Cochlear zinc signaling dysregulation is associated with noise-induced hearing loss, and zinc chelation enhances cochlear recovery.

Exposure to loud noise triggers sensory organ damage and degeneration that, in turn, leads to hearing loss. Despite the troublesome impact of noise-induced hearing loss (NIHL) in individuals and societies, treatment strategies that protect and restore hearing are few and insufficient. As such, identification and mechanistic understanding of the signaling pathways involved in NIHL are required. Biological zinc is mostly bound to proteins, where it plays major structural or catalytic roles; however, there is also a pool of unbound, mobile (labile) zinc. Labile zinc is mostly found in vesicles in secretory tissues, where it is released and plays a critical signaling role. In the brain, labile zinc fine-tunes neurotransmission and sensory processing. However, injury-induced dysregulation of labile zinc signaling contributes to neurodegeneration. Here, we tested whether zinc dysregulation occurs and contributes to NIHL in mice. We found that ZnT3, the vesicular zinc transporter responsible for loading zinc into vesicles, is expressed in cochlear hair cells and the spiral limbus, with labile zinc also present in the same areas. Soon after noise trauma, ZnT3 and zinc levels are significantly increased, and their subcellular localization is vastly altered. Disruption of zinc signaling, either via ZnT3 deletion or pharmacological zinc chelation, mitigated NIHL, as evidenced by enhanced auditory brainstem responses, distortion product otoacoustic emissions, and number of hair cell synapses. These data reveal that noise-induced zinc dysregulation is associated with cochlear dysfunction and recovery after NIHL, and point to zinc chelation as a potential treatment for mitigating NIHL.

Macrophages Promote Repair of Inner Hair Cell Ribbon Synapses following Noise-Induced Cochlear Synaptopathy.

Resident cochlear macrophages rapidly migrate into the inner hair cell synaptic region and directly contact the damaged synaptic connections after noise-induced synaptopathy. Eventually, such damaged synapses are spontaneously repaired, but the precise role of macrophages in synaptic degeneration and repair remains unknown. To address this, cochlear macrophages were eliminated using colony stimulating factor 1 receptor (CSF1R) inhibitor, PLX5622. Sustained treatment with PLX5622 in CX3CR1 GFP/+ mice of both sexes led to robust elimination of resident macrophages (∼94%) without significant adverse effects on peripheral leukocytes, cochlear function, and structure. At 1 day (d) post noise exposure of 93 or 90 dB SPL for 2 hours, the degree of hearing loss and synapse loss were comparable in the presence and absence of macrophages. At 30 d after exposure, damaged synapses appeared repaired in the presence of macrophages. However, in the absence of macrophages, such synaptic repair was significantly reduced. Remarkably, on cessation of PLX5622 treatment, macrophages repopulated the cochlea, leading to enhanced synaptic repair. Elevated auditory brainstem response thresholds and reduced auditory brainstem response Peak 1 amplitudes showed limited recovery in the absence of macrophages but recovered similarly with resident and repopulated macrophages. Cochlear neuron loss was augmented in the absence of macrophages but showed preservation with resident and repopulated macrophages after noise exposure. While the central auditory effects of PLX5622 treatment and microglia depletion remain to be investigated, these data demonstrate that macrophages do not affect synaptic degeneration but are necessary and sufficient to restore cochlear synapses and function after noise-induced synaptopathy.SIGNIFICANCE STATEMENT The synaptic connections between cochlear inner hair cells and spiral ganglion neurons can be lost because of noise over exposure or biological aging. This loss may represent the most common causes of sensorineural hearing loss also known as hidden hearing loss. Synaptic loss results in degradation of auditory information, leading to difficulty in listening in noisy environments and other auditory perceptual disorders. We demonstrate that resident macrophages of the cochlea are necessary and sufficient to restore synapses and function following synaptopathic noise exposure. Our work reveals a novel role for innate-immune cells, such as macrophages in synaptic repair, that could be harnessed to regenerate lost ribbon synapses in noise- or age-linked cochlear synaptopathy, hidden hearing loss, and associated perceptual anomalies.

Developmental Exposure to Polychlorinated Biphenyls Prevents Recovery from Noise-Induced Hearing Loss and Disrupts the Functional Organization of the Inferior Colliculus.

