Biomonitoring on carcinogenic metals and oxidative DNA damage in a cross-sectional study

Oxidative DNA damage is mediated by reactive oxygen species and is supposed to play an important role in various diseases including cancer. The endoge nous amount of reactive oxygen species may be enhanced by the exposure to g enotoxic metals. A cross-sectional study was conducted from 1993 to 1994 in an urban population in Germany to investigate the association between meta l exposure and oxidative DNA damage. The cross-sectional sample of 824 part icipants was recruited from the registry of residents in Bremen, comprising about two-third males and one-third females with an average age of 61.1 ye ars. A standardized questionnaire was used to obtain the occupational and s moking history. The incorporated dose of exposure to metals was assessed by biological monitoring. Chromium, cadmium, and nickel were measured in 593 urine samples. Lead was determined in blood samples of 227 participants. As a biomarker for oxidative DNA damage, 7,8-dihydro-8-oxoguanine has been an alyzed in lymphocytes of 201 participants. Oxidative lesions were identifie d by single strand breaks induced by the bacterial formamidopyrimidine-DNA glycosylase (Fpg) in combination with the alkaline unwinding approach. The concentrations of metals indicate a low body load (median values: 1.0 mug n ickel/l urine, 0.4 mug cadmium/l urine, and 46 mug lead/l blood; 83% of chr omium measures were below the technical detection limit of 0.3 mug/l). The median level of Fpg-sensitive DNA lesions was 0.23 lesions/10(6) bp, A posi tive association between nickel and the rate of oxidative DNA lesions (Fpg- sensitive sites) was observed (odds ratio, 2.15; tertiles 1 versus 3, P < 0 .05), which provides further evidence for the genotoxic effect of nickel in the general population.