Liira J, Riihimäki V, Engström K
Turka Regional Institute of Occupational Health, Finland.
Br J Ind Med. 1990 May;47(5):325-30. doi: 10.1136/oem.47.5.325.
The kinetics of inhaled methyl ethyl ketone (MEK) at a concentration of 200 ppm for four hours were studied in volunteers after swallowing ethanol at a dose of 0.8 g/kg. Ethanol was given either before or at the end of the exposure to MEK. The blood concentrations of MEK, 2-butanol, and 2,3-butanediol were monitored during and after the exposure. MEK concentrations in exhaled air and MEK and 2,3-butanediol concentrations in urine were also measured. Ethanol inhibited the primary oxidative metabolism of MEK and caused an increase in the blood concentrations of MEK and 2-butanol after ingestion. Ethanol ingestion, through higher blood MEK concentrations, also increased the elimination of MEK in the urine and exhaled air. Ethanol taken before exposure to MEK reduced the serum concentration of 2,3-butanediol initially but there was an increase about eight hours after the exposure. Urinary excretion of 2,3-butanediol followed the same pattern. Prior ingestion of ethanol thus seemed to interfere with the metabolism of 2,3-butanediol during and after exposure to MEK.
在志愿者摄入0.8 g/kg剂量的乙醇后,研究了他们在浓度为200 ppm的情况下吸入甲乙酮(MEK)4小时的动力学情况。乙醇在接触MEK之前或接触结束时给予。在接触期间及接触后监测了MEK、2-丁醇和2,3-丁二醇的血药浓度。还测量了呼出气体中的MEK浓度以及尿液中的MEK和2,3-丁二醇浓度。摄入乙醇会抑制MEK的主要氧化代谢,并导致摄入后MEK和2-丁醇的血药浓度升高。通过提高血液中的MEK浓度,摄入乙醇还会增加尿液和呼出气体中MEK的排泄。接触MEK之前摄入乙醇最初会降低2,3-丁二醇的血清浓度,但在接触约八小时后会有所升高。2,3-丁二醇的尿排泄情况也遵循相同模式。因此,预先摄入乙醇似乎会在接触MEK期间及之后干扰2,3-丁二醇的代谢。