Perceptual Consequences of Cochlear Deafferentation in Humans.

Cochlear synaptopathy, a form of cochlear deafferentation, has been demonstrated in a number of animal species, including non-human primates. Both age and noise exposure contribute to synaptopathy in animal models, indicating that it may be a common type of auditory dysfunction in humans. Temporal bone and auditory physiological data suggest that age and occupational/military noise exposure also lead to synaptopathy in humans. The predicted perceptual consequences of synaptopathy include tinnitus, hyperacusis, and difficulty with speech-in-noise perception. However, confirming the perceptual impacts of this form of cochlear deafferentation presents a particular challenge because synaptopathy can only be confirmed through post-mortem temporal bone analysis and auditory perception is difficult to evaluate in animals. Animal data suggest that deafferentation leads to increased central gain, signs of tinnitus and abnormal loudness perception, and deficits in temporal processing and signal-in-noise detection. If equivalent changes occur in humans following deafferentation, this would be expected to increase the likelihood of developing tinnitus, hyperacusis, and difficulty with speech-in-noise perception. Physiological data from humans is consistent with the hypothesis that deafferentation is associated with increased central gain and a greater likelihood of tinnitus perception, while human data on the relationship between deafferentation and hyperacusis is extremely limited. Many human studies have investigated the relationship between physiological correlates of deafferentation and difficulty with speech-in-noise perception, with mixed findings. A non-linear relationship between deafferentation and speech perception may have contributed to the mixed results. When differences in sample characteristics and study measurements are considered, the findings may be more consistent.

Prevalence and associated factors of noise-induced hearing loss among workers in Bishoftu Central Air Base of Ethiopia.

Excessive occupational exposure to noise results in a well-recognized occupational hearing loss which is prevalent in many workplaces and now it is taken as a global problem. Therefore, this study aims to assess the prevalence of noise-induced hearing loss and associated factors among workers in the Bishoftu Central Air Base in Ethiopia. An institutional-based cross-sectional study was conducted among 260 central air base workers through face-to-face interviews, an environment noise survey, and an audiometric test for data collection. Data were entered by Epi-data version 3.1 and SPSS was used to analyze the data. Finally, a statistical analysis such as descriptive and binary logistic regression analysis was applied. A P-value < 0.05 at 95% CI was considered statistically significant. The overall prevalence of noise-induced hearing loss and hearing impairments was 24.6 and 30.9%, respectively. The highest prevalence of noise-induced hearing loss was recorded for workers who were exposed to noise levels greater than 90 dBA. Out of 132 workers exposed to the average noise level of 75 dB A, only 5% of workers were affected with noise-induced hearing loss, while 128 workers exposed to an average noise level equal to or greater than 90 dB A, 19.6% of workers were identified with noise-induced hearing loss. Regarding sex, around 21.9% of male workers were identified with noise-induced hearing loss. Workers who were exposed to a high noise level workplace previously or before the Central Air Base workplace were five times (AOR = 5.0, 95% CI 1.74-14.36) more likely affected by noise-induced hearing loss than those workers not previously exposed. Those workers who were exposed to greater or equal to 90dBA noise level were 4.98 times (AOR = 4.98, 95% CI 2.59-9.58) more likely to be exposed to noise-induced levels than those who were exposed to less than 90dBA noise level. Moreover, male air base workers were 3.5 times more likely exposed to hearing impairment than female workers (AOR = 3.5, 95% CI 1.01-12.0). This study identified that the prevalence of noise-induced hearing loss and hearing impairments was significantly high. So implementation of a hearing conservation program, giving noise education, and supplying adequate hearing protective devices (HPDs) are essentials.

Noise-induced hearing loss alters potassium-chloride cotransporter KCC2 and GABA inhibition in the auditory centers.

