Noise-induced hearing loss

Douglas J Lanska MD MS MSPH

Neuro-Ophthalmology & Neuro-Otology

Updated 05.15.2024
Released 09.10.2001
Expires For CME 05.15.2027

Noise-induced hearing loss

Author: Douglas J Lanska MD MS MSPH

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Noise-induced hearing loss

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Introduction

Overview

The author explains the clinical presentation, pathophysiology, diagnostic work-up, and management of noise-induced hearing loss. Occupational noise exposure is the most important preventable cause of hearing loss in the United States. With acute noise exposure, the threshold shift may be temporary, with hearing gradually returning to baseline levels over the period of approximately a day. However, with repeated noise exposure hearing only partially returns to baseline levels, and the threshold shift becomes permanent and progressive. Other factors may act synergistically with noise exposure to damage cochlear hair cells, including hereditary factors and environmental exposures, such as smoking, secondhand smoke exposure, and exposure to toxic solvents in car paints.

Key points

	• Worldwide, approximately one sixth (16%) of disabling hearing loss in adults is attributable to occupational noise exposure. Occupational noise exposure is the most important preventable cause of hearing loss in the United States, but it accounts for less than 10% of the burden of hearing loss (most of the rest is age-related).
	• Other factors may act synergistically with noise exposure to damage cochlear hair cells, including hereditary factors and environmental exposures such as smoking, secondhand smoke exposure, and exposure to toxic solvents in car paints.
	• Patients with noise-induced hearing loss typically present with gradual, bilateral, high-frequency, sensorineural hearing loss.
	• Noise-induced hearing loss results from cochlear damage, particularly near the base of the cochlea.
	• Audiograms in patients with noise-induced hearing loss show bilateral sensorineural hearing loss, often with a characteristic notch at 4000 Hz.
	• With acute noise exposure, the threshold shift may be temporary, with hearing gradually returning to baseline levels over the period of approximately a day. However, with repeated noise exposure hearing only partially returns to baseline levels, and the threshold shift becomes permanent and progressive.
	• Like most instances of sensorineural hearing loss, there is no effective medical or surgical therapy for noise-induced hearing loss. Therefore, prevention is essential.

Historical note and terminology

Noise-induced hearing loss was described by Italian physician Bernardino Ramazzini (1633–1714) (127). Ramazzini described noise-related hearing loss (and possibly tinnitus) in corn millers and in coppersmiths and recognized that the disorder is irreversible and progressive when exposure to noise continues. He suggested the use of earplugs as a preventive measure for these classes of workers.

Bernardino Ramazzini (1633-1714)

Italian physician Bernardino Ramazzini described noise-related hearing loss (and possibly tinnitus) in corn millers and coppersmiths in the pre-industrial era. (Public domain.)

Noise-induced hearing loss has been more widely recognized since at least the early 19th century as a result of artillery fire or chronic noise exposure in certain occupations (eg, blacksmiths) (110; 151). By the late 19th century, occupational hearing loss was recognized in a broader group of workers (eg, boilermakers and railroad workers) (122). Knowledge of the effects of impulse noise on hearing increased markedly during and after World War II. The United States military established noise exposure regulations in 1956, but civilian occupation standards were not promulgated until 1969 and not adopted widely and enforced until establishment of the Occupational Safety and Health Administration in 1970 (101). The Occupational Safety and Health Administration originally adopted a permissible exposure limit of 90 dBA for an 8-hour, time-weighted, average noise exposure, with an exchange rate designed to allow somewhat higher exposure levels (up to 115 db) for progressively shorter durations. The National Institute for Occupational Safety and Health estimates that approximately 10% of workers are exposed to unsafe noise levels on the job (97).

Hearing loss is categorized commonly according to American National Standards Institute references for signal intensity: normal, 10 to 26 dB; mild loss, 27 to 40 dB; moderate loss, 41 to 55 dB; moderately severe loss, 56 to 70 dB; severe loss, 71 to 90 dB; and profound loss, 91+ dB. Categorization of the degree of hearing loss is generally based on the pure tone average (ie, the average of air-conduction thresholds at 500, 1000, and 2000 Hz) but may be specified for each frequency region (ie, low, mid, or high frequencies on the audiogram).

Clinical manifestations

Presentation and course

	• Occupational noise exposure is the most important preventable cause of hearing loss in the United States but accounts for less than 10% of the burden of hearing loss (most of the rest is age-related).
	• Patients with noise-induced hearing loss typically present with gradual, bilateral, high-frequency sensorineural hearing loss.
	• Noise-induced hearing loss adversely affects quality of life.
	• Tinnitus is common with noise-induced hearing loss typically and, for some patients, may be the most troubling symptom.
	• Noise-induced hearing loss is typically bilateral but may be worse in one ear.

Occupational noise exposure is the most important preventable cause of hearing loss in the United States but accounts for less than 10% of the burden of hearing loss (most of the rest is age-related) (35; 81; 164). Noise-induced hearing loss is generally attributable to unprotected exposures above 95 dBA. It often becomes clinically apparent in middle age when age-related threshold shifts are added to prior noise-induced shifts.

Patients with noise-induced hearing loss typically present with gradual, bilateral, high-frequency sensorineural hearing loss (45; 81). There is usually a history of recreational or occupational noise exposure, usually without hearing protection, occurring over many years. With continued noise exposure, hearing loss is progressive. Rarely, with extreme high-intensity noise damage, permanent hearing loss may develop suddenly and may be accompanied by tympanic membrane, middle ear, and vestibular dysfunction; such exposures are relatively rare in civilian populations, and temporally related hearing loss is obvious from the history (125; 143).

Noise-induced hearing loss adversely affects quality of life (111). Patients may hear vowels better than consonants because vowels have predominantly low-frequency content, whereas consonants have predominantly high-frequency content. High-frequency voices (ie, children's voices) may be difficult for these patients to understand, especially with background noise. Shouting does not help understanding because it primarily increases the intensity level of vowels rather than consonants; in addition, loud sounds are often uncomfortable for such patients because of recruitment. Sounds are also frequently distorted so that a pure tone may be heard as a buzz, broadband noise, or a complex mixture of tones. Some patients experience diplacusis. Furthermore, daily occupational noise exposures of at least 100 dBA and noise-induced hearing losses have been associated with work-related accidents (133; 134) and less vigilance while driving (133).

