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Animal studies demonstrate that noise exposure can permanently damage the synapses between inner hair cells and auditory nerve fibers, even when outer hair cells are intact and there is no clinically relevant permanent threshold shift. Synaptopathy disrupts the afferent connection between the cochlea and the central auditory system and is predicted to impair speech understanding in noisy environments and potentially result in tinnitus and/or hyperacusis. While cochlear synaptopathy has been demonstrated in numerous experimental animal models, synaptopathy can only be confirmed through post-mortem temporal bone analysis, making it difficult to study in living humans. A variety of non-invasive measures have been used to determine whether noise-induced synaptopathy occurs in humans, but the results are conflicting. The overall objective of this article is to synthesize the existing data on the functional impact of noise-induced synaptopathy in the human auditory system. The first section of the article summarizes the studies that provide evidence for and against noise-induced synaptopathy in humans. The second section offers potential explanations for the differing results between studies. The final section outlines suggested methodologies for diagnosing synaptopathy in humans with the aim of improving consistency across studies., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Objective: Short-term noise exposure that induces transient changes in thresholds has induced permanent cochlear synaptopathy in multiple species. Here, the literature was reviewed to gain translational insight into the relationships between noise exposure, ABR metrics, speech-in-noise performance and TTS in humans., Design: PubMed-based literature search, retrieval and review of full-text articles., Study Sample: Peer-reviewed literature identified using PubMed search., Results: Permanent occupational noise-induced hearing loss (NIHL) is frequently accompanied by abnormal ABR amplitude and latency. In the absence of NIHL, there are mixed results for relationships between noise exposure and ABR metrics. Interpretation of speech-in-noise deficits is difficult as both cochlear synaptopathy and outer hair cell (OHC) loss can drive deficits. Reductions in Wave I amplitude during TTS may reflect temporary OHC pathology rather than cochlear synaptopathy. Use of diverse protocols across studies reduces the ability to compare outcomes across studies., Conclusions: Longitudinal ABR and speech-in-noise data collected using consistent protocols are needed. Although speech-in-noise testing may not reflect cochlear synaptopathy, speech-in-noise testing should be completed as part of a comprehensive test battery to provide the objective measurement of patient difficulty.

Objectives: The purpose of this study was to evaluate the relationship between recreational sound exposure and potentially undiagnosed or subclinical hearing loss by assessing sound exposure history, threshold sensitivity, distortion product otoacoustic emission (DPOAE) amplitudes, and performance on the words-in-noise (WIN) test., Design: Survey data were collected from 74 adult participants (14 male and 60 female), 18 to 27 years of age, recruited via advertisements posted throughout the University of Florida campus. Of these participants, 70 completed both the survey and the additional functional test battery, and their preferred listening level was measured in a laboratory setting., Results: There were statistically significant relationships between hearing thresholds and DPOAE amplitude. In contrast, performance on the WIN was not reliably related to threshold sensitivity within this cohort with largely normal hearing. The two most common exposures included bars or dance clubs, followed by music player use. There were no statistically significant relationships between individual or composite measures of recreational sound exposure, including preferred listening level, years of music player use, number of reported sound exposures, previous impulse noise exposure, or previous noise-induced change in hearing, and functional measures including threshold, DPOAE amplitude, and WIN measures. Some subjects were highly consistent in listening level preferences, while others were more variable from song to song., Conclusions: No reliable relationships between common recreational sound exposure or previous noise-induced changes in hearing were found during analysis of threshold sensitivity, DPOAE amplitude, or WIN performance in this cohort. However, the study sample was predominantly female and Caucasian, which limits generalizability of the results.

