Noise-induced Threshold Shift Research Articles

Dolphin short-term auditory fatigue and self-mitigation.

Auditory brainstem responses (ABRs) were measured at 57 kHz in two dolphins warned of an impending intense tone at 40 kHz. Over the course of testing, the duration of the intense tone was increased from 0.5 to 16 s to determine if changes in ABRs observed after cessation of the intense sound were the result of post-stimulatory auditory fatigue or conditioned hearing attenuation. One dolphin exhibited conditioned hearing attenuation after the warning sound preceding the intense sound, but little evidence of post-stimulatory fatigue after the intense sound. The second dolphin showed no conditioned attenuation before the intense sound, but auditory fatigue afterwards. The fatigue was observed within a few seconds after cessation of the intense tone: i.e., at time scales much shorter than those in previous studies of marine mammal noise-induced threshold shifts, which feature measurements on the order of a few minutes after exposure. The differences observed between the two individuals (less auditory fatigue in the dolphin that exhibited the conditioned attenuation) support the hypothesis that conditioned attenuation is a form of "self-mitigation."

Noise-Induced Hearing Threshold Shift Correlated with Body Weight and External-Ear Amplification in Chinchilla: a Preliminary Analysis

BackgroundExternal-ear amplification (EEA) has been shown to vary from 5–19 dB-A in large datasets of pediatric, adolescent, and adult human participants. However, variable EEA is an overlooked characteristic that likely plays a role in individual noise-induced hearing loss (NIHL) susceptibility. A noise exposure varying 5–19 dB-A translates to high-EEA individuals theoretically experiencing 3–4 times greater NIHL risk than low-EEA individuals.ObjectiveThe purpose of this preliminary analysis was to test the hypothesis that higher EEA is correlated with increased noise-induced threshold shift susceptibility.DesignNine chinchillas were exposed to 4-kHz octave-band noise at 89 dB-SPL for 24 h. Auditory brainstem response thresholds were obtained pre-exposure, 24-h post-exposure, and 4-week post-exposure. Relationships between EEA and threshold shift were analyzed.ResultsOpen-ear EEA ranged 11–19 dB-SPL, and occluded-ear EEA ranged 10–21 dB-SPL. Higher occluded-ear EEA was correlated with increased NIHL susceptibility (p = 0.04), as was lower body weight (p = 0.01). Male animals exhibited more threshold shift than female animals (p = 0.02), lower body weight than female animals (p = 0.02), and higher occluded-ear EEA (male mean = 18 dB; female mean = 15 dB).ConclusionsTaken together, increased threshold shift susceptibility was observed in the smallest animals, animals with the highest occluded-ear EEA, and in male animals (which tended to have higher occluded-ear EEA). Given the established relationship between smaller body size and higher occluded-ear EEA, these preliminary results suggest that body size (and occluded-ear EEA; a function of body size) could be a potential, underlying driver of NIHL susceptibility differences, rather than true sex differences.

Evaluation of hidden hearing loss in normal-hearing firearm users.