Tinnitus is common with noise-induced hearing loss typically and, for some patients, may be the most troubling symptom (90; 102; 183; 98; 132; 52; 81). Tinnitus related to noise-induced hearing loss is most often experienced as a high-frequency tone (167). The prevalence of temporary noise-induced tinnitus and permanent tinnitus in high school students is respectively 75% and 18% (47). Tinnitus intensity levels established with loudness matching techniques generally correlate with hearing levels at the frequency of most severe hearing loss (90; 93), although one study concluded just the opposite, ie, that the loudness of tinnitus was inversely correlated with the degree of hearing loss (44). In the presence of normal hearing, however, tinnitus should not necessarily be ascribed to noise exposure, as the presence of tinnitus in those with normal hearing is not associated with present noise level, duration of noise exposure, or cumulative noise exposure (144).

Noise-induced hearing loss is typically bilateral but may be worse in one ear (21; 135; 136; 178; 163; 151; 40). In shotgun or rifle users, noise-induced hearing loss is typically worse on the side opposite the patient's dominant hand (171; 138; 151), whereas handgun users may have worse hearing loss on the same side as the dominant hand. Occupational noise-induced hearing loss can cause and accentuate asymmetry between the right and left ears over time (28).

Prognosis and complications

With acute noise exposure, the threshold shift may be temporary, with hearing gradually returning to baseline levels over the period of approximately a day (125). With repeated noise exposure, hearing only partially returns to baseline levels, and the threshold shift becomes permanent and progressive. Independent risk factors for noise-induced hearing loss include older age, male sex, and greater intensity and duration of noise exposure, whereas the frequency of hearing protector use is a protective factor (12; 118; 108). Common associated symptoms include tinnitus, sound distortion, and diplacusis. Tinnitus at the time of annual occupational audiometric testing may help identify workers at increased risk for developing noise-induced hearing loss; it may occur before development of a 4000 Hz noise notch (52). The most important predictor of later noise-induced hearing loss in occupational settings is the initial temporary threshold shift at 4 kHz (108). Rarely, with extreme high-intensity noise damage, permanent hearing loss may be accompanied by tympanic membrane, middle ear, and vestibular dysfunction.

Prolonged duration of noise exposure over decades and the presence of moderate or severe noise-induced hearing loss are associated with an increased risk of death from cardiovascular disease (48).

Clinical vignette

A 55-year-old man presented with complaints of longstanding, gradually progressive, bilateral hearing loss and constant subjective tinnitus. He had problems understanding his 14-year-old daughter's speech, especially while riding in their car. He denied otalgia and otorrhea. He had served for 2 years in a United States Army maintenance engineering battalion in Vietnam; his service involved amphibious bridging, frequent use of maintenance equipment, and practice on the rifle range. No hearing protection devices were provided to him during his military service. He had also worked with farm machinery but did not use hearing protection. Otoscopic examination was normal. Pure tone findings indicated mild to moderate bilateral sensorineural hearing loss above 2000 Hz, most severe at 4000 Hz. Speech recognition thresholds were 10 dB hearing level bilaterally. Word recognition scores were excellent (96%) at a presentation level of 60 dB hearing level. Communication strategies were reviewed, annual hearing evaluation was recommended, and the consistent use of hearing protection was strongly advised for exposures to high-intensity occupational or recreational noise.

Biological basis

	• Noise-induced hearing loss results from cochlear damage, particularly near the base of the cochlea.
	• Brief exposure to loud noise (ie, hours to days) may produce only a temporary threshold shift, whereas more prolonged exposure results in permanent injury and loss of cochlear hair cells.
	• Genetic and epigenetic factors are significant contributors to noise-induced hearing loss.
	• Various environmental exposures can augment the damaging effect of noise.
	• Nonmodifiable risk factors associated with noise-induced hearing loss include increasing age, male gender, and genetic predisposition.
	• Modifiable risk factors associated with noise-induced hearing loss include voluntary exposure to loud noise, lack of hearing protection, smoking, lack of regular exercise, poor diet, poor dentition, diabetes and impaired fasting glucose, hypertension, and cardiovascular disease.

Anatomic localization

Noise-induced hearing loss results from cochlear damage, particularly near the base of the cochlea.

Pathophysiology

Brief exposure to loud noise (ie, hours to days) may produce only a temporary threshold shift (125). More prolonged exposure results in permanent injury and loss of cochlear hair cells (125).

High-intensity sound waves travel through the cochlear duct, causing damage to the organ of Corti, the spiral ganglion neurons, and the stria vascularis (190). In response to noise damage, hair cells, supporting cells, and spiral ganglion, neurons go through morphological changes and eventual apoptosis, but the supporting cells cannot regenerate (27). Noise-related dysfunction of the stria vascularis leads to ischemia reperfusion injury, which increases the level of damaging reactive oxygen species in the cochlea. Overproduction of reactive oxygen species and cochlear inflammation act synergistically (190). With excessive calcium influx triggering glutamate neurotoxicity at the ribbon synapses, both hair cells and synaptic structures are damaged, triggering intrinsic or extrinsic pathways of apoptosis.

Anatomy of the human ear and the pathophysiology of noise-induced hearing loss

(A) Schematic representation of ear anatomy. The ear consists of three parts: the outer, middle, and inner ear. The outer and middle ear are separated by the tympanic membrane. Sound waves are transduced through the tympanic me...
Contributing factors to noise-induced hearing loss and their interactions

Noise-related dysfunction of the stria vascularis leads to ischemia-reperfusion injury, which increases the level of reactive oxygen species (ROS) in the cochlea. The overproduction of ROS and cochlear inflammation are two bioc...
Molecular pathways underlying noise-induced hearing loss and potential therapeutic opportunities

Signaling pathways involved in (A) inflammation, (B) energy metabolism, (C) oxidative stress, (D) programmed cell death, and (E) excitotoxicity and autophagy are illustrated in separated regions. Protective responses are shown ...

