Noise-induced hearing loss

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Noise-induced hearing loss (NIHL) is hearing decrease caused by loud sound. Evidences of NIHL include a history of exposure to loud sound and a hearing loss in a narrow range of frequencies, such as those from gunfire, power tools, explosions and night club music. The loud sounds result in the over-stimulation of the hearing cells leading to cell death. The two types of loss are one, intense noise incident, or gradually, over time due to exposure to noise.[1] There are certain fields in which workplaces have hazardous levels of noise. Musicians have a very acoustic "workplace," and can develop gradual NIHL through the music they constantly hear. Governmental agencies describe workplace standards to manage noise pollution and protect the hearing of workers. The best, first option for protecting hearing is lowering the volume at the source of the sound.[2] There are, however, ways to mitigate the damage after a period of potentially damaging noise. There are also options to manage hearing loss once it has occurred.

While frogs, fish, and birds with hearing loss regain their hearing naturally, humans and other mammals do not.[citation needed]


The outer ear receives sound, transmitted through the ossicles of the middle ear to the inner ear, where it is converted to a nervous signal in the cochlear and transmitted along the vestibulocochlear nerve

NIHL occurs when too much sound intensity is transmitted into and through the auditory system. An acoustic signal from an energy source, such as a radio, enters into the external auditory canal, and is funneled through to the tympanic membrane (eardrum). The tympanic membrane acts as an elastic diaphragm and drives the ossicular chain of the middle ear system into motion. Then the middle ear ossicles transfer mechanical energy to the cochlea by way of the stapes footplate hammering against the oval window of the cochlea. This hammering causes the fluid within the cochlea (perilymph and endolymph) to push against the stereocilia of the hair cells, which then transmit a signal to the central auditory system within the brain. When the ear is exposed to excessive sound levels or loud sounds over time, the overstimulation of the hair cells leads to heavy production of reactive oxygen species, leading to oxidative cell death. In animal experiments, antioxidant vitamins have been found to reduce hearing loss even when administered the day after noise exposure.[3] They were not able to fully prevent it.

Damage ranges from exhaustion of the "hair" (hearing) cells in the ear to loss of those cells[4]

NIHL is therefore the consequence of overstimulation of the hair cells and supporting structures. Structural damage to hair cells (primarily the outer hair cells) will result in hearing loss that can be characterized by an attenuation and distortion of incoming auditory stimuli.


The ear can be exposed to short periods in excess of 120 dB without permanent harm — albeit with discomfort and possibly pain; but long term exposure to sound levels over 80 dB can cause permanent hearing loss.[5]

There are two basic types of NIHL:

  • NIHL caused by acoustic trauma and
  • gradually developing NIHL.

Acoustic trauma[edit]

NIHL caused by acoustic trauma refers to permanent cochlear damage from a one-time exposure to excessive sound pressure. This form of NIHL commonly results from exposure to high-intensity sounds such as explosions, gunfire, a large drum hit loudly, and firecrackers.

Temporary and permanent hearing loss[edit]

  • PTS (Permanent Threshold Shift): the part of the hearing loss subsequent to an acoustic trauma that will never be recovered. PTS is measured in decibels.
  • TTS (Temporary Threshold Shift): the hearing loss that will be recovered after a couple of days. Also called auditory fatigue. TTS is measured in decibels too.

TTS imperceptibly gives way to PTS.[1]


In addition to hearing loss, other external symptoms of an acoustic trauma can be:

  • Tinnitus[6]
  • Some pain in the ear[7]
  • Hyperacusis[6]
  • Dizziness, vertigo; in case of vestibular damages, in the inner-ear[8]

Physiological response[edit]

The symptoms mentioned above are the external signs of the physiological response to cochlear overstimulation. Here are some elements of this response:

  • Broken and "bent" hairs of the hair-cells; damaged hair-cells degeneration. In humans, dead hair-cells are never replaced; the resulting hearing loss is thus irreparable.[9]
  • Inflammation of the exposed areas. This inflammation causes a bad blood flow in the exposed blood vessels (vascular stasis), and a bad oxygen supply for the liquid inside the cochlea (endolymphatic hypoxia)[10] Those noxious conditions worsen the damaged hair-cells degeneration.
  • Synaptic damages, by excitotoxicity. Noise overstimulation causes an excessive release of glutamate, causing the postsynaptic bouton to swell and burst. However the neuron connection can be repaired, and the hearing loss only caused by the "wiring" (i.e. excitotoxicity) can thus be recovered within 2–3 days.[11]