Homeostatic plasticity, the ability of neurons to maintain their averaged activity constant around a set point value, is thought to account for the central hyperactivity after hearing loss. Here, we investigated the putative role of GABAergic neurotransmission in this mechanism after a noise-induced hearing loss larger than 50 dB in high frequencies in guinea pigs. The effect of GABAergic inhibition is linked to the normal functioning of K + -Cl- co-transporter isoform 2 (KCC2) which maintains a low intracellular concentration of chloride. The expression of membrane KCC2 were investigated before and after noise trauma in the ventral and dorsal cochlear nucleus (VCN and DCN, respectively) and in the inferior colliculus (IC). Moreover, the effect of gabazine (GBZ), a GABA antagonist, was also studied on the neural activity in IC. We show that KCC2 is downregulated in VCN, DCN and IC 3 days after noise trauma, and in DCN and IC 30 days after the trauma. As expected, GBZ application in the IC of control animals resulted in an increase of spontaneous and stimulus-evoked activity. In the noise exposed animals, on the other hand, GBZ application decreased the stimulus-evoked activity in IC neurons. The functional implications of these central changes are discussed.

Hearing protection field attenuation estimation systems and associated training for reducing workers' exposure to noise.

BACKGROUND: Global Burden of Disease studies identify hearing loss as the third leading cause of years lived with a disability. Their estimates point to large societal and individual costs from unaddressed hearing difficulties. Workplace noise is an important modifiable risk factor; if addressed, it could significantly reduce the global burden of disease. In practice, providing hearing protection devices (HPDs) is the most common intervention to reduce noise exposure at work. However, lack of fit of HPDs, especially earplugs, can greatly limit their effectiveness. This may be the case for 40% of users. Testing the fit and providing instructions to improve noise attenuation might be effective. In the past two decades, hearing protection fit-test systems have been developed and evaluated in the field. They are called field attenuation estimation systems. They measure the noise attenuation obtained by individual workers using HPDs. If there is a lack of fit, instruction for better fit is provided, and may lead to better noise attenuation obtained by HPDs. OBJECTIVES: To assess: (1) the effects of field attenuation estimation systems and associated training on the noise attenuation obtained by HPDs compared to no instruction or to less instruction in workers exposed to noise; and (2) whether these interventions promote adherence to HPD use. SEARCH METHODS: We used CENTRAL, MEDLINE, five other databases, and two trial registers, together with reference checking, citation searching, and contact with study authors to identify studies. We imposed no language or date restrictions. The latest search date was February 2024. SELECTION CRITERIA: We included randomised controlled trials (RCTs), cluster-RCTs, controlled before-after studies (CBAs), and interrupted time-series studies (ITSs) exploring HPD fit testing in workers exposed to noise levels of more than 80 A-weighted decibels (or dBA) who use hearing protection devices. The unit 'dBA' reports on the use of a frequency-weighting filter to adjust sound measurement results to better reflect how human ears process sound. The outcome noise attenuation had to be measured either as a personal attenuation rating (PAR), PAR pass rate, or both. PAR pass rate is the percentage of workers who passed a pre-established level of sufficient attenuation from their HPDs, identified on the basis of their individual noise exposure. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed study eligibility, risk of bias, and extracted data. We categorised interventions as fit testing of HPDs with instructions at different levels (no instructions, simple instructions, and extensive instructions). MAIN RESULTS: We included three RCTs (756 participants). We did not find any studies that examined whether fit testing and training contributed to hearing protector use, nor any studies that examined whether age, gender, or HPD experience influenced attenuation. We would have included any adverse effects if mentioned by the trial authors, but none reported them. None of the included studies blinded participants; two studies blinded those who delivered the intervention. Effects of fit testing of HPDs with instructions (simple or extensive) versus fit testing of HPDs without instructions Testing the fit of foam and premoulded earplugs accompanied by simple instructions probably does not improve their noise attenuation in the short term after the test (1-month follow-up: mean difference (MD) 1.62 decibels (dB), 95% confidence interval (CI) -0.93 to 4.17; 1 study, 209 participants; 4-month follow-up: MD 0.40 dB, 95% CI -2.28 to 3.08; 1 study, 197 participants; both moderate-certainty evidence). The intervention probably does not improve noise attenuation in the long term (MD 0.15 dB, 95% CI -3.44 to 3.74; 1 study, 103 participants; moderate-certainty evidence). Fit testing of premoulded earplugs with extensive instructions on the fit of the earplugs may improve their noise attenuation at the immediate retest when compared to fit testing without instructions (MD 8.34 dB, 95% CI 7.32 to 9.36; 1 study, 100 participants; low-certainty evidence). Effects of fit testing of HPDs with extensive instructions versus fit testing of HPDs with simple instructions Fit testing of foam earplugs with extensive instructions probably improves their attenuation (MD 8.62 dB, 95% CI 6.31 to 10.93; 1 study, 321 participants; moderate-certainty evidence) and also the pass rate of sufficient attenuation (risk ratio (RR) 1.75, 95% CI 1.44 to 2.11; 1 study, 321 participants; moderate-certainty evidence) when compared to fit testing with simple instructions immediately after the test. This is significant because every 3 dB decrease in noise exposure level halves the sound energy entering the ear. No RCTs reported on the long-term effectiveness of the HPD fit testing with extensive instructions. AUTHORS' CONCLUSIONS: HPD fit testing accompanied by simple instructions probably does not improve noise attenuation from foam and premoulded earplugs. Testing the fit of foam and premoulded earplugs with extensive instructions probably improves attenuation and PAR pass rate immediately after the test. The effects of fit testing associated with training to improve attenuation may vary with types of HPDs and training methods. Better-designed trials with larger sample sizes are required to increase the certainty of the evidence.

