Hazards to hearing from combined exposure to toluene and noise in rats.

INTRODUCTION: The main risk of hearing impairment from workplace exposure to organic solvents may stem from the potentiation of effects caused by concomitant noise exposure. The aim of the present study was to identify the main hazards from combined long-term, low-level exposure to noise and aromatic organic solvents, like toluene, in rats. MATERIAL AND METHODS: The rats were exposed to steady-state, wide-band noise (WBN) and 0 ppm, 100 ppm, 200 ppm and 500 ppm toluene for 90 days. Hearing was assessed using Auditory Brain Stem Responses (ABR) and Distortion Product Oto-Acoustic Emissions (DPOAE) eight weeks after exposure. The impact of noise composition on the interaction between solvent and noise exposure was investigated in rats exposed for 10 days either to 0 ppm, 500 ppm, 1000 ppm or 1500 ppm toluene and either WBN or impulse noise. ABR and DPOAE tests were performed before and two weeks after exposure. RESULTS: Long-term exposure of rats to WBN and toluene at 500 ppm or less did not show any increase in hearing impairment, compared to the rats exposed to noise only. Synergistic interaction was demonstrated in short-term exposure to 1500 ppm toluene and both to WBN and impulse noise, but hearing impairment was much larger when following exposure to impulse noise. CONCLUSION: In combined exposure to low-levels of noise and toluene, even a long-term exposure did not reveal a potential hazard of hearing impairment. Synergistic interaction in combined short-term exposure to toluene and noise was noted both with respect to WBN and impulse noise, but the impulse noise was much more disruptive than WBN at the same level of noise exposure. The ototoxicity of organic solvents may primarily be a hazard also to human hearing due to the exacerbation of hearing loss by a possible co-exposure to especially harmful noise, such as impulse noise.

No evidence for enhanced noise induced hearing loss after prenatal stress or dexamethasone.

It was recently implied that prenatal stress and fetal exposure to glucocorticoids may interfere with hearing ability and noise induced hearing loss in adulthood. In the present study pregnant Wistar rats were stressed during gestation by Chronic Mild Stress (CMS, a variable schedule of different stressors) or by dexamethasone (a synthetic glucocorticoid, i.e. a pharmacological stressor). At birth, but not at weaning, the dexamethasone offspring exhibited significantly decreased body weight compared to both control offspring and progeny from dams exposed to CMS during pregnancy. As adults, male offspring were exposed to 105 dB sound pressure level (SPL) wide band noise either continuously for eight hours or for two hours per day on three consecutive days. Oto-acoustic emissions and auditory brainstem responses were recorded before and after exposure to noise. Neither prenatal chronic stress nor prenatal dexamethasone exposure was associated with significantly enhanced noise induced hearing loss compared to controls, and these results were consistent in both subsets of animals. Our data do not support previous reports that prenatal exposure to mild stress nor to dexamethasone is detrimental to the hearing organ per se. However, hearing may be modulated by prenatal stressors under certain circumstances, of which the timing and degree are probably the most important.