Gradually developing NIHL[edit]

Further information: Auditory fatigue

Gradually developing NIHL refers to permanent cochlear damage from repeated exposure to loud sounds over a period of time. Unlike NIHL from acoustic trauma, this form of NIHL does not occur from a single exposure to a high-intensity sound pressure level. Gradually developing NIHL can be caused by multiple exposures to any source of excessive volume, such as home and vehicle stereos, concerts, nightclubs, excessive noise in the workplace, and personal media players. The U.S. Department of Labor's Occupational Safety and Health Administration (OSHA) states that exposure to 85 dB(A) of noise, known as an exposure action value, for more than eight hours per day can result in permanent hearing loss.[12] Since decibels are based on a logarithmic scale, every increase of 10 decibels SPL results in a doubling of intensity, meaning hearing loss can occur at a faster rate. Therefore, gradually developing NIHL occurs from the combination of sound intensity and duration of exposure.

Characteristics of the hearing loss[edit]

Exemple of an audiogram.

Both NIHL caused by acoustic trauma and gradually-developed-NIHL can often be characterized by a specific pattern presented in audiological findings. NIHL is generally observed to affect a person's hearing sensitivity in the higher frequencies, especially at 4000 Hz. "Noise-induced impairments are usually associated with a notch-shaped high-frequency sensorineural loss that is worst at 4000 Hz, although the notch often occurs at 3000 or 6000 Hz, as well".[4] Doctoral students at the University of Iowa have termed this notch, specific to a noise-induced etiology, a "muna." The symptoms of NIHL are usually presented equally in both ears.[4]

This typical 4000 Hz notch is due to the transfer function of the ear.[9] Indeed, as any object facing a sound, the ear acts as a passive filter (-although the inner ear is not an absolute passive filter, as the outer hair cells provide active mechanisms). A passive filter is a low pass : the high frequencies are more absorbed by the object, as high frequencies impose a higher pace of compression-decompression to the object. Thus, the high frequency harmonics of a sound are more harmful to the inner-ear.

However, not all audiological results from patients with NIHL match this typical notch. Often a decline in hearing sensitivity will occur at frequencies other than at the typical 3000–6000 Hz range. Variations arise from differences in people's ear canal resonance, the frequency of the harmful acoustic signal, and the length of exposure.[13] As harmful noise exposure continues, the commonly affected frequencies will broaden and worsen in severity.[4] "NIHL usually occurs initially at high frequencies (3, 4, or 6 kHz), and then spreads to the low frequencies (0.5, 1, or 2 kHz)".[14]

Individual fragility towards noise[edit]

There appear to be large differences in individual susceptibility to NIHL.[15] The following factors have been implicated:

  • bad acoustic reflex[9]
  • damages caused by noise exposure early in life[16]
  • a bad general health state: bad cardiovascular function, insufficient intake of oxygen, a high platelet aggregation rate; and most importantly, a high viscosity of the blood[9]
  • cigarette smoking [16]
  • exposure to ototoxic chemicals (medication or chemicals that can damage the ear), including certain solvents and heavy metals[16][17]
  • type 2 diabetes [16]

No "noise training" against NIHL[edit]

The ear can not get more resistant to noise harmfulness by training it to noise.

Perceived harmfulness VS actual harmfulness[edit]

The discomfort threshold is the loudness level from which a sound starts to be felt as "too loud" by an individual. Industry workers tend to have a higher discomfort threshold (i.e. loud sounds do not ache them), but the sound is just as harmful to their ears.[18] At the contrary, industry workers often suffer from NIHL. In fact, the discomfort threshold is not a relevant indicator of the harmfulness of a sound.[18]

Middle ear muscles[edit]

The cochlea is partially protected by the acoustic reflex, but being frequently exposed to noise does not lower the reflex threshold.[18]

No outer-hair-cells sound training[edit]

Cross-section of the cochlea. The inner hair cells are connected to afferent nerve fibers, and the outer hair cells are connected to efferent nerve fibers.

