The World Health Organization estimates that nearly 360 million people have moderate to profound hearing loss from all causes.
Rates of hearing loss has traditionally been attributed to occupational or firearm-related exposure, as well as recreational exposure.
Noise-induced hearing loss (NIHL) is a hearing impairment resulting from exposure to loud sound.
People may have a loss of perception of a narrow range of frequencies or impaired perception of sound including sensitivity to sound or ringing in the ears.
Noise that occurs at work and is associated with hearing loss, it is referred to as occupational hearing loss.
Hearing may deteriorate gradually from chronic and repeated noise exposure-loud music or background noise or suddenly from exposure to impulse noise, which is a short high intensity noise such as a gunshot or airhorn.
Loud sound overstimulates delicate hearing cells, leading to the permanent injury or death of the cells.
Hearing loss in this way, cannot be restored.
Prevention strategies available to avoid or reduce hearing loss: lowering the volume of sound at its source, limiting the time of exposure and physical protection can reduce the impact of excessive noise.
If not prevented, hearing loss can be managed through assistive devices and communication strategies.
The largest burden of NIHL is through occupational exposures.
Additionally,, noise-induced hearing loss pcan also be due to unsafe recreational, residential, social and military service-related noise exposures.
It is estimated that 15% of young people are exposed to sufficient leisure noises-concerts, sporting events, daily activities, personal listening devices, to cause NIHL.
Exposure to excessively high levels from any sound source over time can cause hearing loss.
The first symptom of NIHL may be difficulty hearing a conversation against a noisy background.
The effect of hearing loss on speech perception has two components.
The first component is the loss of audibility, which may be perceived as an overall decrease in volume.
Modern hearing aids compensate this loss with amplification.
The second component is distortion or clarity loss due to selective frequency loss.
Consonants, due to their higher frequency, are typically affected first in noise induced hearing loss: the sounds “s” and “t” are often difficult to hear for those with hearing loss, affecting clarity of speech.
Noise induced hearing loss can affect either one or both ears.
Unilateral hearing loss causes problems with directional hearing, affecting the ability to localize sound.
PTS (Permanent Threshold Shift) measured in decibels is a permanent change of the hearing threshold following an event, which will never recover
TTS (Temporary Threshold Shift) is a temporary change of the hearing threshold the hearing loss that will be recovered after a few hours to couple of days. (Auditory fatigue)
TTS is measured in decibels.
In addition to hearing loss, other external symptoms of an acoustic trauma can be:
Tinnitus Otalgia Hyperacusis Dizziness or vertigo; in the case of vestibular damages, in the inner-ear
Tinnitus is described as hearing a sound when an external sound is not present.
Noise-induced hearing loss can cause high-pitched tinnitus.
An estimated 50 million Americans have some degree of tinnitus in one or both ears; 16 million of them have symptoms serious enough for them to see a doctor or hearing specialist.
As many as 2 million become so debilitated by the unrelenting ringing, hissing, chirping, clicking, whooshing or screeching, that they cannot carry out normal daily activities.
Tinnitus is the largest single category for disability claims in the military, with hearing loss a close second.
The third largest category is post-traumatic stress disorder, which itself may be accompanied by tinnitus and may exacerbate it.
NIHL has implications on quality of life that extend beyond related symptoms and the ability to hear.
2.5 of annual disability-adjusted healthy years are lost each year for every 1,000 noise-exposed U.S. workers because of hearing impairment:These lost years were shared among the 13% of workers with hearing impairment (about 130 workers out of each 1,000 workers.
The negative impacts of NIHL include the ability to reciprocate communication, to socialize and interact with society.
Hearing loss, in general, is not just an issue of volume; individuals may experience difficulty in understanding what is said over the phone, when several people are talking at once, in a large space, or when the speaker’s face cannot be seen.
Hearing loss leads to challenging social interactions can negatively lead to decreased self-esteem, shame, and fear.
Hearing loss is more acutely felt by those who experience hearing impairment or loss earlier in life, rather than later when it is more socially accepted.
Hearing loss affects psychosocial status, regardless of age, can lead to social isolation, which is known to negatively impact one’s overall health and well-being.
Hearing loss impacts can also lead to depression, especially if hearing impairment leads to tinnitus, and to greater risk for deterioration of quality of life.
