Document ID: EPA-HQ-OAR-2019-0055-0139
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2020-01-21T05:00Z

UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
                                                    OFFICE OF AIR AND RADIATION
                                 NATIONAL VEHICLE AND FUEL EMISSIONS LABORATORY
                                                          2000 TRAVERWOOD DRIVE
                                                      ANN ARBOR, MI  48105-2498

10/22/2019

MEMORANDUM

SUBJECT:
Health and Environmental Effects of NOx, Ozone and PM 
FROM:
Ken Davidson and Margaret Zawacki, Assessment and Standards Division
TO:
Cleaner Trucks Initiative - Docket EPA-HQ-OAR-2019-0055

As mentioned in the ANPR, NOX emissions contribute to pollution in the ambient air which can adversely affect human health and the environment.  Additional information on health and environmental effects is provided here. 

Particulate Matter

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 micrometers (um, or 10[-6] meter) in diameter (for reference, a typical strand of human hair is 70 um in diameter and a grain of salt is about 100 um).  Atmospheric particles can be grouped into several classes according to their aerodynamic and physical sizes.  Generally, the three broad classes of particles include ultrafine particles (UFPs, generally considered as particulates with a diameter less than or equal to 0.1 um [typically based on physical size, thermal diffusivity or electrical mobility]), "fine" particles (PM2.5; particles with a nominal mean aerodynamic diameter less than or equal to 2.5 um), and "thoracic" particles (PM10; particles with a nominal mean aerodynamic diameter less than or equal to 10 um).  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 um and greater than 2.5 um).  EPA currently has standards that regulate PM2.5 and PM10. 

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 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.  
        
Health Effects of Particulate Matter
Scientific studies show exposure to ambient PM is associated with a broad range of health effects.  These health effects are discussed in detail in the Integrated Science Assessment for Particulate Matter (PM ISA), which was finalized in December 2009.  The PM ISA summarizes health effects evidence for 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 are associated with a number of adverse health effects and characterizes the weight of evidence for broad health categories (e.g., cardiovascular effects, respiratory effects, etc.).  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 PM can also be found in the rulemaking documents for the most recent review of the PM NAAQS completed in 2012.[,]

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 that "a causal relationship is likely to exist" 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).

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 short-term 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.[,]  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 studies that demonstrated an improvement in community health following reductions in ambient fine particles.

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.

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.

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 post-neonatal period (i.e., 1 month to 12 months of age).  With regard to cancer effects, ``[m]ultiple epidemiologic studies have shown a consistent positive association between PM2.5 and lung cancer mortality, but studies have generally not reported associations between PM2.5 and lung cancer incidence.''[,] 

In addition to evaluating the health effects attributed to short- and long-term exposure to PM2.5, the 2009 PM ISA also evaluated whether specific components or sources of PM2.5 are more strongly associated with specific health effects.  An evaluation of those studies resulted in the 2009 PM ISA concluding that "many [components] of PM can be linked with differing health effects and the evidence is not yet sufficient to allow differentiation of those [components] or sources that are more closely related to specific health outcomes."

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.  The scientific evidence was "inadequate to infer a causal relationship" between long-term exposure to PM10-2.5 and various health effects. [,][,]

For UFPs, 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 also concluded that there was evidence "suggestive of a causal relationship" between short-term exposure to UFPs and respiratory effects, including lung function and pulmonary inflammation, with limited and inconsistent evidence for increases in ED visits and hospital admissions.  Scientific evidence was "inadequate to infer a causal relationship" between short-term exposure to UFPs and additional health effects including premature mortality as well as long-term exposure to UFPs and all health outcomes evaluated.[,]

The 2009 PM ISA conducted an evaluation of specific groups within the general population potentially at increased risk for experiencing adverse health effects related to PM exposures.[,][,][,]  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.

Ozone
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.

