Occupational noise exposure accounts for approximately 16% of all disabling hearing losses, but the true value and societal costs may be grossly underestimated because current regulations only identify hearing impairments in the workplace if exposures result in audiometric threshold shifts within a limited frequency region. Research over the past several decades indicates that occupational noise exposures can cause other serious auditory deficits such as tinnitus, hyperacusis, extended high-frequency hearing loss, and poor speech perception in noise. Beyond the audiogram, there is growing awareness that hearing loss is a significant risk factor for other debilitating and potentially life-threatening disorders such as cardiovascular disease and dementia. This review discusses some of the shortcomings and limitations of current noise regulations in the United States and Europe.

Salicylate's ototoxic properties have been well established, inducing tinnitus and a sensory hearing loss when administered in high doses. Peripherally, acute dosing of salicylate causes frequency dependent reductions in DPOAEs and CAP amplitudes in low (20 kHz) frequencies more than mid frequencies (10-20 kHz), which interestingly corresponds to the pitch of behaviourally-matched salicylate-induced tinnitus. Chronic salicylate dosing affects the peripheral system by causing a compensatory temporary enhancement in DPOAE amplitudes and up-regulation of prestin mRNA and protein expression. Despite salicylate's antioxidant properties, cultured cochlea studies indicate it also impairs spiral ganglion neurons (SGNs) by paradoxically causing an upsurge of superoxide radicals leading to apoptosis. Centrally, salicylate alters γ-aminobutyric acid (GABA) and serotonin mediated neurotransmission in the central nervous system (CNS), which results in classical and non-classical auditory regions showing hyperactivity after salicylate administration. In the auditory cortex (AC) and lateral amygdala (LA), neuron characteristic frequencies (CF) shift upward and downward to mid frequencies (10-20 kHz) altering tonotopy following salicylate administration. Additionally, current source density (CSD) analysis showed enhanced current flow into the supergranular layer of the auditory cortex after a high systemic dose of salicylate. In humans, auditory perception changes following salicylate or aspirin, including decreased word discrimination and temporal integration ability. The results of previous studies have partially identified the mechanisms that are involved in salicylate-induced tinnitus and hearing loss, however to date some interactions remain convoluted. This review discusses current knowledge of salicylate ototoxicity and interactions.

Objective: This article reviews: (1) the evidence related to enhanced central gain as a potential mechanism for the generation of tinnitus and hyperacusis, (2) the neuroplastic changes induced by prolonged, low-level sound stimulation and (3) the clinical effectiveness of various sound therapies and amplification for the treatment of tinnitus and hyperacusis. Design: General literature review. Study sample: Peer-reviewed articles related to auditory neural gain, prolonged low-level noise exposure and effectiveness of sound therapy. Results: A large body of literature exists supporting the enhanced neural gain model of tinnitus and hyperacusis. Neuroplastic changes associated with prolonged low-level noise show evidence of reversing enhanced neural gain, which should theoretically reduce percepts of tinnitus and/or hyperacusis. However, the available clinical evidence assessing the efficacy of sound therapy to reduce tinnitus or hyperacusis lacks controlled clinical trials to accurately assess the effectiveness of sound therapy. Conclusions: The available literature from basic science studies supports the neural gain model of tinnitus and hyperacusis, which conceivably should be effectively managed with sound therapy. However, well-controlled clinical trials are needed before conclusions can be made on the effectiveness of sound therapy for tinnitus and hyperacusis.