The Report on Diesel Exhaust

This page last reviewed July 21, 2015

Findings of the Scientific Review Panel On

The Report on Diesel Exhaust

As Adopted at the Panel's April 22, 1998 Meeting

Pursuant to Health and Safety Code section 39661, the Scientific Review Panel (SRP / Panel) has reviewed the report Proposed Identification of Diesel Exhaust as a Toxic Air Contaminant by the staffs of the California Air Resources Board (ARB or Board) and the Office of Environmental Health Hazard Assessment (OEHHA) describing the public exposure to, and health effects of, diesel exhaust. The Panel members also reviewed the public comments received on this report.

Panel members participated in workshops devoted to discussion of the exposure and health issues associated with diesel exhaust in September 1994, January 1996, July 1997, and March 1998. The SRP reviewed the issues at its meetings in October 1997 and April 1998. A special meeting of the SRP was held on March 11, 1998, to hear testimony on health issues including the quantitative risk assessment from highly respected scientists invited by the Panel. Based on these reviews and information provided at scientific workshops and meetings, the SRP makes the following findings pursuant to Health and Safety Code section 39661:

Exposure Related Conclusions:

  1. Diesel exhaust is a complex mixture of gases and fine particles emitted by a diesel-fueled internal combustion engine.

  2. The gaseous fraction is composed of typical combustion gases such as nitrogen, oxygen, carbon dioxide, and water vapor. However, as a result of incomplete combustion, the gaseous fraction also contains air pollutants such as carbon monoxide, sulfur oxides, nitrogen oxides, volatile organics, alkenes, aromatic hydrocarbons, and aldehydes, such as formaldehyde and 1,3-butadiene and low-molecular weight polycyclic aromatic hydrocarbons (PAH) and PAH-derivatives.

  3. One of the main characteristics of diesel exhaust is the release of particles at a markedly greater rate than from gasoline-fueled vehicles, on an equivalent fuel energy basis. The particles are mainly aggregates of spherical carbon particles coated with inorganic and organic substances. The inorganic fraction primarily consists of small solid carbon (or elemental carbon) particles ranging from 0.01 to 0.08 microns in diameter. The organic fraction consists of soluble organic compounds such as aldehydes, alkanes and alkenes, and high-molecular weight PAH and PAH-derivatives, such as nitro-PAHs. Many of these PAHs and PAH-derivatives, especially nitro-PAHs, have been found to be potent mutagens and carcinogens. Nitro-PAH compounds can also be formed during transport through the atmosphere by reactions of adsorbed PAH with nitric acid and by gas-phase radical-initiated reactions in the presence of oxides of nitrogen.

  4. Diesel exhaust includes over 40 substances that are listed by the United States Environmental Protection Agency (U.S. EPA) as hazardous air pollutants and by the ARB as toxic air contaminants. Fifteen of these substances are listed by the International Agency for Research on Cancer (IARC) as carcinogenic to humans, or as a probable or possible human carcinogen. Some of these substances are: acetaldehyde; antimony compounds; arsenic; benzene; beryllium compounds; bis(2-ethylhexyl)phthalate; dioxins and dibenzofurans; formaldehyde; inorganic lead; mercury compounds; nickel; POM (including PAHs); and styrene.

  5. Almost all of the diesel particle mass is in the fine particle range of 10 microns or less in diameter (PM10). Approximately 94 percent of the mass of these particles are less than 2.5 microns in diameter. Because of their small size, these particles can be inhaled and a portion will eventually become trapped within the small airways and alveolar regions of the lung.

  6. The estimated population-weighted average outdoor diesel exhaust PM10 concentration in California for 1995 is 2.2 microgram per cubic meter (µg/m3). Several independent studies have reported similar outdoor air diesel exhaust PM10 concentrations. The 1995 estimated average indoor exposure concentration is approximately 1.5 µg/m3.

  7. The population time-weighted average total air exposure to diesel exhaust particle concentrations across all environments (including outdoors) is estimated to be 1.5 µg/m3 in 1995. This total exposure estimate may underestimate many Californians' actual total exposure because it excludes elevated exposures near roadways, railroad tracks, and inside vehicles. Near-source exposures to diesel exhaust may be as much as five times higher than the 1995 population time-weighted average total air exposure. It also excludes other routes of exposure to diesel exhaust, such as ingestion and dermal absorption.