Damage to cochlear hair cells is often initially confined to a small area 5 to 10 mm from the base of the cochlea, the area involved in sensing frequencies around 4000 Hz. Hearing at 4000 Hz is important for speech discrimination in noisy environments (125). Considerable cochlear hair cell damage can occur before hearing thresholds are affected. The basis for the relatively selective damage to the basal cochlea is not clear, but mechanical, vascular, and toxic-metabolic theories have been proposed: the mechanical theory postulates shear forces from a "jet effect" at this location, whereas the vascular theory maintains that this region is susceptible to ischemia because it is at the juncture of the main cochlear and cochlear ramus arteries, and one of the toxic-metabolic theories implicates late development of free radicals in mitochondria followed by excitotoxic neural swelling and induction of necrotic and apoptotic cell death in the organ of Corti (89; 193; 59; 83).

Following noise-induced hearing loss, distorted tonotopy (ie, a disruption in the mapping between acoustic frequency and cochlear place) severely degrades the neural representations of speech (particularly in noise) in single- and across-fiber responses in the auditory nerve (129).

Noise-induced functional deficits in hearing in the absence of changes in sensitivity are called "noise-induced hidden hearing loss” (152). Noise exposure that does not lead to permanent threshold shift can nevertheless cause considerable damage around the synapses between inner hair cells and type-I afferent auditory nerve fibers (152). Disruption of these synapses disables the innervated afferent auditory nerve fibers and produces a secondary degeneration of spiral ganglion neurons if the synapses are not reestablished (152). Without a permanent threshold shift, the signal coding deficits resulting from this noise-induced cochlear “synaptopathy” cannot be detected using routine audiological evaluations and may be unrecognized by affected individuals (152). Noise-induced hidden hearing loss first manifests as reduced output of the auditory nerve at high sound levels without affecting the hearing threshold. Whether noise-induced ribbon synapse damage is reversible is unclear, with current debate on this issue. In any case, there are likely to be changes in central coding due to a combination of peripheral deficits and central plasticity (152).

Differences in cerebral glucose metabolism and metabolic and structural connectivity exist between noise‐induced hearing loss subjects and normal subjects (153; 64; 141). In one study, noise‐induced hearing loss subjects showed hypometabolism compared to normal subjects in both insulae and the right superior temporal gyrus (153). In metabolic connectivity analysis, noise‐induced hearing loss subjects showed decreased average strength, global efficiency, and local efficiency when compared with normal subjects.

Brain areas showing hypometabolism in noise-induced hearing loss subjects

Legend: arrow: insula; arrowhead: right superior temporal gyrus. (Source: Shin S, Nam HY. Characteristics of brain glucose metabolism and metabolic connectivity in noise-induced hearing loss. Sci Rep 2023;13[1]:21889. Creative ...

Alterations of the cerebral microstructure in patients with noise-induced hearing loss were examined on sagittal scans using a T1-weighted 3D-FSPGR sequence (fast spoiled gradient-echo) in combination with diffusion tensor imaging (DTI) (64). The white matter structural abnormalities in patients with noise-induced hearing loss were mainly located in the syndesmotic fibers of the temporooccipital region, which affect auditory and language pathways. All DTI parameters (ie, fractional anisotropy, axial diffusivity, mean diffusivity, and radial diffusivity) were significantly different in the left inferior longitudinal fasciculus and the left inferior fronto-occipital fasciculus for mild noise‐induced hearing loss, relatively severe noise‐induced hearing loss, and healthy controls.

Fractional anisotropy maps in noise-induced hearing loss

Fractional anisotropy maps show significant differences between patients with mild noise‐induced hearing loss, relatively severe noise‐induced hearing loss, and healthy controls. The red-yellow highlighted areas indicate lower ...
Axial diffusivity maps in noise-induced hearing loss

Axial diffusivity maps show significant differences between patients with mild noise‐induced hearing loss, relatively severe noise‐induced hearing loss, and healthy controls. The red-yellow highlighted areas indicate higher axi...
Mean diffusivity maps in noise-induced hearing loss

Mean diffusivity maps show significant differences between patients with mild noise‐induced hearing loss, relatively severe noise‐induced hearing loss, and healthy controls. The red-yellow highlighted areas indicate higher mean...
Radial diffusivity maps in noise-induced hearing loss

Radial diffusivity maps show significant differences between patients with mild noise‐induced hearing loss, relatively severe noise‐induced hearing loss, and healthy controls. The red-yellow highlighted areas indicate higher ra...

In addition, the fractional anisotropy values were significantly lower in the corticospinal tracts, the right fronto-pontine tract, the right forceps major, the temporal part of the left superior longitudinal fasciculus, and the left cingulum (hippocampus) of the mild and relatively severe noise‐induced hearing loss groups than in those of the healthy controls. The axial diffusivity values showed diverse changes in the corticospinal tracts, the left inferior fronto-occipital fasciculus, the right anterior thalamic radiation, the right external capsule, the right superior longitudinal fasciculus, and the right superior cerebellar peduncle of the mild and relatively severe noise‐induced hearing loss groups than in those of the healthy controls. However, there were no significant differences among the bilateral auditory cortex regions of interest in the three groups.

Another study of alterations of resting-state functional network connectivity found that (1) compared with healthy controls, those with mild noise‐induced hearing loss showed increased resting-state functional network connectivity within the executive control network and enhanced resting-state functional network connectivity within the default mode network and the visual network; (2) compared with healthy controls, those with relatively severe noise‐induced hearing loss showed decreased resting-state functional network connectivity within the executive control network and auditory network, default mode network, and visual network; and (3) there were no significant changes in resting-state functional network connectivity between those with mild or relatively severe noise-induced hearing loss (141).

