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

1 alveolar regions of the lungs. At the same time, a proliferation of cuboidal type II alveolar cells is
2 observed, replacing thinner type I cells and thickening the alveolar walls. Because of the key role
3 alveoli play in the exchange of gases, these changes may inhibit the efficiency of pulmonary
4 function. Human studies are inadequate to evaluate potential toxic effects resulting from acute
5 exposures.
6 The observed effects from single high-dose or episodic exposures in test animals are
7 consistent with effects seen with lower and more long-term exposures. This suggests that total
· 8 accumulated dose may be one basis for characterizing DE hazards, but this could be too simplistic
9 for all aspects of DE toxicity because dose-rate aspects cannot be ruled out.
10
1 r 12.2.1.2. Effects From Short-Term and Chronic Exposure
12 Based on suggestive evidence from human occupational studies, combined with multiple
13 controlled laboratory animal studies in several species, a high level of confidence exists that
14 chronic exposure to DE constitutes a noncancer respiratory hazard for humans. As DE exposure
15 levels and duration increase, the onset of respiratory symptoms in humans is observable on a
16 limited basis, whereas in animal studies the onset of symptoms is more clear and replicable.
17 Current data do not support confident identification of health hazards other than for the respiratory
18 system. Chapter 5 discusses this topic in more depth.
19 Several studies of workers occupationally exposed to DE on a short-term basis have
20 monitored pulmonary function at the beginning and end of work shifts to see if this marker of
21 respiratory distress has been impaired by exposures. Short-term symptoms are seen (e.g., bus
22 garage workers experienced burning and watering of the eyes, coughing, labored breathing,
23 chest tightness, and wheezing), but no reduction in pulmonary function. A study of stevedores
24 showed an adverse effect on pulmonary function, but normal function returned a few days after
25 DE exposure stopped. It was noted in one study that occupationally exposed smokers appeared
26 to demonstrate larger work-shift respiratory function decrements and increased incidence of
27 respiratory symptoms. Other occupational studies did not find statistically significant effects
28 from short-term exposure, though these studies have limitations thaf reduce the ability to detect
29 responses.
30 Noncancer effects of chronic DE exposure have also been evaluated in epidemiologic
31 studies of occupationally exposed workers (metal and nonmetal miners, railroad yard workers,
32 stevedores, and bus garage mechanics). Some ofthe data indicate an absence of increased
33 respiratory disease associated with exposure. In a few studies, though, a higher prevalence of
34 respiratory symptoms, primarily cough, phlegm,·or chronic bronchitis, was observed among the
35 exposed, but usually without significant changes in pulmonary function. However, two studies,
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