Face the (unamplified) music: Key findings for musicians.

Music is complex. There are risks to hearing health associated with playing due to excessive sound exposure. Face the Music is an on-going cross-sectional project to assess the risks to unamplified classical musicians. Key findings over the first fifteen years are presented based on the research undertaken with a leading conservatoire on more than 5000 classical music students. The work covers hearing health surveillance, education and awareness, sound exposure, and new technology. The future of the research programme is discussed along with opportunities in objective hearing health assessment and new acoustic solutions. A lot has changed in fifteen years, but the research was driven by a change in United Kingdom legislation. It is hoped that the research results can inform future regulation.

Frequency-dependent temporary threshold shifts in the Eastern painted turtle (Chrysemys picta picta).

Testudines are a highly threatened group facing an array of stressors, including alteration of their sensory environment. Underwater noise pollution has the potential to induce hearing loss and disrupt detection of biologically important acoustic cues and signals. To examine the conditions that induce temporary threshold shifts (TTS) in hearing in the freshwater Eastern painted turtle (Chrysemys picta picta), three individuals were exposed to band limited continuous white noise (50-1000 Hz) of varying durations and amplitudes (sound exposure levels ranged from 151 to 171 dB re 1 µPa2 s). Control and post-exposure auditory thresholds were measured and compared at 400 and 600 Hz using auditory evoked potential methods. TTS occurred in all individuals at both test frequencies, with shifts of 6.1-41.4 dB. While the numbers of TTS occurrences were equal between frequencies, greater shifts were observed at 600 Hz, a frequency of higher auditory sensitivity, compared to 400 Hz. The onset of TTS occurred at 154 dB re 1 µPa2 s for 600 Hz, compared to 158 dB re 1 µPa2 s at 400 Hz. The 400-Hz onset and patterns of TTS growth and recovery were similar to those observed in previously studied Trachemys scripta elegans, suggesting TTS may be comparable across Emydidae species.

Risk analysis of noise-induced hearing loss of workers in the automobile manufacturing industries based on back-propagation neural network model: a cross-sectional study in Han Chinese population.

OBJECTIVES: This study aims to predict the risk of noise-induced hearing loss (NIHL) through a back-propagation neural network (BPNN) model. It provides an early, simple and accurate prediction method for NIHL. DESIGN: Population based, a cross sectional study. SETTING: Han, China. PARTICIPANTS: This study selected 3266 Han male workers from three automobile manufacturing industries. PRIMARY OUTCOME MEASURES: Information including personal life habits, occupational health test information and occupational exposure history were collected and predictive factors of NIHL were screened from these workers. BPNN and logistic regression models were constructed using these predictors. RESULTS: The input variables of BPNN model were 20, 16 and 21 important factors screened by univariate, stepwise and lasso-logistic regression. When the BPNN model was applied to the test set, it was found to have a sensitivity (TPR) of 83.33%, a specificity (TNR) of 85.92%, an accuracy (ACC) of 85.51%, a positive predictive value (PPV) of 52.85%, a negative predictive value of 96.46% and area under the receiver operating curve (AUC) is: 0.926 (95% CI: 0.891 to 0.961), which demonstrated the better overall properties than univariate-logistic regression modelling (AUC: 0.715) (95% CI: 0.652 to 0.777). The BPNN model has better predictive performance against NIHL than the stepwise-logistic and lasso-logistic regression model in terms of TPR, TNR, ACC, PPV and NPV (p<0.05); the area under the receiver operating characteristics curve of NIHL is also higher than that of the stepwise and lasso-logistic regression model (p<0.05). It was a relatively important factor in NIHL to find cumulative noise exposure, auditory system symptoms, age, listening to music or watching video with headphones, exposure to high temperature and noise exposure time in the trained BPNN model. CONCLUSIONS: The BPNN model was a valuable tool in dealing with the occupational risk prediction problem of NIHL. It can be used to predict the risk of an individual NIHL.