  8. Diesel engine exhaust contains small carbonaceous particles and a large number of chemicals that are adsorbed onto these particles or present as vapors. These particles have been the subject of many studies because of their adverse effects on human health and the environment. A recent study conducted for the Health Effects Institute showed that, despite a substantial reduction in the weight of the total particulate matter, the total number of particles from a 1991-model engine was 15 to 35 times greater than the number of particles from a 1988 engine when both engines were operated without emission control devices. This suggests that more fine particles, a potential health concern, could be formed as a result of new technologies. Further study is needed since the extent of these findings only measured exhaust from two engines and engine technologies.

  9. The major sources of diesel exhaust in ambient outdoor air are estimated to emit approximately 27,000 tons per year in 1995. On-road mobile sources (heavy-duty trucks, buses, light-duty cars and trucks) contribute the majority of total diesel exhaust PM10 emissions in California. Other mobile sources (mobile equipment, ships, trains, and boats) and stationary sources contribute the remaining emissions.

  10. Significant progress has been made as a result of federal and state regulations that have addressed particulate matter levels from diesel engines. Emissions of on-road mobile source diesel exhaust PM10 in California are expected to decline by approximately 85 percent from 1990 to 2010 as a result of mobile source regulations already adopted by the ARB.

  11. The results of a study funded by the ARB at the University of California, Riverside, indicate that the diesel exhaust from the new fuel tested contained the same toxic air contaminants as the old fuel, although their concentrations and other components may differ. Further research would be helpful to quantify the amounts of specific compounds emitted from a variety of engine technologies, operating cycles, and fuel to characterize better any differences between old and new fuels and technologies.

Health Effects Associated with Diesel Exhaust:

  1. A number of adverse short-term health effects have been associated with exposures to diesel exhaust. Occupational exposures to diesel exhaust particles have been associated with significant cross-shift decreases in lung function. Increased cough, labored breathing, chest tightness, and wheezing have been associated with exposure to diesel exhaust in bus garage workers. A significant increase in airway resistance and increases in eye and nasal irritation were observed in human volunteers following one-hour chamber exposure to diesel exhaust. In acute or subchronic animal studies, exposure to diesel exhaust particles induced inflammatory airway changes, lung function changes, and increased the animals' susceptibility to infection.

  2. A number of adverse long-term noncancer effects have been associated with exposure to diesel exhaust. Occupational studies have shown that there may be a greater incidence of cough, phlegm and chronic bronchitis among those exposed to diesel exhaust than among those not exposed. Reductions in pulmonary function have also been reported following occupational exposures in chronic studies. Reduced pulmonary function was noted in monkeys during long-term exposure. Histopathological changes in the lung of diesel-exposed test animals reflect inflammation of the lung tissue. These changes include dose-dependent proliferations of Type II epithelial cells, marked infiltration of macrophages, plasma cells and fibroblasts into the alveolar septa, thickening of the alveolar walls, alveolar proteinosis, and focal fibrosis.

  3. Studies have shown that diesel exhaust particles can induce immunological reactions and localized inflammatory responses in humans, as well as acting as an adjuvant for pollen allergy. Intranasal challenge with diesel exhaust particles in human volunteers resulted in increased nasal IgE antibody production and a significant increase in mRNA for pro-inflammatory cytokines. Co-exposure to diesel exhaust particles and ragweed pollen resulted in a nasal IgE response greater than that following pollen or diesel exhaust particles alone. Effects of intratracheal, intranasal, and inhalation exposures of laboratory animals are supportive of the findings in humans. These effects include eosinophilic infiltration into bronchi and bronchioles, elevated IgE response, increased mucus secretion and respiratory resistance, and airway constriction.

  4. Based on the animal studies, the U.S. EPA determined a chronic inhalation Reference Concentration value of 5 µg/m3 for noncancer effects of diesel exhaust. This estimate takes into consideration persons who may be more sensitive than others to the effects of diesel exhaust. The report supports the recommendation of 5 µg/m3 as the California Reference Exposure Level (REL) (Table 1). It should be noted that this REL may need to be lowered further as more data emerge on potential adverse noncancer effects from diesel exhaust.

