carbon seque stration in terrestrial ecosy stems, alteration of terrestrial ecos ys tem water cycling, and alteration of terrestrial community composition are likely to be causall y associated with exposure to ozone. 

### 6.1.2.4 Particulate Matter Deposition Particulate matter contributes to adverse effects on vegetation and ecos ys tems, and to soiling and materials damage. These welfare effects result predomina nt ly from exposure to excess amounts of specific chemical species, regardless of their source or predominant form (particle, gas or liquid). The following characterizations of the nature of these environmental effects are based on info rmation contained in the 2009 PM I SA and the 2008 Integrated Science Assessment for Oxides of Nitrogen and Sulfur - Ecological Criteria (secondary NO X/SO X ISA) . 130 , 131

N The concentration at which ozone levels overwhelm a plant’s ability to detoxify or compensate for oxidant exposure varies. Thus, whether a plant is classified as sensitive or tolerant depends in part on the exposure levels being considered. O Per footnote above, ozone impa cts could be occurring in areas where plant species sensitive to ozone have not yet been studied or identified. P The Ozone ISA evaluates the evidence assoc iated with different ozone related health and welfare effects, assigning one of five “weight of evidence” determinations: causal relationship, likely to be a causal relationship, suggestive of a causal relationship, inadequate to infer a causal relationsh ip, and not likely to be a causal relationship. For more information on these levels of evidence, please refer to Table II of the ISA.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 26 

### 6.1.2.4.1 Deposition of Nitrogen and Sulfur Nitrogen and sulfur interactions in the environment are highly complex as shown in Figure 6 - 4 . Both nitrogen and sulfur are essential, and sometimes limiting, nutrients needed for growth and productivity of ecos ys tem components (e.g. algae, plants). In terrestrial and aquatic ecos ys tems excesses of nitrogen or sulfur can lead to acidification and nutrient enrichmen t. 132 In addition, in aquatic ecos ystems, sulfur deposition can increase mercury methylation.

**Figure 6**  **- 4**  **Nitrogen and Sulfur Cycling, and Interactions in the Environment** Source: U.S. EPA, 2008c **6.1.2.4.1.1 Ecological**  **Effects of Acidification** Deposition of nitrogen and sulfur can cause acidification, which alters biogeochemistry and affects animal and plant life in terrestrial and aquatic ecosystems across the U.S. Soil acidification is a natural process, but is often a ccelerated b y acidify ingdeposition, which can decrease concentrations of exchangeable base cations in soils. 133 Biological effects of acidification in terrestrial ecos ys tems are generally linked to aluminum toxicity and decreased ability of plant roots to t ake up base cations. 134 Decreases in the acid neutralizing capacity and increases in inorganic aluminum concentration contribute to declines in zooplankton, macro invertebrates, and fish species richness in aquatic ecosys tems. 135 Geology (particularl y surficia l geology) is the principal factor governing the sensitivity of terrestrial and aquatic ecosystems to acidification from nitrogen and sulfur deposition. 136 Geologic formations having low base cation supply generally underlie the watersheds of acid - sensitive lakes and streams. Other factors contribute to the sensitivity of soils and surface waters***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 27 to acidifying deposition, including topography , soil chemistry , land use, and hydrologic flow path. 137 **6.1.2.4.1.1.1 Aquatic Acidification**  Aquatic effects of acidification have been well studied in the U.S. and elsewhere at various trophic levels. These studies indicate that aquatic biota have been affected by acidification at virtuall y all levels of the food web in acid sensitive aquatic ecos ys tems. Effects have been most clearl y documented for fish, aquatic insects, other invertebrates, and algae. Biological effects are primarily attributable to a combination of low pH and high inorganic aluminum concentrations. Such conditions occur more frequently during rainfall and snowmelt that cause high flows of water and less commonly during low - flow conditions, except where chronic acidity

conditions are severe. Biological effects of episodes include reduced fish condition factorA , changes in species composition and declines in aquatic species richness across multiple taxa, ecosy stems and regions. Because acidification primarily affects the diversity

and abundance of aquatic biota, it also affects the ecosy stem services that are derived from the fish and other aquatic life found in thes e surface waters. Inthe northeastern United States, the surface waters affected b y acidification are a source of food for some recreational and subsistence fishermen and for other consumers with particularly high rates of self

- caught fish consumption, su ch as the Hmong and Chippewa ethnic groups. 138 , 139

**6.1.2.4.1.1.2 Terrestrial Acidification**  Acidifying deposition has altered major biogeochemical processes in the U.S. by increasing the nitrogen and sulfur content of soils, accelerating nitrate and sulfate leaching from soil to drainage waters, depleting base cations (especiall y calcium and magn esium) from soils, and increasing the mobility of aluminum. Inorganic aluminum is toxic to some tree roots. Plants affected b y high levels of aluminum from the soil often have reduced root growth, which restricts the ability

of the plant to take up water and nutrients, especiall y calcium. 140 These direct effects can, in turn, influence the response of these plants to climatic stresses such as droughts and cold temperatures. They

can also influence the sensitivity of plants to other stresses, including ins ect pests and disease leading to increased mortality of canop y trees. 141 Inthe U.S., terrestrial effects of acidification are best described for forested ecosy stems (especiall y red spruce and sugar maple ecos ys tems) with additional information on other plant communities, including shrubs and lichen. 142 Both coniferous and deciduous forests throughout the eastern U.S. are experiencing gradual losses of base cation nutrients from the soil due to accelerated leaching from acidifying deposition. This change in nutrient availability may reduce the qualit y of forest nutrition over the long term. Evidence suggests that red spruce and sugar maple in some areas in the eastern U.S. have experienced declining health because of this deposition. For red spruce, ( Picea rubens ) dieback or decline has been observed across high elevation landscapes of the northeastern U.S., and to a lesser extent, the southeastern U.S., and acidifying deposition has been implicated as a causal factor. 143***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 28 **6.1.2.4.1.2 Ecological Effects from Nitrogen Enrich**  **ment 6.1.2.4.1.2.1**  **Aquatic Enrichment** Eutrophication in estuaries is associated with a range of adverse ecological effects including low dissolved oxygen (DO), harmful algal blooms (HABs), loss of submerged aquatic vegetation (SAV), and low water clarit y. Low DO disrup ts aquatic habitats, causing stress to fish and shellfish, which, in the short - term, can lead to episodic fish kills and, in the long - term, can damage overall growth in fish and shellfish populations. Lo w DO also degrades the aesthetic qualities of surfac e water. In addition to often being toxic to fish and shellfish, and leading to fish kills and aesthetic impairments of estuaries, HABs can, in some instances, also be harmful to human health. SAV provides critical habitat for man y aquatic species in estu aries and, in some instances, can also protect shorelines by reducing wave strength; therefore, declines in SAV due to nutrient enrichment are an important source of concern. Low water clarity is in part the result of accumulations of both algae and sedime nts in estuarine waters. In addition to contributing to declines in SAV, high levels of turbidity also degrade the aesthetic qualities of the estuarine environment. An assessment of estuaries nationwide by the National Oceanic and Atmospheric Administrati on (NOAA) concluded that 64 estuaries ( out of 99 with available data) suffered from moderate or high levels of eutrophication due to excessive inputs of both N and phosphorus. 144 For estuaries in the Mid - Atlantic region, the contribution of atmospheric deposition to total N loads is estimated to range between 10 percent and 58 percent . 145 Estuaries in the eastern United States are an important source of food production, in particular fish and shellfish production. The estuaries are capable of supporting large stocks of resident commercial species, and they

serve as the breeding grounds and interim habitat for several migratory species. Eutrophication in estuaries may also affect the demand for seafood after well - publicized toxic blooms, water - based recreation, and erosion protection provided by SAV. **6.1.2.4.1.2.2 Terrestrial Enrichment**  Terrestrial enrichment occurs when terrestrial ecosy stems receive N loadings in excess of natural background levels, through either atmospheric deposition or direct application. Atmosph eric N deposition is associated with changes in the t ypes and number of species and biodiversity

in terrestrial sy stems. Nitrogen enrichment occurs over a long time period; as a result, it may

take as much as 50 years or more to see changes in ecos ys tem c onditions and indicators. One of the main provisioning services potentially affected by

