Individual Susceptibility to Noise-Induced Hearing loss

Henderson, Donald; Subramaniam, Malini; Boettcher, Flint A.

doi:10.1097/00003446-199306000-00002

Cited by 144 publications

(84 citation statements)

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“…Hearing losses in noise-exposed and/or aging ears are highly variable (Gates and Mills, 2005). This variability may arise from underlying differences in actual noise exposures, as well as the influence of other intrinsic and environmental variables that produce hearing loss on their own or alter NIHL vulnerability (Henderson et al, 1993). Such variables do not lend themselves easily to retrospective quantification.…”

Section: Introductionmentioning

confidence: 99%

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

Kujawa¹,

Liberman²

2006

J. Neurosci.

581

411

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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 (Ն16 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.

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Section: Introductionmentioning

confidence: 99%

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

Kujawa¹,

Liberman²

2006

J. Neurosci.

581

411

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“…In the case of the Patient Two, hearing loss was affected more severely and permanently, while the degree of hearing impairment in the Patient One was lower, with complete recovery after pharmacological treatment. Such differences might be attributed to age (greater hearing impairment with advancing age), sex (male sex more predisposed to NIHL), the source of the damaging noise or the size of any tumor [15][16][17]. Alternatively, according to Nordmann et al, the susceptibility to NIHL depends on recovery or repair processes in the cochlea, rather than the degree of the initial threshold shift [18].…”

Section: Methodsmentioning

confidence: 99%

Increased sensibility to acute acoustic and blast trauma among patients with acoustic neuroma

Mielczarek

Olszewski

2017

Int J Occup Med Environ Health

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The article shows 2 cases of unusual presentation of acute acoustic trauma and blast injury due to occupational exposure. In the case of both patients the range of impaired frequencies in pure tone audiograms was atypical for this kind of causative factor. Both patients had symmetrical hearing before the accident (which was confirmed by provided results of hearing controls during their employment). A history of noise/blast exposure, the onset of symptoms directly after harmful exposure, symmetrical hearing before the trauma documented with audiograms, directed initial diagnosis towards acoustic/blast trauma, however, of atypical course. Acute acoustic and blast trauma and coexisting acoustic neuroma (AN) contributed to, and mutually modified, the course of sudden hearing loss. In the literature there are some reports pointing to a higher sensitivity to acoustic trauma in the case of patients with AN and, on the other hand, indicating noise as one of the causative factors in AN. Int J Occup Med Environ Health 2018;31(3):361 -369

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“…Noise exposure either in short duration impulse form or continuous exposure leads to alterations in the cochlear functions especially when the sound threshold levels are more than 75-85dB. This short duration change in cochlea is reversible if further exposure is prevented and is known as temporary threshold shift (TTS) [8]. However, in continuous exposure permanent changes in cochlear function develops and …”

Section: Introductionmentioning

confidence: 99%

Alterations in Cochlear Function after Exposure to Short Term Broad Band Noise Assessed by Otoacoustic Emissions

Reddy

Khavasi

2014

JCDR

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Individual Susceptibility to Noise-Induced Hearing loss

Cited by 144 publications

References 0 publications

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

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

Increased sensibility to acute acoustic and blast trauma among patients with acoustic neuroma

Alterations in Cochlear Function after Exposure to Short Term Broad Band Noise Assessed by Otoacoustic Emissions

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