Health Effects of Ozone 
This section provides a summary of the health effects associated with exposure to ambient concentrations of ozone.  The information in this section is based on the information and conclusions in the February 2013 Integrated Science Assessment for Ozone (Ozone ISA).  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.   The 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.  In addition, some groups are at increased risk of exposure due to their activities, such as outdoor workers and children.  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.  

Nitrogen Oxides 
Background on Nitrogen Oxides  
Oxides of nitrogen (NOX) refers to nitric oxide (NO) and nitrogen dioxide (NO2).  For the NOX NAAQS, NO2 is the indicator.  Most NO2 is formed in the air through the oxidation of nitric oxide (NO) emitted when fuel is burned at a high temperature.  NOX is a major contributor to secondary PM2.5 formation and NOX along with VOCs are the two major precursors of ozone.  

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 2016 Integrated Science Assessment for Oxides of Nitrogen - Health Criteria (Oxides of Nitrogen ISA).  The primary source of NO2 is motor vehicle emissions, and ambient NO2 concentrations tend to be highly correlated with other traffic-related pollutants.  Thus, a key issue in characterizing the causality of NO2-health effect relationships was evaluating the extent to which studies supported an effect of NO2 that is independent of other traffic-related pollutants. EPA concluded that the findings for asthma exacerbation integrated from epidemiologic and controlled human exposure studies provided evidence that is sufficient to infer a causal relationship between respiratory effects and short-term NO2 exposure.  The strongest evidence supporting an independent effect of NO2 exposure comes from controlled human exposure studies demonstrating increased airway responsiveness in individuals with asthma following ambient-relevant NO2 exposures.  The coherence of this evidence with epidemiologic findings for asthma hospital admissions and ED visits as well as lung function decrements and increased pulmonary inflammation in children with asthma describe a plausible pathway by which NO2 exposure can cause an asthma exacerbation.  The 2016 ISA for Oxides of Nitrogen also concluded that there is likely to be a causal relationship between long-term NO2 exposure and respiratory effects.  This conclusion is based on new epidemiologic evidence for associations of NO2 with asthma development in children combined with biological plausibility from experimental studies.  

In evaluating a broader range of health effects, the 2016 ISA for Oxides of Nitrogen concluded evidence is "suggestive of, but not sufficient to infer, a causal relationship" between short-term NO2 exposure and cardiovascular effects and mortality and between long-term NO2 exposure and cardiovascular effects and diabetes, birth outcomes, and cancer.  In addition, the scientific evidence is inadequate (insufficient consistency of epidemiologic and toxicological evidence) to infer a causal relationship for long-term NO2 exposure with fertility, reproduction, and pregnancy, as well as with postnatal development.  A key uncertainty in understanding the relationship between these non-respiratory health effects and short- or long-term exposure to NO2 is copollutant confounding, particularly by other roadway pollutants.  The available evidence for non-respiratory health effects does not adequately address whether NO2 has an independent effect or whether it primarily represents effects related to other or a mixture of traffic-related pollutants. 

The 2016 ISA for Oxides of Nitrogen concluded that people with asthma, children, and older adults are at increased risk for NO2-related health effects. In these groups and lifestages, NO2 is consistently related to larger effects on outcomes related to asthma exacerbation, for which there is confidence in the relationship with NO2 exposure.  

Diesel Exhaust 
Background on Diesel Exhaust
Diesel exhaust consists of a complex mixture composed of particulate matter, 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 um), of which a significant fraction is ultrafine particles (< 0.1 um).  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, acceleration, deceleration), 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.

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.[,]  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[-5] to 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 ug/m[3] for diesel exhaust measured as diesel particulate matter.  This RfC 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 EPA 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 ug/m[3].  In 2012, EPA revised the annual PM2.5 NAAQS to 12 ug/m[3].  There is a large and extensive body of human data showing a wide spectrum of adverse health effects associated with exposure to ambient PM, of which diesel exhaust is an important component.  The 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.[,][,]  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."  This designation was an update from its 1988 evaluation that considered the evidence to be indicative of a "probable human carcinogen."   
Air Toxics
Heavy-duty vehicle emissions contribute to ambient levels of air toxics that are known or suspected 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."  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 2011 National-scale Air Toxics Assessment and have significant inventory contributions from mobile sources.  

