Noise Exposure and Hearing Loss

Etiology

The source of noise exposure can be occupational or environmental. Occupational noise exposure occurs in areas like mines, factories, rail yards, construction sites, or military bases. Environmental noise exposure occurs on highways, trains, airplanes, and in recreational places like nightclubs, sporting venues, or shooting ranges. Additionally, using earphones or headphones while listening to loud music has increased the risk of early sensorineural hearing loss in young adults.[2]

Noise-induced hearing loss (NIHL) may be acute or chronic. Acute noise exposure, or acoustic trauma, may, depending on the intensity of the exposure, result in reversible or irreversible hearing loss from explosions, loud music, and other short-duration, high-amplitude sounds. Chronic noise exposure, on the other hand, can cause various auditory and nonauditory health problems. Other factors that may affect the severity of acquired sensorineural hearing loss include socioeconomic status, ethnicity, age, tobacco use, exposure to ototoxic drugs, and associated comorbidities such as diabetes and hypertension.[3][4]

Epidemiology

The exact incidence of NIHL is difficult to determine due to the limited data available. The World Health Organization estimates that more than 1 billion people worldwide between the ages of 12 and 35 years are at risk of hearing loss due to recreational exposure to loud sounds. NIHL is more prevalent in males, predominantly due to greater occupational exposure, particularly in lower socioeconomic status populations.[5] Females, however, may be somewhat protected from NIHL by hormonal effects. NIHL is considered the second-most-common cause of occupational illness, affecting roughly one-fifth of American adults with hearing loss.[6][7]

Pathophysiology

The auditory apparatus comprises the outer, middle, and inner ears. The external or outer ear consists of the pinna and the external auditory canal. The pinna localizes sounds and conducts them to the external auditory meatus, the entrance to the external auditory canal. The external auditory canal acts as a resonator that amplifies sounds by 5 to 10 dB in the 2 to 5 kHz frequency range.

The middle ear is separated from the outer ear by the tympanic membrane. It contains the ossicular chain, which amplifies the incoming sound energy by impedance matching, ultimately vibrating the footplate of stapes. This movement is transmitted to the perilymph, causing wave-like motion of the basilar membrane, starting from the base of the cochlea and progressing toward the apex (see Image. Cochlea, Cross-Section). According to the "traveling theory of Von Békésy," the wave propagates along the basilar membrane, and different regions of the cochlea are stimulated depending on the fundamental frequency of the vibration. This forms the basis of the tonotopic or place theory of the cochlea, in which high-frequency sounds produce the greatest displacement of the basilar membrane near the basal end of the cochlea, and low-frequency sounds produce the greatest displacement at the apical end.[8]

The inner ear's tensor tympani and stapedius muscles attenuate sounds via reflex contraction, thereby protecting the cochlea from injury. The stapedius muscle plays a crucial role by attenuating low-frequency sounds greater than 80 to 90 dB through reflexive contraction, with a 100 to 200 ms latency. This delay prevents the stapedius muscle from protecting the cochlea from high-intensity impulse noises like gunshots, which can cause acoustic trauma. For this reason, providing a noise primer before a loud noise will preemptively trigger otoprotective stapedial contraction that may reduce noise-induced cochlear synaptopathy, which is characterized by inner hair cell synaptic losses and leads to tinnitus, hyperacusis, and difficulty hearing in noisy environments.[9][10]

Because of its acute and cumulative effects on the cochlea, noise may be considered a type of toxin, manifesting its effects in proportion to the total dose. The two primary presentations of NIHL are temporary and permanent threshold shifts.

Temporary threshold shift (TTS) occurs after short-term exposure or acoustic trauma and recovers in a few days. TTS happens primarily due to the reversible uncoupling of outer hair cell stereocilia from the tectorial membrane, although specific synaptopathic mechanisms are also believed to be involved. Permanent threshold shift (PTS) occurs after chronic noise exposure or acoustic trauma and is irreversible. PTS occurs due to the loss of outer hair cells, especially at the basal turn, followed by neuronal degeneration of the auditory nerve. The inability of mammalian sensory hair cells to regenerate causes permanent damage. Repeated TTS can also cause PTS.[11]

