eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Inner Ear

Inner Ear, Noise-Induced Hearing Loss

Neeraj N Mathur, MBBS, MS, Professor, Department of Ear, Nose and Throat, Lady Hardinge Medical College and Associated Smt SK and Kalawati, Saran Children's Hospital, University of Delhi, India; Professor and Head, Department of Ear, Nose and Throat, BP Koirala Institute of Health Sciences, Nepal
Peter S Roland, MD, Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director of Clinical Center for Auditory, Vestibular and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Adjunct Professor of Communicative Disorders, University of Texas School of Human Development

Updated: Jul 16, 2009

Introduction

Background

Environmental noise is a common and preventable cause of hearing loss in industrialized societies. Hearing loss that is caused by the noise exposure due to recreational or nonoccupational activities is termed socioacusis. Hearing loss due to injurious noise at workplace is referred to as occupational noise-induced hearing loss (ONIHL). The term acoustic trauma means the hearing loss due to single exposure to intense sound.

ONIHL is a more common cause of noise-induced hearing loss (NIHL) and much more serious problem than socioacusis for the following 2 reasons: (1) The threat of loss of employment may convince people to remain in environments with noise levels higher than they would otherwise accept, and (2) in the workplace, high levels of noise may be sustained on a regular basis for many hours each day over many years. Consequently, occupational noise exposure has drawn the most attention and is the best studied.

Controversy exists regarding what percentage of age-related hearing loss (presbycusis) is a consequence of a lifetime socioacusis and what percentage is solely due to the physiologic aging process.

Sustained exposure to loud noise is associated with adverse consequences other than hearing loss. For instance, sustained exposure to unwanted loud noise is annoying. Homberg has noted that unwanted noise at any level is annoying; at 72 dB, 100% of subjects rated unwanted noise as either "somewhat annoying" or "rather annoying." Even with hearing protection, Melamed reported that 60% of workers rated high levels of unwanted background noise as "highly annoying."¹

Dornie and Laakssonen have investigated the impact of the annoying quality of noise exposure. The annoying quality of loud noise may serve as a warning that it is adversely affecting health, ie, injuring the auditory system. Moreover, the annoying quality of noise reduces processing capacity, thereby increasing the cost of performing a given task. Bhatia reported that individuals who are sensitive to noise show decreased efficacy on multiplication tasks in the presence of unwanted background noise.

Melamed et al have also shown that chronic noise exposure increases fatigue symptoms and postwork irritability.¹ They found that, after the workday was over, these fatigue symptoms and postwork irritability made relaxing and being able to unwind extremely difficult. Noise protection that attenuated the unwanted background noise by 30-33 dB for 7 days produced significant improvement in irritability and fatigue symptoms. Furthermore, urinary cortisol secretion was shown to increase with unwanted background noise. The increased urinary cortisol levels decreased toward normal after 7 days of noise attenuation.

Simply measuring the physical intensity of the stimulus as a sound pressure level cannot assess the potentially damaging effect of noise. The human ear does not respond equally to all frequencies—high frequencies are much more damaging than low frequencies at the same physical intensity levels. Consequently, most sound level meters are equipped with a filter that is designed to de-emphasize the physical contribution from frequencies to which the human ear is less sensitive. This filter is referred to as the A filter, and measurements taken using the A filter are reported as dBA. This is known as the A level on a sound pressure meter.

Pathophysiology

When animals exposed to impulse noise are examined, anatomic changes that range from distorted stereocilia of the inner and outer hair cells to complete absence of the organ of Corti and rupture of the Reissner membrane are found. Generally, no changes are found in the blood vessels, spiral ligament, or limbus. A few minutes after exposure to impulse noise, edema of the stria vascularis appears and may persist for several days.

A cochlear inflammatory response is also initiated in response to acoustic trauma and involves the recruitment of circulating leukocytes to the inner ear.²

Outer hair cells are more susceptible to noise exposure than inner hair cells. Temporary threshold shifts (TTS; see History) are anatomically correlated with decreased stiffness of the stereocilia of outer hair cells. The stereocilia become disarrayed and floppy. Presumably, in such a state they respond poorly. At a minimum, permanent threshold shifts (PTS; see History) are associated with fusion of adjacent stereocilia and loss of stereocilia. With more severe exposure, injury can proceed from a loss of adjacent supporting cells to complete disruption of the organ of Corti. Histopathologically, the primary site of injury appears to be the rootlets that connect the stereocilia to the top of the hair cell. With loss of stereocilia, hair cells die. Death of the sensory cell can lead to progressive Wallerian degeneration and loss of primary auditory nerve fibers.

NIHL and hair cell loss are known to show only moderate correlation because NIHL may reflect not only the sum of dead hair cells but also impaired, but still living, hair cells. High-frequency hair cells in rat cochlea may die relatively rapidly after injury, indicating a linear relation between them, but the low-frequency hair cells may survive without auditory function.

Two general theories have been advanced to account for the mechanism of injury. NIHL from constant noise exposure may be secondary to accumulated microtrauma and have a similar mechanism to injury produced from impulse noise. On the other hand, TTS may be due to metabolic exhaustion. Consequently, TTS is sometimes referred as auditory fatigue. Metabolic exhaustion sustained for prolonged periods may be so profound as to result in cell death. The concept of auditory fatigue as an explanation for TTS (with an opportunity for recovery if the noxious acoustic stimulus is removed) may account for the well-described clinical fact that intermittent noise is much less likely to produce permanent injury than continuous noise at the same intensity level.