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.,,  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[-6] to 7.8 x 10[-6] per ug/m[3] as the unit risk estimate (URE) for benzene.[,]  The International Agency for Research on Cancer (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.,    

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.,  The most sensitive noncancer effect observed in humans, based on current data, is the depression of the absolute lymphocyte count in blood.[,]  EPA's inhalation reference concentration (RfC) for benzene is 30 ug/m[3].  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.,,,  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 ug/m[3] for 1-14 days exposure.[,]

Health Effects of 1,3-Butadiene
EPA has characterized 1,3-butadiene as carcinogenic to humans by inhalation.,  The IARC has determined that 1,3-butadiene is a human carcinogen and the U.S. DHHS has characterized 1,3-butadiene as a known human carcinogen.,,  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 x 10[-5] per ug/m[3].  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.  Based on this critical effect and the benchmark concentration methodology, an RfC for chronic health effects was calculated at 0.9 ppb (approximately 2 ug/m[3]).

Health Effects of Formaldehyde
In 1991, EPA concluded that formaldehyde is a carcinogen based on nasal tumors in animal bioassays. 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.[,][,]

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.,,  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.  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.  Finally, a study of embalmers reported formaldehyde exposures to be associated with an increased risk of myeloid leukemia but not brain cancer. 

Health effects of formaldehyde in addition to cancer were reviewed by the Agency for Toxics Substances and Disease Registry in 1999, supplemented in 2010, and by the World Health Organization.  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, reduced 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.  The draft assessment reviewed more recent research from animal and human studies on cancer and other health effects.  The NRC released their review report in April 2011 (http://www.nap.edu/catalog.php?record_id=13142).  EPA is currently developing a revised draft assessment in response to this review.

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.  The URE in IRIS for acetaldehyde is 2.2 x 10[-6] per ug/m[3].  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.[,]  EPA is currently conducting a reassessment of cancer risk from inhalation exposure to acetaldehyde. Acetaldehyde is currently listed on the IRIS Program Multi-Year Agenda for reassessment within the next few years.  

The primary noncancer effects of exposure to acetaldehyde vapors include irritation of the eyes, skin, and respiratory tract.  In short-term (4 week) rat studies, degeneration of olfactory epithelium was observed at various concentration levels of acetaldehyde exposure.[,]  Data from these studies were used by EPA to develop an inhalation reference concentration of 9 ug/m[3].  Some asthmatics have been shown to be a sensitive subpopulation to decrements in functional expiratory volume (FEV1 test) and bronchoconstriction upon acetaldehyde inhalation.  

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.  The IARC determined in 1995 that acrolein was not classifiable as to its carcinogenicity in humans.  

Lesions to the lungs and upper respiratory tract of rats, rabbits, and hamsters have been observed after subchronic exposure to acrolein.  The agency has developed an RfC for acrolein of 0.02 ug/m3 and an RfD of 0.5 ug/kg-day.  

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.  These data and additional studies regarding acute effects of human exposure to acrolein are summarized in EPA's 2003 Toxicological Review of Acrolein.  Studies in humans indicate that levels as low as 0.09 ppm (0.21 mg/m[3]) for five minutes may elicit subjective complaints of eye irritation with increasing concentrations leading to more extensive eye, nose and respiratory symptoms.  Acute exposures in animal studies report bronchial hyper-responsiveness.  Based on animal data (more pronounced respiratory irritancy in mice with allergic airway disease in comparison to non-diseased mice) 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 ug/m[3] for 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 ug/m[3] and 0.7 ug/m[3], respectively.    

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.  Animal studies have reported respiratory tract tumors from inhalation exposure to benzo[a]pyrene and alimentary tract and liver tumors from oral exposure to benzo[a]pyrene.  In 1997 EPA classified seven PAHs (benzo[a]pyrene, benz[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, dibenz[a,h]anthracene, and indeno[1,2,3-cd]pyrene) as Group B2, probable human carcinogens.  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).[,] These and similar studies are being evaluated as a part of the ongoing IRIS reassessment of health effects associated with exposure to benzo[a]pyrene.

