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Ethanol exacerbates noise-induced cochlear injury: Effects on hearing thresholds and hair cell loss
Seokhwan Lee1, Jieun Kang1, Sung-Won Choi2
1Department of Otorhinolaryngology-Head and Neck Surgery and Biomedical Research Institute, Pusan National University Hospital, Busan, South Korea.
Abstract:
Noise-induced hearing loss (NIHL) is a common auditory disorder, and acute alcohol consumption may exacerbate its severity. This study investigated whether concurrent ethanol exposure worsens NIHL, focusing on auditory brainstem response (ABR) threshold shifts and outer hair cell (OHC) loss in a rat model. Twenty-six male rats were randomly assigned to four groups: control, noise-only, ethanol-only, and noise with ethanol (N + E). Ethanol (1.5 g/kg intraperitoneally) was administered 30 min before a 2 h noise exposure at 116 dB sound pressure level (SPL) in the N + E group. ABR thresholds at multiple frequencies were measured at baseline and at 1, 7, 28, 56, and 84 days post-exposure. Cochlear OHC loss was quantified histologically at 12 weeks post-exposure. The results showed that the N + E group exhibited significantly greater initial ABR threshold shifts across all tested frequencies compared with the noise-only group. Threshold recovery in the N + E group remained incomplete at high frequencies (8-32 kHz) even after 12 weeks, whereas the noise-only group largely recovered to baseline by 12 weeks. All exposure groups exhibited OHC loss relative to controls, including the ethanol-only group. The N + E group had the most extensive OHC loss, particularly in the basal cochlear regions. In conclusion, concurrent ethanol exposure during loud noise leads to more severe and persistent ABR threshold elevations and greater cochlear hair cell loss than noise exposure alone, indicating that ethanol exacerbates NIHL. These findings suggest that alcohol consumption may heighten vulnerability to acoustic trauma in loud recreational settings, underscoring its public health implications.
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