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EPA Says Diesel Exhaust Probably Causes Lung Cancer

AP 3sep02

[EPA Study Executive Report below]

WASHINGTON -- Diesel exhaust from large trucks and other sources probably causes lung cancer, the Environmental Protection Agency concluded Tuesday in a report that buttresses a push to reduce truck emissions through stricter requirements for cleaner diesel fuel.

The EPA report concludes that uncertainties remain about long-term health effects of exposure to diesel exhausts. It said, however, that studies involving both tests on animals and occupational exposure suggest strong evidence of a cancer risk to humans.

"Overall, the evidence for a potential cancer hazard to humans resulting from chronic inhalation exposure to [diesel emissions] is persuasive," said the health impact report released by the EPA.

The report mirrors conclusions made previously in documents from various world health agencies and studies in California, and is particularly significant because the EPA is the federal agency that regulates diesel emissions under the Clean Air Act.

Some environmentalists have expressed worries recently that the Bush administration might have been backing away from a Clinton-era regulation that would establish tougher requirements on emissions from large trucks and a separate rule that virtually would eliminate sulfur from diesel fuel.

EPA Administrator Christie Whitman repeatedly has promised to go ahead with the tougher diesel rules. Last month, with White House approval, the EPA rebuffed attempts by some diesel engine manufacturers to postpone the requirements, approving new penalties against manufacturers who fail to meet an October deadline for making cleaner-burning truck engines.

The engine rule doesn't affect emissions from trucks already on the road, although the separate regulation cutting the amount of sulfur in diesel fuel is expected to produce pollution reductions.

The EPA's 651-page diesel health assessment report had been awaited by environmentalists, health advocates and state air quality regulators who have been pushing for diesel emission reductions.

The report reiterated that environmental exposure to diesel exhausts poses "a chronic respiratory hazard to humans" in the long term including increased asthma and other respiratory problems. In some urban areas diesel exhausts account for as much as a quarter of the airborne microscopic soot, the report said.

As for cancer, the report noted occupational health studies and tests on animals that showed diesel emissions to be a carcinogen, a cancer-causing substance. While there remain uncertainties, the report continued, "it is reasonable to presume that the hazard extends to environmental exposure levels" as well.

"The overall evidence for potential human health effects of diesel exhausts is persuasive," the report said.

"This assessment concludes that [diesel exhaust] is likely to be carcinogenic to humans by inhalation, and that this hazard applies to environmental exposure ... based on the totality of evidence from human, animal and other supporting studies," said the report.

Environmentalists welcomed the study as clear evidence that pollution needs to be curtailed not only from large trucks but also from off-road diesel-powered vehicles. The EPA has yet to deal with those diesel exhaust sources, which include farm tractors and construction equipment.

"To reduce the public's exposure to harmful diesel emissions, the Bush administration should .. fully implement clean air standards for diesel trucks and buses and should pass equivalent standards for diesel construction and farm equipment," said Emily Figdor of the U.S. Public Interest Research Group, a private environmental organization.

Ms. Figdor noted that the report is surfacing just as children across the country are returning to schools, many in diesel-powered buses. "Children riding buses back to school .. need stronger protection against the health impacts of diesel exhaust," she said.

Health Assessment Document For Diesel Engine Exhaust 

EPA/600/8-90/057F May 2002

National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Washington, DC



This Health Assessment Document for Diesel Engine Exhaust (DE) represents EPA’s first comprehensive review of the potential health effects from ambient exposure to exhaust from diesel engines. The assessment was developed to provide information about the potential for DE to pose environmental health hazards, information that would be useful in evaluating regulatory needs under provisions of the Clean Air Act. The assessment identifies and characterizes the potential human health hazards of DE (i.e, hazard assessment) and seeks to estimate the relationship between exposure and disease response for the key health effects (i.e., dose-response assessment). A full exposure assessment and risk characterization, the other two components of a complete risk assessment, are beyond the scope of this document.

The report has nine chapters and three appendices. Chapter 2 provides a characterization of diesel emissions, atmospheric transformation, and human exposures to provide a context for the hazard evaluation of DE. Chapters 3, 4, 5, and 7 provide a review of relevant information for the evaluation of potential health hazards of DE, including dosimetry (Chapter 3), mutagenicity (Chapter 4), noncancer effects (Chapter 5), and carcinogenic effects (Chapter 7). Chapters 6 and 8 contain dose-response analyses to provide insight about the significance of the key noncancer and cancer hazards. Chapter 9 summarizes and characterizes the overall nature of the health hazard potential in the environment and the overall confidence and/or uncertainties associated with the conclusions.


