Hearing impairment due to the cochlear toxicity of several drugs is well documented (Ryback 1993). But until the latest decade there has been only little attention paid to audiologic effects of industrial chemicals. The recent research on chemically-induced hearing disorders has focused on solvents, heavy metals and chemicals inducing anoxia.
Solvents. In studies with rodents, a permanent decrease in auditory sensitivity to high-frequency tones has been demonstrated following weeks of high-level exposure to toluene. Histopathological and auditory brainstem response studies have indicated a major effect on the cochlea with damage to the outer hair cells. Similar effects have been found in exposure to styrene, xylenes or trichloroethylene. Carbon disulphide and n-hexane may also affect auditory functions while their major effect seems to be on more central pathways (Johnson and Nylén 1995).
Several human cases with damage to the auditory system together with severe neurologic abnormalities have been reported following solvent sniffing. In case series of persons with occupational exposure to solvent mixtures, to n-hexane or to carbon disulphide, both cochlear and central effects on auditory functions have been reported. Exposure to noise was prevalent in these groups, but the effect on hearing has been considered greater than expected from noise.
Only few controlled studies have so far addressed the problem of hearing impairment in humans exposed to solvents without a significant noise exposure. In a Danish study, a statistically significant elevated risk for self-reported hearing impairment at 1.4 (95% CI: 1.1-1.9) was found after exposure to solvents for five years or more. In a group exposed to both solvents and noise, no additional effect from solvent exposure was found. A good agreement between reporting hearing problems and audiometric criteria for hearing impairment was found in a subsample of the study population (Jacobsen et al. 1993).
In a Dutch study of styrene-exposed workers a dose-dependent difference in hearing thresholds was found by audiometry (Muijser et al. 1988).
In another study from Brazil the audiologic effect from exposure to noise, toluene combined with noise, and mixed solvents was examined in workers in printing and paint manufacturing industries. Compared to an unexposed control group, significantly elevated risks for audiometric high frequency hearing loss were found for all three exposure groups. For noise and mixed solvent exposures the relative risks were 4 and 5 respectively. In the group with combined toluene and noise exposure a relative risk of 11 was found, suggesting interaction between the two exposures (Morata et al. 1993).
Metals. The effect of lead on hearing has been studied in surveys of children and teenagers from the United States. A significant dose-response association between blood lead and hearing thresholds at frequencies from 0.5 to 4 kHz was found after controlling for several potential confounders. The effect of lead was present across the entire range of exposure and could be detected at blood lead levels below 10 μg/100ml. In children without clinical signs of lead toxicity a linear relationship between blood lead and latencies of waves III and V in brainstem auditory potentials (BAEP) has been found, indicating a site of action central to the cochlear nucleus (Otto et al. 1985).
Hearing loss is described as a common part of the clinical picture in acute and chronic methyl-mercury poisoning. Both cochlear and postcochlear lesions have been involved (Oyanagi et al. 1989). Inorganic mercury may also affect the auditory system, probably through damage to cochlear structures.
Exposure to inorganic arsenic has been implied in hearing disorders in children. A high frequency of severe hearing loss (>30 dB) has been observed in children fed with powdered milk contaminated with inorganic arsenic V. In a study from Czechoslovakia, environmental exposure to arsenic from a coal-burning power plant was associated with audiometric hearing loss in ten-year-old children. In animal experiments, inorganic arsenic compounds have produced extensive cochlear damage (WHO 1981).
In acute trimethyltin poisoning, hearing loss and tinnitus have been early symptoms. Audiometry has shown pancochlear hearing loss between 15 and 30 dB at presentation. It is not clear whether the abnormalities have been reversible (Besser et al. 1987). In animal experiments, trimethyltin and triethyltin compounds have produced partly reversible cochlear damage (Clerisi et al. 1991).
Asphyxiants. In reports on acute human poisoning by carbon monoxide or hydrogen sulphide, hearing disorders have often been noted along with central nervous system disease (Ryback 1992).
In experiments with rodents, exposure to carbon monoxide had a synergistic effect with noise on auditory thresholds and cochlear structures. No effect was observed after exposure to carbon monoxide alone (Fechter et al. 1988).
Experimental studies have documented that several solvents can produce hearing disorders under certain exposure circumstances. Studies in humans have indicated that the effect may be present following exposures that are common in the occupational environment. Synergistic effects between noise and chemicals have been observed in some human and experimental animal studies. Some heavy metals may affect hearing, most of them only at exposure levels that produce overt systemic toxicity. For lead, minor effects on hearing thresholds have been observed at exposures far below occupational exposure levels. A specific ototoxic effect from asphyxiants has not been documented at present although carbon monoxide may enhance the audiological effect of noise.