Strong evidence has now emerged from animal models that noise exposure, even at levels common in occupational and recreational settings, can cause a substantial loss of afferent synapses and nerve terminals innervating the cochlea. Such cochlear synaptopathy does not affect hearing thresholds, and hence is completely undetected in current standard audiological testing. Despite leaving thresholds intact, we hypothesized that by reducing the effective number of auditory-nerve fibers, synaptopathy may degrade suprathreshold coding of temporal information and hence explain the suprathreshold listening problems that many listeners experience despite normal hearing thresholds (NHTs). Consistent with this, we recently documented that among listeners with NHTs, there are large individual differences in the ability to perceive subtle temporal features of clearly audible sounds and that these suprathreshold perceptual differences correlate with suprathreshold coding of temporal information in the auditory brainstem. In further support of this hypothesis, our preliminary data show that individual differences in brainstem temporal coding are already present at the level of the auditory nerve. In the current proposal, we leverage an active hearing conservation program led by the Purdue Audiology Clinic, and a large on-campus student marching band to directly test the effects of occupational and recreational noise-exposure on suprathreshold hearing using parallel behavioral and non-invasive physiological measurements. Further, to directly link the human physiological measures to synaptopathy, we expand on an ongoing NIH project at Purdue that focuses on single-neuron and behavioral characterizations of synaptopathic effects in an animal model (chinchilla) to include our innovative battery of non-invasive measures. This multidisciplinary study is organized in three Specific aims:
In Aim 1, we quantify suprathreshold coding using three distinct non-invasive physiological assays that are designed to be sensitive to synaptopathy in three separate ?high-risk? human groups.
In Aim 2, we quantify suprathreshold perception using behavioral measures of temporal sensitivity and listening in noise in the same ?high-risk? human groups.
In Aim 3, we will relate the same non-invasive physiological measures of coding used in humans (as in Aim 1) to the degree of synaptopathy in the chinchilla model, as well as to objective (noise dosimetry) and questionnaire-based estimates of noise-exposure in the human subjects. Our results will not only evaluate clinically-viable prospective diagnostic measures of synaptopathy, but these data will advance our understanding of the complex relationships between noise exposure, information coding by early parts of the auditory pathway, and perceptual ability.
We now know from animal models that overexposure to noise can cause permanent nerve loss in the inner ear, and that this nerve loss cannot be measured with current clinical hearing testing. Based on our recent findings on how individual human listeners differ in challenging hearing tasks, we hypothesize that this hidden noise-induced nerve loss may be causing difficulty understanding speech in situations with background noise, such as crowded restaurants, busy streets, or sports arenas. In a multidisciplinary translational approach, we test this hypothesis and evaluate prospective clinical measures for hidden noise-induced nerve loss through studies on occupationally and recreationally noise-exposed humans, and simultaneously in an animal model in which nerve loss can be measured directly.