[Research progress in genetics of noise-induced hearing loss].

Noise-induced hearing loss（NIHL） is an acquired sensorineural hearing loss induced by long-term noise exposure. The susceptibility of exposed people may vary even in the same noise environment. With the development of sequencing techniques, genes related to oxidative stress, immunoinflammatory, ion homeostasis, energy metabolism, DNA damage repair and other mechanisms in NIHL have been reported continuously. And some genes may interact with noise exposure indexes. In this article, population studies on NIHL-related gene polymorphisms and gene-environment interactions in the past 20 years are reviewed, aimed to providing evidence for the construction of NIHL-related risk prediction models and the formulation of individualized interventions.

The influencing factors of hearing protection device usage among noise-exposed workers in Guangdong Province: a structural equation modeling-based survey.

BACKGROUND: There are numerous complex barriers and facilitators to continuously wearing hearing protection devices (HPDs) for noise-exposed workers. Therefore, the present study aimed to investigate the relationship between HPD wearing behavior and hearing protection knowledge and attitude, HPD wearing comfort, and work-related factors. METHOD: A cross-sectional study was conducted with 524 noise-exposed workers in manufacturing enterprises in Guangdong Province, China. Data were collected on hearing protection knowledge and attitudes, HPD wearing comfort and behavior, and work-related factors through a questionnaire. Using structural equation modeling (SEM), we tested the association among the study variables. RESULTS: Among the total workers, 69.47% wore HPD continuously, and the attitudes of hearing protection (26.17 ± 2.958) and total HPD wearing comfort (60.13 ± 8.924) were satisfactory, while hearing protection knowledge (3.54 ± 1.552) was not enough. SEM revealed that hearing protection knowledge had direct effects on attitudes (ß = 0.333, p < 0.01) and HPD wearing behavior (ß = 0.239, p < 0.01), and the direct effect of total HPD wearing comfort on behavior was ß = 0.157 (p < 0.01). The direct effect also existed between work shifts and behavior (ß=-0.107, p < 0.05). Indirect relationships mainly existed between other work-related factors, hearing protection attitudes, and HPD wearing behavior through knowledge. Meanwhile, work operation had a direct and negative effect on attitudes (ß=-0.146, p < 0.05), and it can also indirectly and positively affect attitudes through knowledge (ß = 0.08, p < 0.05). CONCLUSION: The behavior of wearing HPD was influenced by hearing protection knowledge, comfort in wearing HPD, and work-related factors. The results showed that to improve the compliance of noise-exposed workers wearing HPD continuously when exposed to noise, the HPD wearing comfort and work-related factors must be taken into consideration. In addition, we evaluated HPD wearing comfort in physical and functional dimensions, and this study initially verified the availability of the questionnaire scale of HPD wearing comfort.

Role of Oxidative Stress in Sensorineural Hearing Loss.

Hearing is essential for communication, and its loss can cause a serious disruption to one's social life. Hearing loss is also recognized as a major risk factor for dementia; therefore, addressing hearing loss is a pressing global issue. Sensorineural hearing loss, the predominant type of hearing loss, is mainly due to damage to the inner ear along with a variety of pathologies including ischemia, noise, trauma, aging, and ototoxic drugs. In addition to genetic factors, oxidative stress has been identified as a common mechanism underlying several cochlear pathologies. The cochlea, which plays a major role in auditory function, requires high-energy metabolism and is, therefore, highly susceptible to oxidative stress, particularly in the mitochondria. Based on these pathological findings, the potential of antioxidants for the treatment of hearing loss has been demonstrated in several animal studies. However, results from human studies are insufficient, and future clinical trials are required. This review discusses the relationship between sensorineural hearing loss and reactive oxidative species (ROS), with particular emphasis on age-related hearing loss, noise-induced hearing loss, and ischemia-reperfusion injury. Based on these mechanisms, the current status and future perspectives of ROS-targeted therapy for sensorineural hearing loss are described.

