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

1 on the following evidence. The epithelium of the terminal and respiratory bronchioles in
2 exposed cats consisted ofthree cell types (ciliated, basal, and Clara cells) compared with only
3 one type (Clara cells) in the controls. The proximal ').Cinar region showed evidence of
4 peribronchial fibrosis and bronchiolar epithelial metaplasia. Type II cell hyperplasia was present
5 in the proximal interalveolar septa. The more distal alveolar ducts and the majority of the rest of
6 the parenchyma were unchanged from controls. Peribronchial fibrosis was greater at the end of 6
7 mo in clean air following exposure, whereas the bronchiolar epithelial metaplasia was most
8 severe at the end of exposure. Following an additional6 mo in clean air, the bronchiolar
9 epithelium more closely resembled the control epithelial cell population.
10 Wallace et al. (1987) used transmission electron microscopy (TEM) to determine the
11 effect of diesel exhaust on the intravascular and interstitial cellular populations of the lungs of
12 exposed rats and guinea pigs. Exposed animals and matched controls were exposed to 0.25,
13 0.75, 1.5, or 6.0 mg/m 3 particulate matter for 2, 6, or 10 weeks or 18 mo. The results inferred the
14 following: (1) exposure to 6.0 mg/m 3 for 2 weeks was insufficient to elicit any cellular response,
15 (2) both species demonstrated an adaptive multicellular response to diesel exhaust, (3) increased
16 numbers of fibroblasts were found in the interstitium from week 6 of exposure through month
17 18, and ( 4) there was no significant difference in either cell type or number in alveolar
18 capillaries, but there was a significant increase at 18 mo in the mononuclear population in the
19 interstitium of both species.
20 Additional means for assessing the adverse effects of diesel exhaust on the lung are to
21 examine biochemical and cytological changes in bronchoalveolar lavage fluid (BALF) and in
22 lung tissue. Fedan et al. (1985) performed studies to determine whether chronic exposure of rats
23 affected the pharmacologic characteristics of the rat's airway smooth muscle. Concentration-
24 response relationships for tension changes induced with acetylcholine, 5-hydroxytryptamine,
25 potassium chloride, and isoproterenol were assessed in vitro on isolated preparations of airway
26 smooth muscle (trachealis). Chrome exposure to diesel exhaust significantly increased the
27 maximal contractile responses to acetylcholine compared with control values; exposure did not
28 alter the sensitivity (EC 50 values) of the muscles to the agonists. Exposures·were to diesel
29 exhaust containing 2 mg/m 3 particulate matter for 7 h/day, 5 days/week for 2 years.
30 Biochemical studies of BALF obtained from hamsters and rats revealed that exposures to
31 diesel exhaust caused significant increases in lactic dehydrogenase, alkaline phosphatase,
32 glucose-6-phosphate dehydrogenase (G6P-DH), total protein, collagen, and protease (pH 5.1)
33 after approximately 1 year and 2 years of exposure (Heinrich et al., 1986a). These responses
34 were generally much greater in rats than in ·hamsters. Exposures were to diesel exhaust
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