Ethanol-induced accumulation of ethylene glycol monoalkyl ethers in rats.

In adult female SPF Sprague-Dawley rats, exposed for 2 hours to 2-methoxy-ethanol (ME, 1600 ppm), 1-acetoxy-2-methoxy-ethane (AME, 800 ppm), 2-ethoxy-ethanol (EE, 420 ppm), or 1-acetoxy-2-ethoxy-ethane (AEE, 170 ppm) the blood level of ME (after ME or AME) or EE (after EE or AEE) was considerably increased after pretreatment with ethanol (20 mmol/kg b.w. i.p.). (ME and EE are metabolites of AME and AEE, respectively.) After i.p. co-administration of ME (10 mmol/kg), EE (10 mmol/kg) or butoxy-ethanol (BE, 2.5 mmol/kg) with ethanol (20 mmol/kg) the blood level of ME, EE, and BE remained nearly constant as long as ethanol levels in blood were above 3 mmol/l. Repeated i.p. dosing (5 times one injection per hour) with EE (4 mmol/kg) or ME (5 mmol/kg) plus ethanol (8 or 10 mmol/kg) each resulted in an almost complete accumulation of both ether compounds in the blood. Blood levels of ethanol were increased significantly after EE, but only slightly after ME administration. The prolonged retention of ME, EE, or BE is due to an inhibition of the degradation of these compounds following the competition with ethanol at the alcohol dehydrogenase, the common metabolizing enzyme. This study has demonstrated that glycol ether derivatives are extremely accumulated as long as only very low levels of ethanol are present in blood. Therefore, it is concluded that the elimination of the investigated glycol ethers after occupational exposure can be retarded in alcoholized employees causing an increased health risk of these chemicals following the consumption of alcoholic beverages.