Hearing impairment and loss of hearing, regardless of source or age, also limits experiencing the many benefits of sound on quality of life.
New studies suggest the effects of nature sounds, such as birds chirping and water, can positively affect an individual’s capacity to recover after being stressed or to increase cognitive focus.
Hearing loss is typically quantified by results from an audiogram; however, the degree of loss of hearing does not predict the impact on one’s quality of life.
The ear can be exposed to short periods of sound in excess of 120 dB without permanent harm.
Long term exposure to sound levels over 85 dB(A) can cause permanent hearing loss.
NIHL caused by acute 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.
Excessive noise levels in cinemas are sufficiently brief that movie-goers do not experience hearing loss.
The discomfort threshold is the loudness level from which a sound starts to be felt as too loud and thus painful by a person.
Industry workers tend to have a higher discomfort threshold (i.e. the sounds must be louder to feel painful than for non-industry workers), but the sound is just as harmful to their ears.
Industry workers often have NIHL because the discomfort threshold is not a relevant indicator of the harmfulness of a sound.
The gradual development of NIHL refers to permanent cochlear damage from repeated exposure to loud sounds over a period of time.
Gradually developing NIHL can be caused by multiple exposures to excessive noise in the workplace or any source of repetitive, frequent exposures to sounds of excessive volume, such as home and vehicle stereos, concerts, nightclubs, and personal media players.
Earplugs have been recommended for those people who regularly attend live music concerts.
It is suggested that increased exposure to loud noise through personal listening devices is a risk factor for noise induced hearing loss.
There are strong correlations between extended duration or elevated usage of personal listening devices and hearing loss.
There are associations between sound-induced hearing loss and playing video games and esports with average measured sound levels during gameplay by subjects averaging 3 hours per week exceeding or nearly exceeding permissible sound exposure levels.
About 22 million workers are exposed to hazardous noise.
Occupational hearing loss is one of the most common occupational diseases: 49% of male miners have hearing loss by the age of 50, and By age of 60, this number goes up to 70%, construction workers also have an elevated risk.
Occupational hearing loss is present in up to 33% of workers, and causes 16% of adult disabling hearing loss worldwide.
Llist of occupations that are most susceptible to hearing loss:
Agriculture Mining Police Construction Manufacturing Utilities Transportation Military Musicians Orchestra conductors
Musicians are exposed to high decibel ranges.
Some rock musicians experience noise-induced hearing loss from their music.
Symphonic musicians suffer from hearing impairment and that the impairment might be ascribed to symphonic music.
The rates of hearing disorders is lower than other occupational groups.
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.
OSHA also states that exposure to impulsive or impact noise should not exceed 140 dB peak sound pressure level.
The National Institute for Occupational Safety and Health (NIOSH) recommends that all worker exposures to noise should be controlled below a level equivalent to 85 dBA for eight hours to minimize occupational noise induced hearing loss.
Every increase by 3 dBA doubles the amount of the noise and halves the recommended amount of exposure time.
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.
Sporting event noise levels may reach 120 dB, and informal studies suggest that people may receive up to a 117% noise dose in one game.
In an attempt to a the stadium louder workers, teams, and fans may be at potential risk for damage to the auditory system.
At Monster Trucking and Stock Car racing events, spectators average noise levels ranged from 95 to 100 dBA at the Monster Truck event and over 100 dBA at the stock car racing event.
Several NASCAR drivers have complete or partial hearing loss and other symptoms from their many years of exposure.
A study of occupational and recreational noise exposure at indoor hockey arenas found noise levels from 81 dBA to 97 dBA, with peak sound pressure levels ranging from 105 dB SPLto 124 dB SPL.
In a study of noise levels at 10 intercollegiate games reachedv120dBA.
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 a sound source, enters into the external auditory canal and is funneled through to the tympanic membrane causing it to vibrate.
The vibration of the tympanic membrane drives the middle ear ossicles, the malleus, incus, and stapes to vibrate in sync with the eardrum.
The middle ear ossicles transfer mechanical energy to the cochlea by way of the stapes footplate hammering against the oval window of the cochlea, effectively amplifying the sound signal.
This hammering causes the fluid within the cochlea’s perilymph and endolymph to be displaced.