Apoptosis (programmed cell death) was observed in noise-exposed cochlea.⁴³ An Src–protein tyrosine kinase (PTK) signaling cascade may be involved in both the metabolic and mechanically induced initiation of apoptosis in the sensory cells of cochlea. They may also be activated in outer hair cells following noise exposure. This knowledge, obtained from studies on chinchillas, has led to trials with Src-PTK inhibitors such as KXI-004, KXI-005, and KXI-174 by placing them on round window membrane and noting its beneficial effect in the prevention of NIHL. This may eventually lead to the development of more effective drugs for the prevention of NIHL.

A study on the fate of outer hair cells after acoustic or ototoxic insults showed that outer hair cell remains are phagocytosed by supporting cells within the epithelium.³

Evidence is available to support both the theory of metabolic exhaustion and the theory of mechanical trauma. Experimental animal studies have shown decreased endolymphatic oxygen tension directly related to the duration of intensity of noise exposure. Decreases in succinic dehydrogenase and glycogen content have been observed. However, mechanical models are more compatible with the observation that the greatest area of injury in occupational NIHL appears to be to that portion of a cochlea sensitive to frequencies of about 4000 cycles per second (Hz).

Recent work has clearly demonstrated the presence of glucocorticoid signaling pathways in the cochlea and their protective roles against noise-induced hearing loss. Therefore, taking advantage of current molecular and pharmacological tools to dissect the role of GC signaling in hearing loss is important.⁴

A gene association study for NIHL in 2 independent noise-exposed populations revealed that PCDH15 and MYH14 may be NIHL susceptibility genes, but further replication in independent sample sets is mandatory.⁵

The equal energy hypothesis assumed that hearing damage is a function of total acoustic energy received. That the hearing organ reacts uniformly to sounds of various intensities and duration, provided that the total sound energy remains constant, is an oversimplification and does not explain noise-induced hearing damage. A study by Pourbakht et al found that, although the total energy of intermittent sound of 125 dB noise was greater than that of continuous 115 dB sound pressure level, the latter was found to cause significantly greater PTS and hair cell loss.⁶

Much acoustic trauma is caused by impulse noise, which is usually due to blast effect and the rapid expansion of gases. Acoustic trauma is often the consequence of an explosion. Impact noise results from the collision of metals. It is highly reverberant, has both peaks and valleys, and is less likely to reach critical levels. Impact noise is more likely to be seen in the context of occupational noise exposure. It is frequency superimposed on a background of more sustained noise. Boettcher has shown that when impact noise is superimposed on continuous noise, the injurious potential is synergistically enhanced.

Animals with large PTS from an initial noise exposure showed less PTS following second noise exposure at a specific intensity compared with animals with little or no previous NIHL, indicating that these animals are less sensitive to subsequent noise exposures. However, total PTS in these ears is higher. This suggests that the major factor responsible for these results is lower effective intensity of the second noise for the ears with large initial PTS.

Other physiologic conditions that affect the likelihood and progression of NIHL have been identified. Evidence appears in the literature that decreased body temperature, increased oxygen tension, decreased free radical formation, and removal of the thyroid gland can all lessen an individual's sensitivity to NIHL. Hypoxia potentiates the noise-induced damages. Good experimental evidence shows that sustained exposure to moderately high levels of noise can reduce an individual's sensitivity to NIHL at higher levels of noise. This process is referred to as sound conditioning. It is at least superficially analogous to the protective effect a deliberate training regimen has for severe physical activity.

Frequency

United States

According to the Occupational Health and Safety Administration (OSHA), 5-10 million Americans are at risk for noise-induced hearing loss (NIHL) because they are exposed to sounds louder than 85 dBA on a sustained basis in the workplace. Forty-eight million Americans engage in shooting sports, the most common cause of nonoccupational NIHL (socioacusis). Dobie reports that 1.8% of American males have handicapping NIHL.⁷

Sex

More males than females are reported to have noise-induced hearing loss (NIHL). However, whether this is a consequence of greater sensitivity to NIHL in the workplace or whether it represents a higher level of exposure to nonoccupational noise is unclear.

Age

No clear-cut differences exist between young and older individuals in their susceptibility to noise-induced hearing loss (NIHL).