NIHL results from the interaction of genetic and environmental factors and is based on the equal-energy principle, which states that equal energy causes equal damage. In essence, higher levels of noise exposure over a short period or equivalent lower levels of noise exposure over a prolonged period will cause similar degrees of cochlear damage. NIHL may occur due to several pathological processes. Metabolic derangements may contribute to NIHL, such as excessive glutamate release damaging inner hair cell synapses or the accumulation of reactive oxygen species damaging DNA and causing cellular death.[12][13][14] Vascular insufficiency may cause cochlear hypoxia and outer hair cell damage depleting the sensory epithelium of the cochlea, especially of the outer hair cells and their associated neurons.[15][16]

History and Physical

A single loud noise exposure may cause acoustic trauma. Characteristics of acoustic trauma include hearing loss, tinnitus, hyperacusis, dizziness, aural fullness, and headache. Concurrent acoustic shock may occur, characterized by otalgia, nausea, anxiety, fatigue, and depression. Contrarily, clinical symptoms from chronic noise exposure are typically limited to hearing loss and tinnitus. Tinnitus, or "ringing in the ears," is the subjective sensation of sound; it is frequently bothersome and is an early indicator of auditory injury. NIHL-associated tinnitus occurs with threshold elevation in the 3 to 6 kHz region of the pure-tone audiogram.[17][18]

Noise exposure may also cause nonauditory symptoms like headache, anxiety, depression, insomnia, poor concentration with daytime sleepiness, increased risk of hypertension and cardiovascular disease in adults, and cognitive decline in children. NIHL causes a maximum reduction in hearing sensitivity in the 3 to 6 kHz range, with recovery towards the normal baseline at 8 kHz and above.[19] 

The 3 factors that must be considered when arriving at a diagnosis of NIHL are the type and degree of noise exposure, the potential for age-related hearing impairment, and possible idiopathic degenerative changes in predisposed individuals. 

NIHL is sensorineural in nature and almost always bilateral with symmetrical or near symmetrical loss except when caused by unilateral noise exposure, such as with firearm use, in which one ear is pointed toward the weapon's muzzle and the other ear is pointed away. Patients with typical NIHL have normal or near-normal speech discrimination scores.[20]

The rate of NIHL due to chronic noise exposure is greatest during the first 10 to 15 years of noise exposure, after which the loss rate decreases gradually without significant progression. Noise exposure alone does not usually cause hearing loss of more than 75 dB in higher frequencies and 40 dB in lower frequencies. Patients with NIHL demonstrate pure-tone audiogram "notching" at 3000, 4000, or 6000 Hz, with recovery at 8000 Hz.[18]

Evaluation

The diagnosis of NIHL should only be made after a comprehensive evaluation and consideration of other possibly contributing to hearing loss; some individuals with occupation-associated NIHL may claim compensation. A battery of audiological tests is required to diagnose NIHL.

Pure-tone Audiometry

Conventional audiometry usually reveals bilateral high-frequency hearing loss with a notch between 3 and 6 kHz and recovery at 8 kHz (see Image. Audiogram, Noise-Induced Hearing Loss). In cases of asymmetrical hearing loss, magnetic resonance imaging of the brain with contrast should be performed to rule out vestibular schwannoma. Asymmetrical hearing loss is characterized by a difference of 15 dB or more in any two frequencies in the range of 2 to 8 kHz, 20 dB or more in any two contiguous frequencies, or more than a 10 dB difference in the 2 kHz frequency.[21]

Hearing in Noise Test 

Sentences are repeated in quiet surroundings and with background noise. Persons with presbycusis and central auditory processing disorder have difficulty hearing in noise. This test also helps determine the signal-to-noise ratio for programming hearing aids.

Speech Audiometry 

Basic speech audiometry is an assessment of the reception, discrimination, and recognition of speech. The speech recognition threshold (SRT) is the minimum hearing level at which an individual can correctly repeat 50% of the speech material. The word recognition score (WR) or speech discrimination score represents the number of words correctly repeated, expressed as a percentage. The SRT scores in quiet and noisy surroundings may be decreased in the early stages of NIHL despite normal audiometry thresholds. This occurs secondary to synaptopathic mechanisms and decreased temporal processing. If SRT scores diverge more than 10 dB from pure-tone audiometry thresholds for speech frequencies, nonorganic hearing loss should be excluded.[22]

Otoacoustic Emissions

Otoacoustic emissions (OAEs) are sounds produced by the movement of outer hair cells within a properly functioning cochlea when stimulated by external sounds. This is an objective, sensitive, and easy-to-use test. Distortion product OAEs can detect early NIHL with 82% sensitivity and 92.5% specificity even when pure-tone audiometry is normal.[23]

Brainstem-evoked Response Audiometry

Brainstem-evoked response audiometry (BERA) is an electrophysiological measurement used to detect noise-induced synaptopathy by revealing a reduction of wave I of the auditory brainstem response. This test is also helpful for identifying individuals with feigned hearing loss, especially those seeking compensation.

