Abstract
Recent studies have reported the induction of lung tumors in rats chronically exposed to levels of diesel-engine emissions which interfered with lung clearance. The present analysis suggests that the mutagenic substances (e.g. dinitropyrenes, polycyclic aromatic hydrocarbons) present in diesel particulates are not major contributors to rat-lung carcinogenesis. The cancers presumably result from lung “overloading” and the ensuing inflammatory response. In the absence of additional data, this putative mechanism of diesel-caused cancer cannot be exptrapolated to other species at risk from exposure to diesel emissions.
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