  5. Diesel exhaust contains genotoxic compounds in both the vapor phase and the particle phase. Diesel exhaust particles or extracts of diesel exhaust particles are mutagenic in bacteria and in mammalian cell systems, and can induce chromosomal aberrations, aneuploidy, and sister chromatid exchange in rodents and in human cells in vitro. Diesel exhaust particles induced unscheduled DNA synthesis in vitro in mammalian cells. DNA adducts have been isolated from calf thymus DNA in vitro following treatment with diesel exhaust particle extracts. DNA adducts have been shown to increase following inhalation exposure of rodents and monkeys to whole diesel exhaust. Elevated levels of DNA adducts have been associated with occupational exposure to diesel exhaust. Results of inhalation bioassays in the rat, and with lesser certainty in mice, have demonstrated the carcinogenicity of diesel exhaust in test animals, although the mechanisms by which diesel exhaust induces lung tumors in animals remains uncertain.

  6. Over 30 human epidemiological studies have investigated the potential carcinogenicity of diesel exhaust. These studies, on average, found that long-term occupational exposures to diesel exhaust were associated with a 40 percent increase in the relative risk of lung cancer. The lung cancer findings are consistent and the association is unlikely to be due to chance. These epidemiological studies strongly suggest a causal relationship between occupational diesel exhaust exposure and lung cancer.

  7. Other agencies or scientific bodies have evaluated the health effects of diesel exhaust. The National Institute of Occupational Safety and Health first recommended in 1988 that whole diesel exhaust be regarded as a potential occupational carcinogen based upon animal and human evidence. The International Agency for Research on Cancer (IARC) concluded that diesel engine exhaust is probably carcinogenic to humans and classified diesel exhaust in Group 2A. Based upon the IARC findings, in 1990, the State of California under the Safe Drinking Water and Toxic Enforcement Act of 1986 (Proposition 65) identified diesel exhaust as a chemical "known to the State to cause cancer." The U.S. EPA has proposed a conclusion similar to IARC in their draft documents. The 1998 draft U.S. EPA document concluded similarly that there was sufficient animal evidence of carcinogenicity and that the human evidence was limited.

  8. There are data from human epidemiological studies of occupationally exposed populations which are useful for quantitative risk assessment. The estimated range of lung cancer risk (upper 95% confidence interval) based on human epidemiological data is 1.3 x 10-4 to 2.4 x 10-3 (µg/m3)-1 (Table 2). After considering the results of the meta-analysis of human studies, as well as the detailed analysis of railroad workers, the SRP concludes that 3 x 10-4 (µg/m3)-1 is a reasonable estimate of unit risk expressed in terms of diesel particulate. Thus this unit risk value was derived from two separate approaches which yield similar results. A comparison of estimates of risk can be found in Table 3.

  9. Based on available scientific information, a level of diesel exhaust exposure below which no carcinogenic effects are anticipated has not been identified.

  10. Based on available scientific evidence, as well as the results of the risk assessment, we conclude that diesel exhaust be identified as a Toxic Air Contaminant.

  11. As with other substances evaluated by this Panel and after reviewing the field of published peer reviewed research studies on diesel exhaust, additional research is appropriate to clarify further the health effects of diesel exhaust. This research may have significance for estimating the unit risk value.

  12. The Panel, after careful review of the February 1998 draft SRP version of the ARB report, Proposed Identification of Diesel Exhaust as a Toxic Air Contaminant, as well as the scientific procedures and methods used to support the data, the data itself, and the conclusions and assessments on which the Report is based, finds this report with the changes specified during our October 16, 1997, meeting and as a result of comments made at the March 11, 1998, meeting, is based upon sound scientific knowledge, methods, and practices and represents a complete and balanced assessment of our current scientific understanding.

For these reasons, we agree with the science presented in Part A by ARB and Part B by OEHHA in the report on diesel exhaust and the ARB staff recommendation to its Board that diesel exhaust be listed by the ARB as a Toxic Air Contaminant.

  I certify that the above is a true and correct copy of the findings adopted by the Scientific Review Panel on April 22, 1998.