Some noise exposures resulting in temporary threshold shift (TTS) result in cochlear synaptopathy. The purpose of this retrospective study was to evaluate a human population that might be at risk for noise-induced cochlear synaptopathy (i.e., "hidden hearing loss"). Participants were firearm users who were (1) at-risk for prior audiometric noise-induced threshold shifts, given their history of firearm use, (2) likely to have experienced complete threshold recovery if any prior TTS had occurred, based on this study's normal-hearing inclusion criteria, and (3) not at-risk for significant age-related synaptopathic loss, based on this study's young-adult inclusion criteria. 70 participants (age 18-25 yr) were enrolled, including 33 firearm users experimental (EXP), and 37 non-firearm users control (CNTRL). All participants were required to exhibit audiometric thresholds ≤20 dB HL bilaterally, from 0.25 to 8 kHz. The study was designed to test the hypothesis that EXP participants would exhibit a reduced cochlear nerve response compared to CNTRL participants, despite normal-hearing sensitivity in both groups. No statistically significant group differences in auditory performance were detected between the CNTRL and EXP participants on standard audiom to etry, extended high-frequency audiometry, Words-in-Noise performance, distortion product otoacoustic emission, middle ear muscle reflex, or auditory brainstem response. Importantly, 91% of EXP participants reported that they wore hearing protection either "all the time" or "almost all the time" while using firearms. The data suggest that consistent use of hearing protection during firearm use can effectively protect cochlear and neural measures of auditory function, including suprathreshold responses. The current results do not exclude the possibility that neural pathology may be evident in firearm users with less consistent hearing protection use. However, firearm users with less consistent hearing protection use are also more likely to exhibit threshold elevation, among other cochlear deficits, thereby confounding the isolation of any potentially selective neural deficits. Taken together, it seems most likely that firearm users who consistently and correctly use hearing protection will exhibit preserved measures of cochlear and neural function, while firearm users who inconsistently and incorrectly use hearing protection are most likely to exhibit cochlear injury, rather than evidence of selective neural injury in the absence of cochlear injury.

A simple approach for marine mammal noise-induced threshold shift prediction from down-the-hole piling noise exposure

In assessing auditory effects on marine mammals from noise exposure, a dual-criterion is currently used by regulators to estimate the noise-induced threshold shift (NITS). Such criterion classifies anthropogenic noise into two mutually exclusive categories: Impulsive and non-impulsive. However, in real world situations, marine mammals are often exposed to complex noise field that contains both impulsive and non-impulsive components, thus makes it difficult or even impossible to accurately assess their NITS from noise exposure. One example is down-the-hole (DTH) pile installation, which generates both impulsive noise from percussive drilling/striking and non-impulsive noise from debris removal simultaneously. In this study, a relatively simple approach is proposed that employs kurtosis values to quantify the impulsiveness of two DTH piling noises datasets for six different marine mammal functional hearing groups. A kurtosis adjustment approach that has been suggested for predict human hearing loss from noise exposure was then used to build correction factors for estimation of NITS of marine mammals exposed to DTH piling noises. Further research on marine mammal NITS from complex noise exposure is needed to validate and improve this model.

Hsp70/Bmi1-FoxO1-SOD Signaling Pathway Contributes to the Protective Effect of Sound Conditioning against Acute Acoustic Trauma in a Rat Model.

Sound conditioning (SC) is defined as “toughening” to lower levels of sound over time, which reduces a subsequent noise-induced threshold shift. Although the protective effect of SC in mammals is generally understood, the exact mechanisms involved have not yet been elucidated. To confirm the protective effect of SC against noise exposure (NE) and the stress-related signaling pathway of its rescue, we observed target molecule changes caused by SC of low frequency prior to NE as well as histology analysis in vivo and verified the suggested mechanisms in SGNs in vitro. Further, we investigated the potential role of Hsp70 and Bmi1 in SC by targeting SOD1 and SOD2 which are regulated by the FoxO1 signaling pathway based on mitochondrial function and reactive oxygen species (ROS) levels. Finally, we sought to identify the possible molecular mechanisms associated with the beneficial effects of SC against noise-induced trauma. Data from the rat model were evaluated by western blot, immunofluorescence, and RT-PCR. The results revealed that SC upregulated Hsp70, Bmi1, FoxO1, SOD1, and SOD2 expression in spiral ganglion neurons (SGNs). Moreover, the auditory brainstem responses (ABRs) and electron microscopy revealed that SC could protect against acute acoustic trauma (AAT) based on a significant reduction of hearing impairment and visible reduction in outer hair cell loss as well as ultrastructural changes in OHCs and SGNs. Collectively, these results suggested that the contribution of Bmi1 toward decreased sensitivity to noise-induced trauma following SC was triggered by Hsp70 induction and associated with enhancement of the antioxidant system and decreased mitochondrial superoxide accumulation. This contribution of Bmi1 was achieved by direct targeting of SOD1 and SOD2, which was regulated by FoxO1. Therefore, the Hsp70/Bmi1-FoxO1-SOD signaling pathway might contribute to the protective effect of SC against AAT in a rat model.

