BLOOD ANTIOXIDANT ENZYMES AS MARKERS OF EXPOSURE OR EFFECT IN COAL-MINERS

Objective-To investigate if blood Cu++/Zn++ superoxide dismutase, glut athione peroxidase, catalase, and total plasma antioxidant activities could be markers of biological activity resulting from exposure to res pirable coal mine dust in active miners, and of pneumoconiosis in reti red miners. Methods-Blood samples were randomly obtained from active s urface workers (n = 30) and underground miners (n = 34), and from reti red miners without (n = 21), and with (n = 33) pneumoconiosis. Antioxi dant enzyme activities and total plasma antioxidants were measured in erythrocytes and plasma. Non-parametric tests were completed by analys es of covariance to compare antioxidants between groups, taking into a ccount potential confounding factors (age, smoking history (pack-years )). Results-Erythrocyte Cu++/Zn++ superoxide dismutase activity was si gnificantly higher in the group of underground miners than the group o f surface workers. The differences in total plasma antioxidants and pl asma glutathione peroxidase activity between both groups were related to age. Glutathione peroxidase activity increased in the plasma of ret ired miners with pneumoconiosis, compared with retired miners without pneumoconiosis. No differences were found either in erythrocyte antiox idant enzyme activities or in total plasma antioxidants between the gr oups of retired miners without and with pneumoconiosis. Conclusions-In this study, erythrocyte Cu++/Zn++ superoxide dismutase activity may b e considered as a marker of effect of respirable coal mine dust in exp osed workers. This result is in agreement with the hypothesis that rea ctive oxygen species are involved in cell injury induced by coal mine dust, and may be predictive of the degree of inflammation and pneumoco niosis induced by coal mine dust. The increase in glutathione peroxida se activity in the plasma of retired miners with pneumoconiosis may be the result of a response to the increasing hydrogen peroxide (H2O2) p roduction due to the disease process.