Abstract

The toxic mechanisms involved in solvent-induced hearing loss are not well-known, even though, today, the disturbances of K⁺ recycling and the generation of reactive oxygen species in the organ of Cori are considered as determinant. The cochleotoxic effects of these pollutants shows up after a long-lasting exposure and ends up by the phagocytosis of outer hair cells (OHCs) initiated by the supporting cells. Because of the lipid peroxidation which takes place within the OHC membranes, the latters are more vulnerable to noise. As a result, a solvent exposure can exacerbate the traumatic effects of noise at the level of the organ of Corti. Such a phenomenon is not the only one capable of explaining the synergistic effects of a co-exposure to noise and solvents. Indeed, solvents can also disturb the function of the middle-ear acoustic reflex which protects against continuous high-intensity noises by contracting the stapes muscle and thereby reduces the amount of acoustic energy penetrating into the cochlea.

Recently, it has been shown that solvents like benzene, toluene, ethylbenzene and xylenes disturb the function of the middle-ear reflex and therefore allow noise to be more cochlea-traumatic. These neuropharmacological effects are likely due to an action of the pollutants on the targeted neuroreceptors of the acoustic reflex circuit. The interaction ‘pollutants vs receptors’ would be determined by the stereo-specificity rather than by the lipophilocity of the molecules. Both cochleotoxic and neuropharmacological phenomena can induce the traumatic effect of the noise on the organ of Corti. Partial disruption of the organ of Corti, or temporary disturbances of the reflex by solvents, both can increase the risk of occupational deafness encountered by co-exposed workers. Despite these statements, the European hearing conservation programs have not changed their concerns about the co-exposures to noise and solvents.