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Chapter 6: Health and Environmental Impacts

6.1 Health and Environmental Effects of 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, 

specifically: particulate matter, ozone, nitrogen oxides (NOX), sulfur oxides (SOX), carbon 

monoxide and air toxics. These pollutants will not be directly regulated by the standards, but the 

standards will 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 highly complex mixture of solid particles and liquid droplets 

distributed among numerous atmospheric gases which interact 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 about 100 μm). Atmospheric particles can be grouped into several 

classes according to their aerodynamic and physical sizes. Generally, the three broad classes of 

particles considered by EPA include ultrafine particles (UFP, aerodynamic diameter <0.1 μm), 

“fine” particles (PM2.5; particles with a nominal mean aerodynamic diameter less than or equal to 

2.5 μm), and “thoracic” particles (PM10; particles with a nominal mean aerodynamic diameter 

less than or equal to 10 μm). Particles that fall within the size range between PM2.5 and PM10, 

are referred to as “thoracic coarse particles” (PM10-2.5, particles with a nominal mean 

aerodynamic diameter less than or equal to 10 μm and greater than 2.5 μm). EPA currently has 

standards that regulate PM2.5 and PM10.

A

Particles span many 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 the latter as “secondary” 

particles. Particle concentration and composition varies by time of year and location, and in 

addition to differences in source emissions, is affected by several weather-related factors, such as 

temperature, clouds, humidity, and wind. 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 primarily by combustion processes and by transformations of 

gaseous emissions (e.g., sulfur oxides (SOX), nitrogen oxides (NOX) and volatile organic 

compounds (VOCs)) in the atmosphere. The chemical and physical properties of PM2.5 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 PM10 standard 

provides protection against effects associated with short-term exposure to thoracic coarse particles (i.e., PM10-2.5).
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vary greatly with time, region, meteorology, and source category. Thus, PM2.5 may include a 

complex mixture of different components including sulfates, nitrates, organic compounds, 

elemental carbon and metal compounds. These particles can remain in the atmosphere for days 

to weeks and travel through the atmosphere hundreds to thousands of kilometers.1 

6.1.1.1.2 Health Effects of Particulate Matter 

Scientific studies show ambient PM is associated with a broad range of health effects. 

These health effects are discussed in detail in the December 2009 Integrated Science Assessment 

for Particulate Matter (PM ISA).

2

 The PM ISA summarizes health effects evidence associated 

with both short- and long-term exposures to PM2.5, PM10-2.5, and ultrafine particles. The PM ISA 

concludes that human exposures to ambient PM2.5 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 ISA’s conclusions pertaining to health effects associated 

with both short- and long-term PM exposures. Further discussion of health effects associated 

with PM2.5 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 PM2.5 and premature mortality and cardiovascular effects and a likely causal 

relationship exists between long- and short-term PM2.5 exposures and respiratory effects. 

Further, there is evidence suggestive of a causal relationship between long-term PM2.5 exposures 

and other health effects, including developmental and reproductive effects (e.g., low birth 

weight, infant mortality) and carcinogenic, mutagenic, and genotoxic effects (e.g., lung cancer 

mortality).C

As summarized in the Final PM NAAQS rule, and discussed extensively in the 2009 PM 

ISA, the available scientific evidence significantly strengthens the link between long- and shortterm exposure to PM2.5 and premature mortality, while providing indications that the magnitude 

of the PM2.5- mortality association with long-term exposures may be larger than previously

estimated.5,6 The strongest evidence comes from recent studies investigating long-term exposure 

to PM2.5 and cardiovascular-related mortality. The evidence supporting a causal relationship 

between long-term PM2.5 exposure and mortality also includes consideration of new studies that 

demonstrated an improvement in community health following reductions in ambient fine 

particles.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 causal relationship, and not likely to be a causal relationship 

(U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental 

Protection Agency, Washington, DC, EPA/600/R-08/139F, Table 1–3). 

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 biologic modes of action or pathways for PM-related cardiovascular and 

respiratory effects (U.S. EPA. (2009). Integrated Science Assessment for Particulate Matter (Final Report). U.S. 

Environmental Protection Agency, Washington, DC, EPA/600/R-08/139F, Chapter 5).
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Several studies evaluated in the 2009 PM ISA have examined the association between 

cardiovascular effects and long-term PM2.5 exposures in multi-city studies conducted in the U.S. 

and Europe. These studies have provided new evidence linking long-term exposure to PM2.5

with an array of cardiovascular effects such as heart attacks, congestive heart failure, stroke, and 

mortality. This evidence is coherent with studies of short-term exposure to PM2.5 that have 

observed associations with a continuum of effects ranging from subtle changes in indicators of 

cardiovascular health to serious clinical events, such as increased hospitalizations and emergency

department visits due to cardiovascular disease and cardiovascular mortality.8

As detailed in the 2009 PM ISA, extended analyses of seminal epidemiological studies,

as well as more recent epidemiological studies conducted in the U.S. and abroad, provide strong 

evidence of respiratory-related morbidity effects associated with long-term PM2.5 exposure. The 

strongest evidence for respiratory-related effects is from studies that evaluated decrements in

lung function growth (in children), increased respiratory symptoms, and asthma development. 

The strongest evidence from short-term PM2.5 exposure studies has been observed for increased 

respiratory-related emergency department visits and hospital admissions for chronic obstructive 

pulmonary disease (COPD) and respiratory infections.9

The body of scientific evidence detailed in the 2009 PM ISA is still limited with respect 

to associations between long-term PM2.5 exposures and developmental and reproductive effects 

as well as cancer, mutagenic, and genotoxic effects. The strongest evidence for an association 

between PM2.5 and developmental and reproductive effects comes from epidemiological studies 

of low birth weight and infant mortality, especially due to respiratory causes during the postneonatal 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 PM2.5 and lung 

cancer mortality, but studies have generally not reported associations between PM2.5 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 previously identified at-risk populations and lifestages (i.e., 

children, older adults, and individuals with pre-existing heart and lung disease) and supports the 

identification of additional at-risk populations (e.g., persons with lower socioeconomic status, 

genetic differences). Additionally, there is emerging, though still limited, evidence for additional 

potentially at-risk populations and lifestages, such as those with diabetes, people who are obese, 

pregnant women, and the developing fetus.16

For PM10-2.5, the 2009 PM ISA concluded that available evidence was suggestive of a 

causal relationship between short-term exposures to PM10-2.5 and cardiovascular effects (e.g., 

hospital admissions and ED visits, changes in cardiovascular function), respiratory effects (e.g., 

ED visits and hospital admissions, increase in markers of pulmonary inflammation), and 

premature mortality. Data were inadequate to draw conclusions regarding the relationships 

between long-term exposure to PM10-2.5 and various health effects. 17,18,19

For ultrafine particles, the 2009 PM ISA concluded that the evidence was suggestive of a 

causal relationship between short-term exposures and cardiovascular effects, including changes 

in heart rhythm and vasomotor function (the ability of blood vessels to expand and contract). It 
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also concluded that there was evidence suggestive of a causal relationship between short-term 

exposure to ultrafine particles and respiratory effects, including lung function and pulmonary

inflammation, with limited and inconsistent evidence for increases in ED visits and hospital 

admissions. Data were inadequate to draw conclusions regarding the relationship between shortterm 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 typically formed through reactions involving VOCs and 

NOX in the lower atmosphere in the presence of sunlight. These pollutants, often referred to as 

ozone precursors, are emitted by many types of pollution sources such as highway and nonroad 

motor vehicles and engines, power plants, chemical plants, refineries, makers of consumer and 

commercial products, industrial facilities, and smaller area sources. 

The science of ozone formation, transport, and accumulation is complex. Ground-level 

ozone is produced and destroyed in a cyclical set of chemical reactions, many of which are 

sensitive to temperature and sunlight. When ambient temperatures and sunlight levels remain 

high for several days and the air is relatively stagnant, ozone and its precursors can build up and 

result in more ozone than typically occurs on a single high-temperature day. Ozone 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 NOX emissions. 

The highest levels of ozone are produced when both VOC and NOX emissions are present 

in significant quantities on clear summer days. Relatively small amounts of NOX enable ozone 

to form rapidly when VOC levels are relatively high, but ozone production is quickly limited by 

removal of the NOX. Under these conditions NOX reductions are highly effective in reducing 

ozone while VOC reductions have little effect. Such conditions are called “NOX-limited.” 

Because the contribution of VOC emissions from biogenic (natural) sources to local ambient 

ozone concentrations can be significant, even some areas where man-made VOC emissions are 

relatively low can be NOX-limited.

Ozone concentrations in an area also can be lowered by the reaction of nitric oxide (NO) 

with ozone, forming nitrogen dioxide (NO2). As the air moves downwind and the cycle 

continues, the NO2 forms additional ozone. The importance of this reaction depends, in part, on 

the relative concentrations of NOX, VOC, and ozone, all of which change with time and location. 