Exposure to combinations of environmental toxins is growing in prevalence; and therefore, understanding their interactions is of increasing societal importance. Here, we examined the mechanisms by which two environmental toxins, polychlorinated biphenyls (PCBs) and high-amplitude acoustic noise, interact to produce dysfunction in central auditory processing. PCBs are well established to impose negative developmental impacts on hearing. However, it is not known whether developmental exposure to this ototoxin alters the sensitivity to other ototoxic exposures later in life. Here, male mice were exposed to PCBs in utero, and later as adults were exposed to 45 min of high-intensity noise. We then examined the impacts of the two exposures on hearing and the organization of the auditory midbrain using two-photon imaging and analysis of the expression of mediators of oxidative stress. We observed that developmental exposure to PCBs blocked hearing recovery from acoustic trauma. In vivo two-photon imaging of the inferior colliculus (IC) revealed that this lack of recovery was associated with disruption of the tonotopic organization and reduction of inhibition in the auditory midbrain. In addition, expression analysis in the inferior colliculus revealed that reduced GABAergic inhibition was more prominent in animals with a lower capacity to mitigate oxidative stress. These data suggest that combined PCBs and noise exposure act nonlinearly to damage hearing and that this damage is associated with synaptic reorganization, and reduced capacity to limit oxidative stress. In addition, this work provides a new paradigm by which to understand nonlinear interactions between combinations of environmental toxins.SIGNIFICANCE STATEMENT Exposure to common environmental toxins is a large and growing problem in the population. This work provides a new mechanistic understanding of how the prenatal and postnatal developmental changes induced by polychlorinated biphenyls (PCBs) could negatively impact the resilience of the brain to noise-induced hearing loss (NIHL) later in adulthood. The use of state-of-the-art tools, including in vivo multiphoton microscopy of the midbrain helped in identifying the long-term central changes in the auditory system after the peripheral hearing damage induced by such environmental toxins. In addition, the novel combination of methods employed in this study will lead to additional advances in our understanding of mechanisms of central hearing loss in other contexts.

What can insects teach us about hearing loss?

Over the last three decades, insects have been utilized to provide a deep and fundamental understanding of many human diseases and disorders. Here, we present arguments for insects as models to understand general principles underlying hearing loss. Despite ∼600 million years since the last common ancestor of vertebrates and invertebrates, we share an overwhelming degree of genetic homology particularly with respect to auditory organ development and maintenance. Despite the anatomical differences between human and insect auditory organs, both share physiological principles of operation. We explain why these observations are expected and highlight areas in hearing loss research in which insects can provide insight. We start by briefly introducing the evolutionary journey of auditory organs, the reasons for using insect auditory organs for hearing loss research, and the tools and approaches available in insects. Then, the first half of the review focuses on auditory development and auditory disorders with a genetic cause. The second half analyses the physiological and genetic consequences of ageing and short- and long-term changes as a result of noise exposure. We finish with complex age and noise interactions in auditory systems. In this review, we present some of the evidence and arguments to support the use of insects to study mechanisms and potential treatments for hearing loss in humans. Obviously, insects cannot fully substitute for all aspects of human auditory function and loss of function, although there are many important questions that can be addressed in an animal model for which there are important ethical, practical and experimental advantages.

Alterations of resting-state functional network connectivity in patients with noise-induced hearing loss: A study based on independent component analysis.

