Health Assessment Document for Diesel Emissions - NSCEP | US ...
Health Assessment Document for Diesel Emissions - NSCEP | US ...
Health Assessment Document for Diesel Emissions - NSCEP | US ...
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1 radicals present on the particle surface, which are potent oxidizing agents <strong>for</strong> bio-organic<br />
2 substrates.<br />
3 The observation that some of the DE-induced rat tumors are different pathologically from<br />
4 what one would expect in humans and that some are similar may also support the thought that<br />
5 multiple MOAs may be present.<br />
6 Given the in<strong>for</strong>mation at hand, dual modes of action are more likely than a single mode.<br />
7 One would be driven by particles and one by the organic/inorganic components, with a shifting<br />
8 influence as the exposure/dose varies from high to low. The role of contributory toxicity from<br />
·9 other constituents, such as N0 2 or oxygen free radicals, among others, is uncertain.<br />
10 It would be ideal if the MOA were in<strong>for</strong>mative about whether all humans were equally<br />
11 susceptible or whether some population subgroups were more or less susceptible. The human<br />
12 evidence, i.e., occupational and population-derived studies, does not provide any particular insight<br />
13 about variations in susceptibility, nor do the animal studies. Neither female versus male nor adult<br />
14 versus children's susceptibility differences are specifically indicated: the <strong>for</strong>mer may have been<br />
15 discemable given the nature of the studies, but there is no study basis to address possible<br />
16 children's risk issues. Later, in this section, a·qualitative discussion about susceptibility is<br />
17 included that acknowledges that toxicological wisdom suggests that background respiratory<br />
18 system conditions could make some in the population more susceptible to chronic effects of DE<br />
19 exposure. Similarly, infants and children could have greater susceptibility simply because their<br />
20 developing organs and defense systems may be less effective at dealing with insults from DE<br />
21 exposure. These suggestions are not unique to DE exposure, though.<br />
22<br />
23 12.2.3. Carcinogenic Hazard <strong>Assessment</strong><br />
24 For inhalation exposure, both human studies and animal bioassays are available to assess<br />
25 the chronic exposure carcinogenic potential <strong>for</strong> DE. In fact, both the human and the animal<br />
26 studies provide evidence that exposure to DE has potential to be carcinogenic to humans under<br />
27 some condition of exposure. Chapters 7 and 8 review these data in detail. A finding· about the<br />
28 hazard potential does not specify the magnitude of the impact, in<strong>for</strong>mation on which is discussed<br />
29<br />
30<br />
in Chapter 11, the carcinogenicity dose-response evaluation section.<br />
31 12.2.3.1. Human Evidence<br />
32 A total of 26 key epidemiologic studies have been evaluated to examine the association<br />
33 between exposure to DE and increased cancer response. The positive human evidence consists of<br />
34 observed increases in lung cancer mortality .in a number of occupational exposure studies and<br />
35 some suggestion of other possible cancer sites. Cohort, .case control, and population-based studies<br />
2/1/98 12-9 DRAFT--DO NOT CITE OR QUOTE