Displacement of the fluid causes movement of the hair cells which are sensory cells in the cochlea and an electrochemical signal to be sent from the auditory nerve (CN VIII) to the central auditory system within the brain to where sound is perceived.
Varied groups of hair cells are responsive to different frequencies.
Hair cells at or near the base of the cochlea are most sensitive to higher frequency sounds while those at the apex are most sensitive to lower frequency sounds.
Biological mechanisms of NIHL from excessive sound intensity: damage to the structures called stereocilia that sit atop hair cells and respond to sound, and damage to the synapses that the auditory nerve makes with hair cells, also termed hidden hearing loss.
Damaged sensory hairs, stereocilia, of the hair cells; damaged hair cells degenerate and die.
Dead hair-cells are never replaced; the resulting hearing loss is permanent.
Inflammation of the exposed areas causes poor blood flow in the exposed blood vessels and poor oxygen supply for the liquid inside the cochlea resulting in endolymphatic hypoxia.
Those noxious conditions worsen the damaged hair cell degeneration.
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 excitotoxicity can thus be recovered within 2–3 days.
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.
Antioxidants however do not seem to be effective in protecting the human ear.
Damage ranges from exhaustion of the hair hearing cells in the ear to loss of those cells.
NIHL is, therefore, the consequence of overstimulation of the hair cells and supporting structures.
The structural damage primarily the outer hair cells resulting in hearing loss that can be characterized by an attenuation and distortion of incoming auditory stimuli.
During hair cell death scarring develops, which prevent potassium rich fluid of the endolymph from mixing with the fluid on the basal domain.
The potassium rich fluid is toxic to the neuronal endings and can damage hearing of the entire ear.
If the endolymph fluid mixes with the fluid on the basal domain the neurons become depolarized, causing complete hearing loss.
The scarring that forms to replace the damaged hair cell are caused by supporting hair cells undergoing apoptosis and sealing the reticular lamina, which prevents fluid leakage.
With extreme acute acoustic trauma, a portion of the postsynaptic dendrite, where the hair cell transfers electrochemical signals to the auditory nerve, can rupture from overstimulation, temporarily stopping all transmission of auditory input to the auditory nerve (excitotoxicity).
Usually, this sort of rupture heals within about five days, resulting in functional recovery of that synapse.
While healing, an over-expression of glutamate receptors can result in temporary tinnitus, repeated ruptures at the same synapse may eventually fail to heal, leading to permanent hearing loss.
Prolonged exposure to high intensity noise has been linked to the disruption of synapses located in the synaptic cleft between inner hair cells and spiral ganglion nerve fibers, leading to a disorder referred to as cochlear synaptopathy or hidden hearing loss.
Cochlear synaptopathy disorder is cumulative and over time, leads to degeneration of the spiral ganglion cells of the inner ear and overall dysfunction in the neural transmission between auditory nerve fibers and the central auditory pathway.
The most common symptom of cochlear synaptopathy is difficulty understanding speech, especially in the presence of surrounding noise.
Cochlear synaptopathy type of hearing impairment is often undetectable by conventional pure tone audiometry (hidden hearing loss).
Acoustic over-exposure can also decrease myelination at specific points on the auditory nerve.
Myelin, surrounding nerve axons, expedites electrical impulses along nerves throughout the nervous system, and its thinning on the auditory nerve significantly slows the transmission of electrical signals from hair cell to auditory cortex, reducing comprehension of auditory stimuli by delaying auditory perception, particularly in noisy environments.
There appear to be large differences in individual susceptibility to NIHL.
Factors implicated:
missing acoustic reflex previous sensorineural hearing loss 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 cigarette smoking exposure to ototoxic chemicals including certain solvents and heavy metals type 2 diabetes
Diagnosis
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 decrease hearing sensitivity in the higher frequencies (audiometric notch) especially at 4000 Hz, but sometimes at 3000 or 6000 Hz..
The symptoms of NIHL are usually presented equally in both ears.
The high frequency harmonics of a sound are more harmful to the inner-ear.
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.
As harmful noise exposure continues, affected frequencies will broaden to lower frequencies and worsen.
NIHL can be prevented through the use of simple, widely available tools: personal noise reduction through the use of ear protection, education, and hearing conservation programs.