Evidence suggests that auditory reflex testing may help detect early noise-induced synaptopathy, but further research is required. The efficacy of high-frequency audiometry (8 to 20 kHz) to detect early NIHL is also under investigation.[24]

Calculating Hearing Loss

Calculating the percentage of hearing loss is performed in three steps and is the basis for determining the magnitude of a compensation claim.[25]  

1. The arithmetic mean of the hearing thresholds for each ear at 500 Hz, 1 kHz, 2 kHz, and 3 kHz determine the pure-tone audiometry threshold average. 
2. The monaural hearing impairment for each ear is calculated by subtracting 25 dB from the pure-tone audiometry threshold average calculated in Step 1 and multiplying the result by 1.5. This calculation assumes that hearing loss becomes a handicap beyond 25 dB and increases at a rate of 1.5% per dB after 25 dB.
3. The hearing handicap is calculated by multiplying the better ear impairment percentage by 5, adding this to the worse ear impairment percentage, and dividing the total by 6.

Table. Hearing handicap calculation worksheet

Treatment / Management

The gold-standard treatment of NIHL is amplification through the use of hearing aids. A hearing aid is recommended if the SRT is more than 25 dB or the word recognition score is less than 80% at presentation levels of 50 dB above the threshold. Noise-induced tinnitus is treated with a tinnitus masker or tinnitus retraining therapy.

Some pharmaceutical agents show promising protective effects against NIHL, including corticosteroids, antioxidants, and neurotrophins. Corticosteroids are helpful in acute acoustic trauma due to their anti-inflammatory effect when administered intravenously, orally, or intratympanically.[26][27] Intravenous corticosteroid regimens may include methylprednisolone 125 mg on the first day of treatment, 80 mg on the second day, and 40 mg on the last day.[28] Alternatively, oral prednisone may be administered at 1 mg/kg up to 60 mg daily for 1 to 2 weeks, with longer courses producing better outcomes in patients who can tolerate high-dose steroids for more than 1 week.[26][29] However, the role of corticosteroids in treating chronic occupational NIHL is unclear.

Hyperbaric oxygen therapy has also proven useful in acoustic trauma, particularly if corticosteroid therapy fails; treatment may consist of 120-minute dives to 200 to 280 kPa daily for 10 days.[28][30][31] Based on the oxidative stress hypotheses, antioxidants like N-acetyl cysteine, D-methionine, and coenzyme Q10 are undergoing clinical trials for use as otoprotective agents.[32][33] Magnesium and vitamins A, E, C, and B12 have also demonstrated protective effects against NIHL in animal models.[34] (A1)

The cornerstone of NIHL management is prevention. Prevention of NIHL involves periodic noise monitoring by exposure assessment, reducing noise exposure in workplaces, and early detection of noise-induced auditory injury. Noise monitoring can be conducted through area noise surveys and personal noise dosimetry. During area noise surveys, a sound pressure level meter is kept in a specific location to sample the noise field. For personal noise dosimetry, the sound pressure level meter is worn on the body with a microphone on the shoulder, 5 in lateral to the ear.

Reducing occupational noise exposure can be achieved via engineering controls, administrative controls, and personal hearing protection. Engineering control measures include enclosures to isolate noise sources from personnel and other barriers to reduce acoustic energy transmission. Regulatory standards determine administrative controls in a given location or jurisdiction. Many countries follow the permissible exposure limit of 85 dBA in workplaces. The dBA is sound pressure measured with A-weighting, an adjusted measurement of noise that considers the sensitivity of the human ear to different sound frequencies. Workers should be educated regarding the necessity of personal hearing protection devices like ear plugs and ear muffs, which can attenuate noise levels by up to approximately 30 dB.