DE is a complex mixture of hundreds of constituents in either a gas or particle form. Gaseous components of DE include carbon dioxide, oxygen, nitrogen, water vapor, carbon monoxide, nitrogen compounds, sulfur compounds, and numerous low-molecular-weight hydrocarbons. Among the gaseous hydrocarbon components of DE that are individually known to be of toxicologic relevance are the aldehydes (e.g., formaldehyde, acetaldehyde, acrolein), benzene, 1,3-butadiene, and polycyclic aromatic hydrocarbons (PAHs) and nitro-PAHs. The particles present in DE (i.e., diesel particulate matter [DPM]) are composed of a center core of elemental carbon and adsorbed organic compounds, as well as small amounts of sulfate, nitrate, metals, and other trace elements. DPM consists of fine particles (fine particles have a diameter <2.5 :m), including a subgroup with a large number of ultrafine particles (ultrafine particles have a diameter <0.1 :m). Collectively, these particles have a large surface area which makes them an excellent medium for adsorbing organics. Also, their small size makes them highly respirable and able to reach the deep lung. A number of potentially toxicologically relevant organic compounds are on the particles. The organics, in general, range from about 20% to 40 % of the particle weight, though higher and lower percentages are also reported. Many of the organic compounds present on the particle and in the gases are individually known to have mutagenic and carcinogenic properties. For example, PAHs, nitro- PAHs, and oxidized PAH derivatives are present on the diesel particles, with the PAHs and their derivatives comprising about 1% or less of the DPM mass.

DE emissions vary 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 emission differences between on-road and nonroad engines simply because the nonroad engines to date are generally of older technology. The mass of particles emitted and the organic components on the particles from on-road diesel engines have been reduced over the years. Available data for on-road engines indicate that toxicologically relevant organic components of DE (e.g., PAHs, nitro- PAHs) emitted from older vehicle engines are still present in emissions from newer engines, though relative amounts have decreased. There is currently insufficient information to characterize the changes in the composition of DE from nonroad diesel engines over time.


DE is emitted from “on-road” diesel engines (vehicle engines) or “nonroad” diesel engines (e.g., locomotives, marine vessels, heavy-duty equipment, etc.). Nationwide, data in 1998 indicated that DE as measured by DPM made up about 6% of the total ambient PM2.5 inventory (i.e., particles with aerodynamic diameter of 2.5 micrometers or less) and about 23% of the inventory, if natural and miscellaneous sources of PM2.5 are excluded. Estimates of the DPM percentage of the total inventory in urban centers are higher. For example, estimates range from 10% to 36% in some urban areas in California, Colorado, and Arizona. Available data also indicate that over the years there have been significant reductions in DPM emissions from the exhaust of on-road diesel engines, whereas limited data suggest that exhaust emissions from nonroad engines have increased.


After emission from the tailpipe, DE undergoes dilution and chemical and physical transformations in the atmosphere, as well as dispersion and transport in the atmosphere. The atmospheric lifetime for some compounds present in DE ranges from hours to days. DPM is directly emitted from diesel-powered engines (primary particulate matter) and can be formed from the gaseous compounds emitted by diesel engines (secondary particulate matter). Limited information is available about the physical and chemical transformation of DE in the atmosphere. It is not clear what the overall toxicological consequences of DE’s transformations are because some compounds in the DE mixture are altered to more toxic forms while others are made less toxic.


DPM mass (expressed as :g DPM/m3) has historically been used as a surrogate measure of exposure for whole DE. Although uncertainty exists as to whether DPM is the most appropriate parameter to correlate with human health effects, it is considered a reasonable choice until more definitive information about the mechanisms of toxicity or mode(s) of action of DE becomes available. In the ambient environment, human exposure to DE comes from both onroad and nonroad engine exhaust. A large percentage of the U.S. population also is exposed to ambient PM2.5, of which DPM is typically a significant constituent. Although this document does not provide an exposure assessment, DE exposure information is included to provide a context for the health effects information. Exposure estimates for the early to mid-1990s suggest that national annual average DE exposure from on-road engines alone was in the range of about 0.5 to 0.8 :g DPM/m3 of inhaled air in many rural and urban areas, respectively. Exposures could be higher if there is a nonroad DE source that adds to the exposure from on-road vehicles. For example, preliminary estimates show that, on a national average basis, accounting for nonroad DE emissions adds another twofold to the on-road exposure. For localized urban areas where people spend a large portion of their time outdoors, the exposures are higher and, for example, may range up to 4.0 :g DPM/m3 of inhaled air.