When NOX levels are relatively high and VOC levels relatively low, NOX forms inorganic 

nitrates (i.e., particles) but relatively little ozone. Such conditions are called “VOC-limited.” 

Under these conditions, VOC reductions are effective in reducing ozone, but NOX reductions can 

actually increase local ozone under certain circumstances. Even in VOC-limited urban areas, 

NOX reductions are not expected to increase ozone levels if the NOX reductions are sufficiently 

large. Rural areas are usually NOX-limited, due to the relatively large amounts of biogenic VOC 

emissions in such areas. Urban areas can be either VOC- or NOX-limited, or a mixture of both, 

in which ozone levels exhibit moderate sensitivity to changes in either pollutant.
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6.1.1.2.2 Health Effects of 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 ISA).

22

The Ozone ISA 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. EThe discussion below highlights the Ozone ISA’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 ISA concludes 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 cardiovascular effects, including decreased cardiac function and 

increased vascular disease, and total mortality are likely to be causally associated with short-term 

exposure to ozone and that evidence is suggestive of a causal relationship between central 

nervous system effects and short-term exposure to ozone. 

For long-term exposure to ozone, the Ozone ISA concludes that respiratory effects, 

including new onset asthma, pulmonary inflammation and injury, are likely to be causally related 

with ozone exposure. The Ozone ISA 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 system effects and total mortality. The 

evidence 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 effects 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., Vitamins 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 respiratory and immune systems. 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 greater 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 

move between locations which have notable different ozone concentrations. Also, the amount of ozone delivered to 

the lung is not only influenced by the ambient concentrations but also by the breathing route and rate.

E The ISA evaluates evidence and draws conclusions on the causal relationship between relevant pollutant exposures 

and 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 more information on these levels of evidence, please refer to Table II in the Preamble of 

the ISA. 
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6.1.1.3 Nitrogen Oxides 

6.1.1.3.1 Background on Nitrogen Oxides 

Nitrogen dioxide (NO2) is a member of the nitrogen oxide (NOX) family of gases. Most 

NO2 is formed in the air through the oxidation of nitric oxide (NO) emitted when fuel is burned 

at a high temperature. NO2 and its gas phase oxidation products can dissolve in water droplets

and further oxidize to form nitric acid which reacts 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. NOX 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 of 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 ISA).

23

 EPA concluded that the findings of epidemiological, controlled 

human exposure, and animal toxicological studies provided evidence that was sufficient to infer 

a likely causal relationship between respiratory effects and short-term NO2 exposure. The 2008 

ISA for Oxides of Nitrogen concluded that the strongest evidence for such a relationship comes 

from epidemiological studies of respiratory effects including increased respiratory symptoms, 

emergency department visits, and hospital admissions. Based on both short- and long-term 

exposure studies, the 2008 ISA 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 NO2-related respiratory effects. Based on findings from controlled 

human exposure studies, the 2008 ISA for Oxides of Nitrogen also drew two broad conclusions 

regarding airway responsiveness following NO2 exposure. First, the NOX ISA concluded that 

NO2 exposure may enhance the sensitivity to allergen-induced decrements in lung function and 

increase the allergen-induced airway inflammatory response following 30-minute exposures of 

asthmatic adults to NO2 concentrations as low as 260 ppb.

24

 Second, exposure to NO2 was found 

to enhance the inherent responsiveness of the airway to subsequent nonspecific challenges in 

controlled human exposure studies of healthy and asthmatic adults. Statistically significant 

increases in nonspecific airway responsiveness were reported for asthmatic adults following 30-

minute exposures to 200-300 ppb NO2 and following 1-hour exposures to 100 ppb NO2.

25

 

Enhanced airway responsiveness could have important clinical implications for asthmatics since 

transient increases in airway responsiveness following NO2 exposure have the potential to 

increase symptoms and worsen asthma control. Together, the epidemiological and experimental 

data sets formed a plausible, consistent, and coherent description of a relationship between NO2

exposures and an array of adverse health effects that range from the onset of respiratory

symptoms to hospital admissions and emergency department visits for respiratory causes, 

especially asthma.

26

 

In evaluating a broader range of health effects, the 2008 ISA for Oxides of Nitrogen

concluded evidence was “suggestive but not sufficient to infer a causal relationship” between 

short-term NO2 exposure and premature mortality and between long-term NO2 exposure and 

respiratory effects. The latter was based largely on associations observed between long-term 

NO2 exposure and decreases in lung function growth in children. Furthermore, the 2008 ISA for 
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Oxides of Nitrogen concluded that evidence was “inadequate to infer the presence or absence of 

a causal relationship” between short-term NO2 exposure and cardiovascular effects as well as 

between long-term NO2 exposure and cardiovascular effects, reproductive and developmental 

effects, premature mortality, and cancer.27 The conclusions for these health effect categories 

were informed by uncertainties in the evidence base such as the independent effects of NO2

exposure within the broader mixture of traffic-related pollutants, limited evidence from 

experimental studies, and/or an overall limited literature base.

6.1.1.4 Sulfur Oxides

6.1.1.4.1 Background

Sulfur dioxide (SO2), a member of the sulfur oxide (SOX) family of gases, is formed from 

burning fuels containing sulfur (e.g., coal or oil), extracting gasoline from oil, or extracting 

metals from ore. SO2 andits gas phase oxidation products can dissolve in water droplets and 

further oxidize to form sulfuric acid which reacts with ammonia to form sulfates, which are 

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 of Sulfur Oxides

This section provides an overview of the health effects associated with SO2. Additional 

information on the health effects of SO2 can be found in the 2008 Integrated Science Assessment 

for Sulfur Oxides – Health Criteria (SOX 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 SO2. The immediate 

effect of SO2 on the respiratory system in humans is bronchoconstriction. Asthmatics are more 

sensitive to the effects of SO2 likely resulting from preexisting inflammation associated with this 

disease. In addition to those with asthma (both children and adults), potentially sensitive groups 

include all children and the elderly. In free-breathing laboratory studies involving controlled 

human exposures to SO2, respiratory effects have consistently been observed following 5-10 min 

exposures at SO2 concentrations ≥ 400 ppb in asthmatics engaged in moderate to heavy 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 SO2 at concentrations between 200 and 1000 ppb, both in terms of 

increasing severity of respiratory symptoms and decrements in lung function, as well as the

percentage of asthmatics adversely affected. 

In epidemiologic studies, respiratory effects have been observed in areas where the mean 

24-hour SO2 levels range from 1 to 30 ppb, with maximum 1 to 24-hour average SO2 values 

ranging from 12 to 75 ppb. Important new multicity studies and several other studies have found 

an association between 24-hour average ambient SO2 concentrations and respiratory symptoms 

in children, particularly those with asthma. Generally consistent associations also have been 

observed between ambient SO2 concentrations and emergency department visits and 

hospitalizations for all respiratory causes, particularly among children and older adults (≥ 65 

years), and for asthma. A limited subset of epidemiologic studies has examined potential 

confounding by copollutants using multipollutant regression models. These analyses indicate 
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that although copollutant adjustment has varying degrees of influence on the SO2 effect 

estimates, the effect of SO2 on respiratory health outcomes appears to be generally robust and 

independent of the effects of gaseous and particulate copollutants, suggesting that the observed 

effects of SO2 on respiratory endpoints occur independent of the effects of other ambient air 

pollutants. 

Consistent associations between short-term exposure to SO2 and mortality have been 

observed in epidemiologic studies, with larger effect estimates reported for respiratory mortality 

than for cardiovascular mortality. While this finding is consistent with the demonstrated effects 

of SO2 on respiratory morbidity, uncertainty remains with respect to the interpretation of these 

observed mortality associations due to potential confounding by various copollutants. Therefore,

EPA has concluded that the overall evidence is suggestive of a causal relationship between shortterm exposure to SO2 and mortality. Significant associations between short-term exposure to 

SO2 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 causal relationship between SO2 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

Information on the health effects of carbon monoxide (CO) can be found in the January

2010 Integrated Science Assessment for Carbon Monoxide (CO ISA).

29

 The CO ISA concludes 

that ambient concentrations of CO are associated with a number of adverse health effects.FThis 

section provides a summary of the health effects associated with exposure to ambient 

concentrations of CO.

G

Controlled human exposure studies of subjects with coronary artery disease show a 

decrease in the time to onset of exercise-induced angina (chest pain) and electrocardiogram 

changes following CO exposure. In addition, epidemiologic studies show associations between 

short-term CO exposure and cardiovascular morbidity, particularly increased emergency room 

visits and hospital admissions for coronary heart disease (including ischemic heart disease, 

 

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 sources, 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.
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myocardial infarction, and angina). Some epidemiologic evidence is also available for increased 

hospital admissions and emergency room visits for congestive heart failure and cardiovascular 

disease as a whole. The CO ISA concludes that a causal relationship is likely to exist between 

short-term exposures to CO and cardiovascular morbidity. It also concludes that available data 

are inadequate to conclude that a causal relationship exists between long-term exposures to CO 

and cardiovascular morbidity. 