Clinical

History

• Noise-induced hearing loss (NIHL) develops slowly after many years of exposure. Susceptibility varies quite widely, but 10 years or more of exposure is generally required for significant hearing loss to occur. In 1990, Dobie listed criteria for the diagnosis of occupation noise-induced hearing loss (ONIHL), as follows:⁸
  • ONIHL is always a neurosensory loss.
  • ONIHL is almost always bilateral.
  • High-frequency losses rarely exceed 75 dB, and low-frequency losses rarely exceed 40 dB.
  • Hearing loss does not progress after noise exposure is discontinued.
  • As hearing loss progresses, the rate of hearing loss decreases.
  • Loss is always greater at the frequencies 3000-6000 Hz than at 500-2000 Hz. Loss is usually greatest at 4000 Hz. The 4000-Hz notch is often preserved even in advanced stages.
  • In stable exposure conditions, losses at 3000, 4000, and 6000 Hz usually reach a maximum level in 10-15 years.
• When hearing loss is limited to the high frequencies, individuals are unlikely to have difficulty in quiet conversational situations. The first difficulty the patient usually notices is trouble understanding speech when a high level of ambient background noise is present. As NIHL progresses, individuals may have difficulty understanding high-pitched voices (eg, women's, children's) even in quiet conversational situations. Conversation on the telephone is generally unimpaired because telephones do not use frequencies above 3000 Hz.
• The aforementioned symptoms are nonspecific symptoms of high-frequency neurosensory hearing loss and do not help to distinguish among etiologies. Consequently, clinical presentation is of no use in distinguishing NIHL from early ototoxicity, genetically mediated progressive losses, or presbycusis.
• Clinically, NIHL begins with a temporary threshold shift (TTS). A TTS is defined by Dobie as a temporary neurosensory hearing loss that recovers almost completely once the noxious stimulus is removed. The amount of time over which recovery occurs is unclear and controversial. Sixteen hours has been used in the past, but some people with TTS require longer periods to recover. Dobie uses a 24-hour threshold; however, some argue that days or months may be required to recover TTS, especially if the case is associated with acoustic trauma. Nonetheless, as a practical matter, Dobie's time limit of 24 hours is commonly used.
• The extent of a TTS is predictable on the basis of the causative noise's intensity, frequency, content, and temporal pattern of exposure (ie, intermittent or continuous). Pure-tone and narrow-band stimuli result in a maximum TTS at or slightly above the center frequency of the noise producing it. However, in occupational situations, TTSs are almost always greatest between 3000-6000 Hz and are often quite narrowly focused at 4000 Hz.
• High-frequency noise is much more damaging than low-frequency noise; therefore, intensity alone cannot predict risk. For this reason, a special scale has been developed for measuring environmental noise when the purpose is to assess its potential to produce hearing loss.
• Continuous stimuli are more damaging than interrupted stimuli. Intermittent noise is more protective for apical lesions induced by low frequencies than for basal lesions induced by high frequencies.
• A clinically important feature of TTS is that it is rarely apparent to the subject because of its relatively low magnitude and relatively high frequency. Repeated TTSs over weeks, months, and years fail to recover completely and thereby become a permanent threshold shift (PTS).
• ONIHL begins with selective loss of hearing at around 4000 Hz. Thresholds are better at both higher and lower frequencies. This is recognized on an audiogram as a notch centered around 4000 Hz and, although not pathognomonic, it is the characteristic audiometric pattern of early NIHL. If exposure is continued, the notch gradually deepens and widens. Eventually, retention of good hearing in the higher frequencies is lost, and the resulting hearing loss appears only as a relatively steep high-frequency loss beginning at 3000 Hz and becoming more severe at each higher frequency over a period of many years. Persistent noise exposure progressively encroaches on the middle frequencies. In the most severe cases, even the lower frequencies may eventually become involved.
• Many patients experience tinnitus associated with both TTS and PTS. Individuals who reliably have ringing in their ears after noise exposure probably have experienced an injury to the auditory system in the form of at least a TTS. Because repeated TTS slowly converts to PTS, postexposure tinnitus and TTS serve as warning signs of impending permanent NIHL.
• Evidence is strong that a significant amount of individual variability exists with respect to susceptibility to NIHL. The auditory system of some individuals seems to be able to withstand longer exposure times to higher loudness levels than the auditory system of others. Thus, norms established for hearing conservation programs, although protecting the group as whole, may not protect the most sensitive individuals. The symptoms of individuals with postexposure tinnitus or hearing loss should be taken seriously. Audiograms immediately after exposure and again 24 hours later should be attained to establish the presence or absence of TTS or PTS. From time to time, such testing may need to be repeated on several occasions.
• The 4-kHZ notch appears to be a consequence of several factors: (1) the fact that human hearing is more sensitive at 1-5 kHz, (2) the fact that the acoustic reflex attenuates loud noises below 2 kHz (as demonstrated by Borg), and (3) nonlinear middle ear function as a result of increased intensities.
• NIHL, especially ONIHL, is generally symmetrical. Occasionally, a work environment results in asymmetrical noise exposure, as seen in tractor drivers with ONIHL in which the left ear is more frequently affected than the right ear. As tractor operators have to monitor equipment mounted on the rear side, most operators look over their right shoulder, exposing their left ear to the noise of the prime mover and exhaust while their right ear is shielded by head shadow.
  • However, work environments, especially indoor environments, have sufficient reverberation so as to produce essentially equal stimulation of both ears.
  • The most common cause of asymmetric NIHL is exposure to firearms, particularly long guns. Right-handed shooters have a more severe hearing loss in the left ear because the left ear faces the barrel while the right ear is tucked into the shoulder and is in the acoustic shadow of the head.

Physical

The physical examination is not important in the evaluation of noise-induced hearing loss (NIHL) except to rule out other causes. The physical examination should include evaluation of the tympanic membranes and external auditory canals. A neurologic examination should be performed to rule out neurologic diseases.

Causes

Noise-induced hearing loss (NIHL) is caused by high levels of ambient noise. OSHA has determined that exposure to loudness levels lower than 85 dBA continuously for an 8-hour workday is unlikely to cause harm. However, sensitive individuals may experience hearing loss even at this or slightly lower levels.