Functional reorganization is a response to auditory deficits or deprivation, and less is known about the overall brain network alterations involving resting-state networks (RSNs) and multiple functional networks in patients with occupational noise-induced hearing loss (NIHL). So this study evaluated resting-state functional network connectivity (FNC) alterations in occupational NIHL using an independent component analysis (ICA). In total, 79 mild NIHL patients (MP), 32 relatively severe NIHL patients (RSP), and 84 age- and education- matched healthy controls (HC) were recruited. All subjects were tested using the Mini-mental State Examination scale, the tinnitus Handicap Inventory scale, the Hamilton Anxiety scale (HAMA) and scanned by T1-3DFSPGR, resting-state functional magnetic resonance imaging sequence in 3.0 T and analysed by the ICA. Seven RSNs were identified, compared with the HC, the MP showed increased FNC within the executive control network (ECN) and enhanced FNC within the default mode network (DMN) and the visual network (VN); compared with the HC, the RSP showed decreased FNC within the ECN and auditory network (AUN), DMN and VN; no significant changes in FNC were found in the MP compared with the RSP. Furthermore, the correlation analysis between the noise exposure time and hearing loss level, HAMA were both negative, and there were no significant correlations between the abnormal RSNs and the hearing level, noise exposure time and HAMA. These findings indicate that different degrees of NIHL involve different alterations in RSNs connectivity and may reveal the neural mechanisms related to emotion-related features and functional abnormalities following long-term NIHL.

Gelatin-Encapsulated Tetrahedral DNA Nanostructure Enhances Cellular Internalization for Treating Noise-Induced Hearing Loss.

Nanoparticle-based drug delivery strategies have emerged as a crucial avenue for comprehensive sensorineural hearing loss treatment. Nevertheless, developing therapy vectors crossing both biological and cellular barriers has encountered significant challenges deriving from various external factors. Herein, the rational integration of gelatin nanoparticles (GNPs) with tetrahedral DNA nanostructures (TDNs) to engineer a distinct drug-delivery nanosystem (designed as TDN@GNP) efficiently enhances the biological permeability and cellular internalization, further resolving the dilemma of noise-induced hearing loss via loading epigallocatechin gallate (EGCG) with anti-lipid peroxidation property. Rationally engineering of TDN@GNP demonstrates dramatic alterations in the physicochemical key parameters of TDNs that are pivotal in cell-particle interactions and promote cellular uptake through multiple endocytic pathways. Furthermore, the EGCG-loaded nanosystem (TDN-EGCG@GNP) facilitates efficient inner ear drug delivery by superior permeability through the biological barrier (round window membrane), maintaining high drug concentration within the inner ear. The TDN-EGCG@GNP actively overcomes the cell membrane, exhibiting hearing protection from noise insults via reduced lipid peroxidation in outer hair cells and spiral ganglion neurons. This work exemplifies how integrating diverse vector functionalities can overcome biological and cellular barriers in the inner ear, offering promising applications for inner ear disorders.

Norepinephrine protects against cochlear outer hair cell damage and noise-induced hearing loss via α2A-adrenergic receptor.

BACKGROUND: The cochlear sympathetic system plays a key role in auditory function and susceptibility to noise-induced hearing loss (NIHL). The formation of reactive oxygen species (ROS) is a well-documented process in NIHL. In this study, we aimed at investigating the effects of a superior cervical ganglionectomy (SCGx) on NIHL in Sprague-Dawley rats. METHODS: We explored the effects of unilateral and bilateral Superior Cervical Ganglion (SCG) ablation in the eight-ten weeks old Sprague-Dawley rats of both sexes on NIHL. Auditory function was evaluated by auditory brainstem response (ABR) testing and Distortion product otoacoustic emissions (DPOAEs). Outer hair cells (OHCs) counts and the expression of α2A-adrenergic receptor (AR) in the rat cochlea using immunofluorescence analysis. Cells culture and treatment, CCK-8 assay, Flow cytometry staining and analysis, and western blotting were to explore the mechanisms of SCG fibers may have a protective role in NIHL. RESULTS: We found that neither bilateral nor unilateral SCGx protected the cochlea against noise exposure. In HEI-OC1 cells, H2O2-induced oxidative damage and cell death were inhibited by the application of norepinephrine (NE). NE may prevent ROS-induced oxidative stress in OHCs and NIHL through the α2A-AR. CONCLUSION: These results demonstrated that sympathetic innervation mildly affected cochlear susceptibility to acoustic trauma by reducing oxidative damage in OHCs through the α2A-AR. NE may be a potential therapeutic strategy for NIHL prevention.

Therapeutic effect of intraperitoneal dexamethasone on noise-induced permanent threshold shift in mice model.