Managing acoustic noise within MRI: A qualitative interview study among Swedish radiographers.

INTRODUCTION: Acoustic noise from magnetic resonance imaging (MRI) can cause hearing loss and needs to be mitigated to ensure the safety of patients and personnel. Capturing MR personnel's insights is crucial for guiding the development and future applications of noise-reduction technology. This study aimed to explore how MR radiographers manage acoustic noise in clinical MR settings. METHODS: Using a qualitative design, we conducted semi-structured individual interviews with fifteen MR radiographers from fifteen hospitals around Sweden. We focused on the clinical implications of participants' noise management, using an interpretive description approach. We also identified sociotechnical interactions between People, Environment, Tools, and Tasks (PETT) by adopting a Human Factors/Ergonomics framework. Interview data were analyzed inductively with thematic analysis (Braun and Clarke). RESULTS: The analysis generated three main themes regarding MR radiographers' noise management: (I) Navigating Occupational Noise: Risk Management and Adaptation; (II) Protecting the Patient and Serving the Exam, and (III) Establishing a Safe Healthcare Environment with Organizational Support. CONCLUSION: This study offers insights into radiographers' experiences of managing acoustic noise within MRI, and the associated challenges. Radiographers have adopted multiple strategies to protect patients and themselves from adverse noise-related effects. However, they require tools and support to manage this effectively, suggesting a need for organizations to adopt more proactive, holistic approaches to safety initiatives. IMPLICATIONS FOR PRACTICE: The radiographers stressed the importance of a soundproofed work environment to minimize occupational adverse health effects and preserve work performance. They acknowledge noise as a common contributor to patient distress and discomfort. Providing options like earplugs, headphones, mold putty, software-optimized "quiet" sequences, and patient information were important tools. Fostering a safety culture requires proactive safety efforts and support from colleagues and management.

Alterations of the cerebral microstructure in patients with noise-induced hearing loss: A diffusion tensor imaging study.

OBJECTIVE: To explore the changes in the cerebral microstructure of patients with noise-induced hearing loss (NIHL) using diffusion tensor imaging (DTI). METHOD: Overall, 122 patients with NIHL (mild [MP, n = 79], relatively severe patients [including moderate and severe; RSP, n = 32], and undetermined [lost to follow-up, n = 11]) and 84 healthy controls (HCs) were enrolled. All clinical data, including age, education level, hearing threshold, occupation type, noise exposure time, and some scale scores (including the Mini-Mental State Examination [MMSE], tinnitus handicap inventory [THI], and Hamilton Anxiety Scale [HAMA]), were collected and analyzed. All participants underwent T1WI3DFSPGR and DTI, and tract-based spatial statistics and region of interest (ROI) analysis were used for assessment. RESULTS: The final sample included 71 MP, 28 RSP, and 75 HCs. The HAMA scores of the three groups were significantly different (p < .05). The noise exposure times, hearing thresholds, and HAMA scores of the MP and RSP were significantly different (p < .05). The noise exposure time was positively correlated with the hearing threshold and negatively correlated with the HAMA scores (p < .05), whereas the THI scores were positively correlated with the hearing threshold (p < .05). DTI analysis showed that all DTI parameters (fractional anisotropy [FA], axial diffusivity [AD], mean diffusivity [MD], and radial diffusivity [RD]) were significantly different in the left inferior longitudinal fasciculus (ILF) and left inferior fronto-occipital fasciculus (IFOF) for the three groups (p < .05). In addition, the FA values were significantly lower in the bilateral corticospinal tract (CST), right fronto-pontine tract (FPT), right forceps major, left superior longitudinal fasciculus (temporal part) (SLF), and left cingulum (hippocampus) (C-H) of the MP and RSP than in those of the HCs (p < .05); the AD values showed diverse changes in the bilateral CST, left IFOF, right anterior thalamic radiation, right external capsule (EC), right SLF, and right superior cerebellar peduncle (SCP) of the MP and RSP relative to those of the HC (p < .05). However, there were no significant differences among the bilateral auditory cortex ROIs of the three groups (p > .05). There was a significant negative correlation between the FA and HAMA scores for the left IFOF/ILF, right FPT, left SLF, and left C-H for the three groups (p < .05). There was a significant positive correlation between the AD and HAMA scores for the left IFOF/ILF and right EC of the three groups (p < .05). There were significantly positive correlations between the RD/MD and HAMA scores in the left IFOF/ILF of the three groups (p < .05). There was a significant negative correlation between the AD in the right SCP and noise exposure time of the MP and RSP groups (p < .05). The AD, MD, and RD in the left ROI were significantly positively correlated with hearing threshold in the MP and RSP groups (p < .05), whereas FA in the right ROI was significantly positively correlated with the HAMA scores for the three groups (p < .05). CONCLUSION: The changes in the white matter (WM) microstructure may be related to hearing loss caused by noise exposure, and the WM structural abnormalities in patients with NIHL were mainly located in the syndesmotic fibers of the temporooccipital region, which affected the auditory and language pathways. This confirmed that the auditory pathways have abnormal structural connectivity in patients with NIHL.