N deposition is grazing opportunities offered b y grasslands for livestock production in the Central U.S. Although N deposition on these grasslands can offer supplement ary nutritive value and promote overall grass production, there are concerns that fertilization may favor invasive grasses and shift the species composition away

from native grasses. This process may ultimatel y reduce the productivity of grasslands for li vestock production. Terrestrial enrichment also affects habitats, for example the Coastal Sage Scrub (CSS) and Mixed Conifer Forest (MCF) habitats which are an integral p art of the California landscape. Togeth er the ranges of these habitats include the d ensely populated and valuable coastline and the mountain areas. Numerous threatened and endangered species at both the state and federal***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 29 levels reside in CSS and MCF. Fire regulation is also an important regulating service that could be affected b y nutri ent enrichment of the CSS and MCF ecos ys tems by encouraging growth of more flammable grasses, increasing fuel loads, and altering the fire cycle. **6.1.2.4.1.3 Vegetation Effects Associated with Gaseous Sulfur Dioxide**  Uptake of gaseous sulfur dioxide in a plant canopy i s a complex process involving adsorption to surfaces (leaves, stems, and soil) and absorption into leaves. SO 2 penetrates into leaves through the stomata, although there is evidence for limited pathways via the cuticle. 146 Pollutants must be transported from the bulk air to the leaf boundary layer in order to get to the stomata. When the stomata are closed, as occurs under dark or drought conditions, resistance to gas uptake is very

high and the plant has a very low degree of susceptibility to injury . In co ntrast, mosses and lichens do not have a protective cuticle barrier to gaseous pollutants or stomates and are generally more sensitive to gaseous sulfur and nitrogen than vascular plants. 147 Acute foliar injury

usually happens within hours of exposure, invol ves a rapid absorption of a toxic dose, and involves collapse or necrosis of plant tissues. Another ty pe of visible injury

is termed chronic injury

and is usually

a result of variable SO 2 exposures over the growing season. Besides foliar injury , chronic exposure to low SO 2 concentrations can result in reduced photosy nthesis, growth, and yield of plants. 148 These effects are cumulative over the season and are often not associated with visible foliar injury . As with foliar injury , these effects vary among s pecies and growing environment. SO 2 is also considered the primary factor causing the death of lichens in many

urban and industrial areas . 149 **6.1.2.4.1.4 Mercury Methylation**  Mercury is a persistent, bioaccumulative toxic metal that is emitted in three forms: gaseous elemental Hg (Hg 0 ), oxidized Hg compounds (Hg +2 ), and particle - bound Hg (Hg P ). Methylmercury

(MeHg) is formed by

microbial action in the top layers of sediment and soils, after Hg has precipitated from the air and deposited into waterbodies or land. Once formed, MeHg is taken up b y aquatic organisms and bioaccumulates up the aquatic food web. Larger predatory fish may have MeHg concentrations many times, ty picall y on the order of one million times, that of the concentrations in the freshwater body in which they

live. The NO X SO X ISA

— Ecological Criteria concluded that evidence is sufficient to infer a causal relationship between sulfur deposition and increased mercury methylation in wetlands and aquatic environments. 150 Specificall y, there appears to be a rel ationship between SO 4 2 - deposition and mercury methylation; however, the rate of mercury methylation varies according to several spatial and biogeochemical factors whose influence has not been full y quantified . Therefore, the correlation between SO 4 2 - dep osition and MeHg cannot yet be quantified for the purpose of interpolating the association across waterbodies or regions. Nevertheless, because changes in MeHg in ecos ys tems represent changes in significant human and ecological health risks, the associati on between sulfur and mercury cannot be neglected. 151 

### 6.1.2.4.2 Deposition of Metallic and Organic Constituents of PM Several significant ecological effects are associated with deposition of chemical constituents of ambient PM such as metals and organics. 152 The trace m etal constituents of PM include cadmium, copper, chromium, mercury , nickel, zinc, and lead. The organics include***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 30 persistent organic pollutants (POPs), polyaromatic hydrocarbons (PAHs) and poly bromiated diphenyl ethers (PBDEs). Exposure to PM for direct e ffects occur via deposition (e.g., wet, dry or occult) to vegetation surfaces, while indirect effects occur via deposition to ecos ys tem soils or surface waters where the deposited constituents of PM then interacts with biological organisms. While both fine and coarse - mode particles may affect plants and other organisms, more often the chemical constituents drive the ecos ys tem response to PM. 153 Ecological effects of PM include direct effects to metabolic processes of plant foliage; contribution to total metal loading resulting in alteration of soil biogeochemistry and microbiology , plant and animal growth and reproduction; and contribution to total organics loading resulting in bioaccumulation and biomagnification. Particulate matter can adversel y impact plants and ecos ys tem services provided by plants by deposition to vegetative surfaces. 154 Particulates deposited on the surfaces of leaves and needles can block light, altering the radiation received by the plant. PM deposition near sources of heav y deposi tion can obstruct stomata limiting gas exchange, damage leaf cuticles and increase plant temperatures. 155 Plants growing on roadsides exhibit impact damage from nearroad PM deposition, having higher levels of organics and heav y metals, and accumulate salt from road de - icing during winter months. 156 In addition, atmospheric PM can convert direct solar radiation to diffuse radiation, which is more uniformly distributed in a tree canop y, allowing radiation to reach lower leaves. 157 Decreases in crop yields (a provisioning service) due to reductions in solar radiation have been attributed to regional scale air pollution in other counties with especiall y severe regional haze. 158 In addition to damage to plant surfaces, deposited PM can be taken up b y plants from so il or foliage. Copper, zinc, and nickel have been shown to be directl y toxic to vegetation under field conditions. 159 The ability of vegetation to take up heavy metals is dependent upon the amount, solubility

and chemical composition of the deposited PM. Uptake of PM by plants from soils and vegetative surfaces can disrupt photos ynthesis, alter pigments and mineral content, reduce plant vigor, decrease frost hardiness and impair root development. Particulate matter can also contain organic air toxic pollutants, including PAHs, which are a class of pol yc yc lic organic matter (POM). PAHs can accumulate in sediments and bioaccumulate in freshwater, flora and fauna. The uptake of organics depends on the plant species, site of deposition, phy sical and chemical p roperties of the organic compound and prevailing environmental conditions. 160 Different species can have different uptake rates of PAHs. For example, zucchini (Cucurbita pepo) accumulated significantly more PAHs than related plant species. 161 PAHs can accumulate to high enough concentrations in some coastal environments to pose an environmental health threat that includes cancer in fish populations, toxicity to organisms living in the sediment and risks to those (e.g., migratory birds) that consume these org anisms. 162 , 163 Atmospheric deposition of particles is thought to be the major source of PAHs to the sediments of L ake Michigan, Chesapeake Bay , Tampa Bay and other coastal areas of the U.S. 164 Contamination of plant leaves b y heav y metals can lead to elevated c oncentrations in the soil. Trace metals absorbed into the plant, frequently bind to the leaf tissue, and then are lost when the leaf drops. As the fallen leaves decompose, the heav y metals are transferred into the soil. 165 , 166 Many

of the major indirect plant responses to PM deposition are chiefly soil - mediated***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 31 and depend on the chemical composition of individual components of deposited PM. Upon entering the soil environment, PM pollutants can alter ecological processes of energy flow and nutrient cycling, inhibit nutrient uptake to plants, change microbial community structure and, affect biodiversity . Accumulation of heav y metals in soils depends on factors such as local soil characteristics, geologic origin of parent soils, and metal bioavailability . Heav y metals, such as zinc, copper, and cadmium, and some pesticides can interfere with microorganisms that are responsible for decomposition of soil litter, an important regulating ecosy stem service that serves as a source of soil nutrients. 167 Surface litter d ecomposition is reduced in soils having high metal concentrations. Soil communities have associated bacteria, fungi, and invertebrates that are essential to soil nutrient cycling processes. Changes to the relative species abundance and community

compositi on are associated with deposited PM to soil biota. 168 Atmospheric deposition can be the primary source of some organics and metals to watersheds. Deposition of PM to surfaces in urban settings increases the metal and organic component of storm water runoff. 169 This atmospherically - associated pollutant burden can then be toxic to aquatic biota. The contribution of atmosphericall y deposited PAHs to aquatic food webs was demonstrated in high elevation mountain lakes with no other anthropogenic contaminant sourc es. 170 Metals associated with PM deposition limit phy toplankton growth, affecting aquatic trophic structure. Long - range atmospheric transport of 47 pesticides and degradation products to the snowpack in seven national parks in the Western U.S. was recently quantified indicating PM - associated contaminant inputs to receiving waters during spring snowmelt. 171 The recentl y completed Western Airborne Contaminants Assessment Project (WACAP) is the most comprehensive database on contaminant transport and PM depositio nal effects on sensitive ecos ys tems in the Western U.S. 172 In this project, the transport, fate, and ecological impacts of anthropogenic contaminants from atmospheric sources were assessed from 2002 to 2007 in seven ecos ys tem components (air, snow, water, se diment, lichen, conifer needles and fish) in eight core national parks. The study concluded that bioaccumulation of semi - volatile organic compounds occurred throughout park ecosy stems, an elevational gradient in PM deposition exists with greater accumulat ion in higher altitude areas, and contaminants accumulate in proximity

to individual agriculture and industry sources, which is counter to the original working h ypothesis that most of the contaminants would originate from Eastern Europe and Asia. 