The contractile effect of the outer hair cells, activated by the efferent nervous system has been proven to provide a protective effect against acoustic trauma.[19] However, we know since 2006 that this protective effect is not affected by any prior sound conditioning.[20]

Indeed, it had been observed that noise conditioning (i.e. exposure to loud non-traumatizing noise) several hours prior to the exposure to traumatizing sound level, significantly reduced the damages inflicted to the hair-cells.[21] The same “protective effect" was also observed with other stressors such as heat-shock conditioning[22] and stress (by restraint) conditioning.[23] This “protective effect" only happens if the traumatizing noise is presented within an optimum interval of time after the sound-conditioning session (-24 hours for a 15min sound-conditioning; no more protection after 48 hours[24]). This “protective effect” had long been thought to involve the active mechanisms of the outer hair cells and the efferent system commanding them;[9] but this has been proven wrong in a 2006 study.[20] This study revealed that the stressor (sound, heat, or stress) conditioning increases the receptibility to glucocorticoid, a kind of anti-inflammatory hormone. The effects of glucocorticoid thus mitigate the inflammation that results from an acoustic trauma. Indeed this inflammation may have noxious effects on the hair-cells, such as vascular stasis in exposed blood vessels.[10] In fact, high doses of corticoids are often prescribed by physicians after an acoustic-trauma[25] in order to mitigate the inflammatory response.

In simpler words, this sound (or other stressors) conditioning is nothing but a kind of pre-emptive medication against cochlea inflammation. It does not make the ear more resistant to noise. It just prevents the inflammation caused by the acoustic trauma, which would cause subsequent damages to hair cells. However, while an anti-inflammatory medication would simply increasing the quantity of anti-inflammatory hormone in the whole body, noise conditioning increases the number of receptors for the anti-inflammatory hormone, and only in the areas where it is much needed (i.e. cochlea).

Physiological response

  • stressor (noise, heat shock or stress) conditioning activates hormonal glands: the HPA axis. Note that the HPA axis is associated to the immune system[26]
  • this HPA axis activation results in the up regulation of glucocorticoid receptors (GR) in the cochlea and the paraventricular nucleus (PVN) of the hypothalamus. Note that the glucocorticoid hormone is a kind of immune-reaction-inhibitor, including the inflammation reaction.
  • This up regulation of GR thus prevents GR down regulation induced by acoustic trauma
  • The protective effect of noise-conditioning is blocked by adrenalectomy or pharmacological treatment with RU486+ metyrapone (a glucocorticoid receptor antagonist).


There is evidence that hearing loss can be minimized by taking megadoses of magnesium for a few days, starting as soon as possible after exposure to the loud noise.[27][28] A magnesium-high diet also seems to be helpful as an NIHL-preventative if taken in advance of exposure to loud noises.[29] Consuming sizable amounts of magnesium can be potentially harmful, so this treatment should be followed with caution.[30]

Researchers at the University of Michigan report that a combination of high doses of vitamins A, C, and E, and magnesium, taken one hour before noise exposure and continued as a once-daily treatment for five days, was very effective at preventing permanent noise-induced hearing loss in animals.[31]

There are currently no medical options for NIHL from noise-exposure which occurred more than a week previously. However, current research for the possible use of drug and genetic therapies look hopeful.[32]


NIHL can easily be prevented through the use of some of the most simple, widely available and economical tools. This includes but is not limited to ear protection (i.e. earplugs and earmuffs), education, and hearing conservation programs. Earplugs and earmuffs can provide the wearer with at least 5 to 10 dB SPL, and up to 20 dB, of attenuation.[4][17] However, use of earplugs is only effective if the users have been educated and use them properly.[17]

Hearing protection programs have been hindered by people not wearing the protection for various reasons, including the desire to converse, uncomfortable devices, lack of concern about the need for protection, and social pressure against wearing protection.[33] In recent years, Buy Quiet programs and initiatives have arisen in an effort to combat occupational noise exposures. These programs promote the purchase of quieter tools and equipment and encourage manufacturers to design quieter equipment.[34]

A systematic review of the effectiveness of interventions to promote the use of hearing protection devices such as earplugs and earmuffs among workers found that tailored interventions improve the average use of such devices when compared with no intervention.[35] Tailored interventions involve the use of communication or other types of interventions that are specific to an individual or a group and aim to change behavior.[35] Mixed interventions such as mailings, distribution of hearing protection devices, noise assessments, and hearing testing are also more effective in improving the use of hearing protection devices compared with hearing testing alone.[35] A 2012 Cochrane review found that education programs about hearing loss were not effective in reducing hearing loss. However, programs that increased the proportion of workers wearing hearing protection equipment did reduce overall hearing loss.[17]