Vesicular Glutamatergic Transmission in Noise-Induced Loss and Repair of Cochlear Ribbon Synapses.

Noise-induced excitotoxicity is thought to depend on glutamate. However, the excitotoxic mechanisms are unknown, and the necessity of glutamate for synapse loss or regeneration is unclear. Despite absence of glutamatergic transmission from cochlear inner hair cells in mice lacking the vesicular glutamate transporter-3 (Vglut3KO ), at 9-11 weeks, approximately half the number of synapses found in Vglut3WT were maintained as postsynaptic AMPA receptors juxtaposed with presynaptic ribbons and voltage-gated calcium channels (CaV1.3). Synapses were larger in Vglut3KO than Vglut3WT In Vglut3WT and Vglut3+/- mice, 8-16 kHz octave-band noise exposure at 100 dB sound pressure level caused a threshold shift (∼40 dB) and a loss of synapses (>50%) at 24 h after exposure. Hearing threshold and synapse number partially recovered by 2 weeks after exposure as ribbons became larger, whereas recovery was significantly better in Vglut3WT Noise exposure at 94 dB sound pressure level caused auditory threshold shifts that fully recovered in 2 weeks, whereas suprathreshold hearing recovered faster in Vglut3WT than Vglut3+/- These results, from mice of both sexes, suggest that spontaneous repair of synapses after noise depends on the level of Vglut3 protein or the level of glutamate release during the recovery period. Noise-induced loss of presynaptic ribbons or postsynaptic AMPA receptors was not observed in Vglut3KO , demonstrating its dependence on vesicular glutamate release. In Vglut3WT and Vglut3+/-, noise exposure caused unpairing of presynaptic ribbons and presynaptic CaV1.3, but not in Vglut3KO where CaV1.3 remained clustered with ribbons at presynaptic active zones. These results suggest that, without glutamate release, noise-induced presynaptic Ca2+ influx was insufficient to disassemble the active zone. However, synapse volume increased by 2 weeks after exposure in Vglut3KO , suggesting glutamate-independent mechanisms.SIGNIFICANCE STATEMENT Hearing depends on glutamatergic transmission mediated by Vglut3, but the role of glutamate in synapse loss and repair is unclear. Here, using mice of both sexes, we show that one copy of the Vglut3 gene is sufficient for noise-induced threshold shift and loss of ribbon synapses, but both copies are required for normal recovery of hearing function and ribbon synapse number. Impairment of the recovery process in mice having only one functional copy suggests that glutamate release may promote synapse regeneration. At least one copy of the Vglut3 gene is necessary for noise-induced synapse loss. Although the excitotoxic mechanism remains unknown, these findings are consistent with the presumption that glutamate is the key mediator of noise-induced synaptopathy.

Influence of risky and protective behaviors connected with listening to music on hearing loss and the noise induced threshold shift among students of the Medical University of Bialystok