### 6.1.2.4.3 Materials Damage and Soiling Building materials including metals, stones, cements, and paints undergo natural weathering processes from exposure to environmental elements (e.g., wind, moisture, temperature fluctuations, sunlight, etc.). Pollution can worsen and accelerate these effects. Deposition of PM is associated with both phy sical damage (materials damage effects) and impaired aesthetic qualities (soiling effects). Wet and dry deposition of PM can ph ys icall y affect materials, adding to the effects of natural weathering processes, b y potentially promoting or accelerating the corrosion of metals, by degrading paints and by

deteriorating building materials such as stone, concrete and marble. 173 The effects of PM are exacerbated b y the pr esence of acidic gases and can be additive or sy nergistic due to the complex mixture of pollutants in the air and surface characteristics of the material. Acidic deposition has been shown to have an effect***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 32 on materials including zinc/galvanized steel and other metal, carbonate stone (as monuments and building facings), and surface coatings (p aints) . 174 The effects on historic buildings and outdoor works of art are of particular concern because of the uniqueness and irreplaceability of many of these objects. 

### 6.1.2.5 Environmental Effects of Air Toxics Emissions from producing, transporting and combusting f uel contribute to ambient levels of pollutants that contribute to adverse effects on vegetation. Volatile organic compounds (VOCs), some of which are considered ai r toxics, have long been suspected to play a role in vegetation damage. 175 Inlaboratory experiments, a wide range of tolerance to VOCs has been observed. 176 Decreases in harvested seed pod weight have been reported for the more sensitive plants, and some studies have reported effects on seed germination, flowering and fruit ripening. Effects of individual VOCs or their role in conjunction with other stressors (e.g., acidification, drought, temperature extremes) have not been well studied. In a recent study of a mixture of VOCs including ethanol and toluene on herbaceous plants, significant effects on seed production, leaf water content and photosy nthetic efficiency

were reported for some plant species. 177 Research suggests an adverse impact of vehicle exhaust on plants, which has in some cases been attributed to aromatic compounds and in other cases to nitrogen oxides. 178 , 179 , 180 The impacts of VOCs on plant reproduction may have long - term implications for biodiversity and survival of native species near major road way s. 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 . 

### 6.2 **Air Quality Impacts of Non -**  **GHG Pollutants** Chapter 5 of this draft RIA presents the projected emissions changes due to the propos al . Once the emissions changes are projected the next step is to look at how the ambient air quality would be impacted b y th ose emissions changes. Although the purpose of this proposal is to address greenhouse gas emissions, this propos al would also impact emissions of criteria and hazardous air pol lutants. No air quality modeling was done for this draft RIA to project the impacts of the propos al . Air quality modeling will be done for the final rule making , however, and those plans are discussed in Section 6.2.2 . 

### 6.2.1 **Current Concentrations of Non**  **- GHG Pollutants**  6.2.1.1 Current Concentrations o f Particulate Matter As described in Chapter 6.1.1.1 , PM causes adverse health effects, and EPA has set national standards to provide requisite protection against those health effects. There are two primary NAAQS for PM 2.5 : an annual standard (1 2 .0 μg/m 3 ) and a 24 - hour standard (35 μg/m 3 ) with a 98 th percentile form , and two secondary NAAQS for PM 2.5 : an annual standard (1 5 .0 μg/m 3 ) and a 24 - hour standard (35 μg/m 3 ) , likewise with a 98 th percentile form . T he initial PM 2.5 standards were set in 1997 and revisions to the standards were finalized in 2006 and in December 2012. The 2006 revision revised the level of the 24 - hour standards from 65 μg/m 3 to 35 ug/m3,***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 33 and the December 2012 rule revised the level of the primary annual PM 2.5 standard from 15 .0 μg/m 3 to 12 .0 μg/m 3

. 181 In 2005 EPA designated 39 nonattainment areas for the 19 97 PM 2.5 NAAQS (70 FR 19844, April 14, 2005) . As of July 2 , 201 4 , over 47 million people lived in the 19 areas that are still designated as nonattainment for the 1997 annual PM 2.5 NAAQS. These PM 2.5 nonattainment areas are comprised of 1 05 full or partia l counties. EPA anticipates making initial area designation decision s for the 2012 primary annual PM 2.5 NAAQS in December 2014, with those designations likel y becoming effective in earl y 2015. 182 On November 13 , 2009 and February 3, 2011, EPA designat ed 32 nonattainment areas for the 2006 24 - hour PM 2.5 NAAQS (74 FR 58688, November 13, 2009 and 76 FR 6056, February 3, 2011 ). As of July 2, 2014, 24 of these areas remain designated as nonattainment, and they are composed of 74 full or partial counties, with a population of over 43 million. In total, there are currently 33 PM 2.5 nonattainment areas with a population of over 61 million people. Q States with PM 2.5 nonattainment areas will be required to take action to bring those areas into attainment in the future. Designated nonattainment areas not currently attaining the 1997 annual PM 2.5 NAAQS are required to attain the NAAQS by 201 5 and will be required to maintain the 1997 annual PM 2.5 NAAQS thereafter . The 2006 24 - hour PM 2.5 nonattainment areas are r equired to attain the 2006 24 - hour PM 2.5 NAAQS in the 201 5 to 2019 time frame and will be required to maintain the 2006 24 - hour PM 2.5 NAAQS thereafter. Areas to be designated nonattainment for the 2012 primary annual PM 2.5 NAAQS will likely be required to attain the 2012 NAAQS in the 20 21 to 20 25 time frame . The heav y - dut y vehicle standards proposed here first apply

to model year 2021 vehicles. 

### 6.2.1.2 Current Concentrations o f Ozone As described in Chapter 6.1.1.2.2 , ozone causes adverse health effects, and EPA has set national ambient air quality standards to protect against those health effects. The primary and secondary NAAQS for ozone are 8 - hour standards with a level of 0.075 ppm. The most recent revision to the ozone standards was in 2008 ; the previous 8 - hour ozone standards, set in 1997, had a level of 0.08 ppm. In 2004, EPA designated nonattainment areas for the 1997 8 - hour ozone NAAQS (69 FR 2 3858, April 30, 2004). R As of July 2, 2014, there were 37 8 - hour ozone nonattainment areas for the 1997 ozone NAAQS , composed of 188 full or partial counties , with a total population of over 1 05 million . Nonattainment designations for the 2008 ozone stan dard s we re finalized on April 30, 2012 and May 31, 2012 . 183 As of July

2, 2014, there were 46 ozone nonattainment areas for the 2008 ozone NAAQS , composed of 227 full or partial counties , with a

Q Data come from Summary Nonattainment Area Population Exposure Report, current as of July 2, 2014 at: http://www.epa.gov/oar/oaqps/greenbk/popexp.html and contained in Docket EPA - HQ - OAR - 2014 - 0827. The 61 million total is calculated by summing, without double counting, the 1997 and 2006 PM 2.5 nonattainment populations contained in the Summary Nonattainment Area Population Exposure report (http://www.epa.gov/oar/oaqps/greenbk/popexp.html). If there is a population associated with both the 1997 and 2006 nonattainment areas, and they are not the same, then the larger of the two populations is included in the sum. R A nonattainment area is defined in the Clean Air Act (CAA) as an area that is violating an ambient standard or is contributing to a nearby area that is violating the standard.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 34 population of over 123 million. As of July 2, 201 4 , over 134 million people are living in ozone nonattainment areas. S States with ozone nonattainment areas are required to take action to bring those areas into attainment . The attainment date assigned to an ozone nonattainment area is based on the area’s classific ation. Areas with higher 3

–year design values are classified at higher levels and subject to more stringent control requirements, but they are also given more time to attain the ozone NAAQS. Most ozone nonattainment areas for the 1997 8 - hour ozone NAAQS we re required to attain in the 2007 to 2013 time frame and then to maintain it thereafter. T T he attainment dates for areas designated nonattainment for the 2008 8 - hour ozone NAAQS are in the 2015 to 203 2 timeframe, depending on the severity of the problem in each area. In addition, EPA is currently working on a review of the ozone NAAQS. U If EP A revises the ozone standards pursuant to that review, the attainment dates associated with areas designated nonattainment for that NAAQS would be 5 or more ye ars after the final rule is promulgated, depending on the severit y of the problem in each area. The heav y - dut y vehicle standards proposed here first apply to model ye ar 2021 vehicles. 

