Noise Induced Hearing Loss

Noise induced hearing loss (NIHL) is permanent sensorineural hearing loss caused by exposure to excessive sound. It is the second most common cause of acquired sensorineural hearing loss after presbycusis. It affects about 10 to 15 percent of adults worldwide and about 16 percent of the world's disabling hearing loss.

Two exposure patterns cause NIHL:

• chronic occupational or recreational noise (sustained levels at or above 85 decibels A-weighted over 8 hours)
• acute acoustic trauma (a single impulse such as an explosion or gunshot of 140 dB or more)

Exposure risk is determined by intensity and duration. It follows an equal energy rule where each 3 dB increase halves the safe exposure time:

• 85 dB for 8 hours
• 88 dB for 4 hours
• 91 dB for 2 hours
• 94 dB for 1 hour
• 100 dB for 15 minutes
• 110 dB for 1.5 minutes

High risk occupations: construction, mining, manufacturing, agriculture, military, aviation, music and entertainment, and others. Recreational sources: personal audio devices at high volume, concerts, firearms, power tools, and motor sports.

Pathology comprises:

• damage to cochlear outer hair cells (initially at the basal turn of the 3 to 6 kilohertz region, with a "noise notch" at 4 kHz)
• mitochondrial oxidative stress and metabolic injury
• glutamate excitotoxicity with cochlear synaptopathy (loss of synapses between inner hair cells and auditory nerve fibres, causing "hidden hearing loss", with normal thresholds and difficulty hearing in noise)
• in severe cases, rupture of the organ of Corti

Susceptibility is increased by smoking, hypertension, diabetes, ototoxic drugs (aminoglycosides, cisplatin, loop diuretics), solvents (toluene, styrene) and vibration.

• Gradual, painless, bilateral and generally symmetrical hearing loss over years, with difficulty understanding speech, particularly in background noise, and difficulty hearing high pitched sounds (female and children voices, birds, alarms).
• Tinnitus (about 50 percent of those with NIHL), often high pitched, which may be the first symptom.
• Temporary threshold shift: transient hearing reduction and tinnitus after exposure (lasting hours to 2 days), which, with repeated exposure, becomes permanent.
• Acute acoustic trauma: sudden hearing loss, severe tinnitus, ear pain and fullness, and sometimes tympanic membrane perforation, ossicular injury and vertigo.
• Hyperacusis and distortion of sound (recruitment); no other otological symptoms; the otoscopic examination is normal.
• Social isolation, communication difficulties, safety hazards at work, and depression.

• History: detailed noise exposure (occupation, hobbies, years, hours per day, use of protection), previous tinnitus, medication, family history and other risks.
• Pure tone audiometry (in a sound treated room, ideally after 14 hours of no noise exposure to avoid temporary threshold shifts): bilateral sensorineural loss with a characteristic notch at 3, 4 or 6 kHz and recovery at 8 kHz. The notch broadens with continued exposure (affecting lower frequencies).
• Thresholds usually do not exceed 75 dB in the high frequencies and 40 dB in the low frequencies in a pure NIHL pattern. Asymmetry beyond 15 dB suggests another cause. Firearm use favours the ear closer to the muzzle, so the left ear is more affected in right handed shooters.
• Speech audiometry and speech in noise testing (cochlear synaptopathy), otoacoustic emissions (reduced or absent), and auditory brainstem response (reduced wave I amplitude with synaptopathy), with tympanometry.
• MRI of the internal auditory canal for asymmetric loss, to exclude retrocochlear pathology.
• Workplace noise survey (dosimetry), and surveillance audiograms with comparison to baseline (a standard threshold shift of 10 dB or more at 2, 3 and 4 kHz).
• Differential diagnosis: presbycusis (more symmetrical, down sloping), ototoxicity, genetic hearing loss, Ménière disease, otosclerosis, and acoustic neuroma.

There is no cure for the permanent loss. Prevention is the primary strategy, and management is rehabilitation.

• Prevention (hearing conservation programme):
  • Engineering noise controls: quieter machinery, enclosures, barriers, maintenance.
  • Administrative controls: limiting exposure time, rotation.
  • Personal protective equipment: foam earplugs (noise reduction rating 20 to 33 dB), earmuffs (25 to 30 dB), and dual protection (earplug plus earmuff) above 105 dB, with training on correct fitting. Custom musician earplugs give flat attenuation.
  • Noise at or above 85 dB (8-hour average) triggers audiometric monitoring (baseline within 6 months of employment and annually), and exposure above 90 dB requires protection.
  • Recreational: keep personal audio device volume below 60 percent for no more than 60 minutes (the "60/60 rule"), use noise cancelling headphones, and wear ear protection at concerts and shooting.
• Acute acoustic trauma and acute noise induced loss: immediate removal from noise, and early high dose corticosteroids (prednisolone 1 mg/kg daily, 60 mg, for 7 to 14 days with taper), started within 24 to 72 hours. Consider intratympanic steroid and hyperbaric oxygen therapy.
• Antioxidant agents (N-acetylcysteine 600 mg twice daily, magnesium, vitamins A, C, E) have been studied but are not established. Tympanic perforation is managed conservatively and repaired if persistent.
• Hearing aids: provide amplification with directional microphones and noise reduction features, fitted early for impairment affecting communication (typically average loss above 25 to 30 dB), with training; assistive listening devices, and cochlear implantation for severe to profound bilateral loss.
• Tinnitus management: sound therapy, counselling, cognitive behavioural therapy, tinnitus retraining therapy and hearing aids.
• Occupational: audiometric surveillance, notification and compensation, fitness for duty, and redeployment away from noise.
• Public health: education and regulation of noise at work and in leisure environments; screening of adolescents.
• Prognosis: loss is cumulative and irreversible, though progression stops when exposure ends (loss from noise does not progress after exposure ceases, apart from age related loss); early detection and prevention are critical.