Available evidence indicates that there are human health hazards associated with exposure to DE. The hazards include acute exposure-related symptoms, chronic exposurerelated noncancer respiratory effects, and lung cancer. The health hazard conclusions are based on exhaust emissions from diesel engines built prior to the mid-1990s. With current engine use including some new and many more older engines (engines typically stay in service for a long time), the health hazard conclusions, in general, are applicable to engines currently in use. As new and cleaner diesel engines, together with different diesel fuels, replace a substantial number of existing engines, the general applicability of the health hazard conclusions will need to be reevaluated. With new engine and fuel technology expected to produce significantly cleaner engine exhaust by 2007 (e.g., in response to new federal heavy duty engine regulations), significant reductions in public health hazards are expected for those engine uses affected by the regulations.

1.6.1. Acute (Short-Term Exposure) Effects

Information is limited for characterizing the potential health effects associated with acute or short-term exposure. However, on the basis of available human and animal evidence, it is concluded that acute or short-term (e.g., episodic) exposure to DE can cause acute irritation (e.g., eye, throat, bronchial), neurophysiological symptoms (e.g., lightheadedness, nausea), and respiratory symptoms (cough, phlegm). There also is evidence for an immunologic effect–the exacerbation of allergenic responses to known allergens and asthma-like symptoms. The lack of adequate exposure-response information in the acute health effect studies precludes the development of recommendations about levels of exposure that would be presumed safe for these effects.

1.6.2. Chronic (Long-Term Exposure) Noncancer Respiratory Effects

Information from the available human studies is inadequate for a definitive evaluation of possible noncancer health effects from chronic exposure to DE. However, on the basis of extensive animal evidence, DE is judged to pose a chronic respiratory hazard to humans. Chronic-exposure, animal inhalation studies show a spectrum of dose-dependent inflammation and histopathological changes in the lung in several animal species including rats, mice, hamsters, and monkeys.

This assessment provides an estimate of inhalation exposure of DE (as measured by DPM) to which humans may be exposed throughout their lifetime without being likely to experience adverse noncancer respiratory effects. This exposure level, known as the reference concentration (RfC) for DE of 5 :g/m3 of DPM was derived on the basis of dose-response data on inflammatory and histopathological changes in the lung from rat inhalation studies. In recognition of the presence of DPM in ambient PM2.5 , it also is appropriate to consider the wealth of PM2.5 human health effects data. In this regard, the 1997 National Ambient Air Quality Standard for PM2.5 of 15 :g/m3 (annual average concentration) also would be expected to provide a measure of protection from DPM, reflecting DPM’s current approximate proportion to PM2.5.

1.6.3. Chronic (Long-Term Exposure) Carcinogenic Effects

This assessment concludes that DE is “likely to be carcinogenic to humans by inhalation” and that this hazard applies to environmental exposures. This conclusion is based on the totality of evidence from human, animal, and other supporting studies. There is considerable evidence demonstrating an association between DE exposure and increased lung cancer risk among workers in varied occupations where diesel engines historically have been used. The human evidence from occupational studies is considered strongly supportive of a finding that DE exposure is causally associated with lung cancer, though the evidence is less than that needed to definitively conclude that DE is carcinogenic to humans. There is some uncertainty about the degree to which confounders are having an influence on the observed cancer risk in the occupational studies, and there is uncertainty evolving from the lack of actual DE exposure data for the workers. In addition to the human evidence, there is supporting evidence of DPM’s carcinogenicity and associated DPM organic compound extracts in rats and mice by noninhalation routes of exposure. Other supporting evidence includes the demonstrated mutagenic and chromosomal effects of DE and its organic constituents, and the suggestive evidence for bioavailability of the DPM organics in humans and animals. Although highexposure chronic rat inhalation studies show a significant lung cancer response, this is not thought predictive of a human hazard at lower environmental exposures. The rat response is considered to result from an overload of particles in the lung resulting from the high exposure, and such an overload is not expected to occur in humans at environmental exposures.

Although the available human evidence shows a lung cancer hazard to be present at occupational exposures that are generally higher than environmental levels, it is reasonable to presume that the hazard extends to environmental exposure levels. While there is an incomplete understanding of the mode of action for DE-induced lung cancer that may occur in humans, there is the potential for a nonthreshold mutagenic mode of action stemming from the organics in the DE mixture. A case for an environmental hazard also is shown by the simple observation that the estimated higher environmental exposure levels are close to, if not overlapping, the lower range of occupational exposures for which lung cancer increases are reported. These considerations taken together support the prudent public health choice of presuming a cancer hazard for DE at environmental levels of exposure. Overall, the evidence for a potential cancer hazard to humans resulting from chronic inhalation exposure to DE is persuasive, even though assumptions and uncertainties are involved. While the hazard evidence is persuasive, this does not lead to similar confidence in understanding the exposure/dose-response relationship.