### 6.2.1.3 Current Concentrations o f Nitrogen Oxides EPA most recently

completed a re view of the primary NAAQS for NO 2 in January 2010. There are two primary

NAAQS for NO 2 : an annual standard ( 53 ppb ) and a 1 - hour standard (100 ppb). EPA promulgated area designations in the Federal Register on February 17, 2012. In this initial round of designations, all areas of the country were designated as “unclassifiable/attainment” for the 2010 NO 2 NAAQS based on data from the existing air quality monitoring network. EPA and state agencies are working to establish an expanded network of NO 2 monito rs, expected to be deplo yed in the 201 3 - 2017 time frame. Once three ye ars of air quality data have been collected from the expanded network, EPA will be able to evaluate NO 2 air quality

in additional locations. 184 , 185 

### 6.2.1.4 Current Concentrations o f Sulfur Oxides EPA most recently

completed a review of the primary SO 2 NAAQS in June 2010. The current primary

NAAQS for SO 2 is a 1 - hour standard of 75 ppb. EPA finalized the initial area designations for 29 nonattainment areas in 16 states in a notice published in the Federal Register

S The 134 million total is calculated by summing, without double counting, the 1997 and 2008 ozone nonattainment populations contained in the Summary Nonattainment Area Population Exposure report (http://www.epa.gov/oar/oaqps/greenbk/popexp.html). If there is a population assoc iated with both the 1997 and 2008 nonattainment areas, and they are not the same, then the larger of the two populations is included in the sum. T The Los Angeles South Coast Air Basin 8 - hour ozone nonattainment area and the San Joaquin Valley Air Basin 8 - hour ozone nonattainment area are designated as Extreme and will have to attain before June 15, 2024. The Sacramento, Coachella Valley, Western M ojave and Houston 8 - hour ozone nonattainment areas are designated as Severe and will have to attain by June 15, 2019. U On November 25, 2014 EPA proposed to update both the primary ozone standard, to protect public health, and the secondary standard, to protect the public welfare. Both standards would be 8 - hour standards set within a range of 65 to 70 parts per billion (ppb). EPA is seeking comment on levels for the health standard as low as 60 ppb. The agency will accept comments on all aspects of the pr oposal, including on retaining the existing standard. (http://www.epa.gov/glo/pdfs/20141125proposal.pdf)***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 35 on August 5, 2013. In this first round of designations, EPA only designated nonattainment areas that were violating the standard based on existing air quality monitoring data provided by the states. The a gency

did not have sufficient inf ormation to designate any area as “attainment” or make final decisions about areas for which additional modeling or monitoring is needed (78 FR 47191, August 5, 2013). EPA anticipates designating areas for the revised SO 2 standard in multiple rounds. 

### 6.2.1.5 Curr ent Concentrations o f Carbon Monoxide There are two NAAQS for CO: an 8 - hour standard (9 ppm) and a 1 - hour standard (35 ppm). The primary

NAAQS for CO were retained in August 2011. There are currentl y no CO nonattainment areas; as of September 27, 2010, all CO nonattainment areas were redesignated to maintenance areas. The designations were based on the existing community- wide monitoring network. EPA is making changes to the ambient air monitoring requirements for CO. The new requirements are expected to result in approximately 52 CO monitors operating near roads within 52 urban areas b y J anuary 2015 (76 FR 54294, August 31, 2011). 

### 6.2.1.6 Current Concentrations of Diesel Exhaust PM Because DPM is part of overall ambient PM and cannot be easily distinguished from overall PM, we do not have direct measurements of DPM in the ambient air. DPM concentrations are estimated using ambient air quality modeling based on DPM emission inventories. DPM concentrations were recently estimated as part of the 2005 NATA. 186 Ambient impacts of mobile source emissions were predicted using the Assessment Sy stem for Population Exposure Nationwide (ASPEN) dispersion model. Concentrations of DPM were calculated at the census tract level in the 2005 NATA. Figure 6 - 5 below summarizes the distribution of ambient DPM concentrations at the national scale. Areas with high concentrations are clustered in the Northeast, Great Lake States, Californi a, and the Gulf Coast States, and are also distributed throughout the rest of the U.S. Table 6 - 1 presents a distribution of ambient DPM concentrations around the country . The median DPM concentration calculated nationwide is 0.53 μg/m 3 . Half of the DPM and diesel exhaust organic gases can be attributed to onroad diesels.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 36 **Figure 6**  **- 5**  **Estim ated County Am** **bient Concentr ation of Diesel Particulate Matter** 

**Table 6**  **- 1**  **Distribution of Census Tract Ambient Concentrations of DPM at the National Scale in 2005 NATA a**  AMBIENT CONCENTRATION ( μg/m3 ) 5 th Percentile 0.03 25 th Percentile 0.17 50 th Percentile 0.53 75 th Percentile 1.22 95th Percentile 2.91 Onroad Contribution to Median Census Tract Concentrations 50% Note: a This table is generated from data contained in the diesel particulate matter Microsoft Access database file found in the Tract - Level Pollutants section of the 2005 NATA webpage (http://www.epa.gov/ttn/atw/nata2005/tables.html).***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 37 

### 6.2.1.7 Current Concentrat ions o f Air Toxics The majority

of Americans continue to be exposed to ambient concentrations of air toxics at levels which have the potential to cause adverse health effects. 187 The levels of air toxics to which people are exposed vary depending on where p eople live and work and the kinds of activities in which they

engage, as discussed in detail in EPA’s most recent Mobile Source Air Toxics (MSAT) Rule. 188 Inorder to identify and prioritize air toxics, emission source types and locations which are of great est potential concern, EPA conducts the National - Scale Air Toxics Assessment (NATA). The most recent NATA was conducted for calendar year 200 5 , and was released in March 2011 . 189 NATA for 200 5 includes four steps: 1) Compiling a national emissions invento ry of air toxics emissions from outdoor sources 2) Estimating ambient concentrations of air toxics across the United States 3) Estimating population exposures across the United States 4) Characterizing potential public health risk due to inhalation o f air toxics including both cancer and noncancer effects According to the NATA for 200 5 , mobile sources were responsible for 43 percent of outdoor toxic emissions and over 50 percent of the cancer risk and noncancer hazard attributable to direct emissions from mobile and stationary sources . V , W , 190 Mobile sources are also large contributors to precursor emissions which react to form secondary concentrations of air toxics . Formaldeh yd e is the largest contributor to cancer risk of all 80 pollutants quantitatively assessed in the 200 5 NATA, and mobile sources were responsible for over 40 percent of primary emissions of this pollutant in 200 5, and are major contributors to formaldehyde precursor emissions . Benzene is also a large contribut or to cancer risk, and mobile sources account for over 70 percent of ambient exposure. Over the ye ars, EPA has implemented a number of mobile source and fuel controls which have resulted in VOC reductions, which also reduced formaldeh yde, benzene and othe r air toxic emissions. 

### 6.2.2 **Impacts of Proposed Standards on**  **Future Air Quality** Air quality

models use mathematical and numerical techniques to simulate the phy sical and chemical processes that affect air pollutants as they disperse and react in the atmospher e. Based on inputs of meteorological data and source information, these models are designed to characterize primary

pollutants that are emitted directly into the atmosphere and secondary pollutants that are formed as a result of complex chemical reactions within the atmosphere.

V NATA also includes estimates of risk attributable to background concentrations, which includes contributions from long - range transport, persistent ai r toxics, and natural sources; as well as secondary concentrations, where toxics are formed via secondary formation. Mobile sources substantially contribute to long - range transport and secondarily formed air toxics. W NATA relies on a Gaussian plume model , Assessment System for Population Exposure Nationwide (ASPEN), to estimate toxic air pollutant concentrations.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 38 Photochemical air quality models have become widely recognized and routinely utilized tools for regulatory

anal ys is by

assessing the effectiveness of control strategies. These models are applied at multiple spatial scales from loc al, regional, national, and global. Full - scale photochemical air quality modeling is necessary

to accurately

project levels of criteria and air toxic pollutant s. For the final rule making , national - scale air quality modeling anal ys e s will be performed to anal yz e the impacts of the standards on PM 2.5 , NO 2 , ozone, and selected air toxics (i.e., benzene, formaldeh yde, acetaldeh yde, naphthalene, acrolein and 1,3 - butadiene). The length of time needed to prepare the necessary emissions inventories, in addition to the processing time associated with the modeling itself, has precluded us from performing air quality

modeling for this proposal. Secti on VII I of the preamble presents projections of the changes in criteria pollutant and air toxic s emissions due to the proposed standards ; the basis for those e stimates is set out in Chapter 5 of the draft RIA . NHTSA also provides its projections in Chapte r 4 of its DEIS. The atmospheric chemistry

related to ambient concentrations of PM 2.5 , ozone and air toxics is very complex, and making predictions based solely on emissions changes is extremely difficult. However, based on the magnitude of the emissions changes predicted to result from the proposed standards, the agencies expect that there will be improvements in ambient air quality , pending a more comprehensive analy sis for the final rule making . For the final rule making , the agencies intend to use a 20 11 - based Community Multi - scale Air Quality

(CMAQ) modeling platform as the tool for the air qualit y modeling. The CMAQ modeling s ys tem is a comprehensive three - dimensional grid - based Eulerian air quality model designed to estimate the formation and fate o f 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.). 191 , 192 , 193 , 194 The CMAQ model is a well - known and well - established tool and is commonly

used b y EPA for regulatory analy ses, and by

States in developing attainment demonstrations for their State Implementation Plans. 195 The CMAQ model version 5.0 was most recentl y peer - reviewed in September of 2011 for the U.S. EPA. CMAQ includes man y science modules that simulate the emission, production, decay, deposition and transport of organic and inorganic gas - phase and particle - phase pollutants in the atmosphere. The agencies intend to use the most recent multi - pollutant CMAQ code available at the time of air quality

modeling (CMAQ version 5.0.2; multipollutant versionX ) which reflects updates to version 5.0 to improve the underl yi ng science algorithms as well as include new diagnostic/scientific modules which are detailed at http://www.cmascenter.org. 196 , 197 , 198 Figure 6 - 6 shows the geographic extent of the modeling domain that will be used for air quality modeling in th e s e anal ys e s. The domain covers the 48 contiguous states along with the southern portions o f Canada and the northern portions of Mexico. This modeling domain contains 25 vertical layers with a top at about 17,60 0 meters, or 50 millibars (mb) and a horizontal resolution of 12 x 12 km.

