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:
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 (g/m3). Several independent studies have reported similar
outdoor air diesel exhaust PM10 concentrations. The 1995 estimated
average indoor exposure concentration is approximately 1.5 g/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 g/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.
13.
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.
14.
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.
15.
Based on the animal studies, the U.S. EPA determined a chronic
inhalation Reference Concentration value of 5 g/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 g/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.
16.
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.
17.
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.
18.
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.
19.
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
(g/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
(g/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.
20.
Based on available scientific information, a level of diesel exhaust
exposure below which no carcinogenic effects are anticipated has not been
identified.
21.
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.
22.
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.
23.
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.
/s/
| Compound | Health Value | Endpoint |
| Acetaldehyde | 9 g/m3 | Respiratory System |
| Diesel Exhaust | 5 g/m3 | Respiratory System |
| Inorganic Lead | 4.6 x 10-4 (g/m3)-1 | Cardiovascular Mortality |
| Perchloroethylene | 35 g/m3 | Alimentary System (Liver) |
| Compound | Unit Risk (g/m3)-1 | Range (g/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 100fiber/m3) |
Lung: 11 - 110 x 10-6 (per 100 fiber/m3) Mesothelioma: 38 - 190 x 10-6 (per 100 fiber/m3) |
| 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 g/m3 | OEHHA, Part B, Section 7.3; bracketed risk bounds |