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

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1 The potency of the other diesel emission samples was not estimated directly because of<br />

2 the weak response in the skin tumor initiation test. Instead, their potency relative to the Nissan<br />

3 engine was estimated as the arithnietic mean of their potency relative to the Nissan in the<br />

4 Salmonella assay in strain TA98, the sister chromatid exchange assay in Chinesehamster ovary<br />

5 cells, and the mutation assay in mouse lymphoma cells. The estimated lifetime cancer risk per<br />

6 microgram per cubic meter of extractable organic matter <strong>for</strong> extracts from these engines are as<br />

7 follows: Volkswagen, 1.3 x 10- 4 ; Oldsmobile 1.2 x 10- 4 ; and Caterpillar, 6.6 x 10- 6 •<br />

8 To convert these values to a lifetime risk per microgram per cupic meter of total DPM,<br />

9 the results were multiplied by the fraction of extractable organic matter in the particles. This<br />

1 0 conversion was based on the assumption that the carcinogenic effects were caused solely by the<br />

11· organic fraction. These fractions were as follows: Nissan, 0.08; Volkswagen, 0.18; Oldsmobile,<br />

12 0.17; and Caterpillar, 0.27. After this adjustment, the resulting estimated potencies per<br />

13 microgram per cubic meter of inhaled DPM varied from 3.5 X 1 o-s <strong>for</strong> theNissan to 1.8 X 1 o- 6 <strong>for</strong><br />

14 the Caterpillar.<br />

15 Harris (1983) developed comparative potency estimates <strong>for</strong> the same four engines used by<br />

16 Albert et al. (1983) but used only two epidemiology-based potency estimates: those <strong>for</strong> coke .<br />

17 oven emissions and <strong>for</strong> roofing tar. He employedpre1iminary data from three ofthe same assays<br />

18 used by Albert et al. (1983)--the Sencar mouse skin tumor initiation assay, enhancement of viral<br />

19 trans<strong>for</strong>mation in Syrian hamster embryo cells, and the L5178 mouse lymphoma test. The mouse<br />

20 lymphoma test was used both with and without metabolic activation, whereas the Salmonella<br />

21 assay was not used.<br />

22 The diesel cancer potency estimates by Harris (1983) were then derived by multiplying<br />

23 the epidemiology-based cancer potency estimates <strong>for</strong> both coke oven emissions and roofing tar<br />

24 by the ratio of their potencies compared with DE particles in each of the four bioassays. For<br />

25 example, the epidemiology-based relative risk of exposure to 1 J.tg/m 3 of coke oven emissions<br />

26 was estimated to equal 4.4 x 10- 4 • In the skin tumor initiation test, 2.1 papillomas per mouse<br />

27 were reported <strong>for</strong> the coke oven sample, compared with 0.53 <strong>for</strong> the Nissan engine extract. The<br />

28 benzene-extractable fraction was assumed to equal 0.06 (slightly less than that in the Albert et<br />

29 al., 1983, studies). The diesel potency estimate using this comparison is then equal to (0.53/2.1)<br />

30 x 0.06 x 4.4 x 10- 4 /J.tg/m 3 , or 6.6 x 10- 6 /J.tg/m 3 DPM. A total of eight comparisons were made <strong>for</strong><br />

31 each engine, four bioassays times two epidemiology-based potency estimates.<br />

32 · The Harris (1983) estimates are not comparable to those of Albert et al. (1983) without<br />

33 adjustment. The unit risk estimates of Albert and co-workers are based on absolute risk during<br />

34 lifetime exposure, whereas Harris reported his values in terms of relative risk per year of<br />

35 exposure. To adjust this to lifetime risk <strong>for</strong> continuous exposure, it is necessary to multiply<br />

2/1/98 11-6 DRAFT --DO NOT CITE OR QUOTE

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