• Experimental data suggest that when exposure is continuous, injury is a consequence of the total amount of energy to which cochlear tissues are exposed. Thus, if sound energy is doubled, the risk of injury can be kept constant if the exposure time is cut roughly in half. Because each 3 dB of loudness increase represents a doubling of sound energy, the amount of damage expected from 8 hours of exposure to 100 dB should be about the same as the amount of damage sustained from 4 hours of exposure to 105 dB. However, this relationship applies only when exposure is constant. Even relatively brief interruptions significantly decrease the amount of damage that is to be expected.
• Moreover, this trade-off between intensity and duration becomes meaningless once the elastic limit of inner ear tissue is exceeded. At this point, rules governing impulse noise come into play. The point at which this occurs in humans is unclear. Available data suggest that brief exposure to relatively high-intensity impulse noise produces less damage than expected from extrapolating the intensity-duration curves established for steady-state noise. For example, young healthy air force personnel exposed for 0.4 seconds to a noise of 153 dB suffered only very slight TTS, much less damage than would have been expected from data obtained from continuous-exposure studies.
• Causative acoustic stimuli can be divided into continuous and intermittent stimuli, which are usually associated with classic NIHL. Intermittent noise is defined as loudness levels that fluctuate more than 20 dBA.
• Acoustic trauma is an extremely loud noise usually resulting in immediate, permanent hearing loss. Such transient noise stimuli are generally less than 0.2 seconds in duration. The 2 types of transient noises are impulse noise, which is usually the result of an explosion, and impact noise, which results from a collision (usually metal on metal). Impact noises are often associated with echoes and reverberations, which produce acoustic peaks and troughs.
• Assessing the degree of noise exposure an individual experiences can be extremely difficult. In most working environments, noise is not continuously sustained and is therefore intermittent. Moreover, many individuals are mobile and move through noise environments of different intensities for various periods during the workday. The American National Standards Institute (ANSI) and the International Organization for Standards (ISO) have set detailed standards for measuring environmental noise.
• Overall, the degree of NIHL is influenced by the following:
  • Intensity of the noise (dBA)
  • The temporal pattern of the noise (continuous, intermittent, transient)
  • The spectral pattern of the noise (frequency content)
  • The duration of exposure to the noise (time weighted average [TWA])
  • Individual susceptibility to the noise
• Continuous exposure to 100 dBA can be expected to produce, on average, the following levels of hearing loss:
  • Five years, 5 dB
  • Twenty years, 14 dB
  • Forty years, 19 dB
• Various nonoccupational noises can produce hearing loss. However, these exposures generally produce minor losses because the exposure times are short. These include the following:
  • Leaf blowers
  • Lawn mowers
  • Chain saws
  • Rock concerts
  • Jet noise
  • Private aircraft
  • Snowmobiles
  • Jet skis
  • Motorcycles
• A study of impulse noise in soldiers exposed to weapon-related noise levels (1.6-16 kHz) found that, after their military service, the soldiers' hearing had significantly deteriorated (an average of 6 dB exclusively at 10 and 12 kHz). Transiently evoked otoacoustic emission (TEOAE) reduction was registered predominantly at 2, 3, and 4 kHz, with greatest decrease at 2 kHz (P <0.02). Reduced TEOAE levels in soldiers exposed to noise may be the first sign of potential hearing loss.
• Although portable radios and cassette, CD, or MP3 players are capable of producing loudness levels greater than 85 dB, they are not commonly adjusted to such high levels, even by adolescents; when they are, exposure times are generally short compared with an 8-hour workday. Dobie has noted an exception to this observation. When portable cassette players are used in the workplace, exposure from the cassette player may be added to the workplace noise and increase the potential for injury.
• Most nonoccupational NIHL is the result of firearm noise. Firearms can produce noise levels of up to 170 dB. Men who had a quiet work environment and engaged in shooting sports had, on average, hearing loss equivalent to that of individuals who had worked for 20 years in a factory with an 89-dBA noise level.

Differential Diagnoses

Inner Ear, Autoimmune Disease
Inner Ear, Genetic Sensorineural Hearing Loss
Inner Ear, Ototoxicity
Inner Ear, Presbycusis
Inner Ear, Sudden Hearing Loss
Middle Ear, Otosclerosis

Workup

Laboratory Studies

No laboratory studies are appropriate in the evaluation of noise-induced hearing loss (NIHL).

Imaging Studies

No imaging studies are appropriate for the study of noise-induced hearing loss (NIHL).

Other Tests

• Audiometric testing is the only diagnostic evaluation relevant to diagnosis of noise-induced hearing loss (NIHL).
  • Pure-tone audiometry at the usual octave intervals should be performed. The interoctave interval of 3000 Hz should always be included as well; 3000 Hz is a sensitive area for NIHL and is a frequency that contributes significantly to speech understanding. The American Medical Association (AMA) guidelines for determining hearing handicap require the amount of hearing loss at 3000 Hz to be included in the calculation.
  • The speech reception threshold (SRT) should also be measured for each ear. Differences between the pure tone average (PTA) (ie, the number of dB of hearing loss at 500, 1000, and 2000 Hz averaged) and the SRT of more than 5-10 dB should bring into question the reliability of the test. Discrimination scored below 60% suggests an etiology other than NIHL.
  • Screening audiometry is performed as part of hearing conservation programs (see Deterrence/Prevention).
  • Because NIHL is compensatable, pseudohypoacusis is more frequently a diagnostic issue when testing patients with alleged NIHL than in many other circumstances. Care should be taken to ensure that accurate, reliable, and repeatable responses are being obtained.
  • A high incidence of exaggerated hearing loss has been found in individuals claiming NIHL as a result of impulse noise. Objective tests of hearing threshold have been used to obtain accurate hearing thresholds in individuals suspected of exaggerating their hearing loss. Cortical evoked response audiometry (CERA) is the most valuable objective test for the following reasons:
    • It has good frequency specificity over the speech frequency range (ie, 500-4000 Hz).
    • It is noninvasive and requires only passive cooperation.
    • It is recorded from a higher auditory level than electrocochleography (ECochG) or brainstem electric response audiometry (BERA) and, therefore, is less subject to organic neurologic disorders.
    • It has a closer correlation with behavioral audiometry thresholds than BERA. CERA must be done in such individuals, especially in the presence of flat audiograms and hearing thresholds of more than 25 dB at 500 Hz.
• Sound level meters are able to evaluate 3 time-averaging characteristics: fast, slow, and peak. The slow setting should be used when measuring sound intensity for purposes of assessing occupational noises.
• OSHA standard for the maximum sound intensity (A level, slow) tolerable over certain lengths of time is listed below. These levels are referred to as the permissible exposure level (PEL).
  • Duration of 16 hours, 85 dBA
  • Duration of 8 hours, 90 dBA
  • Duration of 6 hours, 92 dBA
  • Duration of 4 hours, 95 dBA
  • Duration of 3 hours, 97 dBA
  • Duration of 2 hours, 100 dBA
  • Duration of 1.5 hours, 102 dBA
  • Duration of 1.0 hour, 105 dBA
  • Duration of 30 minutes, 110 dBA
  • Duration of 15 minutes, 115 dBA
• In the jargon of hearing conservation, "the PEL for 4 hours per day is 95 dBA." The reduction in permissible exposure time as the loudness level increases is intended to equalize the risks of NIHL. Consequently, 4 hours of exposure at 95 dB is deemed an equivalent time weighted average (TWA) exposure to 90 dBA for 8 hours.
• The exposure limits set by OSHA have been empirically derived by using both epidemiologic and laboratory data. The standards are believed to be reasonably protective, and the American Academy of Otolaryngology-Head and Neck Surgery has asserted that if exposure to occupational noise did not exceed a TWA of 85 dBA or a dose of 50%, exposure to occupational noise should be excluded as the cause of hearing loss.
• Two methods are used to assess exposure: the amount of noise in a given area can be systemically surveyed, or personal noise dosimetry can be performed.
  • Noise surveys are performed by placing a sound level meter in an area and measuring the loudness level in that location over an 8-hour day.
  • Personal dosimetry is performed by having an individual wear a microphone on the shoulder, approximately 5 inches lateral to the ear. Sophisticated computerized programs are then able to assess the amount of noise exposure that individual receives during the working day. The data obtained must be interpreted with the understanding that reflection of sound off the body adds about 2 dB to the exposure assessment, that bumping or touching the surface microphone increases the dosage measurement, and that the dosimeter is not in the control of the assessing professional.