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.  Chronic (long term) exposure of workers and rodents to naphthalene has been reported to cause cataracts and retinal damage.  EPA released an external review draft of a reassessment of the inhalation carcinogenicity of naphthalene based on a number of recent animal carcinogenicity studies.  The draft reassessment completed external peer review.  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.  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.  
Naphthalene also causes a number of chronic non-cancer effects in animals, including abnormal cell changes and growth in respiratory and nasal tissues.  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 ug/m[3].  The ATSDR MRL for acute exposure to naphthalene is 0.6 mg/kg/day.

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 the rules.  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.
Exposure and Health Effects Associated with Traffic
Locations in close proximity to major roadways generally have elevated concentrations of many air pollutants emitted from motor vehicles.  Hundreds of such studies have been published in peer-reviewed journals, concluding that concentrations of CO, NO, NO2, benzene, aldehydes, particulate matter, black carbon, and many other compounds are elevated in ambient air within approximately 300-600 meters (about 1,000-2,000 feet) of major roadways.  Highest concentrations of most pollutants emitted directly by motor vehicles are found at locations within 50 meters (about 165 feet) of the edge of a roadway's traffic lanes.

A large-scale review of air quality measurements in the vicinity of major roadways between 1978 and 2008 concluded that the pollutants with the steepest concentration gradients in vicinities of roadways were CO, ultrafine particles, metals, elemental carbon (EC), NO, NOX, and several VOCs.  These pollutants showed a large reduction in concentrations within 100 meters downwind of the roadway.  Pollutants that showed more gradual reductions with distance from roadways included benzene, NO2, PM2.5, and PM10.  In the review article, results varied based on the method of statistical analysis used to determine the trend.

For pollutants with relatively high background concentrations relative to near-road concentrations, detecting concentration gradients can be difficult.  For example, many aldehydes have high background concentrations as a result of photochemical breakdown of precursors from many different organic compounds.  This can make detection of gradients around roadways and other primary emission sources difficult.  However, several studies have measured aldehydes in multiple weather conditions and found higher concentrations of many carbonyls downwind of roadways.[,]  These findings suggest a substantial roadway source of these carbonyls.
In the past 15 years, many studies have been published with results reporting that populations who live, work, or go to school near high-traffic roadways experience higher rates of numerous adverse health effects, compared to populations far away from major roads.  In addition, numerous studies have found adverse health effects associated with spending time in traffic, such as commuting or walking along high-traffic roadways.[,][,][,]  The health outcomes with the strongest evidence linking them with traffic-associated air pollutants are respiratory effects, particularly in asthmatic children, and cardiovascular effects.

Numerous reviews of this body of health literature have been published as well.  In 2010, an expert panel of the Health Effects Institute (HEI) published a review of hundreds of exposure, epidemiology, and toxicology studies.  The panel rated how the evidence for each type of health outcome supported a conclusion of a causal association with traffic-associated air pollution as either "sufficient," "suggestive but not sufficient," or "inadequate and insufficient."  The panel categorized evidence of a causal association for exacerbation of childhood asthma as "sufficient."  The panel categorized evidence of a causal association for new onset asthma as between "sufficient" and "suggestive but not sufficient."  "Suggestive of a causal association" was how the panel categorized evidence linking traffic-associated air pollutants with exacerbation of adult respiratory symptoms and lung function decrement.  It categorized as "inadequate and insufficient" evidence of a causal relationship between traffic-related air pollution and health care utilization for respiratory problems, new onset adult asthma, chronic obstructive pulmonary disease (COPD), nonasthmatic respiratory allergy, and cancer in adults and children.  Other literature reviews have been published with conclusions generally similar to the HEI panel's.[,][,][,]  However, in 2014, researchers from the U.S. Centers for Disease Control and Prevention (CDC) published a systematic review and meta-analysis of studies evaluating the risk of childhood leukemia associated with traffic exposure and reported positive associations between "postnatal" proximity to traffic and leukemia risks, but no such association for "prenatal" exposures.  

