Ingestion of ethanol has been shown to increase the hematotoxicity of benzene (300 ppm) in C57B1/6J mice (Baarson et al., 1982). In this study, the effect of ethanol on hematopoietic parameters was examined in mice exposed to low levels of benzene vapors. Urinary trans,trans-muconic acid (t,tMA) was also measured as an indicator of benzene exposure. Male CD-1 mice treated with ethanol (5% alcohol in a liquid diet) for 3 weeks and pair-fed controls were exposed to 10 ppm benzene vapors, 6 h per day, 5 days per week for 2 weeks, starting from the 2nd week of ethanol administration. Urinary t,tMA was measured by HPLC in samples collected during the last 6 h-exposure session, at the end of each week. Hematotoxicity was assessed on hematopoietic progenitors of the bone marrow erythroid lineage (CFU/E, colony-forming unit-erythroid, and BFU/E, burst-forming unit-erythroid) and myeloid lineage (CFU/GM, colony-forming unit-granulocyte/macrophage). Both benzene and ethanol decreased the CFU/E, BFU/E and CFU/GM cells. Cellularity was reduced by 40–50 and 20–30% in benzene- and ethanol-treated mice, respectively. The cell reduction was more severe in animals exposed to benzene in combination with ethanol. The average urinary t,tMA levels were 280±109 µg/ml (mean±SD) in benzene-treated mice and 0.135±0.05 µg/ml in animals given ethanol alone. Mice given both benzene and ethanol showed urinary t,tMA levels significantly lower (63±25 µg/ml) than those measured after administration of benzene alone. Ethanol administration potentiates benzene hematotoxicity and, in addition, may reduce the predictivity of t,tMA measured in mice as a marker of benzene exposure.
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