• Volume/Page
  • Keyword
  • DOI
  • Citation
  • Advanced
   
 
 
 

Journal of the Acoustical Society of America

SECTION LISTING

BROWSE VOLUMES

Year Range: 
Search Issue | RSS Feeds RSS
Previous Issue Next Issue

Nov 1988

Volume 84, Issue S1, pp. S2-S224

Return to All Sections
back to top
RSS Feeds
back to top Session O. Physiological Acoustics II: Ototoxicity of Environmental Chemicals
Invited Papers
FREE

Chemical asphyxiants as sources of ototoxicity (A)

Laurence D. Fechter

J. Acoust. Soc. Am. Volume 84, Issue S1, pp. S37-S38 (1988); (2 pages)

Online Publication Date: 13 Aug 2005

Full Text: | Download PDF

Show Abstract
Total asphyxiation has repeatedly been shown to disrupt cochlear function, but moderate reduction in oxygen delivery has also been suggested as a general mechanism responsible for auditory dysfunction. Several recent experiments in this laboratory using environmental contaminants to produce moderate hypoxia have been used to study the parameters under which reductions in oxygen delivery can disrupt cochlear function. Both transient and permanent impairments have been studied. Acute carbon monoxide exposure increases cochlear blood flow and at higher doses produces transient disruption of the compound action potential. This loss occurs specifically at high frequencies. When carbon monoxide and noise are presented simultaneously, permanent auditory loss results, which is substantially greater than the effect of noise alone. The impairment is greatest at high frequencies and injury to hair cells occurs in the basal turn when white noise is employed. Evidence of ototoxicity by such chemical asphyxiants as butyl nitrite and trimethyltin will also be presented. Taken as a whole, the data do support the hypothesis that environmental agents which impair oxygen delivery and utilization are potent ototoxicants and suggest that hypoxia may be an important mechanism for disrupted auditory function.
FREE

Otoneurologic manifestations following carbon monoxide poisoning (A)

Kazumi Makishima

J. Acoust. Soc. Am. Volume 84, Issue S1, pp. S38-S38 (1988); (1 page)

Online Publication Date: 13 Aug 2005

Full Text: | Download PDF

Show Abstract
Otoneurologic examinations were conducted in the 15 patients who suffered from acute carbon monoxide (CO) poisoning in a coal mine accident. The audiologic and vestibular derangement found in the patients were not significant, but were suggestive of central origin. One victim in the same accident, who had severe psychopathological symptoms and had no otoneurologic complaint, showed moderate histopathological changes in the cerebrum in the presence of no specific change of the inner ears. The effect of CO poisoning on the threshold sensitivity of the auditory responses was studied in a CO poisoning animal model of guinea pigs. Loss of auditory threshold sensitivity was most prominent at the auditory cortex, and was next most severe at the inferior colliculus. There was no loss of sensitivity at the cochlea. Some of the patients mentioned above have been studied again about 25 years after the accident. It is felt that there must be increased and more considerable widespread pathology in the brain following CO poisoning to explain the present audiometric and vestibural pictures.
FREE

Effects of lead acetate on guinea pig—Electrophysiological study of the cochlear function (A)

K. Yamamura, H. Ohno, K. Terayama, N. Yamamoto, and R. Kishi

J. Acoust. Soc. Am. Volume 84, Issue S1, pp. S38-S38 (1988); (1 page)

Online Publication Date: 13 Aug 2005

Full Text: | Download PDF

Show Abstract
Segmental demyelination and axonal degeneration of motor nerves induced by lead exposure are well known in man and animals. The effect of lead acetate exposure to man may involve the cranial nerves, since vertigo and sensory neuronal deafness have been reported among lead workers. However, there are only a few reports concerning the dose effects of lead acetate both on the cochlear and the cranial VIII nerve. The effects of lead acetate on the cochlea and the VIII nerve using CM (cochlear microphonics), AP (action potential), and EP (endocochlear potential) of the guinea pigs are investigated. The results of this experiment were as follows: No changes of CM and EP were found by lead acetate exposure. On the other hand, there were an elevation of threshold but a decrease of maximum output voltage on AP.
Return to All Sections
Close

Home Publications Meetings Contact ASA Site Map Back to Top

Copyright © Acoustical Society of America

close