Hearing loss in industrial workers accumulates from repeated daily (interrupted) exposures to excessive noise over a long period of employment. Most strategies designed to estimate hearing loss rely either upon extrapolations from experimental data acquired from short-term acute exposures or from noninterrupted long-term noise exposures or from epidemiological data with its typically 70 dB or more across-subject variability. Recent discoveries show that the peripheral auditory system can modulate the effects of noise exposure as much as 40 dB. These effects are believed to be partially mediated by the outer hair cell motor system which can be activated by a low-level noise exposure that precedes a hazardous noise exposure, or by interrupting a daily noise exposure regime. The outer hair cell bi-directional transduction system is also responsible for generating cochlear emissions which are now being intensively studied because of their potential use as a noninvasive and objective diagnostic test for noise-induced changes in outer hair cell function. Exposure to high-level impact noise continues to pose a problem to hearing in many industrial environments. Furthermore, there is virtually no experimental data on the accumulation of hearing loss from interrupted high-level impact noise and relatively little data available on the relation between cochlear emissions and noise-induced sensory cell pathology. Similarly, our knowledge of how low-level noise outside the work place affects hearing loss acquired in the work environment is very inadequate. The proposed research is designed to study the issues raised above in an animal model (chinchilla)by using as stimuli: (a) narrow band (400 Hz) impacts with center frequencies between 0.5 and 8.0 kHz to probe a wide frequency extent of the cochlea; (b) broad band impacts; and (c) complex high kurtosis continuous noise. The exposure paradigms will include both interrupted and noninterrupted exposures for 20 days and 5 days respectively. Exposures will be balanced for total energy so that comparisons based on energy can be made with existing data. Pure tone hearing threshold measured using evoked response audiometry and cubic distortion product evoked cochlear emission audiograms and input/output functions will be collected and correlated with sensory cell pathology. The objective is to contribute to: (l) an understanding of how hearing loss accumulates from repeated interrupted impact and complex noise exposures; (2) the development of the distortion product emission as an objective noninvasive diagnostic tool; and (3) an understanding and prediction of individual susceptibility to noise-induced hearing loss.
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