Treatment

Medical Care

No well-recognized and scientifically validated treatments are specifically directed to noise-induced hearing loss (NIHL). The following treatable conditions have been alleged to exacerbate NIHL by some authors, and appropriate management of these considerations might influence the development or progression of NIHL.

• Smoking
• Cardiovascular disease
• Diabetes mellitus
• Hyperlipidemia
• Exposure to ototoxic drugs

If initiated early, medical treatment could have a role in acute acoustic trauma. Animal studies have shown that a combination of hyperbaric oxygenation and corticoid therapies lead to significant improvement in recovery; however, either of these if given alone may not be effective.⁹

In an interesting German study on patients with acoustic trauma, intratympanic administration of a cell-permeable JNK ligand was used because it had shown to prevent hearing loss after acute acoustic trauma in animal models.

For the first application of AM-111 in humans, a clinical phase I/II trial in patients was organized in patients with acute acoustic trauma after exposure to firecrackers in Berlin and Munich on New Year's Eve 2005/2006. Functional and morphological analysis of the treated ears revealed that AM-111 had an excellent otoprotective effect, even when administered hours after the noise exposure. Blocking the signal pathway with D-JNKI-1 is therefore a promising way to protect the morphological integrity and physiological function of the inner ear in various conditions involving acute sensorineural hearing loss.

This trial included 11 randomly selected patients on whom intratympanic treatment with AM-111 at a concentration of 0.4 mg/ml or 2 mg/ml within 24 h after noise exposure was performed. Pure-tone audiometry and otoacoustic emissions were assessed before treatment and on days 3 and 30 thereafter. Based on this clinical experience and on a calculation using an empirically derived exponential hearing recovery function, AM-111 seems to have had a therapeutic effect. A total of 13 adverse events were reported in 5 study participants. None of the adverse events were serious or severe.¹⁰

Surgical Care

Future treatment options

An animal study found that when neural stem cells (cNSCs) were injected into the scala tympani of sound-damaged mice and guinea pigs, and the animals were allowed to recover for up to 6 weeks, some of the cNSCs migrated throughout the cochlea and demonstrated morphological, protein, and genetic characteristics of neural cochlear tissue (eg, spiral ganglion neurons, satellite cells, Schwann cells) and cells of the organ of Corti (pillar cells, supporting cells, and hair cells).¹¹ This suggests that neural stem cell line may derive some information needed from the microenvironment of the cochlea to differentiate into replacement cells in the cochlea. This could help in future treatment development and entirely change the management of hearing loss resulting from damage to these cells.

