Noise-Induced Hearing Loss (NIHL): literature review with a focus on occupational medicine

Metidieri, Mirella Melo; Rodrigues, Hugo Fernandes Santos; Filho, Francisco José Motta Barros de Oliveira; Ferraz, Daniela Pereira; Neto, Antonio Fausto de Almeida; Torres, Sandro

doi:10.7162/s1809-97772013000200015

Cited by 21 publications

(15 citation statements)

References 4 publications

(3 reference statements)

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“…NIHL is a hearing loss that experienced by many workers. Noisy exposure over 85 dB for 8 h is believed to interfere auditory organ function [9,10]. Some recent studies suggest that NIHL hearing loss is due to an increase in the production of toxic ROCs of cochlea [3,11].…”

Section: Discussionmentioning

confidence: 99%

The Association of Reactive Oxygen Species Levels on Noise Induced Hearing Loss of High Risk Workers in Dr. Soetomo General Hospital Surabaya, Indonesia

Purnami

Putri

2018

Indian J Otolaryngol Head Neck Surg

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Excessive noise exposure could increase the production of reactive oxygen species in the cochlea, thus causing the risk of noise-induced hearing loss (NIHL). Noise is commonly found in the industrial sites. However, public places like hospital also can have noisy location which risk the workers of NIHL. To analyzed the correlation of reactive oxygen species and hearing impairment to employees at risk in the hospital. Participants were obtained by identifying the employees in hospital from 3813. They were examined for baseline characteristics, hearing loss and reactive oxygen species. Hearing loss was defined as audiometry and tympanometry level. The statistical test that used in this study is Chi square test (p \ 0.05). The proportion of participant was 42.43 ± 10.72 years old in women (58.33%) and noise levels at Dr. Soetomo General Hospital was 98.15 ± 8.16 dB in range 85.39-112.90 dB. The prevalence of NIHL was 47.92% (audiometry) and 70.83% (otoacoustic emission). Reactive oxygen species estimated 5.55 ± 4.39 ng/ml. Statistical analysis of reactive oxygen species to audiometry (p = 0.993) and reactive oxygen species to otoacoustic emission (p = 0.647). Increased production of reactive oxygen species that cause hearing loss, but there was no correlation between reactive oxygen species and hearing loss in risk worker at the hospital.

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Section: Discussionmentioning

confidence: 99%

The Association of Reactive Oxygen Species Levels on Noise Induced Hearing Loss of High Risk Workers in Dr. Soetomo General Hospital Surabaya, Indonesia

Purnami

Putri

2018

Indian J Otolaryngol Head Neck Surg

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“…Rats were placed in a custom made open field sound-insulated chamber containing a 600 W High Power Horn Tweeter radiating evenly, frequency range 2–20 kHz (Maplin UK) so that both ears were exposed. Bilateral noise exposure was used as it best approximates the noise exposure that occurs in humans ( Metidieri et al, 2013 ). A pure tone of 14.8 kHz was delivered at 110 dB SPL for a total of 9 h (3 h per day over 3 consecutive days) as previously described ( Tagoe et al, 2014 ).…”

Section: Methodsmentioning

confidence: 99%

Saturation of long-term potentiation in the dorsal cochlear nucleus and its pharmacological reversal in an experimental model of tinnitus

Tagoe

Deeping

Hamann

2017

Experimental Neurology

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Animal models have demonstrated that tinnitus is a pathology of dysfunctional excitability in the central auditory system, in particular in the dorsal cochlear nucleus (DCN) of the brainstem. We used a murine model and studied whether acoustic over-exposure leading to hearing loss and tinnitus, affects long-term potentiation (LTP) at DCN multisensory synapses. Whole cell and field potential recordings were used to study the effects on release probability and synaptic plasticity, respectively in brainstem slices. Shifts in hearing threshold were quantified by auditory brainstem recordings, and gap-induced prepulse inhibition of the acoustic startle reflex was used as an index for tinnitus. An increased release probability that saturated LTP and thereby induced metaplasticity at DCN multisensory synapses, was observed 4–5 days following acoustic over-exposure. Perfusion of an NMDA receptor antagonist or decreasing extracellular calcium concentration, decreased the release probability and restored LTP following acoustic over-exposure. In vivo administration of magnesium-threonate following acoustic over-exposure restored LTP at DCN multisensory synapses, and reduced gap detection deficits observed four months following acoustic over-exposure. These observations suggest that consequences of noise-induced metaplasticity could underlie the gap detection deficits that follow acoustic over-exposure, and that early therapeutic intervention could target metaplasticity and alleviate tinnitus.

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“…People with hearing loss often have a prolonged exposure (5-20 years) to loud sounds (over 85 dBA) for several hours a day. Various levels of hearing loss can be measured through audiometric tests 2 , 3) . Exposure to noise is responsible for most cases of disability due to hearing loss 4) .…”

Section: Introductionmentioning

confidence: 99%

Noise‐Induced hearing loss among professional musicians

Pouryaghoub

Mehrdad

Pourhosein

2017

Journal of Occupational Health

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Objectives: After presbycusis, noise exposure is considered the second cause of sensorineural hearing loss. Due to exposure to high-intensity sounds, musicians may be at risk of noise-induced hearing loss (NIHL). Given the importance of good hearing in music career, this study aimed to investigate the frequency of hearing loss and use of protective measures among Iranian musicians.Methods: In this cross-sectional study, 125 musicians, including 21 women (16.8%) and 104 men (83.2%), with at least five years of work experience were recruited. All participants underwent clinical and audiometric examinations. Demographic data, complaints about hearing loss, and information about the use of protective devices were collected through interviews.Results: Audiometric notch in either one or both ears and bilateral hearing loss were present in respectively 42.4% and 19.2% of the participants. The history of tinnitus after performance and ear pain during performance was reported by 64 (51%) and 35 (28%) individuals, respectively. Less than 2% of the participants used hearing protection devices.Conclusions: Long-term exposure to loud sounds puts musicians at risk of hearing loss. However, due to their inadequate knowledge, most musicians never use protective devices to prevent damage to their auditory system.

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Noise-Induced Hearing Loss (NIHL): literature review with a focus on occupational medicine

Cited by 21 publications

References 4 publications

The Association of Reactive Oxygen Species Levels on Noise Induced Hearing Loss of High Risk Workers in Dr. Soetomo General Hospital Surabaya, Indonesia

The Association of Reactive Oxygen Species Levels on Noise Induced Hearing Loss of High Risk Workers in Dr. Soetomo General Hospital Surabaya, Indonesia

Saturation of long-term potentiation in the dorsal cochlear nucleus and its pharmacological reversal in an experimental model of tinnitus

Noise‐Induced hearing loss among professional musicians

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