Health Assessment Document for Diesel Emissions - NSCEP | US ...

1 inconsequential in rats relative to particle overload effects because bioavailability of the organic
2 components is limited by the high-energy binding of these components with the carbon core.
3 resulting in low desorption in the biological environment. The long residence times of particles
4 in human. lungs, however, may allow for greater desorption of organics.
5 The mechanism of action of many P AH carcinogens has been attributed to the reactivity
6 of certain metabolic intermediates with cellular macromolecules and the subsequent formation of
7 DNA adducts. The organics adsorbed to DPM may become available for biotransformation to
8 known reactive intermediates, and macromolecular binding of these metabolites has been
9 demonstrated.
10 Except for some of the DNA adduct studies, the available database does not allow a
11 definitive discussion of the specific mechanism of carcinogenic action for these compounds
12 relative to diesel exhaust specifically but rather is approached from the standpoint of the
13 chemicals per se. Some of the data are derived primarily from in vitro studies that were not
14 specifically concerned with the potential carcinogenicity of diesel exhaust but may be relevant
15 because the compounds of concern are known components of diesel emissions.
16 More than 1 00 carcinogenic or potentially carcinogenic components have been
17 specifically identified in diesel emissions, including various P AHs and nitroarenes such as 1-
18 nitropyrene (1-NP) and dinitropyrenes (DNPs). These compounds are adsorbed to the carbon
19 core of the particulate phase of the exhaust and, if desorbed, may become available for biological
20 processes such as metabolic activation to mutagens. Among compounds identified from diesel
21 exhaust are B[a]P, dibenz[a,h]anthracene, pyrene, chrysene, and nitroarenes.such as 1-NP, 1,3-
22 DNP, 1,6-DNP, and 1,8-DNP, all of which are mutagenic, carcinogenic, or implicated as
23 .. procarcinogens or cocarcinogens (Stenback et al., 1976; Weinstein and Troll, 1977; Thyssen et
24 al., 1981; Pott and StOber, 1983; Howard et al., 1983; Hirose et al., 1984; Nesnow et al., 1984;
25 El-Bayoumy et al., 1988).
26 There is evidence supporting a carcinogenic role for organics in the combustion process.
27 Mumford et al. (1989) reported greatly increased lung cancer mortality in Chinese communes
28 burning so-called "smoky coal," but not wood or smokeless coal, in unvented open-pit fires used
29 for heating and cooking. Particle concentrations ranged from 10 to 25 mg/m 3 in communes
30 burning either smoky coal or wood, but P AH levels were five to six times greater in. the air of
31 communes burning smoky coal. Thus cancer mortality correlated more closely with
32 concentrations of P AHs than with particles. In the case of smokeless coal, both particle and P AH
33 concentrations were low. Demonstration of the carcinogenicity of coke oven emissions in·
34 humans (Lloyd, 1971) also provided evidence for the role of organics, because coke oven
35 particulate matter lacks an insoluble carbon core. It should be recognized, however, that P AH
36 concentrations in these cases are much greater than can be expected from inhalation of DE.,
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