Follow-up

Deterrence/Prevention

• Oxidative stress plays a substantial role in the genesis of noise-induced cochlear injury that causes permanent hearing loss.
• In adults with healthy audiograms, ear vulnerability to noise can be elicited and predicted by the use of objective DPOAE measurements. DPOAEs rely on the contractile properties of the outer hair cells. In response to tonal sound stimuli, these cells can generate retrograde wave sounds, the intensity of which can be captured and recorded by a very sensitive probe microphone in the external auditory canal. Any subclinical dysfunction of the middle ear or cochlea outer hair cells could slightly reduce DPOAEs and could influence the hearing performance in individuals exposed to noise and thus finding reduced DPOAEs in individuals with otherwise healthy pure-tone audiograms could be used in identifying them for their increased vulnerability to noise-induced hearing loss.¹²
• In chinchillas, noise-induced cochlear oxidative stress (NICOS) can be reduced by the following means:
  • Acetyl-L-carnitine (ALCAR) is an endogenous mitochondrial membrane compound that helps maintain mitochondrial bioenergetics and biogenesis in the face of oxidative stress.
  • Carbamathione is a glutamate antagonist.
  • D-methionine (MET) can enhance cellular reduced glutathione (GSH) levels (ie, improve cochlear GSH deficiency state).
• MET’s otoprotective action has a documented role, in a variety of species, against a variety of ototoxic insults including cisplatin-, carboplatin-, aminoglycoside- and noise-induced auditory threshold elevations and cochlear hair cell loss. Also MET can rescue individuals from permanent noise-induced hearing loss when MET is initiated 1 h after noise exposure.¹³
• The studies reveal the potential for the use of NAC in a clinical population exposed to noise.¹⁴ However, as seen experimentally in chinchillas, l-NAC treatments (N -acetyl-l-cysteine) designed to reduce or prevent NIHL has a limited effectiveness. Long-duration exposures at levels that lead to PTS in excess of 50 dB or more with severe loss of OHCs and IHCs in the basal half of the cochlea may lead to the chronic production of excessively high levels of ROS or other free radicals that not only overwhelm the cells endogenous defense mechanisms but also the ability of antioxidant drugs to combat the ROS assault.¹⁵
• In an animal study on guinea pigs, alpha tocopherol has been found to significantly decrease noise-induced auditory brainstem response threshold shifts and attenuate noise-induced outer hair cell stereocilia loss. This also supports the notion that reactive oxygen species (ROS) is involved in metabolic damage of the organ of Corti.
• In a study of guinea pigs, direct infusion of dexamethasone into the perilymphatic space was observed to have a protective effect against noise-induced trauma.
• Deterrence is the only accepted management method for NIHL. OSHA requires hearing conservation programs if noise exposures in the workplace exceed 85 dBA. The Walsh-Haley noise standard requires that engineering or administrative controls be used to ensure that noise levels do not exceed the PEL. If noise levels cannot be brought down to the PEL, hearing protection must be provided. Its use must be enforced.
• Noise levels must be monitored, either with area monitoring or personal dosimetry. Personal dosimetry is required if workers are exposed to variable noise levels.
• Noise levels must be posted in work areas.
• The following features are essential for an adequate hearing conservation program:
  • Hearing conservation programs must include a baseline audiometry performed within 6 months of onset of exposure for all employees. The audiogram must be obtained when the employee has not been exposed to hazardous noise for at least 14 hours.
  • Annual audiometric testing should be performed for workers whose TWAs equal or exceed 85 dBA.
  • Workers exposed to TWA of 85 dBA or higher are required to have annual training about the effects of noise on hearing and the purpose of audiometric testing and hearing protective devices (HPDs).
  • A large number of additional recording and reporting requirements are included in OSHA regulations.
• If exposure to loud environmental noises cannot be avoided, hearing protection should be used. Unfortunately, enforcement has been sporadic. HPDs vary considerably in their effectiveness, comfort, and cost. The following information should be taken into consideration when considering HPDs:
• Only devices that are designed for hearing protection and tested for efficacy should be used. Items such as cotton, tissue paper, and expended cartridge casings provide no meaningful noise attenuation.
• Earplugs are available with attenuation levels from as low as 10 dB to as high as 32 dB. They can be purchased over the counter or custom made. Earplugs can be as effective as earmuffs. However, earplugs are effective only when properly inserted. When earplugs are improperly inserted, noise attenuation may be eliminated or greatly reduced. Earplugs are especially useful when noise exposure is continuously sustained.
• Earmuffs can provide as much attenuation as can earplugs. An advantage of earmuffs is that they are easy to correctly place: whether they are properly inserted or installed is not an issue. Earmuffs are especially useful when exposure to noise is relatively intermittent. Runway workers may need to put on and take off earmuffs many dozens of times a shift. These workers would not likely put earplugs in and out that frequently; if they did, many of those installations would probably be imperfect.
• Earmuffs that permit normal hearing in the absence of a loud noise are now available. The muffs are able to detect the presence of a loud noise and attenuate it before it reaches the human ear. These devices have achieved a much higher level of acceptability among sports shooters because they permit normal hearing except when a firearm is discharged. Sports shooters often worry that their efficiency is impaired if they cannot hear environmental sounds and that their safety is imperiled if they cannot understand what others around them are saying.
• The most effective ear protection is the ear protection the person is willing to wear.

Prognosis

• TTS are reversible, but PTSs are not. No method of treatment is available, and no recovery is expected once a PTS has occurred.
• However, hearing loss should not progress if exposure to the injurious noise is eliminated. Moreover, as the severity of the hearing loss increases, the rate of progression decreases, provided the injurious stimulus remains constant.

Patient Education

For excellent patient education resources, visit eMedicine's Ear, Nose, and Throat Center. Also, see eMedicine's patient education article Hearing Loss and Tinnitus.

Miscellaneous

Medicolegal Pitfalls

• Noise-induced hearing loss (NIHL) frequently becomes a medicolegal issue. A large body of law surrounds the issue of disability secondary to NIHL.
• Workers' compensation claims are frequent in the area of NIHL, and both federal and state laws govern compensation claims. These laws are not uniform.
• The committee on hearing and equilibrium of the American Academy of Otolaryngology has established a computational method to determine hearing handicap. It recognizes that hearing thresholds of 500, 1000, 2000, and 3000 Hz are critical for understanding human conversation, and it uses only those frequencies in the calculation of hearing handicap. The method also recognizes that overall hearing acuity is disproportionately determined by the acuity of the better-hearing ear. Consequently, the calculation heavily favors the better-hearing over the poorer-hearing ear. The method recognizes a 25-dB threshold or better to be normal. The computation is performed as follows:
  • Compute the sum of the hearing threshold levels at 500, 1000, 2000, and 3000 Hz and divide by 4. Subtract 25 from the average. Multiply the result by 1.5 to produce the percent monaural hearing impairment.
  • If the monaural percent figure is the same for both ears, that figure expresses the percent handicap. If the percent monaural hearing impairment is different between ears, apply the formula (5 x % of better ear) + (1 x % poorer ear) divided by 6 = percent hearing handicap.
• The AMA's Guides to the Evaluation of Permanent Impairment provides tables that can convert percent binaural handicap into "percent disability of the whole person."
• Most individuals have hearing loss that has arisen from several causes. Hearing loss due to presbycusis is eventually present in most individuals. Occasionally, a physician is asked to allocate the percent of hearing loss due to noise exposure as distinct from the percent due to other causes. Age correction of audiograms is possible and can be used help allocate or attribute the proportion of hearing loss due to noise-induced PTS. However, age correction of audiograms is not generally considered appropriate for compensation assessment purposes.
• Diagnosis of NIHL should rarely be made on the basis of the audiometric pattern alone. Information about the level of noise exposure should be a part of the diagnosis whenever possible.