ENWEndNote BIBJabRef, Mendeley RISPapers, Reference Manager, RefWorks, Zotero AMA Modzelewska B, Samluk A, Wałejko Ł, Muszyński P, Szczepańska J, Kleszczewska E. Influence of risky and protective behaviors connected with listening to music on hearing loss and the noise induced threshold shift among students of the Medical University of Bialystok. Family Medicine & Primary Care Review. 2017;19(1):44-48. doi:10.5114/fmpcr.2017.65090. APA Modzelewska, B., Samluk, A., Wałejko, Ł., Muszyński, P., Szczepańska, J., & Kleszczewska, E. (2017). Influence of risky and protective behaviors connected with listening to music on hearing loss and the noise induced threshold shift among students of the Medical University of Bialystok. Family Medicine & Primary Care Review, 19(1), 44-48. https://doi.org/10.5114/fmpcr.2017.65090 Chicago Modzelewska, Beata, Anna Samluk, Łukasz Wałejko, Paweł Muszyński, Joanna Szczepańska, and Ewa Kleszczewska. 2017. "Influence of risky and protective behaviors connected with listening to music on hearing loss and the noise induced threshold shift among students of the Medical University of Bialystok". Family Medicine & Primary Care Review 19 (1): 44-48. doi:10.5114/fmpcr.2017.65090. Harvard Modzelewska, B., Samluk, A., Wałejko, Ł., Muszyński, P., Szczepańska, J., and Kleszczewska, E. (2017). Influence of risky and protective behaviors connected with listening to music on hearing loss and the noise induced threshold shift among students of the Medical University of Bialystok. Family Medicine & Primary Care Review, 19(1), pp.44-48. https://doi.org/10.5114/fmpcr.2017.65090 MLA Modzelewska, Beata et al. "Influence of risky and protective behaviors connected with listening to music on hearing loss and the noise induced threshold shift among students of the Medical University of Bialystok." Family Medicine & Primary Care Review, vol. 19, no. 1, 2017, pp. 44-48. doi:10.5114/fmpcr.2017.65090. Vancouver Modzelewska B, Samluk A, Wałejko Ł, Muszyński P, Szczepańska J, Kleszczewska E. Influence of risky and protective behaviors connected with listening to music on hearing loss and the noise induced threshold shift among students of the Medical University of Bialystok. Family Medicine & Primary Care Review. 2017;19(1):44-48. doi:10.5114/fmpcr.2017.65090.

Guidelines for Auditory Threshold Measurement for Significant Threshold Shift.

The purpose of this article is to provide guidelines for determining a Significant Noise-Induced Threshold Shift in clinical trials involving human populations. The article reviews recommendations for the standards to be referenced for human subjects, equipment, test environment, and personnel. Additional guidelines for military populations are provided. Guidelines for the calibration of audiometers, sound booth noise levels, and immitance equipment are provided. In addition the guidance provides specific suggestions for the subjects history before study onset, and otoscopy.Test frequencies for threshold determination and methods of threshold determination are reviewed for both air conduction and bone conduction for both baseline testing and later determination of either a temporary (TTS) or permanent threshold shift (PTS). Once a Significant Noise-Induced Threshold Shift has been determined, subjects should be retested, conductive component should be ruled out or addressed, and the subject should be counseled or referred for additional medical evaluation. Guidance for reporting procedures and the computerized study database are described. Finally, experimental designs suggested for noise-induced otoprotection clinical trials are described.

Temporary and Permanent Noise-induced Threshold Shifts: A Review of Basic and Clinical Observations.

To review basic and clinical findings relevant to defining temporary (TTS) and permanent (PTS) threshold shifts and their sequelae. Relevant scientific literature and government definitions were broadly reviewed. The definitions and characteristics of TTS and PTS were assessed and recent advances that expand our knowledge of the extent, nature, and consequences of noise-induced hearing loss were reviewed. Exposure to intense sound can produce TTS, acute changes in hearing sensitivity that recover over time, or PTS, a loss that does not recover to preexposure levels. In general, a threshold shift ≥10 dB at 2, 3, and 4 kHz is required for reporting purposes in human studies. The high-frequency regions of the cochlea are most sensitive to noise damage. Resonance of the ear canal also results in a frequency region of high-noise sensitivity at 4 to 6 kHz. A primary noise target is the cochlear hair cell. Although the mechanisms that underlie such hair cell damage remain unclear, there is evidence to support a role for reactive oxygen species, stress pathway signaling, and apoptosis. Another target is the synapse between the hair cell and the primary afferent neurons. Large numbers of these synapses and their neurons can be lost after noise, even though hearing thresholds may return to normal. This affects auditory processing and detection of signals in noise. The consequences of TTS and PTS include significant deficits in communication that can impact performance of military duties or obtaining/retaining civilian employment. Tinnitus and exacerbation of posttraumatic stress disorder are also potential sequelae.