Objectives: The purpose of this study was to examine the relationship between noise exposure history, type 1 diabetes mellitus (DM), and suprathreshold measures of auditory function., Design: A cross-sectional study was conducted; 20 normal-hearing participants without type 1 DM were matched on age and sex to 20 normal-hearing participants with type 1 DM (n=40). Participants, all having normal audiometric thresholds, completed noise history questionnaires and a battery of auditory physiological tests including transient evoked otoacoustic emissions, distortion product otoacoustic emissions, and auditory brainstem responses (ABR) at 80 dB nHL and at 2 different stimulus rates in both ears. Amplitude and latency for waves I and V are presented. Statistical analysis included analysis of variance and multivariate linear regression., Results: No statistically significant difference for noise exposure history, otoacoustic emissions (OAE), or ABR findings were found between type 1 DM and matched controls. Males and females showed statistically significant differences for OAE amplitudes and ABR amplitude and latencies. However, no statistically significant relationship was found between noise outcomes and OAE or ABR findings., Conclusions: No statistically significant relationship between noise history and our suprathreshold ABR or OAE findings was indicated for individuals with type 1 DM or matched controls. The lack of evidence of noise related neuropathology might be due to inadequate noise exposure or lack of comorbidities in our DM group. Implications of these findings are discussed.

For decades, we have presumed the death of hair cells and spiral ganglion neurons are the main cause of hearing loss and difficulties understanding speech in noise, but new findings suggest synapse loss may be the key contributor. Specifically, recent preclinical studies suggest that the synapses between inner hair cells and spiral ganglion neurons with low spontaneous rates and high thresholds are the most vulnerable subcellular structures, with respect to insults during aging and noise exposure. This cochlear synaptopathy can be "hidden" because this synaptic loss can occur without permanent hearing threshold shifts. This new discovery of synaptic loss opens doors to new research directions. Here, we review a number of recent studies and make suggestions in two critical future research directions. First, based on solid evidence of cochlear synaptopathy in animal models, it is time to apply molecular approaches to identify the underlying molecular mechanisms; improved understanding is necessary for developing rational, effective therapies against this cochlear synaptopathy. Second, in human studies, the data supporting cochlear synaptopathy are indirect although rapid progress has been made. To fully identify changes in function that are directly related this hidden synaptic damage, we argue that a battery of tests including both electrophysiological and behavior tests should be combined for diagnosis of "hidden hearing loss" in clinical studies. This new approach may provide a direct link between cochlear synaptopathy and perceptual difficulties., (Copyright © 2016 Elsevier B.V. All rights reserved.)

In animals, noise exposures that produce robust temporary threshold shifts (TTS) can produce immediate damage to afferent synapses and long-term degeneration of low spontaneous rate auditory nerve fibers. This synaptopathic damage has been shown to correlate with reduced auditory brainstem response (ABR) wave-I amplitudes at suprathreshold levels. The perceptual consequences of this "synaptopathy" remain unknown but have been suggested to include compromised hearing performance in competing background noise. Here, we used a modified startle inhibition paradigm to evaluate whether noise exposures that produce robust TTS and ABR wave-I reduction but not permanent threshold shift (PTS) reduced hearing-in-noise performance. Animals exposed to 109 dB SPL octave band noise showed TTS >30 dB 24-h post noise and modest but persistent ABR wave-I reduction 2 weeks post noise despite full recovery of ABR thresholds. Hearing-in-noise performance was negatively affected by the noise exposure. However, the effect was observed only at the poorest signal to noise ratio and was frequency specific. Although TTS >30 dB 24-h post noise was a predictor of functional deficits, there was no relationship between the degree of ABR wave-I reduction and degree of functional impairment., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Background: There has been significant discussion in the literature regarding music player use by adolescents and young adults, including whether device use is driving an increase in hearing loss in these populations. While many studies report relatively safe preferred listening levels, some studies with college student participants have reported listening habits that may put individuals at risk for noise-induced hearing loss (NIHL) if those listening habits continue over the long term., Purpose: The goal of the current investigation was to extend listening level data collection sites from urban city settings studied by others to a more rural campus setting., Research Design: This was a prospective study., Study Sample: Participants were 138 students on the University of Florida campus (94 males, 44 females), 18 years or older (mean = 21 years; range: 18-33 years)., Data Collection and Analysis: In this investigation, the current output level (listening level) was measured from personal listening devices used by students as they passed by a recruiting table located in one of three areas of the University of Florida campus. One location was in an open-air campus square; the other two locations were outside the campus recreation building ("gym") and outside the undergraduate library, with participants recruited as they exited the gym or library buildings. After providing written informed consent, participants completed a survey that included questions about demographics and typical listening habits (hours per day, days per week). The output level on their device was then measured using a "Jolene" mannequin., Results: Average listening levels for participants at the three locations were as follows: gym: 85.9 ± 1.4 dBA; campus square: 83.3 ± 2.0 dBA; library: 76.9 ± 1.3 dBA. After adjusting to free-field equivalent level, average listening levels were gym: 79.7 ± 1.4 dBA; campus square: 76.9 ± 2.1 dBA; library: 70.4 ± 1.4 dBA. There were no statistically significant differences between male and female listeners, and there were no reliable differences as a function of race. After accounting for daily and weekly use patterns, 5% were deemed at risk based on the criteria put forward by the Occupational Safety and Health Administration, and 9% were deemed at risk based on the guidance provided by the National Institute for Occupational Safety and Health., Conclusions: Some 5-10% of the participants were deemed at risk; this finding is consistent with other studies using similar methods. It is possible that the same listeners would have selected different listening levels in other noise backgrounds, however. This unknown variable makes it difficult to estimate risk with a single listening level measurement., (American Academy of Audiology)

