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Human and animal studies have shown that toluene can cause hearing loss. In the rat, the outer hair cells are first disrupted by the ototoxicant. Because of their particular sensitivity to toluene, the cochlear microphonic potential (CMP) was used for monitoring the cochlea activity of anesthetized rats exposed to both noise (band noise centered at 4 kHz) and toluene. In the present experiment, the conditions were specifically designed to study the toluene effects on CMP and not those of its metabolites. To this end, 100-microL injections of a vehicle containing different concentrations of solvent were made into the carotid artery connected to the tested cochlea. Interestingly, an injection of 116.2-mM toluene dramatically increased in the CMP amplitude (approximately 4 dB) in response to an 85-dB SPL noise. Moreover, the rise in CMP magnitude was intensity dependent at this concentration suggesting that toluene could inhibit the auditory efferent system involved in the inner-ear or/and middle-ear acoustic reflexes. Because acetylcholine is the neurotransmitter mediated by the auditory efferent bundles, injections of antagonists of cholinergic receptors (AchRs) such as atropine, 4-diphenylacetoxy-N-methylpiperidine-methiodide (mAchR antagonist) and dihydro-beta-erythroidine (nAchR antagonist) were also tested in this investigation. They all provoked rises in CMP having amplitudes as large as those obtained with toluene. The results showed for the first time in an in vivo study that toluene mimics the effects of AchR antagonists. It is likely that toluene might modify the response of protective acoustic reflexes.

The study was carried out to test whether or not cubic distortion otoacoustic emissions were more sensitive than auditory-evoked potentials for assessing styrene-induced hearing losses in the Long-Evans rat. For the purposes of comparison, changes in cubic distortion product otoacoustic emissions (DeltaDPOAE), evoked potential permanent threshold shifts (PTS) and outer hair cell losses were measured in a population of styrene-treated rats. Each rat was exposed to either 650 or 750 ppm of styrene for 4 weeks, 5 days per week, 6 h per day. Only the 750 ppm exposure caused significant hearing losses. For this concentration, DPOAEs appeared as sensitive to styrene as the audiometry performed with evoked potentials, but not more. A high coefficient of correlation [0.84< or =r< or =0.91] between DeltaDPOAE and PTS was obtained across the styrene-induced effects for frequencies ranging from 5 to 12 kHz. This experiment demonstrates that DPOAEs can be used to monitor the ototoxicity induced by styrene even though they cannot be considered as a more sensitive index of cochlear pathology than the evoked potentials, at least under our experimental conditions. Likewise evoked potentials, normal DPOAEs may not guarantee a normal cochlear status and therefore results of DPOAE measurements should be interpreted cautiously. The use of both techniques and the determination of the ratio DeltaDPOAE/PTS may be useful in determining the cause of hearing loss: mechanical or chemical process. Moreover, because of its non-invasive and objective characteristics, the use of DPOAEs could play a greater role in a prevention policy.