eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Inner Ear
Inner Ear, Noise-Induced Hearing Loss
Updated: May 2, 2007
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). 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."
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. 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.
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 (see acoustic trauma). 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 (Hu, 2000). 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.
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).
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.
Hearing loss from sustained exposure to intermittent or continuous noise should be differentiated from acoustic trauma. Acoustic trauma is due to one-time brief exposures followed by immediate permanent hearing loss. The sound stimuli generally exceed 140 dB and are often sustained for less than 0.2 seconds. Acoustic trauma appears to have its pathophysiologic basis in mechanical tearing of membranes and physical disruption of cell walls with mixing of perilymph and endolymph. Damage from impulse noise appears to be a direct mechanical disruption of inner ear tissues because their elastic limit was exceeded. At high energies, acoustic trauma can result in disruption of the tympanic membrane and ossicular injury.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 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.
Sex
More males than females are reported to have 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 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:
- 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 (see A scale).
- 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 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
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 to 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.
More on Inner Ear, Noise-Induced Hearing Loss |
 Overview: Inner Ear, Noise-Induced Hearing Loss |
| Differential Diagnoses & Workup: Inner Ear, Noise-Induced Hearing Loss |
| Treatment & Medication: Inner Ear, Noise-Induced Hearing Loss |
| Follow-up: Inner Ear, Noise-Induced Hearing Loss |
| References |
| Next Page » |
References
American Medical Association. Guides to the Evaluation of Permanent Impairment. 4th ed. Chicago: American Medical Association;1993.
Arslan E, Orzan E. Audiological management of noise induced hearing loss. Scand Audiol Suppl. 1998;48:131-45. [Medline].
Boettcher FA, Henderson D, Gratton MA, et al. Synergistic interactions of noise and other ototraumatic agents. Ear Hear. Aug 1987;8(4):192-212. [Medline].
Canlon B. Protection against noise trauma by sound conditioning. Ear Nose Throat J. Apr 1997;76(4):248-50, 253-5. [Medline].
Chen GD, Liu Y. Mechanisms of noise-induced hearing loss potentiation by hypoxia. Hear Res. Feb 2005;200 (1-2):1-9. [Medline].
Conference report. Consensus conference. Noise and hearing loss. JAMA. Jun 20 1990;263(23):3185-90. [Medline].
DiBiase P, Arriaga MA. Post-traumatic hydrops. Otolaryngol Clin North Am. Dec 1997;30(6):1117-22. [Medline].
Dobie RA. A method for allocation of hearing handicap. Otolaryngol Head Neck Surg. Nov 1990;103(5 (Pt 1)):733-9. [Medline].
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].
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].
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].
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].
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].
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].
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].
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].
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].
Madigan J. Beyond hearing loss. Occup Health Saf. Oct 1998;67(10):84-9. [Medline].
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].
Morata TC. Assessing occupational hearing loss: beyond noise exposures. Scand Audiol Suppl. 1998;48:111-6. [Medline].
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].
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].
Pourbakht A, Yamasoba T. Cochlear damage caused by continuous and intermittent noise exposure. Hear Res. Apr 2003;178(1-2):70-8. [Medline].
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].
Sataloff RT, Sataloff J. Audiologic testing: an overview for occupational physicians. Occup Med. Jul-Sep 1997;12(3):433-47. [Medline].
Sohmer H. Pathophysiological mechanisms of hearing loss. J Basic Clin Physiol Pharmacol. 1997;8(3):113-25. [Medline].
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].
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].
Takemura K, Komeda M, Yagi M, Himeno C, 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].
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].
Further Reading
Keywords
noise-induced hearing loss, NIHL, non-occupational hearing loss, socioacusis, occupational hearing loss, occupational noise-induced hearing loss, ONIHL, acoustic trauma
