Plasma malondialdehyde (MDA) (an indicator of lipid peroxidation) was determined in random samples of workers (age range 25-60 years) exposed to silica dust (n = 31, mean exposure duration 21.3 +/- 8.3 years) or asbestos dust (n = 59, mean exposure duration 15.6 +/- 4.5 years) and in 52 age-matched healthy male controls. MDA levels of both exposed groups were significantly higher than that of the controls and were significantly higher among workers exposed to asbestos than among those exposed to silica dusts. Neither age nor smoking was related to MDA levels among both controls and exposed workers; among the latter group MDA was not significantly correlated with duration of exposure. Mean MDA levels of exposed workers with radiographic signs of lung fibrosis or pleural thickening and of those without such signs were not significantly different, except in the case of asbestos-exposed workers where it was significantly less than that of those without such signs. Differences between mean durations of dust exposure of workers with radiographic signs of lung fibrosis and those without such signs were statistically insignificant. The results suggest the possible involvement of lipid peroxidation on exposure to silica or asbestos dusts in humans and possible development of antioxidant mechanism(s) on prolonged dust exposure and support the opinion that development of pneumoconiosis depends on susceptibility factor(s).