Genetic factors are significant contributors to noise-induced hearing loss (57; 158; 196; 197; 23; 82; 191; 194; 87; 181; 195; 188). Noise sensitivity tends to aggregate in families, and twin studies have implicated a genetic component to noise-induced hearing loss (57). In addition, genetic variation in molecular pathways involved in response to acoustic trauma, and particularly the cellular response to stress, including the heat shock response, detoxification of reactive oxygen species, and aspects of the immune response have significant influence on noise-induced hearing loss (23; 194; 87; 181). Polymorphisms in several genes have been associated with noise-induced hearing loss in various Chinese studies, including: (1) a manganese superoxide dismutase (SOD2) C47T polymorphism; (2) genetic variation in POU4F3, which encodes a member of the POU family of transcription factors that is critical for the maintenance of inner ear hair cells; (3) single-nucleotide polymorphisms in the CASP3 gene; and (4) polymorphisms in the protocadherin related 15 (PCDH15) gene (191; 181; 189; 192; 187). In addition, CDH23, FAS, GJB2, PTPRN2, and SIK3 may be noise-induced hearing loss susceptibility genes (188). Animal studies also provide evidence of gene-environment interactions in the development of noise-induced hearing loss (82).

Epigenetic factors are significant contributors to noise-induced hearing loss. In particular, histone acetylation is involved in the pathogenesis of noise-induced outer hair cell death and the resulting noise-induced hearing loss (19). In an animal model, after exposure to a traumatic noise paradigm sufficient to induce permanent threshold shifts, epigenetic modification of histones has been shown to alter hair cell survival, and histone H3 lysine 9 acetylation was shown to be decreased in the nuclei of outer hair cells and marginal cells of the stria vascularis in the basal region (19). As a result, levels of histone deacetylases 1, 2, and 3 were increased, predominately in the nuclei of cochlear cells. Treatment with a pan-inhibitor of histone deacetylases (SAHA, also named vorinostat) reduced outer hair cell loss and attenuated the permanent threshold shifts (19).

Various environmental exposures can augment the damaging effect of noise (184; 39; 29; 157; 56). For example, smoking (184; 104; 86; 195; 08), secondhand smoke (41), and toxic solvents in car paints (39; 103) may act synergistically with noise exposure to damage cochlear hair cells. Hand-arm vibration may also augment noise-induced hearing loss, specifically, working with vibrating machines in an environment with noise exposure increases the risk of hearing loss (130).

Comorbid conditions can also augment hearing loss due to noise exposure (36). For example, workers with hypertriglyceridemia are at increased risk for noise-induced hearing loss (36).

Nonmodifiable risk factors associated with noise-induced hearing loss include increasing age, male gender, genetic predisposition, and prior noise or vibration exposure; modifiable risk factors include voluntary exposure to loud noise, lack of hearing protection, smoking, lack of regular exercise, poor diet, poor dentition, diabetes and impaired fasting glucose, hypertension, and cardiovascular disease (29; 18; 68; 81; 195; 08). Some of these risk factors may simply be noncausal associations (eg, lack of regular exercise, poor diet, and poor dentition).

In noise-induced hearing loss, changes in brainstem auditory evoked potential latencies suggest an early functional injury of the first auditory pathway afferent neuron (148).

Epidemiology

	• The increase in noise-induced hearing loss has been called a “modern epidemic,” resulting from a combination of recreational noise exposure in young people and occupational noise exposure.
	• Worldwide, approximately one sixth (16%) of disabling hearing loss in adults is attributable to occupational noise exposure.
	• Occupational noise-induced hearing loss is the most prevalent occupational disease in the United States.

The increase in noise-induced hearing loss has been called a “modern epidemic,” resulting from a combination of recreational noise exposure in young people and occupational noise exposure (66). In the 2011 to 2012 National Health and Nutrition Examination Survey, nearly one in four adults (24%) had audiometric notches, suggesting a high prevalence of noise-induced hearing loss (17). The prevalence of notches was higher among men (17). It should be noted, though, that a notched audiogram is not pathognomonic of noise-induced hearing loss because audiometric notches can occur without a history of noise exposure (106).

Worldwide, approximately one sixth (16%) of disabling hearing loss in adults is attributable to occupational noise exposure, with significant variation in different subregions (117). The effects of exposure to occupational noise exposure are higher in males than in females because of differences in both workforce participation and the type of occupations (17; 88). Most of this disability would be preventable with appropriate engineering controls to reduce noise generation or propagation and with appropriate use of hearing protectors.

Occupational noise-induced hearing loss is the most prevalent occupational disease in the world (20), and it disproportionately affects lower socioeconomic countries (198). Occupational noise-induced hearing loss is also the most prevalent occupational disease in the United States (35; 164). Twenty-two million workers in the United States (17%) are exposed to hazardous workplace noise according to 1999 to 2004 data from the National Health and Nutrition Examination Survey (NHANES) (168). In the United States, the prevalence of workplace noise exposure is highest for mining, followed by lumber/wood product manufacturing. High-risk occupations include repair and maintenance, motor vehicle operators, and construction trades. Overall, 34% of the estimated 22 million workers in the United States reporting hazardous workplace exposure reported non-use of hearing protection devices. Somewhat perversely, the proportion of noise-exposed workers who reported non-use of hearing protection devices was highest for healthcare and social services, followed by educational services.

Recreational noise exposure is also an increasing cause of noise-induced hearing loss that results in demonstrable deterioration in hearing and increases in the occurrence of temporary or permanent tinnitus after recreational noise exposures (33; 32).

Smoking is a risk factor for noise-induced hearing loss (184; 104; 86; 195; 08). Current smokers have a higher risk than former smokers, and there is a dose-response relationship between smoking and noise-induced hearing loss (86).

Noise-induced hearing loss has a tremendous economic impact (116). Hearing loss affects more than 13% of the working population, and approximately 20% of this is attributable to noise exposure. If the hearing loss resulting from excessive noise exposure were prevented, the estimated economic benefit in the United States would be $123 billion (rage $58 billion to $152 billion) annually (116).

The prevalence of hearing protection device non-use (using hearing protection devices half the time or less when exposed to hazardous noise) was 53% among all noise-exposed workers in 2014 in self-reported data from the National Health Interview Survey (50).