Animal studies show various neurological effects with in-utero CO exposure. Controlled 

human exposure studies report central nervous system and behavioral effects following low-level 

CO exposures, although the findings have not been consistent across all studies. The CO ISA 

concludes the evidence is suggestive of a causal relationship with both short- and long-term 

exposure to CO and central nervous system effects.

A number of studies cited in the CO ISA have evaluated the role of CO exposure in birth 

outcomes such as preterm birth or cardiac birth defects. The epidemiologic studies provide 

limited evidence of a CO-induced effect on preterm births and birth defects, with weak evidence 

for a decrease in birth weight. Animal toxicological studies have found perinatal CO exposure to 

affect birth weight, as well as other developmental outcomes. The CO ISA concludes the 

evidence is suggestive of a causal relationship between long-term exposures to CO and 

developmental effects and birth outcomes.

Epidemiologic studies provide evidence of associations between ambient CO 

concentrations and respiratory morbidity such as changes in pulmonary function, respiratory

symptoms, and hospital admissions. A limited number of epidemiologic studies considered 

copollutants such as ozone, SO2, and PM in two-pollutant models and found that CO risk 

estimates were generally robust, although this limited evidence makes it difficult to disentangle 

effects attributed to CO itself from those of the larger complex air pollution mixture. Controlled 

human exposure studies have not extensively evaluated the effect of CO on respiratory

morbidity. Animal studies at levels of 50-100 ppm CO show preliminary evidence of altered 

pulmonary vascular remodeling and oxidative injury. The CO ISA concludes that the evidence 

is suggestive of a causal relationship between short-term CO exposure and respiratory morbidity, 

and inadequate to conclude that a causal relationship exists between long-term exposure and 

respiratory morbidity. 

Finally, the CO ISA concludes that the epidemiologic evidence is suggestive of a causal 

relationship between short-term concentrations of CO and mortality. Epidemiologic studies 

provide evidence of an association between short-term exposure to CO and mortality, but limited 

evidence is available to evaluate cause-specific mortality outcomes associated with CO exposure. 

In addition, the attenuation of CO risk estimates which was often observed in copollutant models 

contributes to the uncertainty as to whether CO is acting alone or as an indicator for other 

combustion-related pollutants. The CO ISA also concludes that there is not likely to be a causal 

relationship between relevant long-term exposures to CO and mortality.
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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 hydrocarbons. A number of these gaseous hydrocarbon 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). These particles have a large surface area 

which makes them an excellent medium for adsorbing organics and their small size makes them 

highly respirable. Many of the organic compounds present in the gases and on the particles, such 

as polycyclic organic matter, are individually known to have mutagenic and carcinogenic 

properties. 

Diesel exhaust varies significantly in chemical composition and particle sizes between 

different engine types (heavy-duty, 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 physical 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 Institute for Occupational Safety 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 unit 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 of 

possible lung cancer risk. The outcome was that environmental risks of cancer from long-term 

diesel exhaust exposures could plausibly range from as low as 10-5to as high as 10-3. Because of 

uncertainties, the analysis acknowledged that the risks could be lower than 10-5, and a zero risk 

from diesel exhaust 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/m3for diesel exhaust measured as diesel particulate matter. This RfC 
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does not consider allergenic effects such as those associated 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 time 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 database 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 symptoms (cough and phlegm), 

and neurophysiological symptoms 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 then 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 PM2.5 NAAQS of 15 μg/m3. In

2012, EPA revised the annual PM2.5 NAAQS to 12 μg/m3. 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 PM2.5 NAAQS is 

designed to provide protection from the noncancer health effects and premature mortality

attributed to exposure to PM2.5. 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 locations 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 engines. Of particular 

note since 2011 are three new epidemiology studies which have examined lung cancer in 

occupational populations, for example, truck drivers, underground nonmetal miners and other 

diesel motor related occupations. These studies reported increased risk 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 reinforces the

concern that diesel exhaust exposure likely poses a lung cancer hazard. The findings from these 

newer studies do not necessarily apply 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, in June 2012 the World Health Organization’s International Agency

for Research on Cancer (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.” 
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6.1.1.7 Air Toxics

Heavy-duty vehicle emissions contribute to ambient levels of air toxics known or 

suspected as human or animal carcinogens, or that have noncancer health effects. The 

population experiences an elevated risk of cancer and other noncancer health effects from 

exposure to the class of pollutants known collectively as “air toxics.”36 These compounds 

include, but are not limited to, benzene, 1,3-butadiene, formaldehyde, acetaldehyde, acrolein, 

polycyclic organic matter, and naphthalene. These compounds were identified as national or 

regional risk drivers or contributors in the 2005 National-scale Air Toxics Assessment and have 

significant inventory contributions from mobile sources.37 

6.1.1.7.1 Health Effects of Benzene

EPA’s IRIS database lists benzene as a known human carcinogen (causing leukemia) by

all routes of exposure, and concludes that exposure is associated with additional health effects, 

including genetic changes in both humans and animals and increased proliferation of bone 

marrow cells in mice.38,39,40 EPA states in its IRIS database that data indicate a causal 

relationship between benzene exposure and acute lymphocytic leukemia and suggest a 

relationship between benzene exposure and chronic non-lymphocytic leukemia and chronic 

lymphocytic leukemia. EPA’s IRIS documentation for benzene also lists a range of 2.2 x 10-6to 

7.8 x 10-6as 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. Department 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 lymphocyte count in blood.46,47 EPA’s inhalation reference 

concentration (RfC) for benzene is 30 μg/m3. The RfC is based on suppressed absolute 

lymphocyte counts seen in humans under occupational exposure conditions. In addition, recent 

work, including studies sponsored by the Health Effects Institute (HEI), provides evidence that 

biochemical responses are occurring at lower levels of benzene exposure than previously 

known.48,49,50,51 EPA’s IRIS program has not yet evaluated these new data. EPA does not 

currently have an acute reference concentration for benzene. The Agency for Toxic Substances 

and Disease Registry (ATSDR) Minimal Risk Level (MRL) for acute exposure to benzene is 29 

μg/m3for 1-14 days 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 risk 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.
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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 metabolites by

experimental animals and humans. The specific mechanisms of 1,3-butadiene-induced 

carcinogenesis are unknown; however, the scientific evidence strongly suggests that the 

carcinogenic effects are mediated by genotoxic metabolites. Animal data suggest that females 

may be more sensitive than males for cancer effects associated with 1,3-butadiene exposure; 

there are insufficient data in humans from which to draw conclusions about sensitive 

subpopulations. The URE for 1,3-butadiene is 3 × 10-5per μg/m3.

58 1,3-butadiene also causes a 

variety of reproductive and developmental effects in mice; no human data on these effects are 

available. The most sensitive effect was ovarian atrophy observed in a lifetime bioassay of 

female mice.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/m3).

6.1.1.7.3 Health Effects of Formaldehyde

In 1991, EPA concluded that formaldehyde 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 agency and posted on the Integrated Risk Information System 

(IRIS) database. Since that time, the National Toxicology Program (NTP) and International 

Agency for Research on Cancer (IARC) have concluded that formaldehyde is a known human 

carcinogen.61,62,63

The conclusions by IARC and NTP reflect the results of epidemiologic research 

published since 1991 in combination with previous animal, human and mechanistic evidence. 

Research conducted by the National Cancer Institute reported an increased risk of 

nasopharyngeal cancer and specific lymphohematopoietic malignancies among workers exposed 

to formaldehyde.64,65,66 A National Institute of Occupational Safety and Health study of garment 

workers also reported increased risk of death due to leukemia among workers exposed to 

formaldehyde.67 Extended follow-up of a cohort of British chemical workers did not report 

evidence of an increase in nasopharyngeal or lymphohematopoietic cancers, but a continuing 

statistically significant excess in lung cancers was reported.68 Finally, a study of embalmers 

reported formaldehyde 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 by the Agency for 

Toxics Substances and Disease Registry in 199970 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 

defined exposure concentrations for minimal risk levels (MRLs). The health endpoints reviewed 

included sensory irritation of eyes and respiratory tract, pulmonary function, nasal 

histopathology, and immune system effects. In addition, research on reproductive and 

developmental effects and neurological effects were discussed along with several studies that 

suggest that formaldehyde may increase the risk of asthma – particularly in the young.

EPA released a draft Toxicological Review of Formaldehyde – Inhalation Assessment 

through the IRIS program for peer review by the National Research Council (NRC) and public 

comment in June 2010.73 The draft assessment reviewed more recent research from animal and 
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human studies on cancer and other health effects. The NRC released their review report in April 

201174 (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 of Acetaldehyde

Acetaldehyde is classified in EPA’s IRIS database as a probable human carcinogen, 

based on nasal tumors in rats, and is considered toxic by the inhalation, oral, and intravenous 

routes.75 The URE in IRIS for acetaldehyde is 2.2 × 10-6per μg/m3.

