Potentiation of chemical ototoxicity by noise

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

High-intensity and/or prolonged exposure to noise causes temporary or permanent threshold shifts in auditory perception. Occupational exposure to solvents or administration of clinically important drugs, such as aminoglycoside antibiotics and cisplatin, also can induce permanent hearing loss. The mechanisms by which these ototoxic insults cause auditory dysfunction are still being unraveled, yet they share common sequelae, particularly generation of reactive oxygen species, that ultimately lead to hearing loss and deafness. Individuals are frequently exposed to ototoxic chemical contaminants (e.g., fuel) and noise simultaneously in a variety of work and recreational environments. Does simultaneous exposure to chemical ototoxins and noise potentiate auditory dysfunction? Exposure to solvent vapor in noisy environments potentiates the permanent threshold shifts induced by noise alone. Moderate noise levels potentiate both aminoglycoside- and cisplatin-induced ototoxicity in both rate of onset and in severity of auditory dysfunction. Thus, simultaneous exposure to chemical ototoxins and moderate levels of noise can potentiate auditory dysfunction. Preventing the ototoxic synergy of noise and chemical ototoxins requires removing exposure to ototoxins and/or attenuating noise exposure levels when chemical ototoxins are present.

Original languageEnglish (US)
Pages (from-to)38-46
Number of pages9
JournalSeminars in Hearing
Volume30
Issue number1
DOIs
StatePublished - Feb 2009

Fingerprint

Noise
Aminoglycosides
Hearing Loss
Cisplatin
Auditory Perception
Deafness
Occupational Exposure
Reactive Oxygen Species
Anti-Bacterial Agents
Pharmaceutical Preparations

Keywords

  • Deafness
  • Noise
  • Ototoxic drugs
  • Ototoxins
  • Synergistic effects

ASJC Scopus subject areas

  • Speech and Hearing

Cite this

Potentiation of chemical ototoxicity by noise. / Steyger, Peter.

In: Seminars in Hearing, Vol. 30, No. 1, 02.2009, p. 38-46.

Research output: Contribution to journalArticle

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