Abstract
An analysis of literature data on effects of both diesel exhaust and of particle overload shows that the experimentally induced lung tumors in rats after diesel exposure may be explained by a particulate effect only. This conclusion is also supported by results from inhalation and instillation studies with pure carbon black (Heinrich, 1990; Kawabata, 1986) which showed no difference in the lung tumor inducing potency between diesel exhaust and carbon black. It appears that the surface area of the retained particles plays a decisive role. In contrast to the rat, the observed elevated lung tumor rate in diesel-exposed workers cannot be explained by a particle effect since the predicted extrapolated lung tumor risk for humans based only on the particle phase is much lower than found in an epidemiological study of diesel exposed railroad workers (Garshick et al. 1988). If this increased lung tumor incidence in the railroad workers can be verified in further epidemiological studies in diesel -exposed cohorts then additional effects besides those of the particles must play a role in humans, e.g., effects of the organic compounds or gas phase components.
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