Seminars in Hearing Research

Date: Thursday, December 05, 2024

Location: Nelson Hall, Room 1215

Time: 12:00-1:00pm

Speaker:  Meredith Christine Ziliak, PhD Candidate,BIO  

Title: The Progression of Damage in the Peripheral and Central Auditory Systems Following Small Arms Fire-Like Noise Exposure

Abstract:  Small arms fire-like (SAF) noise is an acute form of noise exposure commonly found in military and law enforcement occupations, as well as recreational activities. While it is well-known that noise exposure damages the auditory system, most studies focus on identifying changes in response to extended narrowband noise exposures. It is still unclear how SAF noise induces damage to the peripheral and central auditory system. Additionally, the studies that have investigated the effects of SAF noise on the auditory systems have primarily looked at either the immediate or longitudinal changes (Altschuler et al., 2019). Therefore, the purpose of this study is to identify the progression of functional changes in the peripheral and central auditory systems in response to SAF noise using distortion product otoacoustic emissions (DPOAEs), thresholds, auditory brainstem responses (ABRs), and middle latency responses (MLRs). We hypothesize SAF noise exposure will result in phases of damage that differentially affect cochlear and neuronal function. Acute damage up to four weeks may resemble phenotypes consistent with traditional noise induced damage such as reduced DPOAEs, thresholds, and wave 1, but early longitudinal damage four weeks and after may resemble electrophysiological phenotypes consistent with aging or damage induced by cellular stress and chronic dysfunction to damaged neurons. To test these hypotheses, F344 rat subjects (3-6 months) were exposed to SAF noise at either 120 dBpSPL (SAF exposure group; n=8; F=4) or 60 dBpSPL (sham group; n=4, F=2). At baseline and 7-, 14-, 28-, and 56-days post-exposure, we measured DPOAEs (f2 = 4, 8, and 10 kHz, f2/f1 = 1.22) (L1 = 60 dB, L1-L2 = 10 dB), ABRs (0.03 ms click, 8 kHz, and 10 kHz), and MLRs (repeated click groupings of decreasing inter-click-intervals, called 1-2-8 clicks). Thresholds were found to be persistently elevated. Distortion product (DP) amplitudes were found to be persistently decreased at 8 and 10 kHz, but not 4 kHz. ABR waveform and peak analysis demonstrated an overall decrease in amplitude with a greater decrease in wave 5. MLR peak analysis demonstrated patterns of damage distinct to each click across days. All measures demonstrated a general trend of damage before minor recovery or plateau. Our findings suggest that the diagnostic profile of SAF noise exposure may differ from previously studied models of noise induced hearing loss. Future work will identify mechanisms of damage at different time points post-exposure through anatomical imaging of biomarkers of damage to associate change in function with structure.

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