The effects of exposure to diesel exhaust (DE) and coal dust (CD) on protective mechanisms, namely production of interferon and detoxification by cytochrome-P450, were studied in mice, following exposure to measured and equal doses of DE and CD for 7 hours per day, 5 days per week for 1 month. The mice were next infected with influenza virus by the intranasal route and the progression of infection was followed. The mice were sacrificed, and the level of production of interferon was estimated by immunofluorescence cell counting. For the metabolic detoxification by cytochrome-P450, the activities of the enzymes ethylmorphine-demethylase (EMDase), 7- ethoxycoumarin-deethylase (7ECDase), and NADPH-cytochrome-c- reductase (NADPH-c-reductase) were measured. The levels of interferon in the serum were not affected by exposure to CD or DE. The values for EMDase in the control rose post infection and were the highest on the fourth day after viral infection. This effect was abolished in the groups exposed to CD and reduced in the mice exposed to DE. NADPH-c-reductase levels also peaked on the fourth day in the controls, and this effect was abolished in the CD and DE exposed groups. 7ECDase levels went down between 1 and 3 days postinfection, and then returned to normal. This pattern was unchanged in mice preexposed to either CD or DE. These patterns were not sustained in the absence of viral infection following exposure to either particle. The authors interpret these results to indicate that the relationship between the two protective mechanisms is altered by exposure to CD and DE particulates under these conditions. The response to CD and DE may be similar in human populations.