The role of micro-noise trauma in the etiology of aging-related changes in the inner ear.

Eleven chinchillas between 1 and 2.4 years of age had the malleus/incus complex removed from one middle ear and then lived in the Washington University animal facilities for 4 years post-surgery. Each animal had one ear (termed ambient-noise) in which the conductive apparatus was intact; the other ear (termed noise-protected) had a 50-60 dB conductive hearing loss. The background sound level in the animal facility was 59 dBA with periodic brief sounds up to 102 dBA. After the 4-year experimental period, both ears were fixed, embedded in plastic and dissected for microscopic examination as flat preparations. The quantitative and qualitative findings in the noise-protected ears were compared to those in the ambient-noise ears. Both groups of ears sustained losses of sensory and supporting cells throughout the organ of Corti. A variable amount of age pigment was found to have accumulated in the outer hair cells and all supporting cells. In the noise-protected ears, inner hair cell loss ranged from 1.0 to 3.1% and averaged 1.7 +/- 0.8%; outer hair cell loss ranged from 1.8 to 6.4% and averaged 3.6 +/- 1.2%. In the ambient-noise ears, inner hair cell loss ranged from 0.7 to 2.8% and averaged 1.6 +/- 0.7%; outer hair cell loss ranged from 1.3 to 5.4% and averaged 3.6 +/- 1.2%. Within-animal comparison of cell losses in the noise-protected and ambient-noise ears revealed no significant difference between the two groups. It is concluded that long-term exposure to micro-noise does not accelerate the spontaneous loss of sensory cells which occurs with aging. Although not quantified, there was no obvious difference in the amount or cellular distribution of age pigment in the two groups. Thus, it appears that the formation of age pigment in the ear is the result of the cells' basic metabolic processes rather than the wear and tear from sensory transduction.