OXIDATIVE DNA-DAMAGE IN PERIPHERAL-BLOOD LYMPHOCYTES OF COAL-WORKERS

Reactive oxygen species are important mediators of both mineral dust-i nduced (malignant) lung disease and in vitro DNA damage. Therefore, we studied in vivo oxidative DNA damage in coal workers who had been chr onically exposed to silica-containing dust. In peripheral blood lympho cytes of 38 retired coal miners (eight with coal workers pneumoconiosi s, 30 references) and 24 age-matched, non-dust-exposed controls 7-hydr o-8-oxo-2'-deoxyguanosine (8-oxodG) was determined by reversed phase h igh-performance liquid chromatography with electrochemical detection. The ratio of 8-oxodG residues to deoxyguanosine (dG) was related to in dividual cumulative dust exposure estimates and pneumoconiotic stage a s established by chest radiography. The ratio of 8-oxodG to dG(x 10(-5 )) in lymphocytes did not differ between miners with coal workers' pne umoconiosis (2.61 +/- 0.44) and miners without coal workers' pneumocon iosis (2.96 +/- 1.86). However, oxidative DNA damage in all miners was higher than in the non-dust-exposed controls (1.67 +/- 1.31). 8-oxodG /dG ratio was not related to individual cumulative coal dust exposure, age or smoking (pack years) when evaluated by multiple linear regress ion. We suggest that oxidative damage to the DNA of peripheral blood l ymphocytes may be introduced by increased oxidative stress responses i n subjects chronically exposed to mineral dusts. Whether this is an im portant pathway in the suggested carcinogenicity of silica is still an open question.