Parameters influencing auditory fatigue among professionals working in the amplified music sector: noise exposure and individual factors.

Objective: Hearing disorders are common among music professionals, as they are frequently exposed to sound levels exceeding 100 dB(A). By assessing auditory fatigue, situations that are deleterious for hearing could be identified, allowing the deployment of preventive measures before permanent impairment occurs. However, little is known about the factors contributing to auditory fatigue.

Effects of co-exposure to CS and noise on hearing and balance in rats: continuous versus intermittent CS exposures.

Background: Carbon disulfide (CS) exacerbates the effect of noise on hearing, and disrupts the vestibular system. The goal of this study was to determine whether these effects are also observed with intermittent CS exposure.

Methods: Rats were exposed for 4 weeks (5 days/week, 6 h/day) to a band noise at 106 dB SPL either alone or combined with continuous (63 ppm or 250 ppm) or intermittent (15 min/h or 2 × 15 min/h at 250 ppm) CS.

Study of potential transfer of aluminum to the brain via the olfactory pathway.

Many employees in the aluminum industry are exposed to a range of aluminum compounds by inhalation, and the presence of ultrafine particles in the workplace has become a concern to occupational health professionals. Some metal salts and metal oxides have been shown to enter the brain through the olfactory route, bypassing the blood-brain barrier, but few studies have examined whether aluminum compounds also use this pathway. In this context, we sought to determine whether aluminum was found in rat olfactory bulbs and whether its transfer depended on physicochemical characteristics such as solubility and granulometry.

Olfactory mucosal necrosis in rats following acute intraperitoneal administration of 1,2-diethylbenzene, 1,2-diacetylbenzene and 2,5-hexanedione.

1,2-Diethylbenzene (1,2-DEB) is used in the manufacture of some plastics. Exposure to 1,2-DEB has been shown to induce peripheral neuropathy in rats. This neurotoxicity is thought to be caused by a metabolite, 1,2-diacetylbenzene (1,2-DAB), a γ-diketone-like compound.

Study of the potential oxidative stress induced by six solvents in the rat brain.

The mechanisms of action involved in the neurotoxicity of solvents are poorly understood. In vitro studies have suggested that the effects of some solvents might be due to the formation of reactive oxygen species (ROS). This study assesses hydroxyl radical (OH) generation and measures malondialdehyde (MDA) levels in the cerebral tissue of rats exposed to six solvents (n-hexane, n-octane, toluene, n-butylbenzene, cyclohexane and 1,2,4-trimethylcyclohexane).