76

 Acetaldehyde is 

reasonably anticipated to be a human carcinogen by the U.S. DHHS in the 13

th Report on 

Carcinogens and is classified as possibly carcinogenic to humans (Group 2B) by the IARC.77,78 

EPA is currently conducting a reassessment of cancer risk from inhalation exposure to 

acetaldehyde.

The primary noncancer effects of exposure to acetaldehyde vapors include irritation of 

the eyes, skin, and respiratory tract.79 In short-term (4 week) rat studies, degeneration of 

olfactory epithelium was observed at various concentration levels of acetaldehyde exposure.80,81 

Data from these studies were used by EPA to develop an inhalation reference concentration of 9 

μg/m3. Some asthmatics have been shown to be a sensitive subpopulation to decrements in 

functional expiratory volume (FEV1 test) and bronchoconstriction upon acetaldehyde 

inhalation.82 The agency is currently conducting a reassessment of the health hazards from 

inhalation exposure to acetaldehyde. 

6.1.1.7.5 Health Effects of Acrolein

EPA most recently evaluated the toxicological and health effects literature related to 

acrolein in 2003 and concluded that the human carcinogenic potential of acrolein could not be 

determined because the available data were inadequate. No information was available on the 

carcinogenic effects of acrolein in humans and the animal data provided inadequate evidence of 

carcinogenicity.

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 have been 

observed after subchronic exposure to acrolein.85 The agency has developed an RfC for acrolein 

of 0.02 μg/m3 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 assessment was completed.

Acrolein is extremely acrid and irritating to humans when inhaled, with acute exposure 

resulting in upper respiratory tract irritation, mucus hypersecretion and congestion. The intense 

irritancy of this carbonyl has been demonstrated during controlled tests in human subjects, who 

suffer intolerable eye and nasal mucosal sensory reactions within minutes of exposure.87 These 

data and additional studies regarding acute effects of human exposure to acrolein are 

summarized in EPA’s 2003 IRIS Human Health Assessment for acrolein.88 Studies in humans 

indicate that levels as low as 0.09 ppm (0.21 mg/m3) for five minutes may elicit subjective 

complaints of eye irritation with increasing concentrations leading to more extensive eye, nose 

and respiratory symptoms. Acute exposures in animal studies report bronchial hyperresponsiveness. Based on animal data (more pronounced respiratory irritancy in mice with 
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allergic airway disease in comparison to non-diseased mice89) and demonstration of similar

effects in humans (e.g., reduction in respiratory rate), individuals with compromised respiratory

function (e.g., emphysema, asthma) are expected to be at increased risk of developing adverse 

responses to strong respiratory irritants such as acrolein. EPA does not currently have an acute 

reference concentration for acrolein. The available health effect reference values for acrolein 

have been summarized by EPA and include an ATSDR MRL for acute exposure to acrolein of 

7 μg/m3for 1-14 days exposure; and Reference Exposure Level (REL) values from the 

California Office of Environmental Health Hazard Assessment (OEHHA) for one-hour and 8-

hour exposures of 2.5 μg/m3and 0.7 μg/m3, respectively.90 

6.1.1.7.6 Health Effects of Polycyclic Organic Matter (POM)

The term polycyclic organic matter (POM) defines a broad class of compounds that 

includes the polycyclic aromatic hydrocarbon compounds (PAHs). One of these compounds, 

naphthalene, is discussed separately below. POM compounds are formed primarily from 

combustion and are present in the atmosphere in gas and particulate form. Cancer is the major 

concern from exposure to POM. Epidemiologic studies have reported an increase in lung cancer 

in humans exposed to diesel exhaust, coke oven emissions, roofing tar emissions, and cigarette 

smoke; all of these mixtures contain POM compounds.9192 Animal studies have reported 

respiratory tract tumors from inhalation exposure to benzo[a]pyrene and alimentary tract and 

liver tumors from oral exposure to benzo[a]pyrene.93 In 1997 EPA classified seven PAHs 

(benzo[a]pyrene, benz[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, 

dibenz[a,h]anthracene, and indeno[1,2,3-cd]pyrene) as Group B2, probable human carcinogens.94 

Since that time, studies have found that maternal exposures to PAHs in a population of pregnant 

women were associated with several adverse birth outcomes, including low birth weight and 

reduced length at birth, as well as impaired cognitive development in preschool children (3 years 

of age).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]pyrene.

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 primarily a product of 

combustion. Acute (short-term) exposure of humans to naphthalene by inhalation, ingestion, or 

dermal contact is associated with hemolytic anemia and damage to the liver and the nervous 

system.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 reassessment 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 not represent official agency opinion and was released solely for the purposes of 

external peer review and public comment. The National Toxicology Program listed naphthalene 

as "reasonably anticipated to be a human carcinogen" in 2004 on the basis of bioassays reporting 

clear evidence of carcinogenicity in rats and some evidence of carcinogenicity in mice.101 
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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 IRIS 

assessment includes noncancer data on hyperplasia and metaplasia in nasal tissue that form the 

basis of the inhalation RfC of 3 μg/m3.

104

 The ATSDR MRL for 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 will be affected by this proposal. Mobile source air toxic 

compounds that would potentially be impacted include ethylbenzene, propionaldehyde, toluene, 

and xylene. Information regarding the health effects of these compounds can be found in EPA’s 

IRIS database.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 major roadways. These studies 

frequently have employed 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 on health effects associated with air quality near 

major roads or traffic in general is summarized. Generally, the section makes use of publications 

that systematically 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 

systematic 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 years, 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 reviews of traffic-related health studies. The HEI 

panel primarily used epidemiology studies for inferring whether there was sufficient evidence 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 

consideration 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.
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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 roadways or other transportation sources. According to the 

Central Intelligence Agency’s World Factbook, in 2010, the United States had 6,506,204 km or 

roadways, 224,792 km of railways, and 15,079 airports. As such, highways represent the 

overwhelming majority of transportation facilities described by this factor in the AHS.

The AHS reports are published every two years, and until 2011 recorded whether homes 

were located near highways 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 roadways. 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 by near-road air quality and health concerns, appears to 

have increased over time.

Figure 6-1 Trends in Populations Near Large Highways, Railroads, and Airports

Furthermore, according to data from the 2008 American Time Use Survey (ATUS), 

conducted by the Bureau of Labor Statistics (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 activity 

brings nearly all 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 2009

P

ercentN

e

arInfrastructure

Million H

o

m

es

Year of American Housing Survey

Million Housing Units

Near 4+ Lane Highway,

Railroad, or Airport
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6.1.1.8.2 Premature Mortality

The HEI panel report concluded that evidence linking traffic-associated air pollution with 

premature mortality from all causes was “suggestive but not sufficient” to infer a causal 

relationship. This conclusion was based largely on several long-term studies that “qualitatively” 

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 Effects

6.1.1.8.3.1 Cardiac Physiology

Exposure to traffic-associated pollutants has been associated with changes in cardiac 

physiology, 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 system’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 system. Overall, the 

panel concluded that the evidence was “suggestive but not sufficient” to infer a causal relation 

between traffic-related pollutants and cardiac function. Studies suggest that the HRV changes 

from traffic-related air pollution result in changes to heart rhythms, which can lead to 

arrhythmia.109,110

6.1.1.8.3.2 Heart Attack and Atherosclerosis

The HEI panel concluded that epidemiologic evidence of the association between trafficrelated 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 entirely 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 parasympathetic 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.
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hospitalization for acute myocardial infarction (i.e., heart attack) were associated with traffic 

exposures and a prospective study finding higher rates of arterial hardening and coronary heart 

disease near traffic.

6.1.1.8.4 Respiratory Effects

6.1.1.8.4.1 Asthma

Pediatric asthma and asthma symptoms 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 symptoms, and 

the effects are frequently statistically significant. Studies have employed both short-term and 

long-term exposure metrics, and a range of different 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 symptoms in children. 

While there is general consistency in studies examining asthma incidence in children, the 

available studies employ different definitions of asthma (e.g., self-reported vs. hospital records), 

methods of exposure assessment, 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 symptoms. The HEI 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-analysis of studies on incident 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 different pollutants ranging from 7-16 percent 

per 10 g/m3of 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 

hypothesis that traffic-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 trafficassociated air pollution. Because of how the panel selected studies for inclusion in review, there 

were only 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 traffic 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 strongly 

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 

studies showed consistently positive associations. As a result, despite the strongly suggestive
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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 Function

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 exhaling. 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 FEV1. FEV1 and PEF reflect the function of the large airways. FVC 

and FEV1, along with their ratio (FVC/FEV1) 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 exhalation 

(FEF75) reflects the status of small airways, 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 high 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 associations 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 causally associated 

with traffic-related exposures was “inadequate and insufficient.” Only 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 systematic reviews. 

