An association between noise exposure and vestibular function has long been suspected. Our wide experience in a major otologic outpatient clinic yielded six patients within the last seven years who presented with Meniere's disease and a history of long-term exposure to noise. Two of the cases are described in detail. Our evaluation in light of the data in the literature suggests that the relationship between vestibular dysfunction and exposure to hazardous noise may be more than coincidental.

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While noise exposure is the most significant contributor to occupational hearing loss, recent evidence points to solvents and their interactions as additional contributors to occupational deafness. Furthermore, due to the metabolic competitive inhibition between aromatic solvents and ethanol, the solvent toxicity can be even enhanced in certain circumstances. So, two dangerous interactions: noise and solvents, solvents and ethanol deserve to be taken into consideration in an exhaustive preventive policy. Based on the investigations reviewed in the present study, it appears that the combined effects of an exposure to noise and solvent exceed the summation of the damage produced by each agent alone. Such a statement can be also made for a combined exposure to solvent and ethanol. It is therefore important to bear in mind that noise effects can be exacerbated by non-acoustic agents. Thus, if our noise regulations have to be more effective, it is necessary to take into consideration the ototoxic effects of noise in a multifactorial environment.

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Hearing loss in workers exposed to organic solvents has been shown to be the effect of interaction between the exposure to solvents and noise. Synergistic interaction has been demonstrated in rats following simultaneous exposure to toluene and noise, but only at high-level toluene exposure. The present study was initiated to investigate the potential interaction of exposure to noise and toluene on the auditory system of the rat, covering a dose-range of toluene exposure (0, 500, 1000, 1500, and 2000 ppm, 6 h/d, 10 d). Exposed to toluene only, the rats exposed at the 1500 and 2000 ppm level developed a mid-frequency ABR threshold shift, whereas rats exposed to 0, 500, and 1000 ppm did not exhibit signs of auditory impairment. Rats exposed to 500 ppm toluene and noise (96 dB SPL, 2h following the daily toluene exposure, 10 d) developed a small, but statistically significant threshold shift, equal to the hearing loss in rats exposed to noise only (0 ppm). Synergistic interaction was evident at the 1000, 1500, and 2000 ppm toluene exposure levels. There was no further hearing loss at the 2000 ppm than at the 1500 ppm level, indicating that a saturation of the auditory impairment had been reached. When acute noise exposure (105 dB SPL, 4 h) followed the toluene exposure by 30 days, interaction was noted at the 1500 ppm toluene exposure level, but not at the 1000 ppm level. However, the latter type of interaction is of indirect nature and should be distinguished from the direct interaction, taking place when toluene is physically present in the cochlea during exposure to noise. Further investigations in animal models should preferentially be carried out as long-term, low-level exposure studies, showing the possible interaction at low exposure levels, where exposure to each factor alone is without any effect.

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An interdisciplinary study was performed to examine the difference between road and rail traffic noise with regard to physiological, subjective, and behavioral responses. In 8 areas where either rail or road noise prevailed, a total of 1 600 persons (18 to 70 years of age) were interviewed; a subgroup of 377 persons was examined during 2 times 5 nights each. In this sleep observation period noise impact and body movements were recorded continuously dur­ing each night. Every morning the subjects stated the position of the windows during the night, they evaluated the qualitative and quantitative parameters of sleep and performed a 4-choice reaction time test. Only the behavior to sleep with open or closed windows was significantly associated with the rating level and the windows were significantly more often closed by the residents primarily exposed to road noise. Whether this indicates a reaction to noise or to concomitant pollutants such as odour is, however, debatable. The fact that none of the other data recorded here revealed any difference between the two types of noise is discussed in view of future studies.

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The effect of noise exposure on the auditory system is well known from animal studies. However, most of the studies concern short-term exposure conditions. The purpose of the present research was to find the dose-effect curve for hearing loss in rats following 5 days of noise exposure. Three groups of eight Wag/Rij rats were exposed to broad band noise at levels of 90, 100 and 110 dB SPL for 8 hours/day and 5 consecutive days. An additional group of eight rats served as the control group. Between three and seven weeks after the exposure, hearing was tested by electrocochleography (CAP) and distortion product otoacoustic emissions (DPOAE). Subsequently, the cochlea were morphologically examined. Only the highest two exposure levels affected hearing. The DPOAE growth curves at 4, 8 and 16 kHz and the CAP growth curves at 4, 8, 12, 16 and 24 kHz were affected after the 110 dB SPL broad band noise. After the 100 dB SPL noise, only the 12 kHz CAP growth curve was affected. At the light microscopic level, OHC damage was not detected in this study.

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Hearing loss is the most common occupational disease in the United States with noise serving as the presumed causative agent in most instances; noise is identified as a prominent factor in approximately 10 million individuals in the United States with hearing impairments. Despite the characterization of noise exposures that yield temporary and permanent threshold shifts and partial elucidation of mechanisms that are responsible for noise-induced hearing loss (NIHL), there remain significant knowledge gaps concerning factors causing NIHL. One such knowledge gap concerns potentiation of NIHL by simultaneous exposure to chemical agents. We have pursued investigation of the exposure conditions that facilitate the potentiation of NIHL by carbon monoxide. The selection of these specific agents is predicated upon the ubiquitous nature of exposure to chemical asphyxiants and a preliminary understanding of the mechanisms by which chemical asphyxiants disrupt hearing. Our data indicate that the potentiation of NIHL by carbon monoxide increases as a function of carbon monoxide concentration at levels of 500 ppm and above, but that the extent of potentiation shows a non­linear relationship to total noise energy with the greatest potentiation shown at moderate noise exposures that produce limited permanent threshold shifts. Further, the potentiation of NIHL by carbon monoxide appears to saturate as noise severity is increased such that at the most severe conditions used, the effects of carbon monoxide on NIHL are obscured totally by the noise effect. Finally, the data presented demonstrate that carbon monoxide is able to impair the recovery of NIHL that normally occurs when periods of silence are interspersed within noise exposure.

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The role of glutathione in carboplatin ototoxicity was investigated in the chinchilla. Chinchillas hearing was tested with both distortion product otoacoustic emissions (DPOAE) and evoked potentials recorded from a chronic electrode in the inferior colliculus (IC). All subjects had an osmotic pump fitted to their right ear and it received buthionine sulfoximine (BSO) at a dose of 15 mM delivered at 5 ml per hour for 14 days. A group (N=4) was given a double dose of carboplatin (25 mg/kg i.p. for 2 days). The pump was implanted three days before the carboplatin dose. The BSO treated ears showed a greater loss in both evoked potential and DPOAE measures, as well as substantially fewer missing hair cells. The results implicate reactive oxygen species (ROS) as a common factor in ototoxic reactions because suppression of glutathione antioxidant leads to greater ototoxic reactions.

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