Health outcomes with few publications suggest the possibility of other effects still lacking sufficient evidence to draw definitive conclusions.  Among these outcomes with a small number of positive studies are neurological impacts (e.g., autism and reduced cognitive function) and reproductive outcomes (e.g., preterm birth, low birth weight).[,][,][,]

In addition to health outcomes, particularly cardiopulmonary effects, conclusions of numerous studies suggest mechanisms by which traffic-related air pollution affects health.  Numerous studies indicate that near-roadway exposures may increase systemic inflammation, affecting organ systems, including blood vessels and lungs.[,][,][,]  Long-term exposures in near-road environments have been associated with inflammation-associated conditions, such as atherosclerosis and asthma.[,][,]  
Several studies suggest that some factors may increase susceptibility to the effects of traffic-associated air pollution.  Several studies have found stronger respiratory associations in children experiencing chronic social stress, such as in violent neighborhoods or in homes with high family stress.[,][,]  

The risks associated with residence, workplace, or schools near major roads are of potentially high public health significance due to the large population in such locations.  According to the 2009 American Housing Survey, over 22 million homes (17.0 percent of all U.S. housing units) were located within 300 feet of an airport, railroad, or highway with four or more lanes.  This corresponds to a population of more than 50 million U.S. residents in close proximity to high-traffic roadways or other transportation sources.  Based on 2010 Census data, a 2013 publication estimated that 19 percent of the U.S. population (over 59 million people) lived within 500 meters of roads with at least 25,000 annual average daily traffic (AADT), while about 3.2 percent of the population lived within 100 meters (about 300 feet) of such roads.  Another 2013 study estimated that 3.7 percent of the U.S. population (about 11.3 million people) lived within 150 meters (about 500 feet) of interstate highways or other freeways and expressways.  On average, populations near major roads have higher fractions of minority residents and lower socioeconomic status.  Furthermore, on average, Americans spend more than an hour traveling each day, bringing nearly all residents into a high-exposure microenvironment for part of the day.

In light of these concerns, EPA has required through the NAAQS process that air quality monitors be placed near high-traffic roadways for determining concentrations of CO, NO2, and PM2.5 (in addition to those existing monitors located in neighborhoods and other locations farther away from pollution sources).  Near-roadway monitors for NO2 begin operation between 2014 and 2017 in Core Based Statistical Areas (CBSAs) with population of at least 500,000.  Monitors for CO and PM2.5 begin operation between 2015 and 2017.  These monitors will further our understanding of exposure in these locations.

EPA and DOT continue to research near-road air quality, including the types of pollutants found in high concentrations near major roads and health problems associated with the mixture of pollutants near roads.  
Environmental Justice
Environmental justice (EJ) is a principle asserting that all people deserve fair treatment and meaningful involvement with respect to environmental laws, regulations, and policies.  EPA seeks to provide the same degree of protection from environmental health hazards for all people.  DOT shares this goal and is informed about the potential environmental impacts of its rulemakings through its NEPA process (see NHTSA's DEIS).  As referenced below, numerous studies have found that some environmental hazards are more prevalent in areas where racial/ethnic minorities and people with low socioeconomic status (SES) represent a higher fraction of the population compared with the general population.  In addition, compared to non-Hispanic whites, some minorities defined by race and ethnicity may have greater incidence of some health problems during certain life stages.  For example, in 2014, about 13 percent of Black, non-Hispanic and 24 percent of Puerto Rican children were estimated to currently have asthma, compared with 8 percent of white, non-Hispanic children.

