Hidden Hearing Loss? No Effect of Common Recreational Noise Exposure on Cochlear Nerve Response Amplitude in Humans

Abstract

This study tested hypothesized relationships between noise exposure and auditory deficits. Both retrospective assessment of potential associations between noise exposure history and performance on an audiologic test battery and prospective assessment of potential changes in performance after new recreational noise exposure were completed.Methods: 32 participants (13M, 19F) with normal hearing (25-dB HL or better, 0.25–8 kHz) were asked to participate in 3 pre- and post-exposure sessions including: otoscopy, tympanometry, distortion product otoacoustic emissions (DPOAEs) (f2 frequencies 1–8 kHz), pure-tone audiometry (0.25–8 kHz), Words-in-Noise (WIN) test, and electrocochleography (eCochG) measurements at 70, 80, and 90-dB nHL (click and 2–4 kHz tone-bursts). The first session was used to collect baseline data, the second session was collected the day after a loud recreational event, and the third session was collected 1-week later. Of the 32 participants, 26 completed all 3 sessions.Results: The retrospective analysis did not reveal statistically significant relationships between noise exposure history and any auditory deficits. The day after new exposure, there was a statistically significant correlation between noise “dose” and WIN performance overall, and within the 4-dB signal-to-babble ratio. In contrast, there were no statistically significant correlations between noise dose and changes in threshold, DPOAE amplitude, or AP amplitude the day after new noise exposure. Additional analyses revealed a statistically significant relationship between TTS and DPOAE amplitude at 6 kHz, with temporarily decreased DPOAE amplitude observed with increasing TTS.Conclusions: There was no evidence of auditory deficits as a function of previous noise exposure history, and no permanent changes in audiometric, electrophysiologic, or functional measures after new recreational noise exposure. There were very few participants with TTS the day after exposure - a test time selected to be consistent with previous animal studies. The largest observed TTS was approximately 20-dB. The observed pattern of small TTS suggests little risk of synaptopathy from common recreational noise exposure, and that we should not expect to observe changes in evoked potentials for this reason. No such changes were observed in this study. These data do not support suggestions that common, recreational noise exposure is likely to result in “hidden hearing loss”.

Effects of Recreational Noise on Threshold and Suprathreshold Measures of Auditory Function

“…Although the present study did not find significant associations between 1-year noise exposure history (L Aeq8760 ) and wave I amplitude of the ABR, or between wave I amplitude and functional measures, it remains possible that deficits may be present in those with louder, longer, or more frequent noise exposure. We suggest that future studies seeking evidence of hidden hearing loss should prioritize prospective documentation of TTS as in the recent report by Grinn et al 55 If possible, the inclusion of participants with exposure to blast and/or weapon fire would present an opportunity to clarify the relationship between wave I amplitude and extreme noise, particularly as related to speech-in-noise abilities. 56 Although data suggest that exposure to blast may result in lingering difficulty with speech-in-noise communication, tinnitus, and reduced quality of life, 57 other data have indicated no significant differences when wave I amplitude was compared for blast-exposed subjects and nonblastexposed controls.…”

Effects of age and hearing loss on perceptual and physiological measures of temporal envelope processing and spatial release from speech-on-speech masking

“…The studies, which are mostly based on measures obtained from young normal-hearing adults with different histories of noise exposure, have provided conflicting results. While some of the studies report findings that support the hypothesis based on cochlear synaptopathy (Grose et al, 2017;Liberman et al, 2016;Stamper et al, 2015;Valderrama et al, 2018), others show no evidence for the presence of temporal-processing deficits expected from cochlear synaptopathy (Grinn et al, 2017;Guest et al, 2017b;Prendergast et al, 2017a;Prendergast et al, 2017b;Spankovich et al, 2014;Yeend et al, 2017).…”

Neural signatures of disordered multi-talker speech perception in adults with normal hearing

“…In animal models, a loss of 1 cochlear afferent synapses disrupts the encoding of rapid timing cues, without affecting thresholds, 2 consistent with observations made in our subject cohort (Parthasarathy and Kujawa, 2018;Shaheen, 3 Valero and Liberman, 2015). In humans, it is impossible to directly assess the status of cochlear afferent 4 synapses in vivo, though indirect proxies for cochlear afferent innervation may be possible (Liberman et 5 al., 2016;Mehraei et al, 2016;Bharadwaj et al, 2015;Guest et al, 2017;Prendergast et al, 2017a;6 Prendergast et al, 2017b;Grinn et al, 2017;Bramhall et al, 2017). Prior work has emphasized the 7 amplitude of ABR wave 1 and extended high frequency hearing thresholds as possible indirect markers of 8 cochlear synapse loss.…”