Noise-induced hearing loss

About: Noise-induced hearing loss is a research topic. Over the lifetime, 2202 publications have been published within this topic receiving 44816 citations. The topic is also known as: noise induced hearing loss & NIHL.

Adding Insult to Injury: Cochlear Nerve Degeneration after “Temporary” Noise-Induced Hearing Loss

Abstract: Overexposure to intense sound can cause temporary or permanent hearing loss. Postexposure recovery of threshold sensitivity has been assumed to indicate reversal of damage to delicate mechano-sensory and neural structures of the inner ear and no persistent or delayed consequences for auditory function. Here, we show, using cochlear functional assays and confocal imaging of the inner ear in mouse, that acoustic overexposures causing moderate, but completely reversible, threshold elevation leave cochlear sensory cells intact, but cause acute loss of afferent nerve terminals and delayed degeneration of the cochlear nerve. Results suggest that noise-induced damage to the ear has progressive consequences that are considerably more widespread than are revealed by conventional threshold testing. This primary neurodegeneration should add to difficulties hearing in noisy environments, and could contribute to tinnitus, hyperacusis, and other perceptual anomalies commonly associated with inner ear damage.

The global burden of occupational noise-induced hearing loss.

Abstract: Background Excessive noise is a global occupational health hazard with considerable social and physiological impacts, including noise-induced hearing loss (NIHL). This paper describes the worldwide morbidity of occupational NIHL in the year 2000. Methods The proportion of the population exposed to occupational noise was estimated using noise exposure data from the US National Institute for Occupational Safety and Health (NIOSH), adjusted by data on the distribution of the work force by occupational category and economic sector, and economic activity rates in each WHO subregion. These values for the exposed population and risk measures for NIHL were used to develop estimates of the attributable fraction (AF) of adult-onset hearing loss resulting from occupational noise exposure. The AFs were applied to WHO estimates of total disability-adjusted life years (DALYs) from adult-onset hearing loss to estimate the DALYs due to occupational noise. Results Worldwide, 16% of the disabling hearing loss in adults (over 4 million DALYs) is attributed to occupational noise, ranging from 7% to 21% in the various subregions. The effects of the exposure to occupational noise are larger for males than females in all subregions and higher in the developing regions. Conclusions Occupational noise is a significant cause of adult-onset hearing loss. The majority of this NIHL burden can be minimized by the use of engineering controls to reduce the generation of noise at its source. Am. J. Ind. Med. 48:446–458, 2005. © 2005 Wiley-Liss, Inc.

Noise-induced hearing loss.

Abstract: Hearing loss caused by exposure to recreational and occupational noise results in devastating disability that is virtually 100 percent preventable. Noise-induced hearing loss is the second most common form of sensorineural hearing deficit, after presbycusis (age-related hearing loss). Shearing forces caused by any sound have an impact on the stereocilia of the hair cells of the basilar membrane of the cochlea; when excessive, these forces can cause cell death. Avoiding noise exposure stops further progression of the damage. Noise-induced hearing loss can be prevented by avoiding excessive noise and using hearing protection such as earplugs and earmuffs. Patients who have been exposed to excessive noise should be screened. When hearing loss is suspected, a thorough history, physical examination and audiometry should be performed. If these examinations disclose evidence of hearing loss, referral for full audiologic evaluation is recommended.

Noise-induced cochlear neuropathy is selective for fibers with low spontaneous rates

Abstract: Acoustic overexposure can cause a permanent loss of auditory nerve fibers without destroying cochlear sensory cells, despite complete recovery of cochlear thresholds (Kujawa and Liberman 2009), as measured by gross neural potentials such as the auditory brainstem response (ABR). To address this nominal paradox, we recorded responses from single auditory nerve fibers in guinea pigs exposed to this type of neuropathic noise (4- to 8-kHz octave band at 106 dB SPL for 2 h). Two weeks postexposure, ABR thresholds had recovered to normal, while suprathreshold ABR amplitudes were reduced. Both thresholds and amplitudes of distortion-product otoacoustic emissions fully recovered, suggesting recovery of hair cell function. Loss of up to 30% of auditory-nerve synapses on inner hair cells was confirmed by confocal analysis of the cochlear sensory epithelium immunostained for pre- and postsynaptic markers. In single fiber recordings, at 2 wk postexposure, frequency tuning, dynamic range, postonset adaptation, first-spike latency and its variance, and other basic properties of auditory nerve response were all completely normal in the remaining fibers. The only physiological abnormality was a change in population statistics suggesting a selective loss of fibers with low- and medium-spontaneous rates. Selective loss of these high-threshold fibers would explain how ABR thresholds can recover despite such significant noise-induced neuropathy. A selective loss of high-threshold fibers may contribute to the problems of hearing in noisy environments that characterize the aging auditory system.

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Abstract: Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age–noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8–16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4–124 weeks) and held with unexposed cohorts for different postexposure times (2–96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4–8 weeks) were 40–50 dB; older-exposed animals (≥16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.