Wilson H K, Robertson S M, Waldron H A, Gompertz D
Br J Ind Med. 1983 Feb;40(1):75-80. doi: 10.1136/oem.40.1.75.
The effect of a dose of alcohol on the kinetics of mandelic acid excretion in four volunteers exposed to 220 mg/m3 styrene has been investigated under controlled exposure chamber conditions. Ethanol inhibited the excretion of mandelic acid, so that the peak excretion was delayed from the end of the exposure period until three hours afterwards. One hour after administration of ethanol blood mandelic acid concentrations were 56% of the levels found during the alcohol-free control exposure, and this was paralleled by a 15-fold rise in phenylethane 1,2 diol, the metabolic precursor of mandelic acid. It is suggested that the inhibition of the oxidation of this diol is related to the change in NAD +/NADH ratio produced by ethanol metabolism. The implications of this ethanol effect on the interpretation of urinary mandelic acid excretion when monitoring workers exposed to styrene are discussed.
在受控暴露舱条件下，研究了剂量酒精对四名暴露于220毫克/立方米苯乙烯环境中的志愿者扁桃酸排泄动力学的影响。乙醇抑制了扁桃酸的排泄，使得排泄峰值从暴露期结束推迟至三小时后。给予乙醇一小时后，血液中扁桃酸浓度为无酒精对照暴露期间所测水平的56%，同时扁桃酸的代谢前体苯乙烷1,2二醇升高了15倍。有人认为，这种二醇氧化的抑制与乙醇代谢产生的NAD +/NADH比值变化有关。文中讨论了这种乙醇效应在监测接触苯乙烯工人时对尿扁桃酸排泄解释的影响。