One new meta-analysis 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 animal 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 typical ambient concentrations. Because there was no 

overlap in the effects studied by epidemiology and toxicology studies, no synthesis review of the 

combined literature was undertaken.
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Since the HEI panel’s publication, a systematic review and meta-analysis of air pollution 

and congenital abnormalities was published.115 In that review, only one study directly included 

nearby traffic in its exposure analysis. As such, there are no systematic reviews that specifically

address traffic’s impact on congenital abnormalities.

6.1.1.8.6 Cancer

6.1.1.8.6.1 Childhood Cancer

Earlier this year, Boothe et al. (2014) published a systematic review and meta-analysis of 

studies of childhood leukemia risks associated for populations near major roads.116 The study 

concluded that childhood leukemia was positively associated with residential exposure during 

childhood, but not 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 

was “inadequate and insufficient” to infer a causal relationship between traffic-related air 

pollution and childhood cancer.

6.1.1.8.6.2 Adult Cancer

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 Effects

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, animal models, and endpoints, making them unsuitable for 

systematic 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, NOX, SOX 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 because it has 

direct significance to people’s enjoyment of daily activities in all parts of the country. 

Individuals value good visibility for the well-being it provides them directly, where they live and 

work, and in places where they enjoy recreational opportunities. Visibility is also highly valued 

in significant natural areas, such as national parks and wilderness areas, and special emphasis is 
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given to protecting visibility in these areas. For more information on visibility see the final 2009 

PM ISA.121

The 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 nearby 

object (e.g., a building) is generally less sensitive to a change in light 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 Important 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 SO2 and NOX have decreased over time due to air 

pollution regulations such as the Acid Rain Program.122 

In the Clean Air Act Amendments of 1977, Congress recognized visibility’s value to 

society by establishing a national goal to protect national parks and wilderness areas from 

visibility impairment caused by manmade pollution.LIn 1999, EPA finalized the regional haze 

 

L

See Section 169(a) of the Clean Air Act. 
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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 I Federal areas

(62 FR 38680-38681, July 18, 1997). These areas are defined in CAA Section 162 as those 

national parks exceeding 6,000 acres, wilderness areas and memorial parks exceeding 5,000 

acres, and all international parks which were in existence on August 7, 1977. 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 PM2.5 causes adverse effects on visibility in other areas that 

are not protected by the Regional Haze Rule, depending on PM2.5 concentrations and other 

factors such as dry chemical composition and relative humidity (i.e., an indicator of the water 

composition of the particles). EPA revised the PM2.5 standards in December 2012 and 

established a target level of protection that is expected to be met through attainment of the 

existing secondary standards for PM2.5. 

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 1988. 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 Mandatory Federal Class I areas 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 employs aerosol measurements at all sites, and optical and 
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scene measurements at some of the sites. Aerosol measurements are taken for PM10 and PM2.5

mass, and for key constituents of PM2.5, such as sulfate, 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 by its 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 sea 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 optical measurements which directly measure light 

extinction or its components. Such measurements are made principally with a nephelometer to 

measure light scattering, some sites also include an aethalometer for light absorption, or a few 

sites use a transmissometer, which measures total light extinction. Scene characteristics are 

typically recorded using digital or video photography and are used to determine the quality of 

visibility conditions (such as effects on color and contrast) associated with specific levels 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 light extinction due to both anthropogenic 

and non-anthropogenic sources) vary regionally across the U.S. Visibility is typically worse in 

the summer months, and the rural East generally has higher levels of impairment than remote 

sites in the West. Figures 9-9 through 9-11 in the PM ISA 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 Ecosystem Effects of Ozone

The welfare effects of ozone can be observed across a variety of scales, i.e. subcellular, 

cellular, leaf, whole plant, population and ecosystem. Ozone effects that begin at small spatial

scales, such as the leaf of an individual plant, when they occur at sufficient magnitudes (or to a 

sufficient degree) can result in effects being propagated along a continuum to larger and larger 

spatial scales. For example, effects at the individual plant level, such as altered rates of leaf gas 

exchange, growth and reproduction can, when widespread, result in broad changes in 

ecosystems, such as productivity, carbon storage, water cycling, nutrient cycling, and community

composition.

Ozone can produce both acute and chronic injury in sensitive species depending on the 

concentration level and the duration of the exposure.124 In those sensitive speciesM, 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.
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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 

photosynthesis and visible injury to leaves. The impairment of photosynthesis, the process by

which the plant makes carbohydrates (its source of energy and food), can lead to reduced crop 

yields, timber production, and plant productivity and growth. Impaired photosynthesis can also 

lead to a reduction in root growth and carbohydrate storage below ground, resulting in other, 

more subtle plant and ecosystems impacts.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 ecosystemsO, resulting in a loss or 

reduction in associated ecosystem goods and services.127 Additionally, visible ozone injury to 

leaves can result in a loss of aesthetic value in areas of special scenic significance like national 

parks and wilderness areas and reduced use of sensitive ornamentals in landscaping.

128

 

The Integrated Science Assessment (ISA) for Ozone presents more detailed information 

on how ozone effects vegetation and ecosystems.129 The ISA concludes that ambient 

concentrations of ozone are associated with a number of adverse welfare effects and 

characterizes the weight of evidence for different effects associated with ozone.PThe ISA 

concludes that visible foliar injury effects on vegetation, reduced vegetation growth, reduced 

productivity in terrestrial ecosystems, reduced yield and quality of agricultural crops, and 

alteration of below-ground biogeochemical cycles are causally associated with exposure to 

ozone. It also concludes that reduced carbon sequestration in terrestrial ecosystems, alteration of 

terrestrial ecosystem water cycling, and alteration of terrestrial community composition are 

likely to be causally associated with exposure to ozone. 

6.1.2.4 Particulate Matter Deposition

Particulate matter contributes to adverse effects on vegetation and ecosystems, and to 

soiling and materials damage. These welfare effects result predominantly 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 information contained in the 2009 PM ISA and the 2008 Integrated Science 

Assessment for Oxides of Nitrogen and Sulfur- Ecological Criteria (secondary NOX/SOX

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 impacts 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 associated with different ozone related health and welfare effects, assigning 

one of five “weight of evidence” determinations: causal relationship, likely to be a causal relationship, suggestive of 

a causal relationship, inadequate to infer a causal relationship, and not likely to be a causal relationship. For more 

information on these levels of evidence, please refer to Table II of the ISA. 
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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 ecosystem components (e.g. algae, plants). In terrestrial and aquatic 

ecosystems excesses of nitrogen or sulfur can lead to acidification and nutrient enrichment.132 In

addition, in aquatic ecosystems, 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 accelerated by acidifying deposition, which can 

decrease concentrations of exchangeable base cations in soils.133 Biological effects of 

acidification in terrestrial ecosystems are generally linked to aluminum toxicity and decreased 

ability of plant roots to take 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 ecosystems. 135

Geology (particularly surficial 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 
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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 virtually all levels of the food web in acid sensitive aquatic ecosystems. Effects 

have been most clearly 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, ecosystems and regions. 

Because acidification primarily affects the diversity and abundance of aquatic biota, it 

also affects the ecosystem services that are derived from the fish and other aquatic life found in 

these surface waters. In the northeastern United States, the surface waters affected by 

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, such 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 (especially calcium and magnesium) from soils, 

and increasing the mobility of aluminum. Inorganic aluminum is toxic to some tree roots. Plants 

affected by 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, especially 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 insect 

pests and disease leading to increased mortality of canopy trees.141 In the U.S., terrestrial effects 

of acidification are best described for forested ecosystems (especially red spruce and sugar maple 

ecosystems) 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 quality 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
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6.1.2.4.1.2 Ecological Effects from Nitrogen Enrichment

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 clarity. Low DO disrupts 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. Low DO also degrades the 

aesthetic qualities of surface 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 many aquatic species in estuaries 

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 sediments 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 

Administration (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 ecosystems receive N loadings in excess of 

natural background levels, through either atmospheric deposition or direct application. 

Atmospheric N deposition is associated with changes in the types and number of species and 

biodiversity in terrestrial systems. 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 ecosystem conditions and 

indicators. One of the main provisioning services potentially affected by N deposition is grazing 

opportunities offered by grasslands for livestock production in the Central U.S. Although N 

deposition on these grasslands can offer supplementary 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 ultimately reduce the productivity of 

grasslands for livestock production.

Terrestrial enrichment also affects habitats, for example the Coastal Sage Scrub (CSS) 

and Mixed Conifer Forest (MCF) habitats which are an integral part of the California landscape. 

Together the ranges of these habitats include the densely populated and valuable coastline and 

the mountain areas. Numerous threatened and endangered species at both the state and federal 
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levels reside in CSS and MCF. Fire regulation is also an important regulating service that could 

be affected by nutrient enrichment of the CSS and MCF ecosystems 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 is a complex process involving 

adsorption to surfaces (leaves, stems, and soil) and absorption into leaves. SO2 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 

contrast, 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, involves a rapid absorption of a 

toxic dose, and involves collapse or necrosis of plant tissues. Another type of visible injury is 

termed chronic injury and is usually a result of variable SO2 exposures over the growing season. 