Objective: Firearm discharges produce hazardous levels of impulse noise that can lead to permanent hearing loss. In the present study, we evaluated the effects of suppression, ammunition, and barrel length on AR-15 rifles., Design: Sound levels were measured left/right of a user's head, and 1-m left of the muzzle, per MIL-STD-1474-D, under both unsuppressed and suppressed conditions., Study Sample: Nine commercially available AR-15 rifles and 14 suppressors were used., Results: Suppressors significantly decreased peak dB SPL at the 1-m location and the left ear location. However, under most rifle/ammunition conditions, levels remained above 140 dB peak SPL near a user's right ear. In a subset of conditions, subsonic ammunition produced values near or below 140 dB peak SPL. Overall suppression ranged from 7-32 dB across conditions., Conclusions: These data indicate that (1) suppressors reduce discharge levels to 140 dB peak SPL or below in only a subset of AR-15 conditions, (2) shorter barrel length and use of muzzle brake devices can substantially increase exposure level for the user, and (3) there are significant left/right ear sound pressure differences under suppressed conditions as a function of the AR-15 direct impingement design that must be considered during sound measurements to fully evaluate overall efficacy.

Many recreational activities are accompanied by loud concurrent sounds and decisions regarding the hearing hazards associated with these activities depend on accurate sound measurements. Sound level meters (SLMs) are designed for this purpose, but these are technical instruments that are not typically available in recreational settings and require training to use properly. Mobile technology has made such sound level measurements more feasible for even inexperienced users. Here, we assessed the accuracy of sound level measurements made using five mobile phone applications or "apps" on an Apple iPhone 4S, one of the most widely used mobile phones. Accuracy was assessed by comparing application-based measurements to measurements made using a calibrated SLM. Whereas most apps erred by reporting higher sound levels, one application measured levels within 5 dB of a calibrated SLM across all frequencies tested.

