Exposure to benzene in various susceptible populations: co-exposures to 1,3-butadiene and PAHs and implications for carcinogenic risk.

摘要

Exposure to benzene in human populations can occur in various work-related settings in which benzene is used or produced, or from traffic emissions resulting from incomplete combustion of fossil fuel, or from other sources. Two scenarios of benzene exposure were studied in 4 susceptible groups in Thailand. The first scenario is work-related exposures primarily to benzene, with the study subjects consisting of petrochemical laboratory workers and gasoline service station attendants, who are exposed at levels of 78.32 and 360.84 microg/m(3), respectively. The second scenario is traffic-related exposure and exposure to incense smoke, where co-exposures to other pollutants occurs, with the study groups consisting of school children attending schools in the city center and exposed to traffic emissions, and temple workers exposed to incense smoke. The individual benzene exposure levels were approximately 19.38 microg/m(3) in city school children and 45.90 microg/m(3) in temple workers. Co-exposures to 1,3-butadiene and polycyclic aromatic hydrocarbons (PAHs) generated from the same sources occurred in the second exposure scenario. 8-OHdG, DNA strand breaks and DNA repair capacity were measured as biomarkers of early effects of carcinogenic compound exposure. Petrochemical laboratory workers and gasoline service stations attendants had significantly higher levels of DNA strand breaks and significantly lower DNA repair capacity compared to controls, while gasoline service station attendants also had significantly higher levels of 8-OHdG than controls. City school children had significantly higher levels of PAH-DNA adducts, 8-OHdG, and DNA strand breaks and significantly lower levels of DNA repair capacity compared to rural children. Temple workers also had significantly higher levels of 8-OHdG and DNA strand breaks and significantly lower levels of DNA repair capacity compared to controls. In all of the study groups, the levels of benzene exposure correlated significantly with 8-OHdG levels, DNA strand breaks, and DNA repair capacity. In school children, PAH levels also correlated significantly with 8-OHdG levels, DNA strand breaks and DNA repair capacity. In temple workers, 1,3-butadiene levels correlated significantly with 8-OHdG and DNA strand breaks, but not with DNA repair capacity, while in the school children they did not correlate significantly with 8-OHdG or DNA strand breaks, and correlated marginally significantly with DNA repair capacity (deletions per metaphase). Multivariate regression analysis identified total PAHs concentrations converted to B[a]P equivalents as the only factor significantly affecting 8-OHdG levels, and total PAHs concentrations converted to B[a]P equivalents, as well as 1,3-butadiene concentrations as the factors significantly affecting DNA repair capacity in the school children. PAHs concentration was identified as the factor most significantly affecting DNA strand breaks in temple workers, followed by benzene concentrations, while DNA repair capacity was also significantly influenced by PAHs concentrations.