Antioxidant use in the prevention of noise-induced hearing loss and ototoxic chemicals in the workplace

• Published in: The Journal of the Acoustical Society of America 2006-11, Vol.120 (5_Supplement), p.3197-3197
• Main Author: MacLean Uberuaga, Sandra C.
• Format: Article
• Language: English
• ISSN: 0001-4966; 1520-8524
• DOI: 10.1121/1.4788063

There have been discoveries in auditory research as to how the cochlea is injured during noise exposure and how it may sometimes be possible to reverse or prevent acute noise damage with medications. There are two primary mechanisms of damage; mechanical, as delicate tissue structures are torn apart when loud blasts occur above 125–130 dB SPL, and metabolic exhaustion, which commonly results from habitual noise exposure. During metabolic exhaustion toxic waste products (free radicals) form as cells in the cochlea are stressed. Our bodies can react to noise trauma by presenting a defense of antioxidant enzymes. However, when these defenses are overwhelmed, the hair cell is subject to serious damage to its nuclear DNA, mitochondria, and membranes. This research has been promising in animal studies. We will discuss pharmacological agents that can be used by the ear to synthesize the toxic products. The next step is well-designed human clinical trials in occupational settings where extreme noise levels cause hearing loss despite the seemingly appropriate use of hearing protection devices (e.g., aircraft carrier decks, mining and petroleum industries). Chemicals and agents that can cause hearing loss in the workplace will also be reviewed.