Reactive oxygen species are important mediators of both mineral dust-induced (malignant) lung disease and in vitro DNA damage.
Therefore, we studied in vivo oxidative DNA damage in coal workers who had been chronically exposed to silica-containing dust.
In peripheral blood lymphocytes of 38 retired coal miners (eight with coal workers pneumoconiosis, 30 references) and 24 age-matched, non-dust-exposed controls 7-hydro-8-oxo-2'-deoxyguanosine (8-oxodG) was determined by reversed phase high-performance liquid chromatography with electrochemical detection.
The ratio of 8-oxodG residues to deoxyguanosine (dG) was related to individual cumulative dust exposure estimates and pneumoconiotic stage as established by chest radiography.
The ratio of 8-oxodG to dG (x 10-5) in lymphocytes did not differ between miners with coal workers'pneumoconiosis (2.61 ± 0.44) and miners without coal workers'pneumoconiosis (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 regression.
We suggest that oxidative damage to the DNA of peripheral blood lymphocytes may be introduced by increased oxidative stress responses in subjects chronically exposed to mineral dusts.
Whether this is an important pathway in the suggested carcinogenicity of silica is still an open question.
Mots-clés Pascal : Mine charbon, Poussière, Silice, Toxicité, Stress oxydatif, Pneumoconiose, DNA, Lymphocyte, Exposition professionnelle, Homme, Marqueur biologique, Médecine travail, Appareil respiratoire pathologie, Poumon pathologie
Mots-clés Pascal anglais : Coal mine, Dust, Silica, Toxicity, Oxidative stress, Pneumoconiosis, DNA, Lymphocyte, Occupational exposure, Human, Biological marker, Occupational medicine, Respiratory disease, Lung disease
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 96-0005575
Code Inist : 002B03L06. Création : 01/03/1996.