A single dose of AC102 restores hearing in a guinea pig model of noise-induced hearing loss to almost prenoise levels.

Although sudden sensorineural hearing loss (SSNHL) is a serious condition, there are currently no approved drugs for its treatment. Nevertheless, there is a growing understanding that the cochlear pathologies that underlie SSNHL include apoptotic death of sensory outer hair cells (OHCs) as well as loss of ribbon synapses connecting sensory inner hair cells (IHCs) and neurites of the auditory nerve, designated synaptopathy. Noise-induced hearing loss (NIHL) is a common subtype of SSNHL and is widely used to model hearing loss preclinically. Here, we demonstrate that a single interventive application of a small pyridoindole molecule (AC102) into the middle ear restored auditory function almost to prenoise levels in a guinea pig model of NIHL. AC102 prevented noise-triggered loss of OHCs and reduced IHC synaptopathy suggesting a role of AC102 in reconnecting auditory neurons to their sensory target cells. Notably, AC102 exerted its therapeutic properties over a wide frequency range. Such strong improvements in hearing have not previously been demonstrated for other therapeutic agents. In vitro experiments of a neuronal damage model revealed that AC102 protected cells from apoptosis and promoted neurite growth. These effects may be explained by increased production of adenosine triphosphate, indicating improved mitochondrial function, and reduced levels of reactive-oxygen species which prevents the apoptotic processes responsible for OHC death. This action profile of AC102 might be causal for the observed hearing recovery in in vivo models.

Synaptic ribbon dynamics after noise exposure in the hearing cochlea.

Moderate noise exposure induces cochlear synaptopathy, the loss of afferent ribbon synapses between cochlear hair cells and spiral ganglion neurons, which is associated with functional hearing decline. Prior studies have demonstrated noise-induced changes in the distribution and number of synaptic components, but the dynamic changes that occur after noise exposure have not been directly visualized. Here, we describe a live imaging model using RIBEYE-tagRFP to enable direct observation of pre-synaptic ribbons in mature hearing mouse cochleae after synaptopathic noise exposure. Ribbon number does not change, but noise induces an increase in ribbon volume as well as movement suggesting unanchoring from synaptic tethers. A subgroup of basal ribbons displays concerted motion towards the cochlear nucleus with subsequent migration back to the cell membrane after noise cessation. Understanding the immediate dynamics of synaptic damage after noise exposure may facilitate identification of specific target pathways to treat cochlear synaptopathy.

[Mechanism of noise induced hidden hearing loss based on proteomics].