The purpose of the study was to which investigate whether dexamethasone, which has anti-inflammatory and immune response suppression roles, could treat noise-induced hearing loss caused by damage to hair cells in the cochlea. The experiment used 8-week-old CBA mice exposed to white noise at an intensity of 110 dB SPL for 2 h, with hearing loss confirmed by the auditory brainstem response test. Dexamethasone was administered by intraperitoneal injection for 5 days, and the therapeutic effect was investigated for 3 weeks. The experimental groups were 3 mg/kg of dexamethasone (3 mpk) and 10 mg/kg of dexamethasone (10 mpk), and the control group was a saline-administered group. The results showed that compared to the control group, the hearing threshold value was recovered by 10 dB SPL compared to the saline group from the 14th day in the 3 mpk group. In the 10 mpk group, thresholds were recovered from the 7th day compared to the saline group. This difference was similar at 4 kHz, and in the case of the 10 mpk group, the threshold was recovered by 20 dB SPL compared to the saline group. The study also confirmed the restoration of nerve cell activity and showed a recovery effect of about 20 µV in the amplitude value change in the 10 mpk group. In conclusion, the study suggests that dexamethasone has a therapeutic effect for noise-induced hearing loss by increasing the activity of nerve cells and showing a recovery effect from hair cells damaged by noise.

Early Loss of Spiral Ganglion Neurons in the Auditory System after Noise Trauma.

INTRODUCTION: Noise-induced hearing loss is one of the most frequent recognized occupational diseases. The time course of the involved pathologies is still under investigation. Several studies have demonstrated an acute damage of the sensory tissue, but only few experiments investigated the degeneration of (type I) spiral ganglion neurons (SGNs), representing the primary neurons in the auditory system. The aim of the present study was to investigate the time course of SGN degeneration within a 7-day period after traumatic noise exposure starting immediately after trauma. METHODS: Young adult normal hearing mice were noise exposed for 3 h with a broadband noise (5-20 kHz) at 115 dB SPL. Auditory threshold shift was measured by auditory brainstem recordings, and SGN densities were analyzed at different time points during the first week after acoustic trauma. RESULTS: Significant reduction of SGN densities was detected and is accompanied by a significant hearing loss. Degeneration starts within hours after the applied trauma, further progressing within days post-exposure. DISCUSSION: Early neurodegeneration in the auditory periphery seems to be induced by direct overstimulation of the auditory nerve fibers. SGN loss is supposed to be a result of inflammatory responses and neural deprivation, leading to permanent hearing loss and auditory processing deficits.

The summating potential polarity encodes the ear health condition.

The summating potential (SP), the DC potential which, along with the AC response, is produced when the hair cells convert the vibrational mechanical energy of sound into electrical signals, is the most enigmatic of the cochlear potentials because its polarity and function have remained elusive for more than seven decades. Despite the tremendous socioeconomic consequences of noise-induced hearing loss and the profound physiological importance of understanding how loud noise exposure impairs the hair cell receptor activation, the relationship between the SP and noise-induced hearing impairment remains poorly characterized. Here, I show that in normally hearing ears, the SP polarity is positive and its amplitude relative to the AC response grows exponentially across frequencies, and becomes negative and decreases exponentially across frequencies following noise-induced hearing injury. Since the SP is thought to be generated by K+ outflow down the gradient through the hair cell basolateral K+ channels, the SP polarity switch to negative values is consistent with a noise-induced shift in the operating point of the hair cells.

The sound of safety: exploring the determinants of prevention intention in noisy industrial workplaces.

Occupational noise exposure is a pervasive issue in many industries, leading to a range of health issues and sleep disturbances among workers. Additionally, there is a strong desire among these workers to prevent industrial accidents. This study, aimed at enhancing worker health and well-being, utilized a survey distributed by the Korean Confederation of Trade Unions to field workers. Data from 1285 workers were collected and analyzed using partial least squares structural equation modeling (PLS-SEM) to identify and understand the factors affecting prevention intention in noisy work environments. Our findings indicate that health problems resulting from occupational noise exposure significantly influence insomnia, perceived severity of potential accidents, perceived benefits of preventive measures, and perceived barriers. Perceived severity was significantly correlated with prevention intention, emphasizing the role of risk perception in motivating preventive behaviors. Perceived benefits were also significantly associated with prevention intention, highlighting the importance of positive outcomes in influencing workers' behaviors. Additionally, perceived barriers showed a significant relationship with prevention intention, suggesting that overcoming these barriers is crucial in promoting preventive behaviors. Demographic factors such as gender displayed a significant association with prevention intention, while age did not. This study provides valuable insights into the multifaceted factors influencing workers' intention to prevent industrial accidents in noisy environments, underlining the importance of comprehensive data collection tools in understanding these dynamics.