A cross-sectional study of a representative sample of the U.S. population comprising 19,730 people included in the U.S. National Health and Nutritional Examination Survey (NHANES) from 1999 to 2016 reported that occupational noise exposure increased from the 2000s to the 2010s, yet hearing protection use remained low (128). Participants self-reported (1) occupational noise exposure lasting more than 4 hours per day for more than 3 months; (2) hearing protective device use; and (3) tinnitus frequency. Audiometric hearing loss was objectively measured. From 1999 to 2004, 13% had occupational noise exposure, but only 41% used hearing protection devices. In the later period (2011-2012 and 2015-2016), 32% had occupational noise exposure (a 2.5-fold increase), but only 33% used hearing protection devices. In a multivariate model, factors independently associated with hearing protection use were younger age, male sex, college education or higher, and white race.

Differential diagnosis

Confusing conditions

Other common causes of sensorineural hearing loss include aging (presbycusis), vascular occlusive disease, trauma, Ménière syndrome, viral infections, meningitis, toxins, and genetic syndromes. Less common causes include acoustic neuroma. Distinguishing among these various causes is facilitated by attention to history (eg, noise or toxin exposure, trauma, etc.), onset and course of hearing loss, whether the hearing loss is unilateral or bilateral, the distribution of hearing loss as a function of sound frequency, associated manifestations (eg, vertigo), and family history.

Noise-induced hearing loss has an insidious onset and is either gradually progressive (with continued noise exposure) or static. Hearing loss with presbycusis or acoustic neuroma is also insidious in onset and gradually progressive. In contrast, hearing loss associated with vascular occlusive disease, trauma, and viral infections has an acute onset and remains static or may improve. Hearing loss associated with ototoxins or meningitis has a subacute onset and is later static once the cause is removed. Hearing loss associated with Ménière syndrome is fluctuating.

Noise-induced hearing loss is typically bilateral but may be more severe in one ear (21; 135; 136; 178; 163; 151; 40). Asymmetric noise-induced hearing loss is common in those using firearms and professional musicians playing stringed instruments. In contrast, hearing loss associated with many of the other conditions is often unilateral (eg, vascular occlusive disease, trauma, Ménière syndrome, viral neurolabyrinthitis, acoustic neuroma). Vascular hearing loss may rarely be bilateral with severe vertebrobasilar occlusive disease. Ménière syndrome is generally unilateral at onset but may progress to bilateral involvement.

The configuration of hearing loss can help suggest an etiology. A notched pattern of high-frequency sensorineural hearing loss with a notch at 4000 or 6000 Hz is suggestive of noise-induced hearing loss (94; 131; 109), whereas a downward-sloping pattern of high-frequency sensorineural hearing loss suggests presbycusis and a low-frequency trough pattern suggests Ménière syndrome. Note, however, that there is no commonly accepted standard definition of an audiometric notch and that audiometric notches can occur in the absence of a positive history of significant noise exposure (107).

Sensorineural hearing loss, notched pattern

Audiogram showing a “4 kHz notch” (or colloquially, a “4K notch”) pattern of sensorineural hearing loss, commonly seen in noise-induced hearing loss. Both ears are shown. (Contributed by James Lanska.)
Sensorineural hearing loss, sloping pattern

Audiogram showing symmetric, gradually sloping, high-frequency sensorineural hearing loss. (Contributed by James Lanska.)
Sensorineural hearing loss, low-frequency trough pattern

Audiogram showing a low-frequency trough pattern of sensorineural hearing loss, commonly seen in Meniere disease. The left ear is shown. (Contributed by James Lanska.)

Ménière syndrome is typically associated with vertigo, which does not occur with noise-induced hearing loss except (rarely) in cases of extreme acute high-intensity noise injuries.

Diagnostic workup

	• Audiograms show bilateral sensorineural hearing loss, often with a characteristic notch at 4000 Hz.
	• Extended high-frequency audiometry (9 to 18 kHz) is more sensitive than conventional audiometry in detecting noise-induced hearing loss, especially in younger workers.
	• Sensorineural hearing loss can be considered asymmetric if the interaural difference in pure tone thresholds is at least 10 dB at two frequencies or at least 15 dB at one frequency.
	• Asymmetric sensorineural hearing loss is fairly common as a result of noise exposure.

Confounding factors. To establish a diagnosis of noise-induced hearing loss incurred during a specific period, it is necessary to assess whether any other plausible cause of hearing loss existed then or subsequently (including noise exposure outside the specified period or outside of the workplace). Noise-induced hearing loss can certainly occur with hearing loss due to other agents, but the diagnosis will be most certain if the following are excluded (105):

	• Substantial exposure to ototoxic substances (eg, solvents)
	• Substantial exposure to ototoxic medications (eg, aminoglycosides, cancer chemotherapy)
	• Current or previous ear diseases
	• Head injury associated with auditory symptoms
	• Familial hearing loss not caused by noise exposure
	• Exposure to high levels of noise during leisure activities or outside the period in question (eg, regular attendance at discotheques, nightclubs, or “raves”)

Medical history. The medical history should include the following (105):

Noise exposure
	• Types and durations of noise exposures • Sound sources of the exposures • Any ear asymmetry in the exposures
Hearing protection
	• Types supplied (if any) or self-supplied • How well it fit • How often it was replaced • How often it was worn • Whether its use was enforced
Temporary threshold shifts
	• Whether and how often periods of temporarily reduced hearing or tinnitus were experienced during the time period in question
Tinnitus symptom
	• Whether tinnitus is currently experienced • If so, when tinnitus started relative to the period in question • The severity of tinnitus symptoms can be assessed according to the following:
		- Guidelines (95) - Tinnitus Handicap Inventory (119) - Tinnitus Functional Index (100) - Tinnitus Impact Questionnaire (03)
Hyperacusis symptom (an intolerance of sounds that most people do not find to be aversive) (177)
	• Whether hyperacusis is experienced • If so, when hyperacusis started relative to the period in question • The severity of hyperacusis symptoms can be assessed according to the following:
		- Hyperacusis Questionnaire (73) - Inventory of Hyperacusis Symptoms (51; 01) - Hyperacusis Impact Questionnaire (02)

Requirement for sufficient noise exposure. It should be established that noise exposure sufficient to produce hearing loss has occurred in at least 10% of individuals. For people who have been exposed mainly to steady broadband noise, a total noise exposure of 90 dB(A) NIL (noise immission level) is considered sufficient to cause noise-induced hearing loss (105). For people who have regularly been exposed to impulsive sounds in non-military occupations, a lower limit of 86 dB(A) NIL should be used (105). Those with active military service have likely been exposed to sounds with the potential to cause hearing loss (105).

