Biomarker studies in northern Bohemia.

Studies were conducted in northern Bohemia to simultaneously evaluate personal exposures to air pollution in the form of respirable particles containing polycyclic aromatic hydrocarbons (PAHs) and biomarkers of exposure, biological effective dose, genetic effects, and metabolic susceptibility. The series of biomarkers included PAH metabolites in urine, urine mutagenicity, PAH-DNA adducts in white blood cells determined by 32P-postlabeling, PAH-albumin adducts determined by enzyme-linked immunosorbent assay (ELISA), DNA damage in lymphocytes detected by comet assay, chromosomal aberrations, sister chromatid exchanges, and glutathione S-transferase M1 (GSTM1) genotypes. For these studies, a group of women who work outdoors about 30% of their daily time was selected. In a pilot study, a group of women from a polluted area of the Teplice district (northern Bohemia) was compared with a group of women from a control district of southern Bohemia (Prachatice). In a follow-up repeated-measures study, a group of nonsmoking women from Teplice was sampled repeatedly during the winter season of 1993 to 1994. Personal exposure monitoring for respirable particles (< 2.5 microns) was conducted for the 24-hr period before collection of blood and urine. Particle extracts were analyzed for carcinogenic PAHs. In the pilot study and in the follow-up study, a highly significant correlation between individual personal exposures to PAHs and DNA adducts was found (r = 0.54, p = 0.016; r = 0.710, p < 0.001, respectively). The comet parameter (percentage DNA in tail; %T) correlated with exposures to respirable particles (r = 0.304, p = 0.015). The GSTM1 genotype had a significant effect on urinary PAH metabolites, urine mutagenicity, and comet parameters (% T and tail moment) when the GSTM1 genotype was considered as a single factor affecting these biomarkers. Multifactor analysis o variance considering exposure and adjusting the data for GSTM1, age, and diet showed that the effect of personal exposures to PAHs on the variability of biomarkers (DNA adducts, comet parameters, urine mutagenicity) might be higher than the effect of the GSTM1 genotype. These results show the importance of considering all potential factors that may affect the biomarkers being analyzed.

DNA adducts and personal air monitoring of carcinogenic polycyclic aromatic hydrocarbons in an environmentally exposed population.

The effect of personal exposure to air pollution on DNA adducts in humans was analyzed in a group (n = 30) of women working outdoors (up to 8 h/day) as postal workers or gardeners in the city of Teplice, Czech Republic (Northern Bohemia), where winter inversions may result in high levels of air pollution from coal combustion. Ten of these women were followed up during the next winter season by repeated personal exposure monitoring and analysis of the DNA adducts in their white blood cells (in four sampling periods). Personal exposure monitoring for respirable particles (< 2.5 microns) was conducted for the 24 h period prior to collection of blood and urine. Particle extracts were analyzed for carcinogenic polycyclic aromatic hydrocarbons (PAH). Urine samples were collected for cotinine analysis to control for exposure to tobacco smoke. DNA isolated from white blood cells was analyzed by 32P-postlabeling with the butanol enrichment procedure. There were 21 non-smokers and nine light smokers in the pilot study (November 1992) and only non-smokers in the follow-up study (winter season 1993/94). In both studies high personal exposure variability between the individuals sampled on the same day was observed. In the pilot study we found a significantly higher (P < 0.05) level of DNA adducts in the 14 non-smoking women sampled on November 24, when their exposure to carcinogenic PAH was also significantly higher (P < 0.05), compared with seven non-smoking women sampled on November 26. We also found a significant correlation (r = 0.541, P < 0.016) between individual exposure to carcinogenic PAH and DNA adducts for the group of non-smokers (n = 21). No significant difference in DNA adduct levels was found between non-smokers and smokers. In the follow-up study, during one sampling period the ambient and personal air monitors exhibited a significantly elevated exposure to respirable particles and carcinogenic PAH. Analyzing data from the follow-up study, a significant effect of personal exposure on DNA adduct levels and their relationship with short-term exposure to carcinogenic PAH was found. The results suggest that DNA adduct levels in white blood cells reflect a short-term environmental exposure.