Besides foliar injury, chronic exposure to low SO2 concentrations can result in reduced 

photosynthesis, 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 

species and growing environment. SO2 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 (Hg0), oxidized Hg compounds (Hg+2), and particle-bound Hg (HgP). 

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 by aquatic organisms and bioaccumulates up the aquatic food web. Larger 

predatory fish may have MeHg concentrations many times, typically on the order of one million 

times, that of the concentrations in the freshwater body in which they live. The NOX SOX 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

Specifically, there appears to be a relationship between SO4

2-

deposition and mercury

methylation; however, the rate of mercury methylation varies according to several spatial and 

biogeochemical factors whose influence has not been fully quantified. Therefore, the correlation 

between SO4

2-

deposition and MeHg cannot yet be quantified for the purpose of interpolating the 

association across waterbodies or regions. Nevertheless, because changes in MeHg in 

ecosystems represent changes in significant human and ecological health risks, the association 

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 metal constituents of PM 

include cadmium, copper, chromium, mercury, nickel, zinc, and lead. The organics include 
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persistent organic pollutants (POPs), polyaromatic hydrocarbons (PAHs) and polybromiated 

diphenyl ethers (PBDEs). Exposure to PM for direct effects occur via deposition (e.g., wet, dry

or occult) to vegetation surfaces, while indirect effects occur via deposition to ecosystem 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 ecosystem 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 adversely impact plants and ecosystem 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 heavy deposition 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 heavy 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 canopy, 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 especially severe regional haze.158

In addition to damage to plant surfaces, deposited PM can be taken up by plants from soil 

or foliage. Copper, zinc, and nickel have been shown to be directly 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 photosynthesis, 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 polycyclic 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, physical and chemical properties 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 organisms.162,163 Atmospheric deposition of particles is thought to be the major 

source of PAHs to the sediments of Lake Michigan, Chesapeake Bay, Tampa Bay and other 

coastal areas of the U.S.164

Contamination of plant leaves by heavy metals can lead to elevated concentrations 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 heavy metals are transferred into the 

soil.165,166 Many of the major indirect plant responses to PM deposition are chiefly soil-mediated 
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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 heavy metals in soils depends on factors such as local soil 

characteristics, geologic origin of parent soils, and metal bioavailability. Heavy 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 ecosystem service that serves 

as a source of soil nutrients.167 Surface litter decomposition 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 composition 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 atmospherically deposited PAHs to aquatic food 

webs was demonstrated in high elevation mountain lakes with no other anthropogenic 

contaminant sources.170 Metals associated with PM deposition limit phytoplankton 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 recently completed Western Airborne Contaminants Assessment Project (WACAP) 

is the most comprehensive database on contaminant transport and PM depositional effects on 

sensitive ecosystems 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 ecosystem components (air, snow, water, sediment, lichen, conifer needles and 

fish) in eight core national parks. The study concluded that bioaccumulation of semi-volatile 

organic compounds occurred throughout park ecosystems, an elevational gradient in PM 

deposition exists with greater accumulation in higher altitude areas, and contaminants 

accumulate in proximity to individual agriculture and industry sources, which is counter to the 

original working hypothesis 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 physical damage (materials damage effects) and 

impaired aesthetic qualities (soiling effects). Wet and dry deposition of PM can physically affect 

materials, adding to the effects of natural weathering processes, by 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 by the presence of 

acidic gases and can be additive or synergistic 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 
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on materials including zinc/galvanized steel and other metal, carbonate stone (as monuments and 

building facings), and surface coatings (paints).

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 fuel contribute to ambient levels 

of pollutants that contribute to adverse effects on vegetation. Volatile organic compounds 

(VOCs), some of which are considered air toxics, have long been suspected to play a role in 

vegetation damage.175 In laboratory 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 photosynthetic 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 roadways. Most of the studies of the impacts of VOCs on 

vegetation have focused on short-term exposure and few studies have focused on long-term 

effects of VOCs on vegetation and the potential for metabolites of these compounds to affect 

herbivores or insects. 

6.2 Air Quality Impacts of Non-GHG Pollutants

Chapter 5 of this draft RIA presents the projected emissions changes due to the proposal. 

Once the emissions changes are projected the next step is to look at how the ambient air quality 

would be impacted by those emissions changes. Although the purpose of this proposal is to 

address greenhouse gas emissions, this proposal would also impact emissions of criteria and 

hazardous air pollutants. No air quality modeling was done for this draft RIA to project the 

impacts of the proposal. Air quality modeling will be done for the final rulemaking, 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 of 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 PM2.5: an annual standard (12.0 μg/m3) and a 24-hour standard (35 μg/m3)

with a 98th percentile form, and two secondary NAAQS for PM2.5: an annual standard (15.0 

μg/m3) and a 24-hour standard (35 μg/m3), likewise with a 98th percentile form. The initial PM2.5

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/m3to 35 ug/m3, 
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and the December 2012 rule revised the level of the primary annual PM2.5 standard from 15.0

μg/m3to 12.0 μg/m3.

181

 

In 2005 EPA designated 39 nonattainment areas for the 1997 PM2.5 NAAQS (70 FR 

19844, April 14, 2005). As of July 2, 2014, over 47 million people lived in the 19 areas that are 

still designated as nonattainment for the 1997 annual PM2.5 NAAQS. These PM2.5 nonattainment 

areas are comprised of 105 full or partial counties. EPA anticipates making initial area 

designation decisions for the 2012 primary annual PM2.5 NAAQS in December 2014, with those 

designations likely becoming effective in early 2015.182 On November 13, 2009 and February 3, 

2011, EPA designated 32 nonattainment areas for the 2006 24-hour PM2.5 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 PM2.5 nonattainment areas 

with a population of over 61 million people.Q 

States with PM2.5 nonattainment areas will be required to take action to bring those areas 

into attainment in the future. Designated nonattainment areas not currently attaining the 1997 

annual PM2.5 NAAQS are required to attain the NAAQS by 2015 and will be required to 

maintain the 1997 annual PM2.5 NAAQS thereafter. The 2006 24-hour PM2.5 nonattainment 

areas are required to attain the 2006 24-hour PM2.5 NAAQS in the 2015 to 2019 time frame and 

will be required to maintain the 2006 24-hour PM2.5 NAAQS thereafter. Areas to be designated 

nonattainment for the 2012 primary annual PM2.5 NAAQS will likely be required to attain the 

2012 NAAQS in the 2021 to 2025 time frame. The heavy-duty vehicle standards proposed here 

first apply to model year 2021 vehicles.

6.2.1.2 Current Concentrations of 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 23858, 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 105 million. Nonattainment designations for the 2008 ozone standards

were 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 PM2.5 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.
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population of over 123 million. As of July 2, 2014, 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 

classification. 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 were required to 

attain in the 2007 to 2013 time frame and then to maintain it thereafter.T The attainment dates 

for areas designated nonattainment for the 2008 8-hour ozone NAAQS are in the 2015 to 2032

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 EPA revises the ozone standards pursuant to that 

review, the attainment dates associated with areas designated nonattainment for that NAAQS 

would be 5 or more years after the final rule is promulgated, depending on the severity of the 

problem in each area. The heavy-duty vehicle standards proposed here first apply to model year 

2021 vehicles.

6.2.1.3 Current Concentrations of Nitrogen Oxides

EPA most recently completed a review of the primary NAAQS for NO2 in January 2010. 

There are two primary NAAQS for NO2: an annual standard (53 ppb) and a 1-hour standard (100 

ppb). EPA promulgated area designations in the Federal Register on February 17, 2012. In this 

initial round of designations, all areas of the country were designated as 

“unclassifiable/attainment” for the 2010 NO2 NAAQS based on data from the existing air quality

monitoring network. EPA and state agencies are working to establish an expanded network of 

NO2 monitors, expected to be deployed in the 2013-2017 time frame. Once three years of air 

quality data have been collected from the expanded network, EPA will be able to evaluate NO2

air quality in additional locations.184,185

6.2.1.4 Current Concentrations of Sulfur Oxides

EPA most recently completed a review of the primary SO2 NAAQS in June 2010. The 

current primary NAAQS for SO2 is a 1-hour standard of 75 ppb. 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 associated 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 Mojave 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 proposal, including on retaining the existing standard. 

(http://www.epa.gov/glo/pdfs/20141125proposal.pdf)
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on August 5, 2013. In this first round of designations, EPA only designated nonattainment areas 

that were violating the standard based on existing air quality monitoring data provided by the 

states. The agency did not have sufficient information to designate any area as “attainment” or 

make final decisions about areas for which additional modeling or monitoring is needed (78 FR 

47191, August 5, 2013). EPA anticipates designating areas for the revised SO2 standard in 

multiple rounds.

6.2.1.5 Current Concentrations of 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 currently no CO 

nonattainment areas; as of September 27, 2010, all CO nonattainment areas were redesignated to 

maintenance areas. The designations were based on the existing community-wide monitoring 

network. EPA is making changes to the ambient air monitoring requirements for CO. The new 

requirements are expected to result in approximately 52 CO monitors operating near roads within 

52 urban areas by January 2015 (76 FR 54294, August 31, 2011). 

