The receptor cells for acoustic stimuli are particularly vulnerable to reduced oxygen tension because of the limited characteristics of blood supply to the inner ear. Electrophysiological data have demonstrated that asphyxiation disrupts audition, but the consequences of mild, prolonged hyposia upon the auditory system have not been investigated.
One aim of this investigation is to determine whether subchronic exposure to chemical asphyxiants at doses relevant to levels widely encountered in occupational and environmental settings produces ototoxicity. Chronic and impulse noise can induce autitory damage, but whether this occurs through mechanical trauma or by metabolic exhaustion is uncertain. Because there are data which show that noise reduces oxygen tension in the endolymph fluid of the scala media and produces vascular damage to the inner ear, it has been hypothesized that noise-induced auditory loss may result from depressed oxygen availability. If noise does disrupt hearing by restricting oxygen to the Corti Organ or if it damages inner ear vascular structures it is logical to assume that noise would potentiate the ototoxic effects of chemical asphyxiant exposure.
The final aim of this proposal will be to specify the nature of the interaction between noise and chemical asphyxiant exposure. The methods to be used include measures of modulation of the acoustic startle reflex by low intensity test stimuli and subsequent histological examination of the inner ear.

National Institute of Health (NIH)
National Institute of Environmental Health Sciences (NIEHS)
Research Project (R01)
Project #
Application #
Study Section
Toxicology Study Section (TOX)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Johns Hopkins University
Schools of Public Health
United States
Zip Code
Liu, Y; Fechter, L D (1997) Toluene disrupts outer hair cell morphometry and intracellular calcium homeostasis in cochlear cells of guinea pigs. Toxicol Appl Pharmacol 142:270-7
Liu, Y; Rao, D; Fechter, L D (1997) Correspondence between middle frequency auditory loss in vivo and outer hair cell shortening in vitro. Hear Res 112:134-40
Fechter, L D; Liu, Y; Pearce, T A (1997) Cochlear protection from carbon monoxide exposure by free radical blockers in the guinea pig. Toxicol Appl Pharmacol 142:47-55
Liu, Y; Fechter, L D (1996) Comparison of the effects of trimethyltin on the intracellular calcium levels in spiral ganglion cells and outer hair cells. Acta Otolaryngol 116:417-21
Liu, Y; Fechter, L D (1995) Trimethyltin disrupts loudness recruitment and auditory threshold sensitivity in guinea pigs. Neurotoxicol Teratol 17:281-7
Fechter, L D; Liu, Y (1995) Elevation of intracellular calcium levels in spiral ganglion cells by trimethyltin. Hear Res 91:101-9
Liu, Y; Fechter, L D (1995) MK-801 protects against carbon monoxide-induced hearing loss. Toxicol Appl Pharmacol 132:196-202
Fechter, L D; Liu, Y (1994) Trimethyltin disrupts N1 sensitivity, but has limited effects on the summating potential and cochlear microphonic. Hear Res 78:189-96
Fechter, L D (1993) Effects of acute styrene and simultaneous noise exposure on auditory function in the guinea pig. Neurotoxicol Teratol 15:151-5
Clerici, W J; Chertoff, M E; Brownell, W E et al. (1993) In vitro organotin administration alters guinea pig cochlear outer hair cell shape and viability. Toxicol Appl Pharmacol 120:193-202

Showing the most recent 10 out of 24 publications