Noise-Induced "Toughening" Effect in Wistar Rats: Enhanced Auditory Brainstem Responses Are Related to Calretinin and Nitric Oxide Synthase Upregulation.

An appropriate conditioning noise exposure may reduce a subsequent noise-induced threshold shift. Although this “toughening” effect helps to protect the auditory system from a subsequent traumatic noise exposure, the mechanisms that regulate this protective process are not fully understood yet. Accordingly, the goal of the present study was to characterize physiological processes associated with “toughening” and to determine their relationship to metabolic changes in the cochlea and cochlear nucleus (CN). Auditory brainstem responses (ABR) were evaluated in Wistar rats before and after exposures to a sound conditioning protocol consisting of a broad-band white noise of 118 dB SPL for 1 h every 72 h, four times. After the last ABR evaluation, animals were perfused and their cochleae and brains removed and processed for the activity markers calretinin (CR) and neuronal nitric oxide synthase (nNOS). Toughening was demonstrated by a progressively faster recovery of the threshold shift, as well as wave amplitudes and latencies over time. Immunostaining revealed an increase in CR and nNOS levels in the spiral ganglion, spiral ligament, and CN in noise-conditioned rats. Overall, these results suggest that the protective mechanisms of the auditory toughening effect initiate in the cochlea and extend to the central auditory system. Such phenomenon might be in part related to an interplay between CR and nitric oxide signaling pathways, and involve an increased cytosolic calcium buffering capacity induced by the noise conditioning protocol.

Multiplicative noise effects on electroconvection in controlling additive noise by a magnetic field

We report multiplicative noise-induced threshold shift of electroconvection (EC) in the presence of a magnetic field H. Controlling the thermal fluctuation (i.e., additive noise) of the rodlike molecules of nematic liquid crystals by H, the EC threshold is examined at various noise levels [characterized by their intensity and cutoff frequency (f(c))]. For a sufficiently strong H (i.e., ignorable additive noise), a modified noise sensitivity characterizing the shift problem is in good agreement with experimental results for colored as well as white noise (f(c)→∞); until now, there was a large deviation for (sufficiently) colored noises. The present study shows that H provides us with ideal conditions for studying the corresponding Carr-Helfrich theory considering pure multiplicative noise.

Is this STS work-related? ISO 1999 predictions as an adjunct to clinical judgment.

Physicians and audiologists are often asked to decide whether standard threshold shifts (STSs) are work-related; epidemiological data can inform these decisions. Predictions of ISO (2013) for both age-related and noise-induced threshold shifts, for the 2, 3, and 4 kHz average used in calculating OSHA STSs, are presented, in tables, graphs, and an Excel spreadsheet calculator. Specifically, the ISO 1999 model estimates age-related thresholds based on age and sex; it estimates noise-induced threshold shifts based on noise level and duration. It specifies that to estimate the final hearing thresholds for a person of given percentile, age, sex, and noise exposure, the expected age-related threshold is to be added to the expected noise-induced threshold shift. Examples show how these data can predict the relative contributions of aging and occupational noise to an STS. Early-career STSs, especially with high levels of noise exposure, are more likely to be primarily noise-induced. After the first decade of exposure, most STSs will be primarily age-related. Given a worker's age, sex, and occupational noise exposure history, ISO 1999 estimates of the expected contributions of aging and noise can supplement clinical judgment.

Noise-induced hearing loss in marine mammals: A review of temporary threshold shift studies from 1996 to 2015.

One of the most widely recognized effects of intense noise exposure is a noise-induced threshold shift—an elevation of hearing thresholds following cessation of the noise. Over the past twenty years, as concerns over the potential effects of human-generated noise on marine mammals have increased, a number of studies have been conducted to investigate noise-induced threshold shift phenomena in marine mammals. The experiments have focused on measuring temporary threshold shift (TTS)—a noise-induced threshold shift that fully recovers over time—in marine mammals exposed to intense tones, band-limited noise, and underwater impulses with various sound pressure levels, frequencies, durations, and temporal patterns. In this review, the methods employed by the groups conducting marine mammal TTS experiments are described and the relationships between the experimental conditions, the noise exposure parameters, and the observed TTS are summarized. An attempt has been made to synthesize the major findings across experiments to provide the current state of knowledge for the effects of noise on marine mammal hearing.