X CMAQ version 5.0.2 was released in April 2014. It is available from the Community Modeling and Analysis Sy stem (CMAS) website: http://www.cm ascenter.org.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 39 **Figure 6**  **- 6**  **Map of the CM**  **AQ 12 -**  **km US**  **Modeling Domain** The key inputs to the CMAQ model include emissions from anthropogenic and biogenic sources, meteorological data, and initial and boundary conditions. The 2011 CMAQ meteorological inputs will be derived from Versio n 3.4 of the Weather Research Forecasting Model (WRF). 199 These inputs included hourly - varyinghorizontal wind components (i.e., speed and direction), temperature, moisture, vertical diffusion rates, and rainfall rates for each grid cell in each vertical laye r. Details of the annual 2011 meteorological model simulation and evaluation will be described in more detail within the final RIA , the technical support document for the final rule making air quality modeling , and NHTSA’s Final Environmental Impact Stat ement . The lateral boundary

and initial species concentrations are provided by a three dimensional global atmospheric chemistry model, the GEOS - CHEM model 200 (standard version 8 - 03 - 02 with 8 - 02 - 01 chemistry . The global GEOS - CHEM model simulates atmospheric chemical and ph ys ical processes driven by assimilated meteorological observations from the NASA’s Goddard Earth Observing Sy stem (GEOS - 5; additional information available at: http://gmao.gsfc.nasa.gov/GEOS/ and http://wiki.seas.harvard.edu/geos - chem/index.php/GEOS -***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 40 5). This model was run for 2011 with a grid resolution of 2.0 degrees x 2.5 degrees (latitude longitude). The predictions were used to provide one - way dy namic boundary

conditions at one hour inter vals and an initial concentration field for the CMAQ simulations. A GEOS - Chem evaluation was conducted for the purpose of validating the 2011 GEOS - Chem simulation for predicting selected measurements relevant to their use as boundary conditions for CMAQ . This evaluation included using satellite retrievals paired with GEOS - Chem grid cells. 201 More information is available about the GEOS - CHEM model and other applications using this tool at: http://www - as.harvard.edu/chemistry /trop/geos. 

### 6.3 **Changes in Atmospheri**  **c CO 2**  

### Concentrations, **Global Mean Temperature**  **, Sea Level Rise**  **, and Ocean pH Associated with the**  **Program’s GHG Emissions Reductions**  **6.3.1 Introduction**  The impact of GHG emissions on the climate has been reviewed in the 2009 Endangerment and Cause or Contribute F indings for Greenhouse Gases Under Section 202(a) of the Clean Air Act, the 2012 - 2016 light - dut y vehicle rulemaking, the 2014 - 2018 heav y - dut y vehicle GHG rulemaking , and the 2017 - 2025 light - duty vehicle rulemaking . See 74 FR at 66496; 75 FR at 25491; 76 FR at 57294; 77 FR at 62894 . This section briefl y discusses again some of the climate impact context for transportation emissions. Once emitted, GHGs that are the subject of this regulation can remain in the atmosphere for decades to millennia, meaning th at 1) their concentrations become well - mixed throughout the global atmosphere regardless of emission origin, and 2) their effects on climate are long lasting. GHG emissions come mainly from the combustion of fossil fuels (coal, oil, and gas), with addition al contributions from the clearing of forests, agricultural activities, cement production, and some industrial activities. Transportation activities, in aggregate, were the second largest contributor to total U.S. GHG emissions in 2010 (27 percent of total emissions). Y EPA Administrator relied on thorough and peer - reviewed assessments of climate change science prepared b y the Intergovernmental Panel on Climate Change (“IPCC”), the United States Global Change Research Program (“USGCRP”), and the Nation al Research Council of the National Academies (“NRC”) Z as the primary scientific and technical basis for the Endangerment and Cause or Contribute Findings for Greenhouse Gases Under Section 202(a) of the Clean Air Act (74 FR 66496, December 15, 2009). T hese assessments comprehensivel y address the scientific issues EPA Administrator had to examine, providing her both data and information on a wide range of issues pertinent to the Endangerment Finding. These assessments have been rigorousl y reviewed b y th e expert community , and also by United States government agencies and scientists, including by EPA itself.

Y U.S. EPA (2012) Inventory of U.S. Greenhouse Gas Emissions and Sinks: 1990

–2010. EPA 430 - R - 12 - 001. Available at http://epa.gov/climatechange/emissions/downloads12/US - GHG - Inventory - 2012 - Main - Text.pdf Z For a complete list of core references from IPCC, USGCRP/CCSP, NRC and others relied upon for development of the TSD for EPA’s Endangerment and Cause or Contribute Findings see Section 1(b), specifically, Table 1.1 of the TSD. (Docket EPA - HQ - OAR - 2010 - 0799 )***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 41 Based on these assessments, EPA Administrator determined that the emissions from new motor vehicles and engines contributes to elevated concentration s of greenhouse gases, that these greenhouse gases cause warming; that the recent warming has been attributed to the increase in greenhouse gases; and that warming of the climate endangers the public health and welfare of current and future generations . T he D.C. Circuit has emphaticall y upheld the reasonableness of these findings. Coalition for Responsible Regulation v. EPA , 684 F. 3d 102, 121 (D.C. Cir. 2012) upholding all of EPA’s findings and stating “EPA had before it substantial record evidence that anthropogenic emissions of greenhouse gases ‘very likel y’ caused warming of the climate over the last several decades. EPA further had evidence of current and future effects of this warming on public health and welfare. Rel yi ng again upon substantial s cientific evidence, EPA determined that anthropogenicall y induced climate change threatens both public health and public welfare. It found that extreme weather events, changes in air quality, increases in food and water - borne pathogens, and increases in temperatures are likely to have adverse health effects. The record also supports EPA’s conclusion that climate change endangers human welfare b y creating risk to food production and agriculture, forestry, energy, infrastructure, ecos ys tems, and wildlife. Substantial evidence further supported EPA’s conclusion that the warming resulting from the greenhouse gas emissions could be expected to create risks to water resources and in general to coastal areas as a result of expected increase in sea level.”) A number of major peer - reviewed scientific assessments have been released since the administrative record concerning the Endangerment Finding closed following EPA’s 2010 Reconsideration Denial 202

. These assessments include the “Special Report on Managing the Ri sks of Extreme Events and Disasters to Advance Climate Change Adaptation” 203 , the 2013 - 14 Fifth Assessment Report (AR5) 204 , the 2014 National Climate Assessment report205 , the “Ocean Acidification: A National Strategy to Meet the Challenges of a Changing Ocean” 206 , “Report on Climate Stabilization Targets: Emissions, Concentrations, and Impacts over Decades to Millennia” 207 , “National Security Implications for U.S. Naval Forces” (National Security Implications) 208 , “Understanding Earth’s Deep Past: Lessons for Our Clim ate Future” 209 , “Sea Level Rise for the Coasts of California, Oregon, and Washington: Past, Present, and Future” 210 , “Climate and Social Stress: Implications for Security Anal ys is” 211 , and “Abrupt Impacts of Climate Change” (Abrupt Impacts) assessments 212