Objective: To explore the mechanism of noise-induced hidden hearing loss by proteomics. Methods: In October 2022, 64 SPF male C57BL/6J mice were divided into control group and noise exposure group with 32 mice in each group according to random sampling method. The noise exposure group was exposed to 100 dB sound pressure level, 2000-16000 Hz broadband noise for 2 h, and the mouse hidden hearing loss model was established. Auditory brainstem response (ABR) was used to test the change of hearing threshold of mice on the 7th day after noise exposure, the damage of basal membrane hair cells was observed by immunofluorescence, and the differentially expressed proteins in the inner ear of mice in each group were identified and analyzed by 4D-Label-free quantitative proteomics, and verified by Western blotting. The results were statistically analyzed by ANOVA and t test. Results: On the 7th day after noise exposure, there was no significant difference in hearing threshold between the control group and the noise exposure group at click and 8000 Hz acoustic stimulation (P>0.05) . The hearing threshold in the noise exposure group was significantly higher than that in the control group under 16000 Hz acoustic stimulation (P<0.05) . Confocal immunofluorescence showed that the basal membrane hair cells of cochlear tissue in noise exposure group were arranged neatly, but the relative expression of C-terminal binding protein 2 antibody of presynaptic membrane in middle gyrus and basal gyrus was significantly lower than that in control group (P<0.05) . GO enrichment analysis showed that the functions of differentially expressed proteins were mainly concentrated in membrane potential regulation, ligand-gated channel activity, and ligand-gated ion channel activity. KEGG pathway enrichment analysis showed that differentially expressed proteins were significantly enriched in phosphatidylinositol 3 kinase-protein kinase B (PI3K-Akt) signaling pathway, NOD-like receptor signaling pathway, calcium signaling pathway, etc. Western blotting showed that the expression of inositol 1, 4, 5-trisphosphate receptor 3 (Itpr3) was increased and the expression of solute carrier family 38 member 2 (Slc38a2) was decreased in the noise exposure group (P<0.05) . Conclusion: Through proteomic analysis, screening and verification of the differential expression proteins Itpr3 and Slc38a2 in the constructed mouse noise-induced hidden hearing loss model, the glutaminergic synaptic related pathways represented by Itpr3 and Slc38a2 may be involved in the occurrence of hidden hearing loss.

Sensitivity of Methods for Diagnosing Noise-Induced Hearing Loss in Cases of Exposures Including Intense Low-Frequency Noise.

Exposure to intense low-frequency sounds, for example inside tanks and armoured vehicles, can lead to noise-induced hearing loss (NIHL) with a variable audiometric pattern, including low- and mid-frequency hearing loss. It is not known how well existing methods for diagnosing NIHL apply in such cases. Here, the audiograms of 68 military personnel (mostly veterans) who had been exposed to intense low-frequency noise (together with other types of noise) and who had low-frequency hearing loss (defined as a pure-tone average loss at 0.25, 0.5 and 1 kHz ≥20 dB) were used to assess the sensitivity of three diagnostic methods: the method of Coles, Lutman and Buffin, denoted CLB, which depends on the identification of a notch or bulge in the audiogram near 4 kHz, and two methods specifically intended for diagnosing NIHL sustained during military service, the rM-NIHL method, which depends on the identification of a notch or bulge in the audiogram near 4 kHz and/or a hearing loss at high frequencies greater than expected from age alone, and the MLP(18) method based on a multi-layer perceptron. The proportion of individuals receiving a positive diagnosis for either or both ears, which provides an approximate measure of sensitivity, was 0.40 for the CLB method, 0.79 for the rM-NIHL method and 1.0 for the MLP(18) method. It is concluded that the MLP(18) method is suitable for diagnosing NIHL sustained during military service whether or not the exposure includes intense low-frequency sounds.

Noise-induced synaptic loss and its post-exposure recovery in CBA/CaJ vs. C57BL/6J mice.

Acute noise-induced loss of synapses between inner hair cells (IHCs) and auditory nerve fibers (ANFs) has been documented in several strains of mice, but the extent of post-exposure recovery reportedly varies dramatically. If such inter-strain heterogeneity is real, it could be exploited to probe molecular pathways mediating neural remodeling in the adult cochlea. Here, we compared synaptopathy repair in CBA/CaJ vs. C57BL/6J, which are at opposite ends of the reported recovery spectrum. We evaluated C57BL/6J mice 0 h, 24 h, 2 wks or 8 wks after exposure for 2 h to octave-band noise (8-16 kHz) at either 90, 94 or 98 dB SPL, to compare with analogous post-exposure results in CBA/CaJ at 98 or 101 dB. We counted pre- and post-synaptic puncta in immunostained cochleas, using machine learning to classify paired (GluA2 and CtBP2) vs. orphan (CtBP2 only) puncta, and batch-processing to quantify immunostaining intensity. At 98 dB, both strains show ongoing loss of ribbons and synapses between 0 and 24 h, followed by partial recovery, however the extent and degree of these changes were greater in C57BL/6J. Much of the synaptic recovery is due to transient reduction in GluA2 intensity in synaptopathic regions. In contrast, CtBP2 intensity showed only transient increases (at 2 wks). Neurofilament staining revealed transient extension of ANF terminals in C57BL/6J, but not in CBA/CaJ, peaking at 24 h and reverting by 2 wks. Thus, although interstrain differences in synapse recovery are dominated by reversible changes in GluA2 receptor levels, the neurite extension seen in C57BL/6J suggests a qualitative difference in regenerative capacity.