Multimedia

Media file 1:

References

1. Melamed S, Rabinowitz S, Green MS. Noise exposure, noise annoyance, use of hearing protection devices and distress among blue-collar workers. Scand J Work Environ Health. Aug 1994;20(4):294-300. [Medline].

2. Tornabene SV, Sato K, Pham L, Billings P, Keithley EM. Immune cell recruitment following acoustic trauma. Hear Res. Dec 2006;222(1-2):115-24. [Medline].

3. Abrashkin KA, Izumikawa M, Miyazawa T, et al. The fate of outer hair cells after acoustic or ototoxic insults. Hear Res. Aug 2006;218(1-2):20-9. [Medline].

4. Jin DX, Lin Z, Lei D, Bao J. The role of glucocorticoids for spiral ganglion neuron survival. Brain Res. Jun 24 2009;1277:3-11. [Medline].

5. Konings A, Van Laer L, Wiktorek-Smagur A, et al. Candidate gene association study for noise-induced hearing loss in two independent noise-exposed populations. Ann Hum Genet. Mar 2009;73(2):215-24. [Medline].

6. Pourbakht A, Yamasoba T. Cochlear damage caused by continuous and intermittent noise exposure. Hear Res. Apr 2003;178(1-2):70-8. [Medline].

7. Dobie RA. The relative contributions of occupational noise and aging in individual cases of hearing loss. Ear Hear. Feb 1992;13(1):19-27. [Medline].

8. Dobie RA. A method for allocation of hearing handicap. Otolaryngol Head Neck Surg. Nov 1990;103(5 (Pt 1)):733-9. [Medline].

9. Fakhry N, Rostain JC, Cazals Y. Hyperbaric oxygenation with corticoid in experimental acoustic trauma. Hear Res. Aug 2007;230(1-2):88-92. [Medline].

10. Suckfuell M, Canis M, Strieth S, Scherer H, Haisch A. Intratympanic treatment of acute acoustic trauma with a cell-permeable JNK ligand: a prospective randomized phase I/II study. Acta Otolaryngol. Sep 2007;127(9):938-42. [Medline].

11. Parker MA, Corliss DA, Gray B, et al. Neural stem cells injected into the sound-damaged cochlea migrate throughout the cochlea and express markers of hair cells, supporting cells, and spiral ganglion cells. Hear Res. Oct 2007;232(1-2):29-43. [Medline].

12. Job A, Raynal M, Kossowski M, et al. Otoacoustic detection of risk of early hearing loss in ears with normal audiograms: a 3-year follow-up study. Hear Res. May 2009;251(1-2):10-6. [Medline].

13. Campbell KC, Meech RP, Klemens JJ, et al. Prevention of noise- and drug-induced hearing loss with D-methionine. Hear Res. Apr 2007;226(1-2):92-103. [Medline].

14. Bielefeld EC, Kopke RD, Jackson RL, Coleman JK, Liu J, Henderson D. Noise protection with N-acetyl-l-cysteine (NAC) using a variety of noise exposures, NAC doses, and routes of administration. Acta Otolaryngol. Sep 2007;127(9):914-9. [Medline].

15. Hamernik RP, Qiu W, Davis B. The effectiveness of N-acetyl-L-cysteine (L-NAC) in the prevention of severe noise-induced hearing loss. Hear Res. May 2008;239(1-2):99-106. [Medline].

16. American Medical Association. Guides to the Evaluation of Permanent Impairment. 4^th ed. Chicago: American Medical Association; 1993.

17. Arslan E, Orzan E. Audiological management of noise induced hearing loss. Scand Audiol Suppl. 1998;48:131-45. [Medline].

18. Boettcher FA, Henderson D, Gratton MA, Danielson RW, Byrne CD. Synergistic interactions of noise and other ototraumatic agents. Ear Hear. Aug 1987;8(4):192-212. [Medline].

19. Canlon B. Protection against noise trauma by sound conditioning. Ear Nose Throat J. Apr 1997;76(4):248-50, 253-5. [Medline].

20. Chen GD, Liu Y. Mechanisms of noise-induced hearing loss potentiation by hypoxia. Hear Res. Feb 2005;200(1-2):1-9. [Medline].

21. Conference report. Consensus conference. Noise and hearing loss. JAMA. Jun 20 1990;263(23):3185-90. [Medline].

22. DiBiase P, Arriaga MA. Post-traumatic hydrops. Otolaryngol Clin North Am. Dec 1997;30(6):1117-22. [Medline].

23. Harris KC, Hu B, Hangauer D, Henderson D. Prevention of noise-induced hearing loss with Src-PTK inhibitors. Hear Res. Oct 2005;208(1-2):14-25. [Medline].

24. Hone SW, Norman G, Keogh I, Kelly V. The use of cortical evoked response audiometry in the assessment of noise-induced hearing loss. Otolaryngol Head Neck Surg. Feb 2003;128(2):257-62. [Medline].

25. Hou F, Wang S, Zhai S, Hu Y, Yang W, He L. Effects of alpha-tocopherol on noise-induced hearing loss in guinea pigs. Hear Res. May 2003;179(1-2):1-8. [Medline].

26. Hu BH, Guo W, Wang PY, Henderson D, Jiang SC. Intense noise-induced apoptosis in hair cells of guinea pig cochleae. Acta Otolaryngol. Jan 2000;120(1):19-24. [Medline].

27. Konopka W, Pawlaczyk-Luszczynska M, Sliwinska-Kowalska M, Grzanka A, Zalewski P. Effects of impulse noise on transiently evoked otoacoustic emission in soldiers. Int J Audiol. Jan 2005;44(1):3-7. [Medline].

