Ethical considerations in noise-induced hearing loss research

Animal studies have shown that glutathione peroxidase 1 (GPx1) is highly expressed in the sensory epithelium of the inner ear, and a targeted mutation of the gene for Gpx1 was found to increase noise-induced hearing loss in mice.1 Based on these observations and given the overlapping role of oxidative stress and cellular injury in noise-induced hearing loss, Jonathan Kil and colleagues2 examined the prophylactic benefits of the administration of ebselen, a GPx1 mimic, in a randomised trial of 83 participants who were exposed to 4 h of standardised sound calibrated to cause a temporary elevation of hearing thresholds, the results of which are published in The Lancet. Decades of research on noise-exposed human beings and animals have shown that acoustic overexposure leads to hair cell damage, threshold elevation, and degraded frequency tuning.3,4 Until 2009, the general agreement was that hair cells were the primary targets of noise, and that death of cochlear neurons was secondary to hair cell degeneration.5 Indeed, hair cell loss can be detected within hours of acoustic exposure, whereas loss of spiral ganglion neurons is not detectable for years.6,7 Hence, the loss of primary auditory neurons was thought to be a delayed downstream consequence of hair cell loss.