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  • Updated 10.21.2020
  • Released 09.10.2001
  • Expires For CME 10.21.2023

Noise-induced hearing loss

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 has been recognized since at least the early 19th century as a result of artillery fire or chronic noise exposure in certain occupations (eg, blacksmiths) (90; 125). By the late 19th century occupational hearing loss was recognized in a broader group of workers (eg, boilermakers and railroad workers) (101). 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 (83). 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 (80).

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).

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