28. Kumar A, Mathur NN, Varghese M, Mohan D, Singh JK, Mahajan P. Effect of tractor driving on hearing loss in farmers in India. Am J Ind Med. Apr 2005;47(4):341-8. [Medline].

29. Lamm K, Lamm H, Arnold W. Effect of hyperbaric oxygen therapy in comparison to conventional or placebo therapy or no treatment in idiopathic sudden hearing loss, acoustic trauma, noise-induced hearing loss and tinnitus. A literature survey. Adv Otorhinolaryngol. 1998;54:86-99. [Medline].

30. Lusk SL. Noise exposures. Effects on hearing and prevention of noise induced hearing loss. AAOHN J. Aug 1997;45(8):397-408; quiz 409-10. [Medline].

31. Madigan J. Beyond hearing loss. Occup Health Saf. Oct 1998;67(10):84-9. [Medline].

32. Morata TC. Assessing occupational hearing loss: beyond noise exposures. Scand Audiol Suppl. 1998;48:111-6. [Medline].

33. Perez R, Freeman S, Sohmer H. Effect of an initial noise induced hearing loss on subsequent noise induced hearing loss. Hear Res. Jun 2004;192(1-2):101-6. [Medline].

34. Picard M, Banville R, Barbarosie T, Manolache M. Speech audiometry in noise-exposed workers: the SRT-PTA relationship revisited. Audiology. Jan-Feb 1999;38(1):30-43. [Medline].

35. Prasher D, Sulkowski W. The role of otoacoustic emissions in screening and evaluation of noise damage. Int J Occup Med Environ Health. 1999;12(2):183-92. [Medline].

36. Sataloff RT, Sataloff J. Audiologic testing: an overview for occupational physicians. Occup Med. Jul-Sep 1997;12(3):433-47. [Medline].

37. Sohmer H. Pathophysiological mechanisms of hearing loss. J Basic Clin Physiol Pharmacol. 1997;8(3):113-25. [Medline].

38. Stewart M, Konkle DF, Simpson TH. The effect of recreational gunfire noise on hearing in workers exposed to occupational noise. Ear Nose Throat J. Jan 2001;80(1):32-4, 36, 38-40. [Medline].

39. Subratty AH, Hooloman NK. Role of circulating inflammatory cytokines in patients during an acute attack of bronchial asthma. Indian J Chest Dis Allied Sci. Jan-Mar 1998;40(1):17-21. [Medline].

40. Takemura K, Komeda M, Yagi M, et al. Direct inner ear infusion of dexamethasone attenuates noise-induced trauma in guinea pig. Hear Res. Oct 2004;196(1-2):58-68. [Medline].

41. Teie PU. Noise-induced hearing loss and symphony orchestra musicians: risk factors, effects, and management. Md Med J. Jan 1998;47(1):13-8. [Medline].

42. Tornabene SV, Sato K, Pham L, Billings P, Keithley EM. Immune cell recruitment following acoustic trauma. Hear Res. Dec 2006;222(1-2):115-24. [Medline].

43. Hu BH, Guo W, Wang PY, Henderson D, Jiang SC. Intense noise-induced apoptosis in hair cells of guinea pig cochleae. Acta Otolaryngol. Jan 2000;120(1):19-24. [Medline].

Keywords

hearing loss, noise-induced hearing loss, NIHL, non-occupational hearing loss, socioacusis, environmental noise, noise exposure, occupational hearing loss, occupational noise-induced hearing loss, ONIHL, acoustic trauma, workplace noise

Contributor Information and Disclosures

Author

Neeraj N Mathur, MBBS, MS, Professor, Department of Ear, Nose and Throat, Lady Hardinge Medical College and Associated Smt SK and Kalawati, Saran Children's Hospital, University of Delhi, India; Professor and Head, Department of Ear, Nose and Throat, BP Koirala Institute of Health Sciences, Nepal
Neeraj N Mathur, MBBS, MS is a member of the following medical societies: Association of Otolaryngologists of India, Cochlear Implant Group of India, Indian Medical Association, National Academy of Medical Sciences, India, Neuro-Otologic and Equlibriometric Society of India, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Peter S Roland, MD, Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director of Clinical Center for Auditory, Vestibular and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Adjunct Professor of Communicative Disorders, University of Texas School of Human Development
Peter S Roland, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American Auditory Society, American Laryngological Rhinological and Otological Society, American Neurotology Society, American Otological Society, North American Skull Base Society, and Society of University Otolaryngologists-Head and Neck Surgeons
Disclosure: Alcon labs Honoraria Speaking and teaching; GSK Honoraria Speaking and teaching; Advanced Bionics Honoraria Board membership; Cochlear corp Honoraria Board membership; Med El corp travel grants Consulting

Medical Editor

S Valentine Fernandes, MBBS, MCPS, FRCSEd, FRACS, FACS, Conjoint Senior Clinical Lecturer, Department of Otorhinolaryngology, Newcastle University; Senior Consultant Surgeon, Department of Otorhinolaryngology-Head and Neck Surgery, John Hunter, Toronto Private and Kurri Hospitals, Australia
S Valentine Fernandes, MBBS, MCPS, FRCSEd, FRACS, FACS is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American College of Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gerard J Gianoli, MD, Clinical Associate Professor, Department of Otolaryngology-Head and Neck Surgery, Tulane University School of Medicine; Vice President, The Ear and Balance Institute; Chief Executive Officer, Ponchartrain Surgery Center
Gerard J Gianoli, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Neurotology Society, American Otological Society, Society of University Otolaryngologists-Head and Neck Surgeons, and Triological Society
Disclosure: Nothing to disclose.

CME Editor

Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo  Consulting; Medvoy Ownership interest Management position

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)