Noise induced threshold shifts after noise exposure: Are bats special?

We conducted psychophysical and neurophysiological experiments to test the hypothesis that big brown bats suffer less severe temporary threshold shifts after noise exposure than other small mammals that also hear high frequency sounds. Five big brown bats were trained in psychophysical detection experiments to obtain thresholds to FM sweeps spanning the frequency range of their echolocation calls. Bats were then exposed to 115 dB of broadband noise for one hour, and thresholds re-measured 20 min and 24 hour after exposure. For all bats, threshold elevations at 20 min post-exposure were 3 dB or less, while at 24 hour post-exposure, thresholds were similar to those obtained pre-exposure. Local field potentials were recorded in the cochlear nucleus of anesthetized big brown bats before and after noise exposure. Neural thresholds to FM sweeps and to single tone frequencies were unaffected by noise exposure. These data suggest that big brown bats are an excellent model system to study naturally occurring immunity to noise damage. [Work supported by ONR and the Capita Foundation.]

Prolonged noise exposure-induced auditory threshold shifts in rats

Noise-induced hearing loss (NIHL) initially increases with exposure duration, but eventually reaches an asymptotic threshold shift (ATS) once the exposure duration exceeds 18–24 h. Equations for predicting the ATS have been developed for several species, but not for rats, even though this species is extensively used in noise exposure research. To fill this void, we exposed rats to narrowband noise (NBN, 16–20 kHz) for 5 weeks starting at 80 dB SPL in the first week and then increasing the level by 6 dB per week to a final level of 104 dB SPL. Auditory brainstem responses (ABR) were recorded before, during, and following the exposure to determine the amount of hearing loss. The noise induced threshold shift to continuous long-term exposure, defined as compound threshold shift (CTS), within and above 16–20 kHz increased with noise level at the rate of 1.82 dB threshold shift per dB of noise level (NL) above a critical level (C) of 77.2 dB SPL i.e. CTS = 1.82(NL-77.2). The normalized amplitude of the largest ABR peak measured at 100 dB SPL decreased at the rate of 3.1% per dB of NL above the critical level of 76.9 dB SPL, i.e., %ABR Reduction = 3.1%(NL-76.9). ABR thresholds measured >30 days post-exposure only partially recovered resulting in a permanent threshold shift of 30–40 dB along with severe hair cell loss in the basal, high-frequency region of the cochlea. In the rat, CTS increases with noise level with a slope similar to humans and chinchillas. The critical level (C) in the rat is similar to that of humans, but higher than that of chinchillas.

Perilymphatic Gentamicin Trafficking through Basolateral Channels May Underlie Enhanced Ototoxicity by Noise‐Induced Threshold Shifts

Objectives: (1) Demonstrate gentamicin uptake from perilymph into hair cells via basolateral channels such as the postsynaptic acetylcholine receptor (nAChR) and the TRPA1 in neonatal mice in vivo and in vitro. (2) Recognize alternative gentamicin trafficking pathways to the well established endolymphatic mechanoelectrotransducer channel underlying aminoglycoside ototoxicity. Methods: Neonatal mice were intraperitoneally injected with fluorescently-conjugated Gentamicin-Texas Red (GTTR), prior to fixation 30 minutes later. Cochlear explants were treated with GTTR 1 µg/mL, with or without 100 µM acetylcholine or cinnamaldehyde then fixed, and analyzed. Fluorescence intensities were measured by calculating the mean gray value of each cell with Image J. Student t test was used to determine any significant differences in fluorescence values between treatment groups. Results: Application of acetylcholine increased GTTR uptake by wildtype outer hair cells (OHC) in vivo and in vitro. These results were also replicated in Myo7a8J/8J mice, which lack functional mechanoelectrotransducer channels. Application of cinnamaldehyde (TRPA1 agonist) also increased GTTR uptake in OHCs in wildtype, myo7a8J/8J mice and guinea pigs. Conclusions: Endolymphatic gentamicin trafficking via the mechanoelectrotransducer (MET) channel is a well established mechanism of ototoxicity. Noise-induced threshold shifts (NITS) have been shown to damage the mechanically gated tip link, thus closing MET channel. However, aminoglycoside hair cell uptake is enhanced by NITS. This suggests one or more aminoglycoside entry route(s) into hair cells in addition to, and independent of, the MET channel. The results of this study support perilymphatic trafficking of gentamicin via basolateral channels including the nAChR Ca2+ channel, and TRPA1.

