AbstractThe effects of long‐term inhalation of diluted diesel exhaust on aryl hydrocarbon hydroxylase activity (AHH) and cytochrome P‐450 content in lung and liver microsomes were investigated in male Fischer‐344 rats and compared with repeated parenteral administration of organic solvent extracts of hydrocarbons adsorbed on the diesel particulate surface during the combustion process. The animals were exposed to concentrations of 750 μg m−3or 1500 μg m−3of diesel particulates from a 5.7L GM diesel engine 20 h per day, 5 1/2 days per week for up to 9 months or treated by repeated IP injections of diesel particulate extract (dissolved in corn oil) from the same engine at several dose levels for 4 days. No significant effects of long‐term inhalation exposure were observed in liver microsomal AHH activity. A slight decrease in lung microsomal AHH activity was found in rats following 6 months of exposure to diesel exhaust at the particulate concentration of 1500 μg m−3. The total mass of particles deposited in the lung during the inhalation exposure was estimated and an equivalent dose of extractable hydrocarbons was administered intraperitoneally; no increase in AHH activity was observed in the lung or liver microsomes. In contrast, 1.4‐to 9‐fold increases in AHH activity were observed in liver and lung microsomes of rats pretreated by intraperitoneal doses 10‐50 times larger than the most conservative estimate of the deposited lung burden. No changes in cytochrome P‐450 content were observed in the microsomes of rat liver after inhalation or injection treatment studies. The data indicate that hydrocarbons adsorbed on inhaled diesel particles are not effective as enzyme inducers primarily due to their absence in quantities necessary for enzyme induction which is further potentiated by the lack of their availability for
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