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 System 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, 

California, 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/m3. Half of the DPM and diesel 

exhaust organic gases can be attributed to onroad diesels. 
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Figure 6-5 Estimated County Ambient Concentration of Diesel Particulate Matter

Table 6-1 Distribution of Census Tract Ambient Concentrations of DPM at the National Scale in 2005 NATAa

AMBIENT CONCENTRATION 

(μg/m3)

5

th Percentile 0.03

25th Percentile 0.17

50th Percentile 0.53

75th 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). 
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6.2.1.7 Current Concentrations of 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 people 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 In order to identify and prioritize air toxics, emission source types and 

locations which are of greatest potential concern, EPA conducts the National-Scale Air Toxics 

Assessment (NATA). The most recent NATA was conducted for calendar year 2005, and was 

released in March 2011.

189

 NATA for 2005 includes four steps:

1) Compiling a national emissions inventory 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 of air toxics including 

both cancer and noncancer effects

According to the NATA for 2005, 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.

Formaldehyde is the largest contributor to cancer risk of all 80 pollutants quantitatively assessed 

in the 2005 NATA, and mobile sources were responsible for over 40 percent of primary

emissions of this pollutant in 2005, and are major contributors to formaldehyde precursor 

emissions. Benzene is also a large contributor to cancer risk, and mobile sources account for 

over 70 percent of ambient exposure. Over the years, EPA has implemented a number of mobile 

source and fuel controls which have resulted in VOC reductions, which also reduced 

formaldehyde, benzene and other air toxic emissions. 

6.2.2 Impacts of Proposed Standards on Future Air Quality

Air quality models use mathematical and numerical techniques to simulate the physical 

and chemical processes that affect air pollutants as they disperse and react in the atmosphere. 

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 air 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. 
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Photochemical air quality models have become widely recognized and routinely utilized tools for 

regulatory analysis by assessing the effectiveness of control strategies. These models are applied 

at multiple spatial scales from local, regional, national, and global. 

Full-scale photochemical air quality modeling is necessary to accurately project levels of 

criteria and air toxic pollutants. For the final rulemaking, national-scale air quality modeling 

analyses will be performed to analyze the impacts of the standards on PM2.5, NO2, ozone, and 

selected air toxics (i.e., benzene, formaldehyde, acetaldehyde, 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. 

Section VIII of the preamble presents projections of the changes in criteria pollutant and 

air toxics emissions due to the proposed standards; the basis for those estimates is set out in 

Chapter 5 of the draft RIA. NHTSA also provides its projections in Chapter 4 of its DEIS. The 

atmospheric chemistry related to ambient concentrations of PM2.5, 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 analysis for the final rulemaking.

For the final rulemaking, the agencies intend to use a 2011-based Community Multi-scale 

Air Quality (CMAQ) modeling platform as the tool for the air quality modeling. The CMAQ 

modeling system is a comprehensive three-dimensional grid-based Eulerian air quality model 

designed to estimate the formation and fate of oxidant precursors, primary and secondary PM 

concentrations and deposition, and air toxics, over regional and urban spatial scales (e.g., over 

the contiguous U.S.).191,192,193 ,194 The CMAQ model is a well-known and well-established tool 

and is commonly used by EPA for regulatory analyses, and by States in developing attainment 

demonstrations for their State Implementation Plans.195 The CMAQ model version 5.0 was most 

recently peer-reviewed in September of 2011 for the U.S. EPA.

CMAQ includes many science modules that simulate the emission, production, decay, 

deposition and transport of organic and inorganic gas-phase and particle-phase pollutants in the 

atmosphere. 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 underlying 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 these analyses. The domain covers the 48 contiguous states along with the southern 

portions of Canada and the northern portions of Mexico. This modeling domain contains 25

vertical layers with a top at about 17,600 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 

System (CMAS) website: http://www.cmascenter.org.
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Figure 6-6 Map of the CMAQ 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 Version 3.4 of the Weather Research Forecasting 

Model (WRF).199 These inputs included hourly-varying horizontal wind components (i.e., speed 

and direction), temperature, moisture, vertical diffusion rates, and rainfall rates for each grid cell 

in each vertical layer. 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 rulemaking air quality modeling, and NHTSA’s Final Environmental Impact 

Statement. 

The lateral boundary and initial species concentrations are provided by a threedimensional global atmospheric chemistry model, the GEOS-CHEM model200 (standard version 

8-03-02 with 8-02-01 chemistry. The global GEOS-CHEM model simulates atmospheric 

chemical and physical processes driven by assimilated meteorological observations from the 

NASA’s Goddard Earth Observing System (GEOS-5; additional information available at: 

http://gmao.gsfc.nasa.gov/GEOS/ and http://wiki.seas.harvard.edu/geos-chem/index.php/GEOS-
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5). This model was run for 2011 with a grid resolution of 2.0 degrees x 2.5 degrees (latitudelongitude). The predictions were used to provide one-way dynamic boundary conditions at onehour intervals 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 Atmospheric CO2 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 Findings for Greenhouse Gases Under Section 202(a) of 

the Clean Air Act, the 2012-2016 light-duty vehicle rulemaking, the 2014-2018 heavy-duty

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 briefly 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 that 1) their concentrations become well-mixed throughout the 

global atmosphere regardless of emission origin, and 2) their effects on climate are long lasting. 

GHG emissions come mainly from the combustion of fossil fuels (coal, oil, and gas), with 

additional contributions from the clearing of forests, agricultural activities, cement production, 

and some industrial activities. Transportation activities, in aggregate, were the second largest 

contributor to total U.S. GHG emissions in 2010 (27 percent of total emissions).Y

EPA Administrator relied on thorough and peer-reviewed assessments of climate change 

science prepared by the Intergovernmental Panel on Climate Change (“IPCC”), the United States 

Global Change Research Program (“USGCRP”), and the National Research Council of the 

National Academies (“NRC”) Zas the primary scientific and technical basis for the 

Endangerment and Cause or Contribute Findings for Greenhouse Gases Under Section 202(a) of 

the Clean Air Act (74 FR 66496, December 15, 2009). These assessments comprehensively 

address the scientific issues 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 rigorously reviewed by the 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)
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Based on these assessments, EPA Administrator determined that the emissions from new 

motor vehicles and engines contributes to elevated concentrations 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. The D.C. Circuit has emphatically 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 likely’ 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. Relying again upon substantial scientific evidence, EPA 

determined that anthropogenically induced climate change threatens both public health and 

public welfare. It found that extreme weather events, changes in air quality, increases in foodand 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 by creating risk to food production and agriculture, forestry, energy, infrastructure, 

ecosystems, 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 Denial202. These assessments include the “Special Report on Managing the 

Risks 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 Climate 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 Analysis”211, and “Abrupt Impacts of 

Climate Change” (Abrupt Impacts) assessments212.

EPA has reviewed these assessments and finds that in general, the improved 

understanding of the climate system 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 system or other systems impacted by the climate. The Abrupt 

Impacts report did find less cause for concern 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 ecosystems, 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 
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ice retreat 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 generally 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 likely (>95 percent 

confidence) that human influences have been the dominant cause of recent warming. Moreover, 

the IPCC found that the last 30 years were likely (>66 percent confidence) the warmest 30 year 

period in the Northern Hemisphere of the past 1400 years, that the rate of ice loss of worldwide 

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 

years, and that concentrations of carbon dioxide and several 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, increased 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, food 

insecurity linked to warming, drought, and flooding, especially for poor populations, reduced 

access to drinking and irrigation water for those with minimal capital in semi-arid regions, and 

decreased biodiversity in marine ecosystems, especially in the 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 

system. Limiting climate change will require substantial and sustained reductions of greenhouse 

gases emissions.”

Finally, the recently released National Climate Assessment stated, “Climate change is 

already affecting the American people in far reaching ways. Certain types of extreme weather 

events with links to climate change have become more frequent and/or intense, including 

prolonged periods of heat, heavy 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, 

comprehensively cover and synthesize thousands of individual studies to obtain the majority

conclusions from the body of scientific literature and undergo a rigorous and exacting standard 

of review by the peer expert community and U.S. government.

Based on modeling analysis performed by EPA, reductions in CO2 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 

will 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 CO2 concentrations based on the emission reductions estimated 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 
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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 CO2 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 CO2 concentrations, global mean surface 

temperature and sea-level rise to 2100 using the GCAM (Global Change Assessment Model, 

formerly MiniCAM), integrated assessment modelAA,213 coupled with the MAGICC (Model for 

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 MAGICC 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 by applying the estimated 

emissions reductions from the proposal’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 Specifically, the annual CO2, N2O, CH4, NOX and SO2

emissions reductions estimated 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 reference 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 significantly and thus emissions 

reductions remain relatively constant from 2050 through 2100. 