. EPA has reviewed these assessments and finds that in general, the improved understanding of the climate sy stem they present are consistent with the assessments underlying the 2009 Endangerment Finding. The most recent assessments to be released were the IPCC AR5 assessments between September 2013 and April 2014, the NRC Abrupt Impacts assessment in December of 2013, and the U.S. National Climate Assessment in May of 2014 . The NRC Abrupt Impacts report examines the potential for tipping points, thresholds beyond which major and rapid changes occur in the Earth’s climate sy stem or other s ys tems impacted by the climate. The Abrupt Impacts report did find less cause for concer n than some previous assessments regarding some abrupt events within the next century such as disruption of the Atlantic Meridional Overturning Circulation (AMOC) and sudden releases of high - latitude methane from hydrates and permafrost, but found that the potential for abrupt changes in ecos ys tems, weather and climate extremes, and groundwater supplies critical for agriculture now seem more likely , severe, and imminent. The assessment found that some abrupt changes were already underway (Arctic sea***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 42 ice re treat and increases in extinction risk due to the speed of climate change), but cautioned that even abrupt changes such as the AMOC disruption that are not expected in this century can have severe impacts when they happen. The IPCC AR5 assessments are also generall y consistent with the underlying science supporting the 2009 Endangerment Finding. For example, confidence in attributing recent warming to human causes has increased: the IPCC stated that it is extremely likel y (>95 percent confidence) that human influences have been the dominant cause of recent warming. Moreover, the IPCC found that the last 30 years were likel y (>66 percent confidence) the warmest 30 ye ar period in the Northern Hemisphere of the past 1400 years, that the rate of ice loss of wo rldwide glaciers and the Greenland and Antarctic ice sheets has likely increased, that there is medium confidence that the recent summer sea ice retreat in the Arctic is larger than has been in 1450 ye ars, and that concentrations of carbon dioxide and seve ral other of the major greenhouse gases are higher than they

have been in at least 800,000 years. Climate - change induced impacts have been observed in changing precipitation patterns, melting snow and ice, species migration, negative impacts on crops, inc reased heat and decreased cold mortality , and altered ranges for water - borne illnesses and disease vectors. Additional risks from future changes include death, injury , and disrupted livelihoods in coastal zones and regions vulnerable to inland flooding, f ood insecurity linked to warming, drought, and flooding, especiall y for poor populations, reduced access to drinking and irrigation water for those with minimal capital in semi - arid regions, and decreased biodiversity in marine ecos ys tems, especially in th e Arctic and tropics, with implications for coastal livelihoods. The IPCC determined that “[c]ontinued emissions of greenhouse gases will cause further warming and changes in all components of the climate sy stem. Limiting climate change will require subs tantial and sustained reductions of greenhouse gases emissions.” Finally , the recentl y released National Climate Assessment stated, “Climate change is already affecting the American people in far reaching way s. Certain ty pes of extreme weather events with links to climate change have become more frequent and/or intense, including prolonged periods of heat, heav y downpours, and, in some regions, floods and droughts. In addition, warming is causing sea level to rise and glaciers and Arctic sea ice to melt, and oceans are becoming more acidic as they absorb carbon dioxide. These and other aspects of climate change are disrupting people’s lives and damaging some sectors of our economy .” Assessments from these bodies represent the current state of knowledge, c omprehensivel y cover and sy nthesize thousands of individual studies to obtain the majority conclusions from the body of scientific literature and undergo a rigorous and exacting standard of review b y the peer expert community and U.S. government. Based on modeling anal ysis performed b y EPA, reductions in CO 2 and other GHG emissions associated with this proposed rule will affect future climate change. Since GHGs are well - mixed in the atmosphere and have long atmospheric lifetimes, changes in GHG emissions w ill affect atmospheric concentrations of greenhouse gases and future climate for decades to millennia, depending on the gas. This section provides estimates of the projected change in atmospheric CO 2 concentrations based on the emission reductions estimat ed for this proposed rule, compared to the reference case. In addition, this section analyzes the response to the changes in GHG concentrations of the following climate - related variables: global mean***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 43 temperature, sea level rise, and ocean pH. See Chapter 5 in this RIA for the estimated net GHG emissions reductions over time. 

### 6.3.2 **Projected Change in Atmospheric CO 2**  

### Concentrations, Global Mean **Surface Temperature and Sea Level Rise** To assess the impact of the emissions reductions from the proposed alternative, EPA estimated changes in projected atmospheric CO 2 concentrations, global mean surface temperature and sea - level rise to 2100 using the GCAM (Global Change Assessment Model, formerl y MiniCAM), integrated assessment model AA , 213 coupled with the MAGICC (Model f or the Assessment of Greenhouse - gas Induced Climate Change) simple climate model. BB , 214 , 215 GCAM was used to create the globally and temporally

consistent set of climate relevant emissions required for running MAGICC. MAGICC was then used to estimate the projected change in relevant climate variables over time. Given the magnitude of the estimated emissions reductions associated with the proposal, a simple climate model such as MAGI CC is appropriate for estimating the atmospheric and climate response. 

### 6.3.2.1 Methodology Emissions reductions associated with this proposal were evaluated with respect to a baseline reference case. An emissions scenario was developed b y applying the estimated emissions reductions from the proposa l’s proposed alternative relative to the baseline to the GCAM reference (no climate policy) scenario (used as the basis for the Representative Concentration Pathway

RCP4.5). 216 Specificall y, the annual CO 2 , N 2 O , CH 4 , NO X and SO 2 emissions reductions estimat ed from this proposed rule were applied as net reductions to the GCAM global baseline net emissions for each substance. The emissions reductions past 2050 for all emissions were scaled with total U.S. road transportation fuel consumption from the GCAM ref

erence scenario. This was chosen as a simple scale factor given that both direct and upstream emissions changes are included in the emissions reduction scenario provided. Road transport fuel consumption past 2050 does not change significantl y and thus em issions reductions remain relatively constant from 2050 through 2100. The GCAM reference scenario 217 depicts a world in which global population reaches a maximum of more than 9 billion in 2065 and then declines to 8.7 billion in 2100 while global

AA GCAM is a long - term , global integrated assessment model of energy, economy, agriculture and land use that considers the sources of emissions of a suite of greenhouse gases (GHG's), emitted in 14 globally disaggregated regions, the fate of emissions to the atmosphere, and the consequences of changing concentrations of greenhouse related gases for climate change. GCAM begins with a representation of demographic and economic developments in each region and combines these with assumptions about technology deve lopment to describe an internally consistent representation of energy, agriculture, land - use, and economic developments that in turn shape global emissions. BB MAGICC consists of a suite of coupled gas - cycle, climate and ice - melt models integrated into a s ingle framework. The framework allow s the user to determine changes in greenhouse - gas concentrations, global - mean surface air temperature and sea - level resulting from anthropogenic emissions of carbon dioxide (CO 2 ), methane (CH 4 ), nitrous oxide (N 2 O), reac tive gases (CO, NO X , VOCs), the halocarbons (e.g. HCFCs, HFCs, PFCs) and sulfur dioxide (SO 2 ). MAGICC emulates the global - mean temperature responses of more sophisticated coupled Atmosphere/Ocean General Circulation Models (AOGCMs) with high accuracy.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 44 GDP grows by

an order of magnitude and global energy consumption triples. The reference scenario includes no explicit policies to limit carbon emissions, and therefore fossil fuels continue to dominate global energy consumption, despite substantial growth in nuclear and renewable energy . Atmospheric CO 2 concentrations rise throughout the century and reach 760 to 820 ppmv by

2100, depending on climatic parameters, with total radiative forcing increasing more than 5 Watts per square meter (W/m 2 ) above 1990 levels by 2100. Forest land declines in the reference scenario to accommodate increases in land use for food and bioenergy crops. Even with the assumed agricultural productivity increases, the amount of land devoted to crops increases in the first half of the cent ury due to increases in population and income (higher income drives increases in land - intensive meat consumption). After 2050 the rate of growth in food demand slows, in part due to declining population. As a result the amount of cropland and also land u se change (LUC) emissions decline as agricultural crop productivity continues to increase. The GCAM reference scenario uses non - CO 2 and pollutant emissions implemented as described in Smith and Wigley (2006); land - use change emissions as described in Wis e et al. (2009); and updated base - ye ar estimates of global GHG emissions. This scenario was created as part of the Climate Change Science Program (CCSP) effort to develop a set of long - term global emissions scenarios that incorporate an update of economic and technology data and utilize improved scenario development tools compared to the IPCC Special Report on Emissions Scenarios (SRES) (IPCC 2000). Using MAGI CC 5.3 v2, 218 the change in atmospheric CO 2 concentrations, global mean temperature, and sea level were projected at five - year time steps to 2100 for both the reference (no climate policy) scenario and the emissions reduction scenario specific to the proposed alternative of this proposal. To capture some of the uncertainty in the climate sy stem, the changes in projected atmospheric CO 2 concentrations, global mean temperature and sea level were estimated across a range of plausible climate sensitivities, 1.5°C to 6.0°C. CC The range as illustrated in Chapter 10, Box 10.2, Figure 2 of the IPCC’s Working Group I is approximately consistent with the 10 - 90 percent probability distribution of the individual cumulative distributions of climate sensitivity . 219 Other uncertainties, such as uncertainties regardi ng the carbon cycle, ocean heat uptake, or aerosol forcing, were not addressed. MAGI CC calculates the forcing response at the global scale from changes in atmospheric concentrations of CO 2 , CH 4 , N 2 O, HFCs, and tropospheric ozone. It also includes the effects of temperature changes on stratospheric ozone and the effects of CH 4 emissions on stratospheric water vapor. Changes in CH 4 , NO X , VOC, and CO emissions affect both O 3 concentrations and CH 4 concentrations. MAGI CC includes the relative climate forcing effects of changes in sulfate concentrations due to changing SO 2 emissions, including both the direct effect of sulfate particles

