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 5.6.2.6. Other Noncancerous Effects<br />
2 Essentially no effects (based on the weight of evidence of a number of studies) were<br />
3 noted <strong>for</strong> reproductive and teratogenic effects in mice, rats, rabbits, and monkeys; clinical<br />
4 chemistry and hematology in the rat, cat, hamster, and monkeys; and enzyme induction in the rat<br />
· 5 and mouse (Tables 5-10 through 5-12 and 5-14).<br />
6<br />
7 5.6.3. Comparison of Filtered and Unfiltered <strong>Diesel</strong> Exhaust<br />
8 The compariso!l of the toxic responses in laboratory animals exposed to whole diesel<br />
9 exhaust or filtered exhaust containing no particles demonstrates across laboratories that diesel<br />
1 0 particles are the principaf etiologic agent of noncancerous health effects in laboratory animals<br />
11 exposed to diesel exhaust (Table 5-15). Whether the particles act additively or synergistically<br />
12 with the gases cannot be determined from the designs of the studies. Under equivalent exposure<br />
13 regimens, hamsters have lower levels of retained DPM in their lungs than rats and mice do and<br />
14 consequently less pulmonary function impairment and·pulmonary pathology. These differences<br />
15 may result from a lower intake rate ofDPM, lower deposition rate and/or more rapid clearance<br />
16 rate, or lung tissue that is less susceptible to the cytotoxicity of DPM. Observations of a<br />
17 decreased respiration in hamsters when exposed by inhalation favor lower intake and deposition<br />
18 rates.<br />
19<br />
20 5.6.4. Interactive Effects of <strong>Diesel</strong> Exhaust<br />
21 . There is no direct evidence that diesel exhaust interacts with other substances in an<br />
22 exposure environment, other than an impaired resistance to respiratory tract infections. Young<br />
23 animals were not more susceptible. In several ways, animals with laboratory-induced<br />
24 emphysema were more resistant. There is experimental evidence that both inorganic and organic<br />
25 compounds can be adsorbed onto carbonaceous particles. When such substances become<br />
26 affiliated with particles, these substances can be carried deeper into the lungs where they might<br />
27 have a more direct and potent effect on epithelial cells or on AM ingesting the particles. Few<br />
28 specific studies to test interactive effects of diesel exhaust with atmospheric contaminants, other<br />
29 than coal dust, have been conducted. Coal dust and DPM had an additive effect only.<br />
30<br />
31 5.6.5. Summary<br />
32 The principal noncancerous health hazard to humans from exposure to diesel exhaust is a<br />
33 structural, functional, or biochemical injury to the lung. Current knowledge indicates that the<br />
34 carb_onaceous core of the diesel particle is the prime c;ausative agent of lung injury. The limg<br />
35 injury appears to be mediated by a progressive impairment of AMs. Because noncancerous<br />
36 pulmonary effects occur at lower doses than those inducing tumors in rats and appear to be<br />
211/98 5-86 DRAFT--DO NOT CITE OR QUOTE