Audiometry. Audiograms of individuals with noise-induced hearing loss typically show bilateral sensorineural hearing loss, often with a characteristic notch at 4000 Hz, colloquially, a “4K notch” or "noise notch" (12; 125; 118; 52; 94; 75; 81; 109; 105).

Sensorineural hearing loss, notched pattern

Audiogram showing a “4 kHz notch” (or colloquially, a “4K notch”) pattern of sensorineural hearing loss, commonly seen in noise-induced hearing loss. Both ears are shown. (Contributed by James Lanska.)

The 4 kHz notch was defined as one in which hearing thresholds at 2 and 8 kHz are both at least 10 dB HL lower than (better than) the threshold at 4 kHz (185). A 6000 Hz notch is variable and of limited importance (94; 109), but in some cases there is a marked notch spanning the range of 4000 Hz to 6000 Hz (71). With progression of sensorineural hearing loss, this "noise notch" at 4000 Hz deepens, and hearing loss extends into lower frequencies. With narrowband noise exposure (eg, siren or whistle), hearing loss may instead be centered approximately one-half octave above the frequency of the exposure. However, audiogram notching is not entirely specific to noise-induced hearing loss: among those with a notched audiogram, almost one third do not have a history of occupational noise exposure, and approximately 11% do not have a history of exposure to any source of noise (120). Discordance between audiogram notching and noise exposure history was greater in women than in men. Speech discrimination is not affected until late in the disease process. Otoacoustic emissions may provide earlier identification of noise-induced damage than pure tone thresholds alone and may identify cochlear dysfunction extending beyond the frequency range suggested by the audiogram (11).

In a high-risk subgroup of personal-listening-device users (ie, daily use 2 hours or more at 91 dB or higher), pure tone audiometry showed increased hearing thresholds at 4000 Hz and 6000 Hz, potentially indicating an early manifestation of noise-induced hearing loss (65).

Extended high-frequency audiometry (9 to 18 kHz) is more sensitive than conventional audiometry in detecting noise-induced hearing loss, especially in younger workers (160; 99).

Although various definitions have been proposed in the literature, sensorineural hearing loss can be considered asymmetric if the interaural difference in pure tone thresholds is at least 10 dB at two frequencies or at least 15 dB at one frequency (178). Asymmetric sensorineural hearing loss is fairly common in general and also as a result of noise exposure (21; 135; 136; 178). However, asymmetric sensorineural hearing loss can rarely indicate retrocochlear pathology, such as acoustic neuroma (178; 10). Patients with asymmetric sensorineural hearing loss may be followed with serial audiograms (every 6 months) if they have known significant asymmetric noise exposure, no recent changes in hearing or word recognition, and no associated symptoms (eg, vertigo) (178). Patients without a history of significant asymmetric noise exposure or other known cause of asymmetric sensorineural hearing loss as well as those with progression of asymmetric sensorineural hearing loss should undergo brainstem auditory evoked potential testing (178). MRI imaging is not a cost-effective screening technique for acoustic neuroma among all patients with asymmetric sensorineural hearing loss; it should be reserved for cases with a high clinical suspicion or cases with abnormal or inconclusive results from brainstem auditory evoked potential testing (178).

For occupational screening for auditory deficits due to noise exposure, there is no clear relationship between distortion product otoacoustic emission amplitude and pure tone audiometry results (186). Distortion-product otoacoustic emissions are commonly preserved despite elevated pure tone audiometry thresholds. Consequently, distortion product otoacoustic emissions cannot replace pure tone audiometry in occupational screening programs.

Quantification of noise-induced hearing loss. Quantification of noise-induced hearing loss is based on comparison of the measured hearing threshold levels with the age-associated hearing levels for a non-noise-exposed population, as specified in ISO 7029, usually using the 50th percentile (67; 105).

Management

	• Because there is no effective medical or surgical therapy for noise-induced hearing loss, prevention is essential.
	• At-risk subjects should use hearing protection.
	• In professional orchestras and bands, more than 50% of musicians have a hearing loss of 15 dBA or more, with the greatest losses among the string and brass players.
	• There is contradictory evidence that hearing loss prevention programs are effective in the long term.
	• Individuals are reluctant to wear hearing protection, and many do not wear it consistently or, in some cases, do not use it correctly. In an occupational setting, the Occupational Safety and Health Administration requires baseline and annual audiometric pure-tone air-conduction threshold testing of both ears at 500, 1000, 2000, 3000, 4000, and 6000 Hz for employees exposed to at least 50% of the permissible noise exposure level.
	• Annual testing as part of a workplace hearing conservation program can increase awareness of noise exposure and effectively influence most participants to change their hearing protection habits at home and work.
	• Unfortunately, most companies give inadequate attention to environmental noise controls and instead rely primarily on hearing protectors to prevent hearing loss.
	• Recreational noise exposure is usually less frequent and of shorter duration than occupational noise exposure, but it may readily compound occupational noise damage.
	• Sound does not have to be annoying or painful to cause hearing loss over time. Hearing protection should be worn if individuals have to raise their voices to easily carry on a conversation.
	• Hearing protection devices commonly available include earmuffs or ear plugs.
	• Affected patients may be fitted with hearing aids (or cochlear implants for profound hearing loss), but this does not generally restore hearing to normal, and sounds are often distorted.

