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

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et al., 1987; Benhamou et al., 1988; Hayes et al., 1989; Steenland et al., 1990;<br />

Gustavsson et al., 1990; Emmelin et al., 1993). Some ofthese studies did adjust <strong>for</strong><br />

the confounding effects of smoking, asbestos, and other exposures. Furthermore, a<br />

recent publication by HEI ( 1995) demonstrates this strength of association in graphic<br />

presentation (Figures 8-1 and 8-2). Although the studies had smaller increases in<br />

lung cancer risk and only some of the studies considered by HEI (1995) are<br />

considered in this chapter, it demonstrates the lung cancer excesses consistently all<br />

across the various populations.<br />

Consistency: Five cohort studies and nine (including one :q.ested case-control) case- ·<br />

control studies of lung cancer conducted in several populations in the United States<br />

and Europe consistently found the same effect (i.e., lung cancer).<br />

Specificity: All of the above-mentioned studies found the same specific effect (i.e.,<br />

lung cancer).<br />

Biological gradient: The biological gradient, which refers to the dose-response<br />

relationship, was observed in the cohorts of Canadian railway workers (Howe et al.,<br />

1983), heavy bulldozer operators (Wong et al., 1985), and truck drivers who had<br />

enrolled in the American Cancer Society's prospective mortality study (Boffetta and<br />

Stellman, 1988). In th,e case-control studies, a dose response was observed in railroad<br />

workers (Garshick et al., 1988; Hayes et al., 1989; Steenland et al., 1990). Although<br />

other studies failed to observe a dose response, these studies were methodologically<br />

limited due to confounding by other exposures and lack of either quantitative data on<br />

exposure or surrogate data on dose.<br />

Biological plausibility: Because diesel exhaust consists of a carbon core particle<br />

with surface layers of organics and gases, the tumorigenic activity may reside in one,<br />

some, or all of these components. As explained in Chapter 9, there is clear evidence<br />

that the organic constituents have the capacity to interact with DNA and give rise to<br />

mutations, chromosomal aberrations, and cell trans<strong>for</strong>mations, all well-established<br />

steps in the process of carcinogenesis. Furthermore, these organic chemicals include<br />

a variety of polycyclic aromatic hydrocarbons and nitroaromatics, many of which are<br />

known to be pulmonary carcinogens. Alternatively, Vostal (1986) suggests that<br />

"diesel" particles themselves induce lung cancer, most likely via an epigenetic<br />

mechanism, if they are present at sufficiently high doses: This makes a convincing<br />

argument <strong>for</strong> biological plausibility of lung cancer occurrence under some condition<br />

of exposure.<br />

When the same causal inference criteria were applied to the seven case-control<br />

studies in which risk of bladder cancer was assessed, the results were:<br />

2/1198<br />

• Temporality: There is temporality of exposure to diesel exhaust prior to the<br />

occurrence of bladder cancer.<br />

8-67 DRAFT--DO NOT CITE OR QUOTE

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