Concentrations of many air pollutants are elevated near high-traffic roadways.  If minority populations and low-income populations disproportionately live near such roads, then an issue of EJ may be present.  We reviewed existing scholarly literature examining the potential for disproportionate exposure among minorities and people with low SES, and we conducted our own evaluation of two national datasets: the U.S. Census Bureau's American Housing Survey for calendar year 2009 and the U.S. Department of Education's database of school locations.

Publications that address EJ issues generally report that populations living near major roadways (and other types of transportation infrastructure) tend to be composed of larger fractions of nonwhite residents.  People living in neighborhoods near such sources of air pollution also tend to be lower in income than people living elsewhere.  Numerous studies evaluating the demographics and socioeconomic status of populations or schools near roadways have found that they include a greater percentage of minority residents, as well as lower SES (indicated by variables such as median household income).  Locations in these studies include Los Angeles, CA; Seattle, WA; Wayne County, MI; Orange County, FL; and the State of California [,][,][,][,][,]  Such disparities may be due to multiple factors.

People with low SES often live in neighborhoods with multiple stressors and health risk factors, including reduced health insurance coverage rates, higher smoking and drug use rates, limited access to fresh food, visible neighborhood violence, and elevated rates of obesity and some diseases such as asthma, diabetes, and ischemic heart disease.  Although questions remain, several studies find stronger associations between air pollution and health in locations with such chronic neighborhood stress, suggesting that populations in these areas may be more susceptible to the effects of air pollution.[,][,][,]  Household-level stressors such as parental smoking and relationship stress also may increase susceptibility to the adverse effects of air pollution.[,]
More recently, three publications report nationwide analyses that compare the demographic patterns of people who do or do not live near major roadways.[,][,]  All three of these studies found that people living near major roadways are more likely to be minorities or low in SES.  They also found that the outcomes of their analyses varied between regions within the U.S.  However, only one such study looked at whether such conclusions were confounded by living in a location with higher population density and how demographics differ between locations nationwide.  In general, it found that higher density areas have higher proportions of low income and minority residents.
 
We analyzed two national databases that allowed us to evaluate whether homes and schools were located near a major road and whether disparities in exposure may be occurring in these environments.  The American Housing Survey includes descriptive statistics of over 70,000 housing units across the nation.  The study survey is conducted every two years by the U.S. Census Bureau.  The second database we analyzed was the U.S. Department of Education's Common Core of Data, which includes enrollment and location information for schools across the U.S.
 
In analyzing the 2009 AHS, we focused on whether or not a housing unit was located within 300 feet of "4-or-more lane highway, railroad, or airport."  We analyzed whether there were differences between households in such locations compared with those in locations farther from these transportation facilities.  We included other variables, such as land use category, region of country, and housing type.  We found that homes with a nonwhite householder were 22-34 percent more likely to be located within 300 feet of these large transportation facilities than homes with white householders.  Homes with a Hispanic householder were 17-33 percent more likely to be located within 300 feet of these large transportation facilities than homes with non-Hispanic householders.  Households near large transportation facilities were, on average, lower in income and educational attainment, more likely to be a rental property and located in an urban area compared with households more distant from transportation facilities.

In examining schools near major roadways, we examined the Common Core of Data from the U.S. Department of Education, which includes information on all public elementary and secondary schools and school districts nationwide.  To determine school proximities to major roadways, we used a geographic information system (GIS) to map each school and roadways based on the U.S. Census's TIGER roadway file.  We found that minority students were overrepresented at schools within 200 meters of the largest roadways, and that schools within 200 meters of the largest roadways also had higher than expected numbers of students eligible for free or reduced-price lunches.  For example, Black students represent 22 percent of students at schools located within 200 meters of a primary road, whereas Black students represent 17 percent of students in all U.S. schools.  Hispanic students represent 30 percent of students at schools located within 200 meters of a primary road, whereas Hispanic students represent 22 percent of students in all U.S. schools.