Early detection of noise-induced auditory damage may be achieved by routine audiometric examinations and health education. All employees working in noisy environments should have a baseline audiogram within 6 months of starting work. If a 10 dB or more standard threshold shift in hearing average at test frequencies of 2, 3, and 4 kHz in either ear is noted, the employee should be enrolled in a hearing conservation program.[8][35](B2)

Differential Diagnosis

The differential diagnosis of NIHL includes many common causes of sensorineural hearing loss and inorganic or functional hearing loss.

Presbycusis is age-related hearing loss, with high-frequency, down-sloping hearing loss (see Image. Audiogram, Presbycusis). Presbycusis may be sensory, where there is damage or death of cochlear sensory hair cells, or metabolic, where there is reduced functioning of the stria vascularis.[36]

Hereditary hearing impairment causing progressive degeneration traditionally manifests in childhood or early adolescence. Structural anomalies such as an enlarged vestibular aqueduct or Mondini deformity may be present.[37]

Hearing loss resulting from previous infections like labyrinthitis, meningitis, or encephalitis with cochlear ossification may mimic NIHL.

Hearing loss from central nervous system dysfunction, such as following a posterior circulation cerebrovascular accident, is typically characterized by the sudden onset of hearing loss and is frequently associated with other neurological deficits.[38] Cerebellopontine angle tumors may cause hearing loss; hearing loss is usually slowly progressive and unilateral, sometimes with associated tinnitus, vertigo, and headache (see Image. Audiogram, Vestibular Schwannoma).[39]

Auditory neuropathy and synaptopathy result in defective neural processing of auditory stimuli. The defect may be with inner hair cell activity, auditory nerve signal transmission, or dysfunction at the synapses of the inner hair cells with the auditory nerve. Patients with this disorder have difficulty hearing in noisy environments and suffer from directional hearing loss, usually bilateral. Audiological evaluation reveals abnormal BERA with the presence of OAEs.[40]

The general presentation of the person with feigned hearing loss is of exaggerated hearing difficulty but with normal vocal volume. There may be a lack of the required eye contact or observed lip movements that patients with organic hearing loss need to understand speech. An SRT better than the PTA by more than 10 to 15 dB suggests functional hearing loss, which may be confirmed with a Stenger test.[41][22]

Prognosis

The natural history of NIHL indicates that the greatest progression of hearing loss occurs in the first 10 to 15 years, following which hearing levels tend to stabilize somewhat. NIHL generally does not progress after the cessation of noise exposure.

As NIHL is a permanent and irreversible condition, prevention is critical. Noise exposure should be regulated carefully by following the maximum allowable daily noise exposure or permissible exposure limit (PEL). For an 8-hour workday, OSHA regulations require employers to use engineering controls when exposures exceed 90 dBA, and administrative controls, such as hearing protection and annual hearing monitoring, when exposures exceed 85 dBA. For exposures longer or shorter than 8 hours, the PEL is increased or decreased by 5 dB for each halving or doubling of sound exposure, respectively.

The United States National Institute for Occupational Safety and Health recommends that the highest permissible level of noise exposure in the workplace be an average of 85 dB over an 8-hour workday; for exposures other than 8 hours, the PEL is increased or decreased by 3 dB for each halving or doubling of sound exposure, respectively. For example, the PEL for a 4-hour workday would be 88 dB, and for a 16-hour workday, it would be 82 dB.[42][43]

The World Health Organization also recommends daily noise exposure limits, suggesting that levels should not exceed 70 dB over 24 hours or 85 dB over 1 hour to avoid hearing impairment.[44]

Complications

The effects of loud noise exposure are pathological, psychological, and sociological. Apart from the well-known auditory effects of hearing loss, tinnitus, and vertigo, noise also has systemic effects on metabolism, including increasing cortisol and norepinephrine levels, among other hormones.[45][46][47] These derangements significantly increase the risk of hypertension, ischemic heart disease, myocardial infarction, and stroke.[48]

Chronic noise exposure also impairs sleep, increasing the risk of workplace accidents. Additionally, there is an increase in the incidence of depression and generalized anxiety disorder in individuals with chronic noise exposure. Excessive noise may also affect family life, causing irritability, annoyance, confusion, and lack of concentration.[49] 

NIHL can affect interpersonal communication, thereby diminishing self-esteem and interfering with relationships. It can also reduce attention and cognition, increasing the risk of dementia. Noise may affect work performance, but this seems to depend on individual predisposition. The financial burden and compensation cost for employers for hearing loss can be high.