As distortion product otoacoustic emissions (DPOAEs) and temporary threshold shifts (TTS) are both presumed to originate in outer hair cells of the cochlea, the proposed study is a direct and non-invasive physiologic approach to the question of TTS mechanisms. The goal of this study is to assess the predictive value of DPOAEs' ability to identify physiologic changes in hair cell function in humans exposed to acoustic overstimulation. It is hypothesized that acoustic overstimulation will result in the decreased amplitude of DPOAEs. The rationale behind this approach is based on the assumption that the output of cochlear transducers is modified (decreased) as a result of acoustic overexposure. The proposed study will use acoustic overstimulation adequate to produce TTS. If this approach proves efficacious, future studies will examine the power of DPOAEs to identify subclinical effects of acoustic overexposure at exposure levels not adequate to produce TTS. No activity is reported.