To prevent NIHL: turn down the volume on devices, move away from the source of noise, and wear hearing protectors in loud environments.
The WHO cites that nearly half of those affected by hearing loss could have been prevented through primary prevention efforts.
Personal noise reduction devices can be passive, active or a combination.
Passive ear protection includes earplugs or earmuffs which can block noise up to a specific frequency.
Earplugs and earmuffs can provide the wearer with 10 dB to 40 dB of attenuation.
Use of earplugs is only effective if the users have been educated and use them properly; without proper use, protection falls far below manufacturer ratings.
Workers in general industry who are exposed to noise levels above 85 dBA are required by the Occupational Safety and Health Administration (OSHA) to be in a hearing conservation program (HCP), which includes noise measurement, noise control, periodic audiometric testing, hearing protection, worker education, and record keeping.
No medication has been proven to prevent or repair NIHL in humans.
There is evidence that hearing loss can be minimized by taking high doses of magnesium for a few days, starting as soon as possible after exposure to the loud noise.
The ear can not get more resistant to noise harmfulness by training it to noise.
The cochlea is partially protected by the acoustic reflex, but being frequently exposed to noise does not lower the reflex threshold.
Noise conditioning by exposure to loud non-traumatizing noise, several hours prior to the exposure to traumatizing sound level, significantly reduces the damages inflicted to the hair-cells.
Such a 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 15 min. sound-conditioning).
This protective effect involves the active mechanisms of the outer hair cells and the efferent system commanding them.
Glucocorticoids mitigate the inflammation from an acoustic trauma that can lead to hearing loss.
Sound conditioning is a pre-emptive effort against cochlea inflammation.
It does not make the ear more resistant to noise, but reduces the inflammation caused by the acoustic trauma, which would cause subsequent damages to hair cells.
Noise conditioning increases the number of receptors for the anti-inflammatory hormone, in the cochlea.
Noise stress noise conditioning activates hormonal glands: the HPA axis.
The HPA axis is associated to the immune system.
HPA axis activation results in the up regulation of glucocorticoid receptors (GR) in the cochlea and the paraventricular nucleus (PVN) of the hypothalamus.
Treatment with a combination of prednisolone and piracetam appeared to rescue patients with acute trauma after exposure to gunshots.
Trials using antioxidants after a traumatic noise event to reduce reactive oxygen species have displayed promising results.
Injections with allopurinol, lazaroids, α-D-tocopherol, and mannitol were found to reduce the threshold shift after noise exposure.
Another antioxidant, Ebselen, has been shown to have promising results for both TTS and PTS.
A combination therapy with hyperbaric oxygen therapy (HBO) and corticosteroids has been found to be effective for acute acoustic trauma.
Acute noise exposure causes inflammation and lower oxygen supply in the inner ear.
Corticosteroids hinder the inflammatory reaction and hyperbaric oxygen therapy provides an adequate oxygen supply.
This combination therapy has been shown to be effective when initiated within three days after acoustic trauma.
No established clinical treatments exist to reverse the effects of permanent NIHL.
Many studies have been conducted looking at regeneration of hair cells in the inner ear.
Management for NIHL options include counseling, amplification, and other assisted listening devices, such as frequency modulation (FM) systems.
FM systems can enhance the use of hearing aids and overcome the effects of poor listening conditions because the signal is sent from the microphone worn by the speaker directly to the listener.
The prognosis has improved with recent advancements in digital hearing aid technology, such as directional microphones, and open-fit hearing aids.
Hearing aids can mask or cover up the tinnitus, and many with hearing loss and tinnitus find relief by using hearing aids.
The use of hearing aids to increase quality of life.
The World Health Organization estimated in 2015 that 1.1 billion young people are at risk for hearing loss caused by unsafe listening practices.
The over-exposure to excessive loud noise is partially attributed to recreational exposure, such as the use of personal audio devices with music at high volumes for long durations, or social settings such as bars, entertainment and sporting events.
Occupational noise exposure is the main risk factor for work-related hearing loss.
Audiometric records show that about 33% of working-age adults with a history of occupational noise exposure have evidence of noise-induced hearing damage, and 16% of noise-exposed workers have material hearing impairment.