The GCAM reference scenario217 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 development 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 single 

framework. The framework allows the user to determine changes in greenhouse-gas concentrations, global-mean 

surface air temperature and sea-level resulting from anthropogenic emissions of carbon dioxide (CO2), methane 

(CH4), nitrous oxide (N2O), reactive gases (CO, NOX, VOCs), the halocarbons (e.g. HCFCs, HFCs, PFCs) and 

sulfur dioxide (SO2). MAGICC emulates the global-mean temperature responses of more sophisticated coupled 

Atmosphere/Ocean General Circulation Models (AOGCMs) with high accuracy.
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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 CO2 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/m2) 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 century 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 use change (LUC) emissions decline as agricultural crop productivity continues to 

increase. 

The GCAM reference scenario uses non-CO2 and pollutant emissions implemented as 

described in Smith and Wigley (2006); land-use change emissions as described in Wise et al. 

(2009); and updated base-year 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 MAGICC 5.3 v2,218 the change in atmospheric CO2 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 system, the 

changes in projected atmospheric CO2 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 regarding the 

carbon cycle, ocean heat uptake, or aerosol forcing, were not addressed. 

MAGICC calculates the forcing response at the global scale from changes in atmospheric 

concentrations of CO2, CH4, N2O, HFCs, and tropospheric ozone. It also includes the effects of 

temperature changes on stratospheric ozone and the effects of CH4 emissions on stratospheric 

water vapor. Changes in CH4, NOX, VOC, and CO emissions affect both O3 concentrations and 

CH4 concentrations. MAGICC includes the relative climate forcing effects of changes in sulfate 

concentrations due to changing SO2 emissions, including both the direct effect of sulfate particles 

 

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 Science 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.
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6-45

and the indirect effects related to cloud interactions. However, MAGICC does not calculate the 

effect of changes in concentrations of other aerosols such as nitrates, black carbon, or organic 

carbon, making the assumption that the sulfate cooling effect is a proxy for the sum of all the 

aerosol effects. Therefore, the climate effects of changes in PM2.5 emissions and precursors 

(besides SO2) presented in Chapter 5 were not included in the calculations in this chapter. 

MAGICC also calculates all climate effects at the global scale. This global scale captures the 

climate effects of the long-lived, well-mixed greenhouse gases, but does not address the fact that 

short-lived climate forcers such as aerosols and ozone can have effects that vary with location 

and timing of emissions. Black carbon in particular is known to cause a positive forcing or 

warming effect by absorbing incoming solar radiation, but there are uncertainties about the 

magnitude of that warming effect and the interaction of black carbon (and other co-emitted 

aerosol species) with clouds. See 77 FR 38890, 38991-993 (June 29, 2012). While black carbon 

is likely to be an important contributor to climate change, it would be premature to include 

quantification of black carbon climate impacts in an analysis of the proposal’s standards at this 

time. See generally, EPA, Response to Comments to the Endangerment Finding Vol. 9 Section 

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 

recently published EPA Report to Congress on Black Carbon. Additionally, the magnitude of 

PM2.5 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 CO2 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, by 2100 the concentration of atmospheric CO2 is 

projected to be reduced by approximately 1.1 to 1.2 parts per million 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 MAGICC do not include the possible effects of accelerated ice 

flow in Greenland and/or Antarctica; including these effects would show correspondingly larger 

benefits of mitigation. 

Figure 6-7 provides the results over time for the estimated reductions in atmospheric CO2

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 in global mean sea level rise associated 

with the proposal. The range of reductions in global mean temperature and sea level rise due to 

uncertainty in climate sensitivity is larger than that for CO2 concentrations because CO2

concentrations are only weakly coupled to climate sensitivity through the dependence on 

temperature of the rate of ocean absorption of CO2, whereas the magnitude of temperature 

change response to CO2 changes (and therefore sea level rise) is more tightly coupled to climate 

sensitivity in the MAGICC model. 
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6-46

Figure 6-7 Estimated Projected Reductions in Atmospheric CO2 Concentrations (parts per million by 

volume) from the Baseline for the Proposed Alternative of the Heavy-Duty Proposal (climate sensitivity (CS) 

cases ranging from 1.5-6°C)

Figure 6-8 Estimated Projected Reductions in Global Mean Surface Temperatures from the Baseline for the 

Proposed Alternative of the Heavy-Duty Proposal (climate 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

ppm

v

Change in CO2 Concentration

(Primary Alternative - 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

degrees C

Change in Global Mean Temperature

(Primary Alternative - Baseline)

CS 1.5

CS 2.0

CS 2.5

CS 3.0

CS 4.5

CS 6.0
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6-47

Figure 6-9 Estimated Projected Reductions in Global Mean Sea Level Rise from the Baseline for the 

Proposed Alternative of the Heavy-Duty Proposal (climate 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 respectively, across all climate sensitivities. The projected reductions 

are small relative to the change in temperature (1.8 – 4.8 oC) and sea level rise (23 – 56 cm) from 

1990 to 2100 from the MAGICC simulations for the GCAM reference case. However, this is to 

be expected given the magnitude of emissions reductions expected from the proposal in the 

context of global emissions. These reductions are quantifiable, directionally consistent, and will 

contribute to reducing the risks associated with climate change. Notably, these effects are 

occurring everywhere 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 any given GHG mitigation action when taken alone or when considered in isolation.

EPA also notes that a substantial portion of CO2 emitted into the atmosphere is not removed by 

natural processes for millennia, and therefore each unit of CO2 not emitted into the atmosphere 

due to this rule avoids essentially permanent climate change on centennial time scales. 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 

MAGICC, so projected reductions in sea level rise may be similarly underestimated.220 If other 

uncertainties besides climate sensitivity were included in the analysis, 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 analysis, changes in ocean pH are 

related to the change in the atmospheric concentration of carbon dioxide (CO2) 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

cm

Change in Global Mean Sea Level Rise

(Primary Alternative - Baseline)

CS 1.5

CS 2.0

CS 2.5

CS 3.0

CS 4.5

CS 6.0
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6-48

for CO2 System Calculations CO2SYS,221 version 1.05, a program which performs calculations 

relating parameters of the carbon dioxide (CO2) system in seawater. The program was 

developed by Ernie Lewis at Brookhaven National Laboratory and Doug Wallace at the Institut 

für Meereskunde in Germany, supported by the U.S. Department of Energy, Office of Biological 

and Environmental Research, under Contract No. DE-ACO2-76CH00016.

The CO2SYS program uses two of the four measurable parameters of the CO2 system 

[total alkalinity (TA), total inorganic CO2 (TC), pH, and either fugacity (fCO2) or partial 

pressure of CO2 (pCO2)] 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 scenarios: the 

baseline scenario at a climate sensitivity of 3 degrees for which the CO2 concentrations was 

calculated to be 784.87 in 2100, the proposed alternative relative to the baseline with a CO2

concentration of 784.11, and a calculation for 1990 with a CO2 concentration of 353.63. 

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 baseline scenario pH was 

+0.0004 units (more basic). For comparison, the difference between the baseline 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 and 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 Millero (1987)224

3) Choice of fCO2 or pCO2: pCO2 

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 variety 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 CO2 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 0.0006 pH units in 2100. Thus, this analysis indicates the projected 

decrease in atmospheric CO2 concentrations from the proposed alternative yields an increase in 

ocean pH. Table 6-2 contains the projected changes in ocean pH based the change in 

atmospheric CO2 concentrations which were derived from the MAGICC modeling.
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6-49

Table 6-2 Impact of the Proposal’s GHG Emissions Reductions on Ocean pH 

CLIMATE 

SENSITIVITY

DIFFERENCE 

IN CO2

A

YEAR PROJECTED 

CHANGE 

3.0 -1.2 ppmv 2100 0.0006

Note:

a Represents the change in atmospheric CO2 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 analysis 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 small differences in 

climate effects (CO2 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 on 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 of climate change, which complicates quantification and cost-benefits assessments. 

Changes in climate variables are a meaningful proxy for changes in the risk of all potential 

impacts--including those that can be monetized, and those that have not been monetized but can 

be quantified in physical 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 subsequent sea level rise).

Table 6-3 Impact of GHG Emissions Reductions on Projected Changes in Global Climate Associated with the 

Proposal (Based on a Range of Climate Sensitivities from 1.5-6°C) 

VARIABLE UNITS YEAR PROJECTED CHANGE 

Atmospheric CO2

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 +0.0006

a

Note:

a The value for projected change in ocean pH is based on a climate sensitivity of 3.0.
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6-50

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86 U.S. EPA. (2003). Integrated Risk Information System File of Acrolein. Office of Research and Development, 

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124 73 FR 16486 (March 27, 2008).

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126 73 FR 16492 (March 27, 2008).

127 73 FR 16493-16494 (March 27, 2008). 

128 73 FR 16490/ 16497 (March 27, 2008).

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137 U.S. Environmental Protection Agency (U.S. EPA). 2008. Integrated Science Assessment for Oxides of Nitrogen 

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