Colored Noise-Induced Threshold Shifts and Phase Diagrams in Electroconvections

We report noise-induced threshold shifts and phase diagrams in electroconvections (ECs) in a nematic liquid crystal by controlling the frequency band (i.e., cutoff frequency fc) of noise. A crucial relationship between the internal characteristic time (i.e., charge relaxation time τσ) of the EC system and the correlation time [τN = 1/(2πfc)] of the external colored noise is found, which determines the role of noise in the nonequilibrium EC system. Modified numerical results using the relationship are quantitatively compared with the present experimental results. From the relationship, two types of phase diagrams can be classified in white-like and colored noises.

Hot Topics—Hidden hearing loss: Permanent cochlear-nerve degeneration after temporary noise-induced threshold shift

The classic view of sensorineural hearing loss (SNHL) is that the “primary” targets are hair cells, and that cochlear-nerve loss is “secondary” to hair cell degeneration. Our work in mouse and guinea pig has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of cochlear-nerve/hair-cell synapses. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained hidden for two reasons: (1) the spiral ganglion cells, the cochlear neural elements commonly assessed in studies of SNHL, survive for years despite loss of synaptic connection with hair cells, and (2) the degeneration is selective for cochlear-nerve fibers with high thresholds. Although not required for threshold detection in quiet (e.g., threshold audiometry, auditory brainstem response threshold), these high-threshold fibers are critical for hearing in noisy environments. Our research suggests that (1) primary neural degeneration is an important contributor to the perceptual handicap in SNHL, and (2) noise exposure guidelines should be re-evaluated, as they are based on the faulty premise that threshold audiograms are the most sensitive measures of noise damage.

D-methionine pre-loading reduces both noise-induced permanent threshold shift and outer hair cell loss in the chinchilla

Objective: This study tested multiple dosing epochs of pre-loaded D-methionine (D-met) for otoprotection from noise-induced hearing loss (NIHL). Design: Auditory brainstem response (ABR) thresholds were measured at baseline, 1 day, and 21 days following a 6-hour 105 dB sound pressure level (SPL) octave band noise (OBN) exposure. Outer hair cell (OHC) counts were measured after day 21 sacrifice. Study sample: Three groups of five Chinchillas laniger each were given a 2-day regimen comprising five doses of D-met (200 mg/kg/dose) intraperitoneally (IP) starting 2, 2.5, or 3 days prior to noise exposure. A control group (n = 5) received five doses of equivalent volume saline IP starting 2.5 days prior to noise exposure. Results: ABR threshold shifts from baseline to day-21 post-noise exposure were reduced in all D-met groups versus controls, reaching significance (p < 0.05) in the 3-day group. D-met groups showed reduced OHC loss relative to controls at day-21 post-noise exposure, reaching significance (p < 0.05) at all frequency regions in the 3-day group and at the 2, 4, and 8 kHz frequency regions in the 2.5-day group. Conclusions: D-met administration in advance of noise-exposure, without further administration, significantly protects from noise-induced ABR threshold shift and OHC loss.

The prevalence of noise-induced hearing threshold shifts in adolescents: The Ohrkan-study

Background: While noise exposure at the workplace is regulated to minimize the risk of hearing loss, leisure noise exposure is likely to pose a risk for hearing as well. However, valid recent data ...