Mechanisms of ototoxicity by chemical contaminants: prospects for intervention.
Noise Health 1999 Jan-Mar; 1(2):10-27
OSHA has promulgated noise exposure standards (29 CFR 1910.95) and established regulations for hearing conservation programs (Hearing Conservation Amendment [46 Fed. Reg. 4078 (1981);48 Fed. Reg.9776 (1983)]) designed to protect workers in many occupations from noise induced hearing loss (NIHL). However, the promulgation of these standards has not eliminated NIHL as one of the 10 most common workplace "diseases" in the US (CDC, MMWR, 1986) or "the most" common workplace disease (US Dept. HHS, NIOSH, 1996). In one extreme example, a NIOSH Health Hazard Evaluation Report (HHE88-0290-2460) cited by Tubbs (1995), reported that audiometric studies over 400 firefighters showed normal hearing in only 40% of those employed less than 6 years with no normal audiograms found in those employed more than 20 years. Tubbs (1995) notes that NIHL in this population exceeds that which would be predicted based upon noise exposure data. Among explanations offered for this difference include inadequacy of the 5 dB exchange rule (by which sound intensity may be increased by 5 dB when noise duration is cut in half), the narrow band of noise generated by critical noise sources such as sirens, and the interaction of toxicants at the fire site with noise exposure. There are many different reasons why occupational noise exposure still produces profound health deficits. These problems of accurate noise characterisation, problems in equating noise exposures of varying time durations using the "equal-energy principle" (selection of an appropriate relationship between duration and intensity of exposure), and significant individual (and idiopathic) differences in susceptibility that might relate to genetic factors and to unrecognised environmental factors. This paper focuses on one such environmental factor that has not received adequate attention; the potentiation of NIHL by simultaneous exposure to chemical ototoxicants such as chemical asphyxiants, [carbon monoxide (CO) and cyanide], and organic solvents. The primary questions that must be addressed relate to the mechanism(s) and the exposure conditions under which these chemicals potentiate temporary and permanent hearing impairments under permissible noise exposure conditions. This focus can provide insights in the nature of the interaction and will provide opportunities for selective pharmacological treatments designed to protect workers. In addition to characterising the doses that lead to potentiation of NIHL and evaluating the equal energy principle when a chemical toxicant is present, it must also be determined how the noise spectrum influences the nature of the interaction with chemical asphyxiants.
Hearing-protection; Noise-induced-hearing-loss; Synergistic-effects; Organic-solvents; Ototoxicity;
University of Oklahoma Health Sciences Center, Oklahoma Center for Toxicology, Department of Pharmacology and Toxicology, Oklahoma City, Oklahoma 73190
Disease and Injury: Hearing Loss
Noise & Health
University of Oklahoma, Health Sciences Center, Oklahoma Center for Toxicology, Oklahoma City, Oklahoma