Overall, there is substantial evidence that people who live or attend school near major roadways are more likely to be of a minority race, Hispanic ethnicity, and/or low SES.  
Visibility
Visibility can be defined as the degree to which the atmosphere is transparent to visible light.  Visibility impairment is caused by light scattering and absorption by suspended particles and gases.  Visibility is important because it has direct significance to people's enjoyment of daily activities in all parts of the country.  Individuals value good visibility for the well-being it provides them directly, where they live and work, and in places where they enjoy recreational opportunities.  Visibility is also highly valued in significant natural areas, such as national parks and wilderness areas, and special emphasis is given to protecting visibility in these areas.  For more information on visibility see the final 2009 PM ISA.

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 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. 

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.  In 1999, EPA finalized the regional haze program 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.  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.  

EPA has also concluded that PM2.5 causes adverse effects on visibility in other areas that are not targeted by the Regional Haze Rule, such as urban areas, 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.  
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.  In those sensitive species, effects from repeated exposure to ozone throughout the growing season of the plant tend to accumulate, so that even low concentrations experienced for a longer duration have the potential to create chronic stress on vegetation.  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.  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 ecosystems, resulting in a loss or reduction in associated ecosystem goods and services.  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.  

The most recent ISA for Ozone presents more detailed information on how ozone affects vegetation and ecosystems.  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.  The 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. 
Atmospheric Deposition
Wet and dry deposition of ambient particulate matter delivers a complex mixture of metals (e.g., mercury, zinc, lead, nickel, aluminum, and cadmium), organic compounds (e.g., polycyclic organic matter, dioxins, and furans) and inorganic compounds (e.g., nitrate, sulfate) to terrestrial and aquatic ecosystems.  The chemical form of the compounds deposited depends on a variety of factors including ambient conditions (e.g., temperature, humidity, oxidant levels) and the sources of the material.  Chemical and physical transformations of the compounds occur in the atmosphere as well as the media onto which they deposit.  These transformations in turn influence the fate, bioavailability and potential toxicity of these compounds.  

Adverse impacts to human health and the environment can occur when particulate matter is deposited to soils, water, and biota.  Deposition of heavy metals or other toxics may lead to the human ingestion of contaminated fish, impairment of drinking water, damage to terrestrial, freshwater and marine ecosystem components, and limits to recreational uses.  Atmospheric deposition has been identified as a key component of the environmental and human health hazard posed by several pollutants including mercury, dioxin and PCBs.   

The ecological effects of acidifying deposition and nutrient enrichment are detailed in the Integrated Science Assessment for Oxides of Nitrogen and Sulfur-Ecological Criteria. Atmospheric deposition of nitrogen and sulfur contributes to acidification, altering biogeochemistry and affecting animal and plant life in terrestrial and aquatic ecosystems across the United States.  The sensitivity of terrestrial and aquatic ecosystems to acidification from nitrogen and sulfur deposition is predominantly governed by geology.  Prolonged exposure to excess nitrogen and sulfur deposition in sensitive areas acidifies lakes, rivers and soils.  Increased acidity in surface waters creates inhospitable conditions for biota and affects the abundance and biodiversity of fishes, zooplankton and macroinvertebrates and ecosystem function.  Over time, acidifying deposition also removes essential nutrients from forest soils, depleting the capacity of soils to neutralize future acid loadings and negatively affecting forest sustainability.  Major effects in forests include a decline in sensitive tree species, such as red spruce (Picea rubens) and sugar maple (Acer saccharum).  In addition to the role nitrogen deposition plays in acidification, nitrogen deposition also leads to nutrient enrichment and altered biogeochemical cycling.  In aquatic systems increased nitrogen can alter species assemblages and cause eutrophication.  In terrestrial systems nitrogen loading can lead to loss of nitrogen-sensitive lichen species, decreased biodiversity of grasslands, meadows and other sensitive habitats, and increased potential for invasive species.  

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.  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 on materials including zinc/galvanized steel and other metal, carbonate stone (as monuments and building facings), and surface coatings (paints).  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.
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, some of which are considered air toxics, have long been suspected to play a role in vegetation damage.  In laboratory experiments, a wide range of tolerance to VOCs has been observed.  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. 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.[,],