Abstract
This study was carried out in order to investigate the human genetic effects of exposure to benzene in 66 male workers of a refinery population and the results compared with 33 control workers in the same refinery, not known to have had exposure to benzene. Questionnaires were used to determine various life style factors such as smoking, drinking and exposure to ionising radiation as examples of known confounding variables. In addition, experiments were designed to investigate the mechanism of benzene carcinogenicity using cell transformation techniques, together with a molecular dosimetry approach in an attempt to identify and quantify any interaction with benzene metabolites and DNA. The results from the human studies showed no difference between the groups when effects such as mitogen-induced blastogenesis, proliferative rate index, sister chromatid exchange and urine mutagenicity were measured. There was a suggestion of a decrease in mitogenic response with age in both exposed and control individuals in the mitogen induced blastogenesis experiments, which was consistent with other studies. Although no difference in the number of revertant colonies in strain TA 98 and 100 was demonstrated between the high and low urinary phenol groups there was a correlation between the number of revertants and the ages of the individuals as a whole. One statistical test used in the examination of the chromosome aberration data suggested a statistically significant increase in aberrations in the exposed group to the control groups, and this increase could be the result of benzene exposure. Cell transformation studies using C3H10T1/2 cell lines did not indicate that benzene had any initiating carcinogenic properties in vitro using the two stage model of carcinogenesis. Furthermore, molecular dosimetry studies using C[14]-labelled benzene in vivo demonstrated only a very weak interation between benzene metabolites and rat liver DNA. All the methods used in this study generated negative data except for that to detect chromosome damage. This method showed a slight increase in damage in exposed workers by comparison with the controls suggesting that benzene may be a weak clastogen at low doses.