Background: Human hearing is sensitive to sounds from as low as 20 Hz to as high as 20,000 Hz in normal ears. However, clinical tests of human hearing rarely include extended high-frequency (EHF) threshold assessments, at frequencies extending beyond 8000 Hz. EHF thresholds have been suggested for use monitoring the earliest effects of noise on the inner ear, although the clinical usefulness of EHF threshold testing is not well established for this purpose., Purpose: The primary objective of this study was to determine if EHF thresholds in healthy, young adult college students vary as a function of recreational noise exposure., Research Design: A retrospective analysis of a laboratory database was conducted; all participants with both EHF threshold testing and noise history data were included. The potential for "preclinical" EHF deficits was assessed based on the measured thresholds, with the noise surveys used to estimate recreational noise exposure., Study Sample: EHF thresholds measured during participation in other ongoing studies were available from 87 participants (34 male and 53 female); all participants had hearing within normal clinical limits (≤25 HL) at conventional frequencies (0.25-8 kHz)., Results: EHF thresholds closely matched standard reference thresholds [ANSI S3.6 (1996) Annex C]. There were statistically reliable threshold differences in participants who used music players, with 3-6 dB worse thresholds at the highest test frequencies (10-16 kHz) in participants who reported long-term use of music player devices (>5 yr), or higher listening levels during music player use., Conclusions: It should be possible to detect small changes in high-frequency hearing for patients or participants who undergo repeated testing at periodic intervals. However, the increased population-level variability in thresholds at the highest frequencies will make it difficult to identify the presence of small but potentially important deficits in otherwise normal-hearing individuals who do not have previously established baseline data., (American Academy of Audiology.)

Free radical formation in the cochlea plays a key role in the development of noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant formation of both reactive oxygen species and reactive nitrogen species 7-10 days after noise exposure. Reduction in cochlear blood flow as a result of free radical formation has also been described. Here we report that the antioxidant agents vitamins A, C, and E act in synergy with magnesium to effectively prevent noise-induced trauma. Neither the antioxidant agents nor the magnesium reliably reduced NIHL or sensory cell death with the doses we used when these agents were delivered alone. In combination, however, they were highly effective in reducing both hearing loss and cell death even with treatment initiated just 1 h before noise exposure. This study supports roles for both free radical formation and noise-induced vasoconstriction in the onset and progression of NIHL. Identification of this safe and effective antioxidant intervention that attenuates NIHL provides a compelling rationale for human trials in which free radical scavengers are used to eliminate this single major cause of acquired hearing loss.

Firearms produce peak sound pressure levels (peak SPL) between ∼130 and 175 dB peak SPL, creating significant risk of noise-induced hearing loss (NIHL) in those exposed to firearm noise during occupational, recreational, and/or military operations. Noise-induced tinnitus and hearing loss are common in military service members, public safety officers, and hunters/shooters. Given the significant risk of NIHL due to firearm and other noise sources, there is an interest in, and demand for, interventions to prevent and/or treat NIHL in high-risk populations. However, research and clinical trial designs assessing NIHL prevention have varied due to inconsistent data from the literature, specifically with end point definitions, study protocols, and assessment methodologies. This article presents a scoping review of the literature pertaining to auditory changes following firearm noise exposure. Meta-analysis was not possible due to heterogeneity of the study designs. Recommendations regarding audiologic test approach and monitoring of populations at risk for NIHL are presented based on critical review of the existing literature. [ABSTRACT FROM AUTHOR]

With advances in the understanding of mechanisms of noise injury, the past 30 years have brought numerous efforts to identify drugs that prevent noise-induced hearing loss (NIHL). The diverse protocols used across investigations have made comparisons across drugs difficult. A systematic review of the literature by Hammill [(2017). Doctoral thesis, The University of Texas at Austin] identified original reports of chemical interventions to prevent or treat hearing loss caused by noise exposure. An initial search returned 3492 articles. After excluding duplicate articles and articles that did not meet the systematic review inclusion criteria, a total of 213 studies published between 1977 and 2016 remained. Reference information, noise exposure parameters, species, sex, method of NIHL assessment, and pharmaceutical intervention details for these 213 studies were entered into a database. Frequency-specific threshold shifts in control animals (i.e., in the absence of pharmaceutical intervention) are reported here. Specific patterns of hearing loss as a function of species and noise exposure parameters are provided to facilitate the selection of appropriate pre-clinical models. The emphasis of this report is octave band noise exposure, as this is one of the most common exposure protocols across pharmacological otoprotection studies. [ABSTRACT FROM AUTHOR]

