Occupational exposure to mineral fibres. Biomarkers of oxidative damage and antioxidant defence and associations with DNA damage and repair

Abstract

In order to study the effect of mineral wool exposure on oxidative DNA damage and lipid peroxidation, an epidemiological study was conducted in a mineral wool factory in Slovakia. Altogether 141 subjects were investigated (21-58 years old), 43 controls (20 men and 23 women: 27 non-smokers, 16 smokers) and 98 exposed (75 men and 23 women: 61 non-smokers, 37 smokers). We found higher malondialdehyde (MDA) levels in the group of all exposed workers (P = 0.025) and in exposed non-smokers (P = 0.003) and a significantly suppressed activity of ceruloplasmin oxidase (P = 0.02, P < 0.02, respectively) and catalase (CAT) (P = 0.04, P = 0.01, respectively) in these groups. The activity of glutathione S-transferase (GST) was affected by exposure to mineral wool; levels were significantly lower in all exposed subjects (P = 0.04), in the exposed non-smokers (P = 0.03) and in exposed men (P < 0.01). Concentrations of vitamin C in plasma and the ferric-reducing activity of plasma (FRAP) were not affected by the mineral wool exposure. There was a significant negative correlation between the activity of glutathione peroxidase (GPX) and MDA in the whole group (P < 0.01) and in the exposed group and between CAT activity and MDA in all subjects (P < 0.01). GST activity correlated inversely with oxidized pyrimidines in lymphocyte DNA, in almost all subgroups. We found significant negative correlations between DNA repair and GPX in all subjects (P = 0.03) as well as in control men (P < 0.03) and between DNA repair and CAT in all control subjects (P < 0.02) and in control men (P < 0.01). Interestingly, we found a positive correlation between DNA repair and MDA in all subjects (P < 0.01) and in all exposed subjects (P < 0.03). The presented results indicate that mineral wool exposure induces an increase in oxidative damage to biomolecules especially in the group of male non-smokers. However, optimal levels of antioxidants could have a protective effect. Biomarkers such as MDA, antioxidant enzymes and antioxidant vitamins measured in blood may be useful biomarkers of oxidative stress and antioxidant protection. We do not recommend FRAP as a marker of antioxidant status as interference from other constituents can provide false or confusing results. Our study supports the idea that there might also be other mechanisms by which antioxidant enzymes (especially GST) protect cells against oxidative DNA damage.