CC 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 most recent IPCC AR5 assessment states that climate sensitivity is “likely” to be in the range of 1 .5°C to 4.5°C, “extremely unlikely” to be less than 1°C, and “very unlikely” to be greater than 6 °C .” Intergovernmental Panel on Climate Change (IPCC). 2013. Climate Change 2013: The Physical Sci ence Basis. Contribution of Working Group I to the Fifth Assessment Report of the Intergovernmental Panel on Climate Change. Cambridge University Press, Cambridge, United Kingdom and New York, NY, USA.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 45 and the indirect effects related to cloud interactions. However, MAGICC does not calculate the effect of changes in c oncentrations of other aerosols such as nitrates, black carbon, or organic carbon, making the assumption that the sulfate cooling effect is a prox y for the sum of all the aerosol effects. Therefore, the climate effects of changes in PM 2.5 emissions and pr ecursors (besides SO 2 ) presented in Chapter 5 were not included in the calculations in this chapter. MAGI CC also calculates all climate effects at the global scale. This global scale captures the climate effects of the long - lived, well - mixed greenhouse ga ses, but does not address the fact that short - lived climate forcers such as aerosols and ozone can have effects that vary with location and timing of emissions. Black carbon in particular is known to cause a positive forcing or warming effect b y absorbing incoming solar radiation, but there are uncertainties about the magnitude of that warming effect and the interaction of black carbon (and other co - emitted aerosol species) with clouds. See 77 FR 38890, 38991 - 993 (June 29, 2012). While black carbon is lik ely to be an important contributor to climate change, it would be premature to include quantification of black carbon climate impacts in an anal ys is of the proposal’s standards at this time. See generally , EPA, Response to Comments to the Endangerment Fin ding Vol. 9 S ection 9.1.6.1, the discussion of black carbon in the endangerment finding at 74 FR at 66520, EPA’s discussion in the recent proposal to revise the PM NAAQS (77 FR at 38991 - 993), and the recentl y published EPA Report to Congress on Black Carbo n. Additionally , the magnitude of PM 2.5 emissions changes (and therefore, black carbon emission changes) related to these standards are small in comparison to the changes in the pollutants which have been included in the MAGICC model simulations. To compute the changes in atmospheric CO 2 concentration, global mean temperature, and sea level rise specifically attributable to the impacts of the proposal, the difference in emissions between the proposal and the baseline scenario was subtracted from the GCAM reference emissions scenario. As a result of the proposal’s emissions reductions from the proposed alternative relative to the baseline case, b y 2100 the concentration of atmospheric CO 2 is projected to be reduced by approximately 1.1 to 1.2 parts per mill ion by volume (ppmv), the global mean temperature is projected to be reduced by approximately 0.0026 to 0.0065 °C, and global mean sea level rise is projected to be reduced by approximately 0.023 to 0.057 cm. For sea level rise, the calculations in MAGI CC do not include the possible effects of accelerated ice flow in Greenland and/or Antarctica ; including these effects would show correspondingl y larger benefits of mitigation . Figure 6 - 7 provides the results over time for the estimated reductions in atmospheric CO 2 concentration associated with the proposal compared to the baseline scenario . Figure 6 - 8 provides the estimated change in projected global mean temperatures associated with the proposal. Figure 6 - 9 provides the estimated reductions i n global mean sea level rise associated with the proposal. The range of reductions in global mean temperature and sea level rise due to uncertaint y in climate sensitivity is larger than that for CO 2 concentrations because CO 2 concentrations are onl y weakl y coupled to climate sensitivity through the dependence on temperature of the rate of ocean absorption of CO 2 , whereas the magnitude of temperature change response to CO 2 changes (and therefore sea level rise) is more tightly coupled to climate sensitivity in the MAGICC model.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 46 **Figure 6**  **- 7**  **Estim ated Projected Reductions in Atm**  **ospheric CO 2**  **Concentrations (parts per million by volum**  **e) from the Baseline for the Proposed Alternative of the Heavy -**  **Duty Proposal (clim ate sensitivity (CS)**  **cases ranging from 1.5**  **- 6°C)** 

**Figure 6**  **- 8**  **Estim ated Projec**  **ted Reductions in Global Mean Surface Temperatures from the Baseline for the**  **Proposed Alternative of the Heavy -**  **Duty Proposal (clim ate sensitivity (CS) cases ranging from** **1.5 -**  **6°C)**

-1.4 -1.2 -1.0 -0.8 -0.6 -0.4 -0.2 0.0

2000 2020 2040 2060 2080 2100**p p** **m v**  

## Change **in CO 2**  

## Concentr**ation (Primary Alt**  **ernative -**  **Baseline)**

CS 1.5 CS 2.0 CS 2.5 CS 3.0 CS 4.5 CS 6.0

-0.007 -0.006 -0.005 -0.004 -0.003 -0.002 -0.001 0.000

2000 2020 2040 2060 2080 2100**d e** **g r** **e e** **s C**  

## Change **in Global Mean T emper**  **ature (Primary Alt**  **ernative -**  **Baseline)**

CS 1.5 CS 2.0 CS 2.5 CS 3.0 CS 4.5 CS 6.0***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 47 **Figure 6**  **- 9**  **Estim ated**  **Projected Reductions in Global Mean Sea Level Rise from the Baseline for the**  **Proposed Alternative of the Heavy -**  **Duty Proposal (clim ate sensitivity (CS) cases ranging from** **1.5 -**  **6°C)** The results in Figure 6 - 8 and Figure 6 - 9 show reductions in the projected global mean temperature and sea level respectivel y, across all climate sensitivi ties. The projected reductions are small relative to the change in temperature (1.8

– 4.8 oC) and sea level rise (2 3

– 5 6 cm) from 1990 to 2100 from the MAGI CC simulations for the GCAM reference case. However, this is to be expected given the magnitude of emissions reductions expected from the proposal in the context of global emissions. These reductions are quantifiable, directionally consistent, and will contribute to reducing the risks associated with climate change. Notabl y, these effects are occur ring every

where around the globe, so benefits that appear to be marginal for any one location, such as a reduction in sea level rise of half a millimeter, can be sizable when the effects are summed along thousands of miles of coastline. Climate change is a global phenomenon and EPA recognizes that this one national action alone will not prevent it; EPA notes this would be true for an y given GHG mitigation action when taken alone or when considered in isolation. EPA also notes that a substantial portion of CO 2 emitted into the atmosphere is not removed b y natural processes for millennia, and therefore each unit of CO 2 not emitted into the atmosphere due to this rule avoids essentially permanent climate change on centennial time scales. Again, it should be noted that the calculations in MAGICC do not include the possible effects of accelerated ice flow in Greenland and/or Antarctica: the recent NRC report estimated a likely sea level increase for the A1B SRES scenario of 0.5 to 1.0 meters, almost double the estimate from MAGI CC, so projected reductions in sea level rise may be similarl y underestimated. 220 If other uncertainties besides climate sensitivity were included in the anal ys is, the resulting ranges of projected changes would likely be slightly

larger. 