John R. Froines, Ph.D.
Acting Chairman
Scientific Review Panel





Compound Health Value End Point
Acetaldehyde 9 µg/m3 Respiratory System
Diesel Exhaust 5 µg/m3 Respiratory System
Inorganic Lead 4.6 x 10-4 ( µg/m3)-1 Cardiovascular Mortality
Perchloroethylene 35 µg/m3 Alimentary System (Liver)
µg/m3:  Microgram Per Cubic Meter



FROM 1984 TO 1998

(In Order of Cancer Potency)

Compound Unit Risk (µg/m3)-1 Range (µg/m3)-1
Dioxins 3.8 x 101 2.4 x 101 to 3.8 x 101
Chromium VI 1.5 x 10-1 1.2 x 10-2 to 1.5 x 10-1
Cadmium 4.2 x 10-3 2.0 x 10-3 to 1.2 x 10-2
Inorganic Arsenic 3.3 x 10-3 6.3 x 10-4 to 1.3 x 10-2
Benzo[a]pyrene 1.1 x 10-3 1.1 x 10-3 to 3.3 x 10-3
Diesel Exhaust 3 x 10-4 1.3 x 10-4 to 2.4 x 10-3
Nickel 2.6 x 10-4 2.1 x 10-4 to 3.7 x 10-3
1,3-Butadiene 1.7 x 10-4 4.4 x 10-6 to 3.6 x 10-4
Ethylene Oxide 8.8 x 10-5 6.1 x 10-5 to 8.8 x 10-5
Vinyl Chloride 7.8 x 10-5 9.8 x 10-6 to 7.8 x 10-5
Ethylene Dibromide 7.1 x 10-5 1.3 x 10-5 to 7.1 x 10-5
Carbon Tetrachloride 4.2 x 10-5 1.0 x 10-5 to 4.2 x 10-5
Benzene 2.9 x 10-5 7.5 x 10-6 to 5.3 x 10-5
Ethylene Dichloride 2.2 x 10-5 1.3 x 10-5 to 2.2 x 10-5
Inorganic Lead 1.2 x 10-5 1.2 x 10-5 to 6.5 x 10-5
Perchloroethylene 5.9 x 10-6 3.0 x 10-7 to 1.1 x 10-5
Formaldehyde 6.0 x 10-6 2.5 x 10-7 to 3.3 x 10-5
Chloroform 5.3 x 10-6 6.0 x 10-7 to 2.0 x 10-5
Acetaldehyde 2.7 x 10-6 9.7 x 10-7 to 2.7 x 10-5
Trichloroethylene 2.0 x 10-6 8.0 x 10-7 to 1.0 x 10-5
Methylene Chloride 1.0 x 10-6 3.0 x 10-7 to 3.0 x 10-6
Asbestos 1.9 x 10-4
(per 100 fiber/m3)
Lung: 11 - 110 x 10-6 (per 100 fiber/m3) Mesothelioma: 38 - 190 x 10-6
(per 100 fiber/m3)
µg/m3:  Microgram Per Cubic Meter

Method Unit Risk / Range Basis of Assessment Reference
Epidemiologic Analysis 3 x 10-4 Based on Smoking-Adjusted Pooled RR Smith, 1998
Epidemiologic Analysisb 3.6 x 10-4 to 2.4 x 10-3 Case-Control Study of Garshick et al., 1987 OEHHA, Part B, Section 7.3.3
Epidemiologic Analysis 2.8 x 10-4 to 1.8 x 10-3 Cohort Study of
Garshick et al., 1988
OEHHA, Part B, Section 7.3.4
Epidemiologic Analysis 1.3 to 7.2 x 10-4 Cohort Study, Time Varying Conc., Roof (3,50) Pattern OEHHA, Part B,
Appendix D
Epidemiologic Analysis 3.8 x 10-4 to 1.9 x 10-3 Cohort Study, Time Varying Conc., Ramp (1,50) Pattern OEHHA, Part B,
Appendix D
Epidemiologic Analysis 1.4 x 10-3 London Transport Studyc Harris, 1983
Epidemiologic Analysis 2 x 10-3 Epidemiologic Data of Garshick (Top End of U.S. EPA's Range) U.S. EPA, 1998
Epidemiologic Analysis 1.3 x 10-4 to 1.3 x 10-2 Using Smoking-Adjusted RR and Exposures of 5 or 500 µg/m3 OEHHA, Part B,
Section 7.3;
Bracketed Risk
a) Bolded values are included in OEHHA's range of risk.
b) Obtained by applying Harris' slope of 5 x 10-4 ( µg/m3 x yr)-1 to California life table.

Air Toxics Program
Particulate Emissions from Diesel-Fueled Engines as a TAC
Toxic Emisisons from Diesel-Fueled Engines