Like most instances of sensorineural hearing loss, there is presently no effective medical or surgical therapy for noise-induced hearing loss. Therefore, prevention is essential (156). Hearing loss prevention and interventions have been shown to modestly reduce noise exposure and hearing loss (173). Unfortunately, present health promotion initiatives for prevention of noise-induced hearing loss are insufficient (15; 30; 172; 53). At-risk subjects should use hearing protection. This includes workers in the following fields: workers in heavy industry, foundry workers, textile industry workers, mill workers, truck drivers, heavy equipment operators, construction workers, machine operators and assemblers, auto factory workers, bottling plant workers, civilian pilots, soldiers and military aviators and aircrew, users of firearms, users of power tools, professional musicians and sound technicians, miners, farmers and other agricultural workers, foresters, fisheries workers, firefighters, and dentists) (46; 61; 38; 40; 69; 70; 76; 79; 123; 172; 09; 37; 63; 72; 96; 142; 155; 25; 58; 157; 124; 139; 42; 75; 121; 149; 13; 55; 112; 137; 161; 92).

Unfortunately, there is limited knowledge of the risks and associated health consequences of noise exposure in the general population, as well as a high rate of self-exposure to hazardous noise, complicating prevention efforts (159). Those with risk-taking behavior are more likely to engage in risky noise behavior. Risky noise behavior is associated with age, gender (males), race, ethnicity, and general risk propensity.

There are limited long-term data on the utility of interventions to prevent occupational noise-induced hearing loss (147).

Most occupational standards specify an 8-hour noise exposure limit of 85 dBA, although this limit assumes that some workers exposed at the limit will develop hearing loss (114). Note that A-weighted decibels, abbreviated dBA, indicate the relative loudness of sounds in air as perceived by the human ear; in the A-weighted system, the decibel values of sounds at low frequencies are reduced compared with unweighted decibels, in which no correction is made for audio frequency. To eliminate the risk of hearing loss, a 24-hour equivalent continuous level limit of 70 dBA is appropriate (114). For recreational sounds, an 8-hour noise exposure limit of 80 dBA, corresponding to a 24-hour equivalent continuous level of 75 dBA, will virtually eliminate the risk of recreationally induced hearing loss in adults (114).

Dentists are exposed to dangerous noise levels when high-volume suction is used; presumably, the same would be true for dental hygienists (112). Although practicing dentists report sensorineural hearing loss at a rate broadly in line with national averages in most studies, they reported a higher prevalence of tinnitus symptoms (112), a significant positive correlation was found in other studies between years of experience as a dentist and reduced hearing capacity (06).

In professional orchestras and bands, more than 50% of musicians have a hearing loss of 15 dBA or more, with the greatest losses among the string and brass players (40; 121; 149; 55). Noise-induced hearing loss is also common in student musicians (131; 49; 182) and correlates with the duration of daily practice but without clear associations with specific instruments (131). Hearing loss among musicians can potentially be reduced by in-ear monitors. Given the similarity between preferred listening levels and known monitor output levels, this potential benefit may not be realized if not used optimally (43). Unfortunately, a significant proportion of musicians use earplugs either inconsistently or not at all, and most find their use difficult or impossible (121). Brass players are least likely to use hearing protection, most likely to report difficulties with usage, and most likely to report hearing loss at a young age (younger than 50 years of age) (121).

Unfortunately, a systematic review of the effectiveness of nonpharmaceutical interventions for preventing occupational noise exposure or occupational hearing loss compared to no intervention or alternative interventions found that there is contradictory evidence that hearing loss prevention programs are effective in the long term (179; 53). Low-quality evidence suggests that stricter legislation can reduce noise levels in workplaces, with substantial reductions demonstrated in some individual circumstances, but there are no controlled studies of the effectiveness of such measures in preserving hearing (179). The limited success of hearing loss prevention programs may be explained by limited use of hearing protection, suboptimal knowledge of noise as a hazard, workplace noisiness, and the benefits of hearing protection devices among some workers (142; 53). Even when full-shift equivalent noise levels are well above the level at which hearing protection devices are required, usage rates are often quite low (37). Improvements are needed in the implementation, reinforcement, and evaluations of technical interventions and long-term effects. Properly worn hearing-protection devices significantly protect against noise-induced hearing loss (78). However, education and workplace requirements for use of hearing protection devices are critical because many affected individuals are reluctant to wear hearing protection (80; 46; 45; 79; 96), and many who wear it do not wear it consistently or in some cases do not use if correctly (45; 79; 96; 146; 50; 128). If feasible, environmental controls should be placed to control noise exposure (30; 46; 53). Concurrent with engineering controls, a range of hearing protection devices should be available free of charge, and hearing protection training should be reviewed, particularly for lower-skilled workers (142; 146).

In certain military and civilian occupations, there are significant barriers to utilization of hearing protection (139). In a military setting, barriers include concerns that hearing protection (1) compromises situational awareness and interferes with detection and localization of auditory warnings, (2) impedes exchange of information, including perception of orders, (3) is incompatible with other gear, and (4) is difficult to fit (04). Similarly, among firefighters, barriers include concerns that hearing protection (1) impedes exchange of information, including perception of orders during emergency situations, (2) is incompatible with other gear, including other required safety equipment (eg, face mask respirators and helmets), and (3) was generally forgotten when gearing up, in part because the perceived risk of occupational hearing loss was small compared with other job-related hazards (62; 139).

In an occupational setting, the Occupational Safety and Health Administration requires baseline and annual audiometric pure-tone air-conduction threshold testing of both ears at 500, 1000, 2000, 3000, 4000, and 6000 Hz for employees exposed to at least 50% of the permissible noise exposure level (24). Testing is generally scheduled at least 14 hours after the employee's last noise exposure to minimize the effect of temporary threshold shifts; if this is not possible, employees should wear hearing protection until tested. If an employee's noise exposure exceeds the Occupational Safety and Health Administration’s permissible exposure level, employers may need to establish environmental controls to reduce noise, issue hearing protectors, or rotate employees to less noisy tasks for part of the work day. Hearing protection is recommended for time-weighted average sound exposure levels of 85 dBA or more; it is required for levels of 90 dBA or more. Hearing protection is also required if a worker has experienced a significant threshold shift, even if occupational exposure is less than 90 dBA time-weighted average. Hearing protection must decrease the employee's noise exposure to less than 85 dBA time-weighted average. Some employers issue hearing protection even when the Occupational Safety and Health Administration standards are met because even at somewhat lower noise levels, some employees may develop permanent noise-induced hearing loss (125). The Occupational Safety and Health Administration regulations do not cover a variety of workers exposed to excessive noise, including farmers, construction workers, and employees of small businesses (34; 166), situations where noise levels often exceed recommended levels (77; 113).

