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Adverse effects of noise on hearing: basic mechanisms.

Bohne-BA; Harding-GW
Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, R01-OH-003973, 2008 Oct; :1-22
Our studies addressed the damaging effects of workplace noise on the structure of the hearing organ, the organ of Corti (OC), and how these structural changes correlate with hearing loss. Noise is a significant problem in the lives of many individuals. NIOSH and the National Institute on Deafness and other Communication Disorders (NIDCD) estimate that at least 30 million American workers are exposed to hazardous levels of occupational noise. Since the beginning of the war on terrorism, a large number of military personnel have been e}"'Posed to hazardous noise during their military service and an increasing number of them have developed noise-induced hearing loss (NIHL). It has been estimated that approximately 10 million Americans have NIHL. The human costs for hearing impairment, including limited job opportunities and lost productivity, and economic costs for workers' compensation and hearing aids, add up to billions of dollars per year. Depending on the frequency content, intensity and duration of the noise, the individual human or animal may sustain a temporary threshold shift (TIS) or a permanent threshold shift (PTS). Several hypotheses exist on the pathogenesis of TTS and PTS, but none have been proven unequivocally. No hypothesis has attempted to explain how workplace noise damages then destroys sensory cells, supporting cells and nerve fibers in the cochlea. It is not known why noise exposure causes different patterns of cell loss in the apical and basal halves of the Oc. The lack of knowledge about mechanisms of noise-induced hair-cell death has hindered identification of noise-protective agents that could be used to ameliorate NIHL in workers. Chinchillas were functionally tested [i.e., auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) pre- and one or more times post-exposure. Their cochleae were fixed in-vivo, embedded in plastic and dissected as flat preparations. Cochleae length was measured and differential counts of missing and dying hair cells (HCs) were made throughout the cochleae. Changes in auditory function after exposure to high-frequency [i.e., 4-kHz octave band of noise (OBN)] or low-frequency (i.e., O.S-kHz OBN) noise were compared to structural changes in the Oc. It was found that immediately after a moderate noise exposure (i.e., < 3 h recovery), shifts in ABR thresholds and DPOAE levels reflected pathology in the supporting cells of the OC, as well as in the HCs. After recovery from a moderate exposure, ABR PTSs detected focal HC losses whereas DPOAE permanent level shifts (PLSs) did not. These results strongly suggest that DPOAE PI, Ss cannot be used to monitor noise-exposed humans in order to identify beginning outer hair cell (OHC) losses in their cochleae. By injecting a solution of tracer particles into the endolymphatic space (US) in-vivo, it was shown that the barrier function of the reticular lamina breaks down temporarily after a damaging noise exposure. This was determined by noting the distribution of tracer particles in the ES and the OC at 0 d and 28 d of recovery. When the OC was damaged by noise such that OHCs degenerated, endolymph containing the injected tracer particles entered the OC and spread within its fluid spaces. The continuing loss of sensory cells that often occurs post-noise e}"'P0sure appears to be due in part to an acute breakdown of the reticular lamina and endolymph contamination of the Oc. This mechanism may also account for the formation of focal OHC losses in restricted regions of the Oc. Losses of HCs occur in focal OC regions after exposure to a low-frequency (O.S-kHz) or a high-frequency (4-kHz) OBN. The distribution of focal HC lesions is different in the apical and basal halves of the Oc. We have shown that exposure level makes a difference in the development of focal lesions. A focal lesion is defined as a region in which SO% or more of the OHCs and/or inner hair cells (IHCs) are missing over a distance of at least 0.03 mm. It appears that the mechanisms for the formation of OHC focal lesions differ in the basal and apical halves of the OC, both during and after the exposure. The mechanism(s) for the formation of pure IHC focal lesions appears to be different from those leading to the formation of OHC focal lesions. Neither the ABR threshold shifts (ISs) nor the DPOAE level shifts (LSs) consistently showed a difference in rate of recovery with post-exposure time between ears that developed a PTS and those that did not. Thus, when examined in detail, the notion that delayed recovery from ABRTS and/or DPOAE LS might indicate that the ear had an increased susceptibility to noise was not supported. Using morphological criteria and in-vivo treatment with the vital dye, trypan blue, we determined what death pathways chinchilla OHCs follow after exposure to typical workplace noise [i.e., 4-kHz OBN or O.S-kHz OBN at 80-9S dB sound pressure level (SPL)]. The apex-to-base patterns of HC death were determined at 0 and 30 days post-exposure. We compared changes in auditory function to losses of HCs and other types of structural damage. We discovered that some noise-damaged OHCs had a morphological appearance that was distinct from apoptosis, oncosis and autophagy. If this newly discovered pathway dominates OHC death following moderate noise exposures, this information will revolutionize thinking about the mechanism(s) of noise damage. Our results have provided information on the basic mechanisms of damage from moderate noise so that drugs can be identified that will prevent or minimize noise-induced HC death.
Noise; Hearing; Hearing-loss; Hazards; Exposure-levels; Military-personnel; Workers; Work-environment; Auditory-system; Pathology; Monitors; Noise-induced-hearing-loss; Animals; Animal-studies; Laboratory-animals
Barbara A. Bohne, Ph.D., Washington University School of Medicine, Dept. of Otolaryngology, Box 8115, 660 South Euclid A venue, St. Louis, MO 63110
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National Institute for Occupational Safety and Health
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Washington University, St. Louis