Noise exposure that causes a temporary threshold shift but no permanent threshold shift can cause degeneration of synaptic ribbons and afferent nerve fibers, with a corresponding reduction in wave I amplitude of the auditory brainstem response (ABR) inanimals.This formof underlying damage, hypothesized to also occur in humans, has been termed synaptopathy, and it has been hypothesized that there will be a hidden hearing loss consisting of functional deficits at suprathreshold stimulus levels. This study assessed whether recreational noise exposure history was associated with smaller ABR wave I amplitude and poorer performance on suprathreshold auditory test measures.Noise exposure historieswere collected from 26 men and 34women with hearing thresholds ≤ 25 dB hearing loss (HL; 250 Hz to 8 kHz), and a variety of functional suprathreshold hearing tests were performed. Wave I amplitudes of click-evoked ABR were obtained at 70, 80, 90, and 99 dB (nHL) and tone-burst evoked ABR were obtained at 90 dB nHL. Speech recognition performance was measured in quiet and in competing noise, using theWords in Noise test, and the NU-6 word list in broadband noise (BBN). In addition, temporal summation to tonal stimuli was assessed in quiet and in competing BBN. To control for the effects of subclinical conventional hearing loss, distortion product otoacoustic emission amplitude, an indirect measure of outer hair cell integrity, was measured. There was no statistically significant relationship between noise exposure history scores andABRwave I amplitude in eithermen or women for any of the ABR conditions. ABR wave I amplitude and noise exposure history were not reliably correlated with suprathreshold functional hearing tests. Taken together, this study found no evidence of noise-induced decreases inABR wave I amplitude or signal processing in noise in a cohort of subjects with a history of recreational noise exposure. [ABSTRACT FROM AUTHOR]

Abstract: Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7–10days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss. [Copyright &y& Elsevier]

Objectives: This study had two objectives. First, baseline audiometric data was assessed for associations with noise exposure history. Seconds, subjects were followed prospectively to assess potential auditory effects of new loud recreational activities. Material and methods: Testing included tympanometry, pure-tone and speech reception thresholds, word-in-noise tests, and ABR and DPOAE measurements. All tests were completed at baseline, and repeated the day after a "loud" recreational event and one week later. Results: There was no reliable relationship between recreational noise history and auditory test metrics. After acute event exposures, a variety of dose-dependent temporary changes were observed across metrics. Final tests one week later showed recovery. Conclusions: Recreational noise was not correlated with chronic or acute changes in function or evoked potential amplitude. However, two subjects with 16-hr exposures had changes in function, indicating hazardous exposures for which hearing protection was needed. [ABSTRACT FROM AUTHOR]

Objectives: Noise exposures that produce robust temporary threshold shift (TTS) reduce auditory brainstem response (ABR) wave-I amplitude. This study evaluated whether these ABR reductions were associated with functional hearing-in-noise deficits. Material and methods: ABR threshold and amplitude, otoacoustic emissions, and hearing-in-noise were assessed in rats before and after noise exposure (106 or 109 dB SPL octave band noise, 8-16 kHz, 2 h). Hearing-in-noise was assessed at various signal-to-noise ratios (SNR). Results: The 106 dB SPL exposure had no effect on ABR or hearing-in-noise after 2 weeks. In contrast, the 109-dB SPL noise reduced ABR wave-1 amplitude at 16-24 kHz and showed hearing-in-noise deficits in the poorest SNR condition, despite threshold recovery. Conclusions: Reduced wave-I amplitude and poorer hearing- in-noise were observed after noise exposure producing robust (>30 dB) TTS at 24 hrs post exposure. Future studies should assess effects of lower level, repeated, exposures that model occupational noise. [ABSTRACT FROM AUTHOR]