Annual testing as part of a workplace hearing conservation program can increase awareness of noise exposure and effectively influence the majority of participants to change their hearing protection habits at both home and work (84).

Unfortunately, most companies give inadequate attention to environmental noise controls and instead rely primarily on hearing protectors to prevent hearing loss (30; 31; 53). However, in the absence of noise controls at the source, exposed workers remain at unnecessary risk (31; 53). Still, there is poor-quality evidence that stricter legislation implementation can reduce noise levels in workplaces, and controlled studies of engineering control interventions in the field have not been conducted (174).

About two fifths of employees (38%) do not use hearing protectors routinely (30). There is moderate-quality evidence that training of proper insertion of earplugs significantly reduces noise exposure at short-term follow-up (174). Hearing protection use correlates with the completeness of company hearing protection programs, suggesting that underuse of hearing protection by employees is “in some substantial part, attributable to incomplete or inadequate company efforts” (30). Nevertheless, there is poor-quality evidence that the better use of hearing protection devices as part of hearing loss prevention programs reduces the risk of hearing loss (174).

Recreational noise exposure is usually less frequent and of shorter duration than occupational noise exposure, but it may readily compound occupational noise damage. Many power tools, lawnmowers, firearms, sound speakers, and personal music players (eg, MP3 players) exceed safe sound exposure levels (171; 122; 138; 163; 145; 16; 14; 22; 150; 74; 85; 180; 115; 165; 169; 26; 176). For example, approximate dBA sound levels are 90 for a lawnmower, 100 for a chain saw, 120 for a rock concert, and 140 for a shotgun blast. The impulsive noise of firearms may be particularly damaging to the cochlea (162; 170). The main hearing loss-related risk factor for teenagers is exposure to recreational noise: frequent attendance at discotheques and pop-music concerts; use of personal stereos; and noise exposure in school workshops (91; 60; 47; 165; 169; 140). In a randomized, single-blind clinical trial, earplug use has been demonstrated to be effective in preventing temporary hearing loss after loud music exposure. Unfortunately, most students are unconcerned about potential effects of loud noise, and the use of hearing protection is minimal (less than 5%) (47).

Sound does not have to be annoying or painful to cause hearing loss over time. Hearing protection should be worn if individuals have to raise their voices to converse easily. Hearing protection devices commonly available include earmuffs or ear plugs. Earmuffs usually have higher noise-reduction ratings than earplugs; they can be worn in combination in extremely high noise environments, but the maximum noise reduction is approximately 50 dB because of bone conduction through the skull (125) and combination use of earplugs and earmuffs disrupts sound localization (154). Some individuals find earmuffs to be hot, cumbersome, or cosmetically unappealing, any of which can adversely affect usage (07). Training in earplug insertion is important for good attenuation (175). For difficult-to-fit external auditory canals, custom earplugs can be made from earmold impressions. Special ear plugs are also available for special needs (eg, for cosmetic considerations, hunting, singing, or specific work environments). In military situations, active noise cancellation earmuffs equipped for communication purposes seem to be the best protection for soldiers during military exercises (126). Misfit earplugs or earmuffs are much less effective and may not adequately protect hearing. Hearing aids (most of which are vented), cotton balls, and earplugs designed for swimming are all inadequate for hearing protection.

Affected patients may be fitted with hearing aids (or cochlear implants for profound hearing loss), but this does not generally restore hearing to normal, and sounds are often distorted.

There is no good evidence that pharmacological interventions help prevent hearing loss due to noise exposure (54). Even when drugs (eg, corticosteroids) or other treatments (eg, hyperbaric oxygen therapy) are discussed, it is not based on well-conducted randomized controlled trials, or even any trials whatsoever (05). Nevertheless, improved understanding of the biochemical processes underlying noise-induced hearing loss, and animal experiments, have raised hopes for potential therapeutic targets that can be addressed with intratympanic, intracochlear, or systemic delivery (190).

Drug delivery routes to the inner ear

Abbreviations: CCA: common cochlear artery; CNS: central neural system; IHCs: inner hair cells; OC: organ of Corti; OHCs: outer hair cells; OW: oval window; RW: round window; SM: scala media; SP: spiral prominence; ST: scala ty...

Media

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Noise-induced hearing loss

Differential Diagnosis

aging
presbycusis
vascular occlusive disease
trauma
Ménière syndrome
- viral infections
- meningitis
- toxins
- genetic syndromes
- acoustic neuroma
- vertigo
- ototoxins
- viral neurolabyrinthitis

Also Relevant

Autoimmune sensorineural hearing loss
Hearing loss in infants and children
Objective tinnitus
Otic capsule dysplasia
Presbycusis
- Pure-tone audiometry (audiogram)
- Sensorineural hearing loss
- Subjective tinnitus
- Sudden deafness
- Vestibular schwannoma

Clinical Categories

Neuro-Ophthalmology & Neuro-Otology

Noise-induced hearing loss

Noise-induced hearing loss

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Anatomic localization

Pathophysiology

Epidemiology

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Media

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Giant cell arteritis

Ischemic optic neuropathy

Transient visual loss

Vestibular schwannoma

Ophthalmic electrophysiology

Hyperventilation syndrome

Benign paroxysmal positional vertigo

Cortical blindness

Noise-induced hearing loss

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Anatomic localization

Pathophysiology

Epidemiology

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Media

References

Contributors

Author

Patient Profile

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Questions or Comment?

Also in This Category

Giant cell arteritis

Ischemic optic neuropathy

Transient visual loss

Vestibular schwannoma

Ophthalmic electrophysiology

Hyperventilation syndrome

Benign paroxysmal positional vertigo

Cortical blindness

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