Given a carcinogenicity hazard, EPA typically performs a dose-response assessment of the human or animal data to develop a cancer unit risk estimate that can be used with exposure information to characterize the potential cancer disease impact on an exposed population. The DE human exposure-response data are considered too uncertain to derive a confident quantitative estimate of cancer unit risk, and with the chronic rat inhalation studies not being predictive for environmental levels of exposure, EPA has not developed a quantitative estimate of cancer unit risk.

In the absence of a cancer unit risk, simple exploratory analyses were used to provide a perspective of the range of possible lung cancer risk from environmental exposure to DE. The analyses make use of reported lung cancer risk increases in occupational epidemiologic studies, and the differences between occupational and environmental exposure. The purpose of having a risk perspective is to illustrate and have a sense of the possible significance of the lung cancer hazard from environmental exposure. The risk perspective cannot be viewed as a definitive quantitative characterization of cancer risk nor is it suitable for estimation of exposure-specific population risks.


Even though the overall evidence for potential human health effects of DE is persuasive, many uncertainties exist because of the use of assumptions to bridge data and knowledge gaps about human exposures to DE and the general lack of understanding about underlying mechanisms by which DE causes observed toxicities in humans and animals. A notable uncertainty of this assessment is whether the health hazards identified from studies using emissions from older engines can be applied to present-day environmental emissions and related exposures, as some physical and chemical characteristics of the emissions from certain sources have changed over time. Available data are not sufficient to provide definitive answers to this question because changes in DE composition over time cannot be confidently quantified, and the relationship between the DE components and the mode(s) of action for DE toxicity is/are unclear. While recognizing the uncertainty, for this assessment a judgment is made that prioryear toxicologic and epidemiologic findings can be applied to more current exposures, both of which use DPM mass in air as the measure of DE exposure.

Other uncertainties include the assumptions that health effects observed at high doses may be applicable to low doses, and that toxicologic findings in laboratory animals generally are predictive of human responses. In the absence of a more complete understanding of how DE may cause adverse health effects in humans and laboratory animals, related assumptions (i.e., the presence of a biological threshold for chronic respiratory effects based on cumulative dosage and absence of a threshold for lung cancer stemming from subtle and irreversible effects) are considered reasonable and prudent.

Although parts of this assessment, particularly the noncancer RfC estimate, have been derived with a generic consideration of sensitive subgroups within the population, the actual spectrum of the population that may have a greater susceptibility to DE is unknown and cannot be better characterized until more information is available regarding the adverse effects of DPM in humans. Increased susceptibility, for example, could result from above-average increases in DE deposition and retention in the respiratory system or intrinsic differences in respiratory system tissue sensitivity. There is no DE-specific information that provides direct insight to the question of differential human susceptibility. Given the nature of DE’s noncancer effects on the respiratory system it would be reasonable, for example, to consider possible vulnerable subgroups to include infants/children, the elderly, or individuals with preexisting health conditions, particularly respiratory conditions.

In developing a perspective on the possible significance of the environmental cancer hazard of DE, this assessment uses information about the differences in the magnitude of DE exposures between the occupational and environmental settings. Although an appreciation for differences in exposure is needed only at an order-of-magnitude level for this assessment, one should recognize that individual exposure is a function of both the variable concentrations in the environment and the related breathing and particle retention patterns of the individual. Because of variations in these factors across the population, different subgroups could receive lower or higher exposure to DE than those groups mentioned in this assessment. Lastly, this assessment considers only potential heath effects from exposures to DE alone. Effects of DE exposure could be additive to or synergistic with concurrent exposures to many other air pollutants. However, in the absence of more definitive data demonstrating interactive effects (e.g., potentiation of allergenicity effects, potentiation of DPM toxicity by ambient ozone and oxides of nitrogen) from combined exposures to DE and other pollutants, it is not possible to address this issue. Further research is needed to improve the knowledge and data on DE exposures and potential human health effects, and thereby reduce uncertainties of future assessments of the DE health effects data.

source: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=29060 3sep02

complete report as PDF from EPA: http://oaspub.epa.gov/eims/eimscomm.getfile?p_download_id=36223 [8MB]

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