In combined exposure with ototoxic chemicals, potentiation of noise induced hearing loss (NIHL) may certainly be a hazard (Sliwinska-Kowalska et al. 2007). However, as impulsive noise has the potential to induce hearing loss even at low levels of daily noise exposure (LEX, 8h), the greatest risk for hearing loss from combined exposures seems to be from simultaneous exposure to ototoxic chemicals and impulsive noise. Toluene exposure may cause hearing loss in rats at high levels of exposure without exposure to noise, but in combination with exposure to noise synergistic interaction may potentiate the hearing loss, especially in combined exposure to impulsive noise (Lund & Kristiansen 2008). The mechanisms involved in the ototoxicity of toluene and other aromatic organic solvents have not been fully elucidated, but toluene may act to impair the auditory medial efferent system, thereby augmenting the acoustic energy absorbed by the cochlea in response to the noise exposure (Lataye et al. 2007). However, in another experiment toluene treatment did not modify the responses in the cochlea in rats with non-functional middle ear muscles, although toluene did instead inhibit the action of the middle ear reflex, possibly by their anticholinergic effect on the efferent motor neurons (Campo et al. 2007). Altogether, exposure to organic solvents appears in general to have additive rather than synergistic effects in combined exposure with noise, while asphyxiants like carbon monoxide (CO) appear capable of true synergistic effects on NIHL (Fechter 2004). CO exposure by itself does not seem to have persisting effects on the hearing of rats, but it does potentiate the effects of NIHL at exposure levels of 500 ppm and higher. The potentiation of noise by CO may not be related to a specific effect of CO on the auditory cells, but may instead reduce the cell's ability to repair the noise induced damage (Chen & Fechter 1999). The combined effect of impulsive noise and both toluene and CO may reveal the full potential for NIHL from impulse noise exposure, because the functional protective mechanisms as well as the repair processes may be hampered. Nevertheless, this combination of exposures does appear to be a rather realistic scenario in the working environment. In order to test this hypothesis, groups of rats were exposed to impulsive noise, CO and toluene. The hearing was tested before and after exposure by assessment oto-acoustic emissions over 30 frequencies between 1 and 70 kHz, and cochleograms was made on 3-4 animals in each group.
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