Cigarette smoking protects mononuclear blood cells of carcinogen exposed workers from additional work exposure-induced DNA single strand breaks.

DNA single-strand breaks in mononuclear blood cells (MNC) of taxi drivers, painters, ethylene oxide-exposed sterilization workers, metal workers, and car mechanics were detected by alkaline filter elution and compared to smoking and non-smoking control persons. Cigarette smoking caused a small but statistically significant increase in control persons (13.5%). In all occupationally exposed groups except the car mechanics, statistically significant increases of DNA single-strand breaks were detected in non-smokers compared to non-smoking controls or comparing groups with high and low exposure. For non-smoking workers the increase in DNA single-strand breaks was found to be 22% for taxi drivers, 60% for painters, 70% for ethylene oxide-exposed workers, and 69% for metal workers compared to control persons. For smokers, however, the increase in DNA single-strand breaks caused by additional occupational exposure was smaller and did not reach statistical significance in any of the occupational groups investigated in this study. Since a high level of glutathione may help to detoxify electrophilic DNA-damaging agents we measured the concentration of total glutathione in MNC of smoking and non-smoking control persons. The glutathione concentration was 13% higher in smokers, but statistical significance was weak (p < 0.05; t-test). Thus cigarette smoking, which represents a highly significant risk factor in carcinogenesis by itself, protects on the other hand against some additional genotoxic insults.