In the workplace[edit]

Further information: Industrial noise

About 30 million workers are exposed to hazardous noise, with an additional 9 million exposed to solvents and metals that put them at risk for hearing loss.[36] In the United States, there are 9 million workers at risk for hearing loss due to regular exposure to sounds of 85 dB or greater.[17] Occupational hearing loss is one of the most common occupational diseases. 49% of male miners have hearing loss by the age of 50.[36] By the age of 60, this number goes up to 70%.[36] Construction workers also suffer an elevated risk. A screening program focused on construction workers employed at US Department of Energy facilities found 58% with significant abnormal hearing loss due to noise exposures at work.[37] Occupational hearing loss is present in up to 33% of workers overall.[38] Occupational exposure to noise causes 16% of adult disabling hearing loss worldwide.[17]

The following is a list of occupations that are most susceptible to hearing loss:[36]

Among musicians[edit]

Musicians, from classical orchestras to rock groups, are exposed to high decibel ranges.[39][40] Some rock musicians experience noise-induced hearing loss from their music,[41] and some studies have found that "symphonic musicians suffer from hearing impairment and that the impairment might be ascribed to symphonic music."[42]

Music-induced hearing loss is still a controversial topic for hearing researchers.[43] While some studies have shown that the risk for hearing loss increases as music exposure increases,[43] other studies found little to no correlation between the two.[43] Experts at the 2006 "Noise-Induced Hearing Loss in Children at Work and Play" Conference agreed that further research into this field was still required before making a broad generalization about music-induced hearing loss.[43]

Given the extensive research suggesting that industrial noise exposure can cause sensorineural hearing loss a link between hearing loss and music exposures of similar level and duration (to industrial noise) seems highly plausible. Determining which individuals or groups are at risk for such exposures may be a difficult task. Recent research suggests that despite concerns about the proliferation of personal music players, in fact discos, concerts and live music events may be more hazardous to youth's hearing.[44][45] People from ages to 6-19 have an approximately 15% rate of hearing loss.[38]

Workplace standards[edit]

The Occupational Safety and Health Administration (OSHA) describes standards for occupational noise exposure in articles 1910.95 and 1926.52. OSHA states that an employer must implement hearing conservation programs for employees if the noise level of the workplace is equal to or above 85 dB(A) for an averaged eight-hour time period.[4] OSHA also states that "exposure to impulsive or impact noise should not exceed 140 dB peak sound pressure level".[5] The United States Department of Defense (DoD) instruction 605512 has some differences from OSHA 1910.95 standard, for example, OSHA 1910.95 uses a 5 dB exchange rate and DoD instruction 605512 uses a 3 dB exchange rate.

There are programs that seek to increase compliance and therefore effectiveness of hearing protection rules; the programs include the use of hearing tests and educating people that loud sound is dangerous[33]

Employees are required to wear hearing protection when it is identified that their eight-hour time weighted average (TWA) is above the exposure action value of 90 dB. If subsequent monitoring shows that 85 dB is not surpassed for an eight-hour TWA, the employee is no longer required to wear hearing protection.[12]

In the European Union, directive 2003/10/EC mandates that employers shall provide hearing protection at noise levels exceeding 80 dB(A), and that hearing protection is mandatory for noise levels exceeding 85 dB(A).[46] Both values are based on 8 hours per day, with a 3 dB exchange rate.

A 2012 Cochrane review found low-quality evidence that legislation to reduce noise in the workplace was successful in reducing exposure both immediately and long-term.[17]


For people living with NIHL, there are several management options that can improve the ability to communicate. Management programs for people with NIHL include counseling and the use of hearing aids and FM systems.[clarification needed] With proper amplification and counseling, the prognosis is excellent for people with NIHL.[citation needed] The prognosis has improved with the recent advancements in digital hearing aid technology, such as directional microphones, open-fit hearing aids, and more advanced algorithms. Annual audiological evaluations are recommended to monitor any changes in a patient's hearing and to modify hearing-aid prescriptions.

See also[edit]



Organisations and awareness-raising initiatives

Noise from power sources


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External links[edit]