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化学窒息剂与噪音

Chemical Asphyxiants and Noise.

作者信息

Fechter Laurence D., Chen Guang-Di, Rao Deepa

机构信息

Center for Toxicology, The University of Oklahoma, Health Sciences Center, P.O. Box 26901, Oklahoma City, OK 73190, USA., Email:

出版信息

Noise Health. 2002;4(14):49-61.

PMID:12678928
Abstract

The damaging effects of noise on auditory function can be altered significantly by exposure to additional agents that may or may not by themselves be ototoxic. This chapter focuses on the ability of chemical asphyxiants present in both occupational settings and ambient environments to potentiate noise induced hearing loss in a laboratory animal model. Since the chemical agents under study do not produce permanent impairment of hearing by themselves, the finding of auditory impairment in excess of that which is produced by noise exposure alone can be defined as noise potentiation. This chapter focuses both on the exposure conditions that favour such potentiation and also on potential mechanisms for potentiation. The data show that low to moderate exposure levels of carbon monoxide (CO) and hydrogen cyanide can potentiate noise induced hearing loss (NIHL) and the relationship between such levels and those permitted in work environments is provided. Finally, evidence is presented that free oxygen radicals may be responsible for potentiation of NIHL by the chemical asphyxiants. First, the ability of a free radical spin trap agent, PBN, to prevent the adverse effects of CO is demonstrated. Then, in an additional experiment, electron paramagnetic spin resonance is used to demonstrate a high level of free radicals in the cochlea with combined exposure to CO + noise while individual exposures to CO and noise do not produce free radicals at levels detectable by this method.

摘要

噪声对听觉功能的损害作用可因接触其他可能具有或不具有耳毒性的物质而发生显著改变。本章重点关注职业环境和周围环境中存在的化学窒息剂在实验动物模型中增强噪声性听力损失的能力。由于所研究的化学物质本身不会导致永久性听力损伤,因此,超过单独噪声暴露所致的听觉损伤可定义为噪声增强效应。本章重点探讨有利于这种增强效应的暴露条件以及潜在的增强机制。数据表明,低至中度水平的一氧化碳(CO)和氰化氢可增强噪声性听力损失(NIHL),并给出了这些水平与工作环境中允许水平之间的关系。最后,有证据表明,自由基可能是化学窒息剂增强NIHL的原因。首先,证明了自由基自旋捕获剂PBN预防CO不良影响的能力。然后,在另一项实验中,利用电子顺磁共振证明,在CO + 噪声联合暴露时,耳蜗中存在高水平的自由基,而单独暴露于CO和噪声时,该方法检测不到可导致自由基的水平。

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