KSR1 Knockout Mouse Model Demonstrates MAPK Pathway's Key Role in Cisplatin- and Noise-induced Hearing Loss.

Hearing loss is a major disability in everyday life and therapeutic interventions to protect hearing would benefit a large portion of the world population. Here we found that mice devoid of the protein kinase suppressor of RAS 1 (KSR1) in their tissues (germline KO mice) exhibit resistance to both cisplatin- and noise-induced permanent hearing loss compared with their wild-type KSR1 littermates. KSR1 is a scaffold protein that brings in proximity the mitogen-activated protein kinase (MAPK) proteins BRAF, MEK1/2 and ERK1/2 and assists in their activation through a phosphorylation cascade induced by both cisplatin and noise insults in the cochlear cells. KSR1, BRAF, MEK1/2, and ERK1/2 are all ubiquitously expressed in the cochlea. Deleting the KSR1 protein tempered down the MAPK phosphorylation cascade in the cochlear cells following both cisplatin and noise insults and conferred hearing protection of up to 30 dB SPL in three tested frequencies in male and female mice. Treatment with dabrafenib, an FDA-approved oral BRAF inhibitor, protected male and female KSR1 wild-type mice from both cisplatin- and noise-induced hearing loss. Dabrafenib treatment did not enhance the protection of KO KSR1 mice, providing evidence dabrafenib works primarily through the MAPK pathway. Thus, either elimination of the KSR1 gene expression or drug inhibition of the MAPK cellular pathway in mice resulted in profound protection from both cisplatin- and noise-induced hearing loss. Inhibition of the MAPK pathway, a cellular pathway that responds to damage in the cochlear cells, can prove a valuable strategy to protect and treat hearing loss.

Association between occupational noise exposure level and pure-tone audiometry abnormalities among Metropolitan Manila Development Authority employees: A cross-sectional study.

Traffic enforcers are exposed to various occupational health and safety hazards, including noise pollution, which may lead to occupational hearing loss. This cross-sectional study aimed to estimate the prevalence of hearing loss and to assess the relationship between occupational noise exposure level (ONEL) and abnormalities in air conduction thresholds among Metropolitan Manila Development Authority (MMDA) employees along Epifanio delos Santos Avenue, Philippines. Eight-hour ONELs were measured among 108 participants working with greater than 5 years of service. Participants had hearing evaluations using pure tone audiometry (PTA) to calculate the prevalence of hearing loss. Generalized linear models with a Poisson distribution were fitted to estimate the association between ONEL and audiologic abnormalities, controlling for confounding factors. Approximately 16% of employees had hearing loss. The prevalence of hearing loss was higher with ONEL exposures greater than 85 A-weighted decibels (dBA), with traffic enforcers exposed to higher ONELs than office workers. ONELs greater than 85 dBA were related to audiologic abnormalities at different frequencies in PTA. The prevalence of audiologic abnormalities at 4000 Hz and 6000 Hz was 48% higher (adjusted prevalence ratio [aPR], 1.48; 95% CI, 1.12-1.96) and 25% higher (aPR, 1.25; 95% CI, 1.00-1.55), respectively, among participants with ONELs greater than 85 dBA than with ONELs less than or equal to 85 dBA. Participants exposed to ONELs greater than 85 dBA, more likely traffic enforcers, may have increased risk of audiologic abnormalities. Regular ONEL monitoring is warranted for occupational risk assessment of traffic enforcers. A hearing conservation program may need to be considered for this population. Additional studies are needed to determine trends in hearing deterioration among traffic enforcers.