Noise pollution is a major public hazard. Previous studies have shown that environmental noise affects the reorganization of the auditory cortex and leads to behavioral abnormality; however, the effects of long-term environmental noise exposure on the inner ear and hearing remain to be elucidated. In this study, we simulated environmental noise with a long-term 70 dB sound pressure level "white" noise, observed its effect on the inner ears of C57BL/6J mice, and developed an in vitro model for mechanistic studies. We found that environmental noise increased the hearing threshold, decreased the auditory response amplitude, and aggravated the range and extent of age-related hearing loss (ARHL), especially in the intermediate frequency band in mice. Cochlear ribbon synapse is the primary site of inner ear injury caused by environmental noise. We also verified, through an in vitro simulation of the excitatory toxicity of glutamate and aging effects, that the activation of NLRP3 inflammasome plays a vital role in the cochlear ribbon synaptic damage. Our results show that long-term exposure to low-intensity environmental noise can lead to hearing loss via the disruption of ribbon synapses, which is caused by an inflammatory reaction. Additionally, environmental noise can further aggravate the progression of ARHL. This study expounded the pathogenesis of the inner ear damage caused by environmental noise exposure and provides a new direction for the prevention and treatment of hearing loss.

Long-term exposure to low-intensity environmental noise aggravates age-related hearing loss via disruption of cochlear ribbon synapses.

Objective: To determine if decreased Cu/Zn superoxide dismutase (SOD1) levels in inner pillar cells is associated and diminished inner hair cell ribbon synapse plasticity in presbycusis. Methods: We evaluated the auditory brainstem responses (ABRs) of 2-, 5-, 6-, and 7-month-old C57BL/6J mice. ABRs were obtained using clicks and 4-, 12-, and 32-kHz tone bursts. Cochleae were collected immediately after audiometric assessment for Western blot analysis. The inner and outer hair cells and the inner hair cell ribbon synapses were separately counted. Frozen tissue sections were exposed to immunofluorescent staining for examine of SOD1 expression in the cochlea. Results: ABR thresholds were elevated in the 6- and 7-month groups. The maximal elevation was detected at 32 kHz. Distortion product otoacoustic emission amplitudes decreased in the mice at 5 months. SOD1 levels in the cochlea decreased as the mice aged. A reduction of SOD1 in the inner pillar cells was detected. Hair cell counting showed an apparent decrease in OHCs from 6 months onwards. The mean number of ribbon synapses was 17.2 ± 1.4, 17.7 ± 2.74, 12.8 ± 0.95, and 9.7 ± 3.08 in the 2-, 5-, 6-, and 7-month groups, respectively. This number significantly decreased with increasing age (P < 0.05). Conclusion: Our study revealed that age-related hearing loss (ARHL) of C57BL/6J mice was caused by multi-site degeneration in the cochlea. Decreased expression of SOD1 in the cochlea is consistent with changes in the hearing threshold. Decreased SOD1 levels in the inner pillar cells may lead to diminished basilar membrane vibration and a reduction in the number of ribbon synapses, which plays an essential role in age-related hearing loss (ARHL).

Decreased levels of superoxide dismutase in inner pillar cells contribute to ribbon synapse impairment in presbycusis.

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Decreased levels of superoxide dismutase in inner pillar cells contribute to ribbon synapse impairment in presbycusis.