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[通过摄入卤代烃增加人和动物血液中的一氧化碳含量(作者译)]

[Increased blood-CO-content in humans and animals by incorporated halogenated hydrocarbons (author's transl)].

作者信息

Fodor G G, Roscovanu A

出版信息

Zentralbl Bakteriol Orig B. 1976 Jul;162(1-2):34-40.

PMID:186984
Abstract

Contrarily to the general opinion about the harmlessness of dichloromethane, clear functional disturbances of the central nervous system could be recorded by means of effect investigations as well in humans as in animals. The depressive effect on the REM-sleep of albino rats was especially well recognisable, similarly as with carbon monoxide exposure. Surprisingly the analytical investigations of the blood of these animals showed a clearly elevated blood-CO-content after exposure to dichloromethane. Further experiments during which albino rats were exposed three hours along to a dichloromethane-concentration equal to the TLV (1750 mg/m3!!) resulted in a blood-COHb-level of about 13%, corresponding to over 30 mug CO/ml blood. So high blood-COHb-levels are obtained after a three-hour-exposure to 120 ppm CO. Following these findings, a number of halogenated and oxygenated hydrocarbon compounds of the methane and ethane series were investigated relatively to their CO-forming capacity. Only the di- and trihalogenated methane derivatives were found leading to an increased blood-COHb-level. After a three hours-exposure to 1000 ppm respectively the jodoalkanes yielding about 23% COHb were strongestly, the bromoalkanes with about 20% COHb more strongly and the chloroalkanes with about 12% COHb strongly implicated in the endogenous CO-formation. By means of detailed experiments with human volunteers (non-smokers) it resulted that after eight-hours-exposure to 500 ppm dichloromethane (TLV) a mean value for CO-content in blood of about 30 mug/ml corresponding to 12% COHb was obtained, in one case raising as high as 60 mug CO/1 ml blood or 24% COHb. After an eight-hours-exposure to 100 ppm of the halocarbon, the blood-COHb-level reached 5%. The elimination was very slow, so that 24 to 26 hours were necessary to reestablish the original blood-COHb-level. These results show that the actually TLV for dichloromethane e.g. 1750 mg/m3 has to be revised, because a fifth of this value already leads to a blood-COHb-content equal to that produced by the TLV for carbon monoxide and that also eventually arising problems due to gas mixtures have to be considered and thoroughly investigated.

摘要

与二氯甲烷无害的普遍观点相反,通过对人和动物的效应研究,可以记录到中枢神经系统明显的功能紊乱。对白化病大鼠快速眼动睡眠的抑制作用尤其明显,这与一氧化碳暴露时的情况类似。令人惊讶的是,对这些动物血液的分析研究表明,接触二氯甲烷后,血液中的一氧化碳含量明显升高。进一步的实验中,将白化病大鼠暴露在相当于阈限值(1750毫克/立方米!!)的二氯甲烷浓度下三小时,结果血液中的碳氧血红蛋白水平约为13%,相当于每毫升血液中一氧化碳含量超过30微克。在接触120 ppm一氧化碳三小时后才会达到如此高的碳氧血红蛋白水平。基于这些发现,对甲烷和乙烷系列的一些卤代烃和含氧烃化合物的一氧化碳生成能力进行了研究。结果发现,只有二卤代和三卤代甲烷衍生物会导致血液中碳氧血红蛋白水平升高。分别接触1000 ppm三小时后,生成约23%碳氧血红蛋白的碘代烷烃与内源性一氧化碳生成的关联最强,生成约20%碳氧血红蛋白的溴代烷烃关联较强,生成约12%碳氧血红蛋白的氯代烷烃关联较弱。通过对人类志愿者(非吸烟者)进行的详细实验发现,接触500 ppm二氯甲烷(阈限值)八小时后,血液中一氧化碳含量的平均值约为每毫升30微克,相当于12%的碳氧血红蛋白,在一个案例中高达每毫升血液60微克一氧化碳或24%的碳氧血红蛋白。接触100 ppm卤代烃八小时后,血液中的碳氧血红蛋白水平达到5%。消除过程非常缓慢,因此需要24到26小时才能恢复到原来的血液碳氧血红蛋白水平。这些结果表明,二氯甲烷目前的阈限值(例如1750毫克/立方米)必须进行修订,因为该值的五分之一就已经会导致血液中的碳氧血红蛋白含量与一氧化碳阈限值所产生的含量相当,而且还必须考虑并深入研究最终因混合气体而产生的问题。

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