### 6.3.3 **Estimated Projected Change in Ocean pH** For this proposal, EPA analyzes another key climate - related variable and calculates projected change in ocean pH for tropical waters. For this anal ys is, changes in ocean pH are related to the change in the atmosph eric concentration of carbon dioxide (CO 2 ) resulting from the emissions reductions associated with the proposed alternative. EPA used the program developed

-0.06 -0.05 -0.04 -0.03 -0.02 -0.01 0.00

2000 2020 2040 2060 2080 2100**c m**  

## Change **in Global Mean Sea Level Rise (Primary Alt**  **ernative -**  **Baseline)**

CS 1.5 CS 2.0 CS 2.5 CS 3.0 CS 4.5 CS 6.0***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 48 for CO 2 Sy stem Calculations CO2SYS, 221 version 1.05, a program which performs calculations relating p arameters of the carbon dioxide (CO 2 ) system in seawater. The program was developed b y Ernie Lewis at Brookhaven National L aboratory and Doug Wallace at the Institut für Meereskunde in Germany , supported by the U.S. Department of Energy , Office of Biologi cal and Environmental Research, under Contract No. DE - ACO2 - 76CH00016. The CO2SYS program uses two of the four measurable parameters of the CO 2 sy stem [total alkalinity

(TA), total inorganic CO 2 (TC), pH, and either fugacit y (fCO 2 ) or partial pressure of CO 2 (pCO 2 )] to calculate the other two parameters given a specific set of input conditions (temperature and pressure) and output conditions chosen by the user. EPA utilized the Excel version ( Pierrot et al. 2006 ) 222 of the program to compute pH for three scen arios: the baseline scenario at a climate sensitivity of 3 degrees for which the CO 2 concentrations was calculated to be 784. 8 7 in 2100, the proposed alternative relative to the baselin e with a CO 2 concentration of 784 .11 , and a calculation for 1990 with a CO 2 concentration of 353. 6 3 . Using the set of seawater parameters detailed below, EPA calculated pH levels for the three scenarios. The pH of the emissions standards relative to the baselin e scenario pH was + 0. 0004 units (more basic). For comparison, th e difference between the baselin e scenario in 2100 and the pH in 1990 was - 0.30 pH units (more acidic). The CO2SYS program required the input of a number of variables and constants for each scenario for calculating the result for both the reference case a nd the proposal’s emissions reduction baseline cases. EPA used the following inputs, with justification and references for these inputs provided in brackets: 1) Input mode: Single - input 2) Choice of constants: Mehrbach et al. (1973) 223 , refit by Dickson and Mill ero (1987) 224 3) Choice of fCO 2 or pCO 2 : pCO 2 4) Choice of KSO4: Dickson (1990) 225 Choice of KSO4: Dickson (1990) 226 5) Choice of pH scale: Total scale Choice of pH scale: Total scale 6) [B] T value: Uppstrom, 1974 The program provides several choices of constants for saltwater that are needed for the calculations. EPA calculated pH values using all choices and found that in all cases the choice had an indistinguishable effect on the results. In addition, EPA ran the model using a variet y of other required input values to test whether the model was sensitive to these inputs. EPA found the model was not sensitive to these inputs in terms of the incremental change in pH calculated for each climate sensitivity case. The input values are derived from certified reference materials of sterilized natural sea water (Dickson, 2003, 2005, and 2009). 227 Based on the projected atmospheric CO 2 concentration reductions that would result from this proposal’s baseline case ( 1.2 ppmv for a climate sensitivity of 3.0), the modeling program calculates an increase in ocean pH of approximately 0.000 6 pH units in 2100. Thus, this analy sis indicates the projected decrease in atmospheric CO 2 concentrations from the proposed alternative yiel ds an increase in ocean pH. Table 6 - 2 contains the projected changes in ocean pH based the change in atmospheric CO 2 concentrations which were derive d from the MAGI CC modeling.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 49 **Table 6**  **- 2**  **Impact of the Proposal’s GHG Emissions Reductions on Ocean pH** CLIMATE SENSITIVITY DIFFERENCE

IN CO 2 A YEAR PROJECTED CHANGE **3.0** - 1.2 ppmv 2100 0. 000 6 Note: a Represents the change in atmospheric CO 2 concentrations in 2100 based on the difference from the proposed alternative relative to the base case from the GCAM reference scenario used in the MAGICC modeling. 

### 6.3.4 **Summary of Climate Analyses** EPA’s anal ys is of the impact of the proposal’s emissions reductions on global climate conditions is intended to quantify these potential reductions using the best available science. While EPA’s modeling results of the impact of this proposal alone show sm all differences in climate effects (CO 2 concentration, global mean temperature, sea level rise, and ocean pH), in comparison to the total projected changes, they yield results that are repeatable and directionally consistent within the modeling frameworks used. The results are summarized in Table 6 - 3 , Impact of GHG Emissions Reductions o n Projected Changes in Global Climate Associated with the Proposal . These projected reductions are proportionally representative of changes to U.S. GHG emissions in the transportation sector. While not formally estimated for this proposal, a reduction in projected global mean temperature and sea level rise implies a reduction in the risks associated with climate change. The figures for these variables illustrate that across a range of climate sensitivities projected global mean temperature and sea level rise increase less in the proposed alternative scenario than in the reference (no climate policy) case. The benefits of GHG emissions reductions can be characterized both qualitatively and quantitatively , some of which can be monetized (see Chapter 9 ). There are substantial uncertainties in modeling the global risks o f climate change, which complicates quantification and cost - benefits assessments. Changes in climate variables are a meaningful prox y for changes in the risk of all potential impacts -- including those that can be monetized, and those that have not been mone tized but can be quantified in ph ys ical terms (e.g., water availability ), as well as those that have not yet been quantified or are extremely difficult to quantify

(e.g., forest disturbance and catastrophic events such as collapse of large ice sheets and s ubsequent sea level rise). **Table 6**  **- 3**  **Impa ct of GHG Emissions Reductions o**  **n Projected Changes in Global Climate Associated with the**

**Proposal ( Based**  **o n**  **a Range**  **o f Clim**  **ate Sensitivities from 1.5**  **- 6°C)**  VARIABLE UNITS YEAR PROJECTED CHANGE **Atmospheric CO 2**  **Concentration** ppmv 2100 - 1.1 to - 1.2 **Global Mean Surface Temperature**  oC 2100 - 0.0026 to - 0.0065 **Sea Level Rise** cm 2100 - 0.023 to - 0.057 **Ocean pH** pH units 2100 + 0. 000 6 a Note: a The value for projected change in ocean pH is based on a climate sensitivity of 3.0.***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

6 - 50 

## References 1 U.S. EPA (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F, 2009. 2 U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washingto n, DC, EPA/600/R - 08/139F. 3 78 FR 3086 (January 15, 2013) pages 3103 - 3104. 4 77 FR 38890 (June 29, 2012) pages 38906 - 38911. 5 78 FR 3086 (January 15, 2013) pages 3103 - 3104. 6 U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F, Chapter 6 (Section 6.5) and Chapter 7 (Section 7.6). 7 78 FR 3103 (January 15, 2013). 8 78 FR 3103 (January 15, 2013). 9 78 FR 3103 - 3104 (January 15, 2013). 10 78 FR 3104 (January 15, 2013). 11 U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139 F. pg 2 - 13. 12 U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F. Chapter 8 and Chapter 2. 13 77 FR 38890, (June 29, 2012) page 38910. 14 78 FR 3086 (January 15, 2013) page 3104. 15 U.S. EPA. (2011). Policy Assessment for the Revie w of the PM NAAQS. U.S. Environmental Protection Agency, Washington, DC, EPA/452/R - 11 - 003. Section 2.2.1. 16 U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F. Chapter 8 and Chapter 2 (Section 2.4.1). 17 U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F. Section 2.3.4 and Table 2 - 6. 18 78 FR 3167 - 8 (January 15, 2013). 19 77 FR 38947 - 51 (June 29, 2012). 20 U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 08/139F. Section 2.3.5 and Table 2 - 6. 21 78 FR 3121 (January 15, 2013). 22 U.S. EPA. Integrated Science Assessment of Ozone and Related Photochemical O xidants (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R - 10/076F, 2013. The ISA is available at http://cfpub.epa.gov/ncea/isa/recordisp lay.cfm?deid=247492#Dow nload . 23 U.S. EPA (2008). Integrated Science Assessment for Oxides of Nitrogen

– Health Criteria (Final Report). EPA/600/R - 08/071. Washington, DC, U.S. EPA. Retrieved on March 19, 2009 from http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=194645 . 24 U.S. EPA (2008). Integrated Science Assessment for Oxides of Nitrogen

– Health Criteria (Final Report). EPA/600/R - 08/071. Washington, DC: U.S. EPA, Section 3.1.3. 1. 25 U.S. EPA (2008). Integrated Science Assessment for Oxides of Nitrogen

– Health Criteria (Final Report). EPA/600/R - 08/071. Washington, DC: U.S. EPA, Section 3.1.3.2. 26 U.S. EPA (2008). Integrated Science Assessment for Oxides of Nitrogen

– Health Crite ria (Final Report). EPA/600/R - 08/071. Washington, DC: U.S. EPA, Section 3.1.7. 27 U.S. EPA (2008). Integrated Science Assessment for Oxides of Nitrogen

– Health Criteria (Final Report). EPA/600/R - 08/071. Washington, DC: U.S. EPA. 28 U.S. EPA (2008). Integrated Science Assessment (ISA) for Sulfur Oxides

– Health Criteria (Final Report). EPA/600/R - 08/047F. Washington, DC, U.S. EPA. Retrieved on March 19, 2009 from http://cfpub.ep a.gov/ncea/cfm/recordisplay.cfm?deid=198843 .***** E.O. 12866 Review –**  **REVISED –**  **Do Not Cite, Quote, or Release During Review *****

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