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Year : 2002  |  Volume : 4  |  Issue : 14  |  Page : 49--61

Chemical asphyxiants and noise

Center for Toxicology, University of Oklahoma Health Sciences Center,Oklahoma City OK 73190, USA

Correspondence Address:
Laurence D Fechter
Center for Toxicology, The University of Oklahoma, Health Sciences Center, P.O. Box 26901, Oklahoma City, OK 73190
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Source of Support: None, Conflict of Interest: None

PMID: 12678928

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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.


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