While noise exposure is the most significant contributor to occupational hearing loss, evidence gained over the last 10 years, has pointed to organic solvents as additional contributors to occupational hearing disorders. Despite the implications of this finding, no significant measure has been undertaken to limit exposure to occupational solvents, or to occupational solvents and noise, within the European community. Guidelines for improving hearing protection of people exposed to solvents, or to solvents and noise, are addressed in the present article. Recently, it has been shown that the lowest-observed-adverseeffect level (LOAEL) of styrene was 300 ppm in active (working wheel) rats, and that the same amount of styrene-induced hearing loss (SIHL) can be obtained with styrene concentration difference of 200 ppm between active and sedentary (inactive) rats. Supported by a reasonable safety factor (SF) of 10, the authors proposed to decrease the French threshold limit value of styrene from 50 to 30 ppm (RfD = LOAEL/SF) to ensure a higher level of protection for human hearing. It is widely acknowledged that outer hair cells in the organ of Corti can be considered as the first target tissue of solvents, while little is known about the action of aromatic solvents on the auditory efferent system. In a recent experiment using both the cochlear microphonic and compound action potentials, the authors have shown that toluene can inhibit the action of the middle ear reflex by modifying the cholinergic receptors. It is likely that toluene affects the cholinergic receptors at the brainstem level. By its anticholinergic-like effect, toluene could allow higher acoustic energy penetration into the cochlea exposed to both noise and solvent. Based on this phenomenon, the authors recommend the use of hearing protection for the lower exposure action value: Lex, 8h = 80 dB(A) in noisy environments polluted by solvents.

From previous in vivo investigations, it has been shown that toluene can mimic the effects of cholinergic receptor antagonists and may thereby modify the response of protective acoustic reflexes. The current study aimed to define the relative effects of aromatic solvents on the middle ear and inner ear acoustic reflexes. Toward this end, the cochlear microphonic (CMP) elicited with a band noise centered at 4 kHz, and the compound action potential (CAP) elicited with 4-kHz tone pips was measured in rats. Both potentials were recorded before, during, and after triggering the protective reflexes by a 110-dB SPL contralateral octave band noise centered at 12.5 kHz (12.5 kHz-OBN). In several rats, the middle ear muscles were severed to identify the relative effects of toluene on the two reflexes. While the reflex elicitor was capable of decreasing both the CMP and CAP amplitudes, an injection of 116.2 mM toluene cancelled this suppressor effect induced by the contralateral sound. In the rats with nonfunctional middle ear muscles, a solvent injection did not modify the electrophysiological responses of the cochlea. Different solvents were tested to study the relationship of the chemical structure of the solvents on the acoustic reflexes. The present study showed that aromatic solvents can inhibit the action of the middle ear reflex by their anticholinergic effect on the efferent motoneurons. An aromatic nucleus and the presence of one side chain of no more than 3 C seem to be required in the solvent structure to inhibit the efferent motoneurons.

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