Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

TLDR

Age‑related and noise‑induced hearing losses are multifactorial, and recent evidence indicates that prior noise damage can worsen age‑related hearing loss. The study aimed to determine whether early noise exposure accelerates age‑related hearing loss in mice. CBA/CaJ mice were exposed to an 8–16 kHz, 100 dB, 2‑hour noise band at ages 4–124 weeks, then monitored for 2–96 weeks post‑exposure alongside unexposed controls. Mice exposed early in life exhibited progressive cochlear neural degeneration and accelerated age‑related hearing loss after long post‑exposure periods, even when initial noise‑induced threshold shifts were minimal, indicating that sublethal noise‑induced changes heighten vulnerability to aging.

Abstract

Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8-16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4-124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4-8 weeks) were 40-50 dB; older-exposed animals (> or =16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.