Noise-induced hearing loss in the contralateral ear during otologic and neurotologic surgeries.

OBJECTIVE: Noise-induced hearing loss in the non-surgical ear during otologic/neurotologic surgery has not been well studied. The purpose of this study was to evaluate changes in hearing that may occur in the contralateral (i.e., non-surgical) ear after various otologic/neurotologic surgeries due to noise generated by drills. We hypothesized that otologic/neurotologic surgeries, longer in duration, would suggest longer drilling times and result in decreased hearing in the contralateral ear as evidenced by a change post-operative pure tone air conduction thresholds when compared to pre-operative thresholds. METHODS: A retrospective chart review at a tertiary referral center. Adult patients (18-75 years old) who underwent otologic/neurotologic surgeries from May 1, 2016 through May 1, 2021 were considered for inclusion. Surgeries included vestibular schwannoma resection (translabyrinthine, middle cranial fossa, or retrosigmoid approaches), endolymphatic sac/shunt and labyrinthectomy for Meniere's disease, and tympanomastoid surgery for middle ear pathology (e.g., cholesteatoma). Patient characteristics obtained through record review included age, sex, surgical procedure, pre-operative and post-operative audiometric thresholds and word recognition scores (WRS) for the contralateral ear, and duration of surgery. RESULTS: No significant differences were observed for change in audiometric thresholds in the contralateral ear for any surgery when considering individual frequencies. Additionally, no significant change in WRS was observed for any surgical approach. CONCLUSIONS: The risk of hearing loss in the non-surgical ear during various otologic/neurotologic surgeries appears to be minimal when measured via routine clinical tests.

Recreational music exposure and hearing health in young adults.

OBJECTIVE: This study aimed to compare daily and total recreational music exposure levels and extended-spectrum audiogram results in young adults without pre-existing hearing problems. DESIGN: The study included healthy volunteers aged 18-25 with no known ear disease or hearing loss. Participants completed a questionnaire, underwent otoscopic and tympanometric examinations, and determined preferred music volumes in an audiometry booth using calibrated music samples of their preferred genres. Hearing thresholds up to 16 kiloHertz (kHz) were measured. Daily music exposure for each participant was normalized to 8 h to calculate a time-weighted average of 8 h (TWA8). Total exposure (TE) was calculated by multiplying TWA8 by the number of years of music listening. RESULTS: A total of 32.4% of participants had TWA8s above 65 dB. Their hearing thresholds at 125, 250, 500, and 16,000 Hz and the average of 125 Hz-8 kHz were significantly higher. Participants with TWA8s above 65 dB were also more prone to speaking loudly and experiencing communication difficulties on the phone. Those with a TE of more than 400 experienced significantly more speech discrimination difficulty in noisy environments and temporary hearing loss/tinnitus after exposure to loud music. Participants with a TE above 700 had worse thresholds at 4, 14, and 16 kHz frequencies, as well as 125-8000 Hz and 500-4000 Hz averages compared to those with a TE below 700. CONCLUSIONS: This study provides evidence that recreational music with much lower exposure levels than the universally accepted TWA8 of 85 dB could negatively impact hearing in healthy young adults. Therefore, maintaining a maximum TWA8 of 65 dB is recommended.

Recovery rate after acute acoustic trauma: a case series and meta-analysis.

OBJECTIVE: Steroids given systemically, locally, or both are the mainstay of treatment for acute acoustic trauma (AAT). The overall recovery rate (full, partial, and none) is undetermined. STUDY DESIGN: Original case series and systematic literature review. SETTING: Case series of a tertiary referral center and a systematic literature review. METHODS: Cases of AAT between 2012 and 2022 were retrospectively analyzed for demographics, acoustic trauma characteristics, treatment modality and delay and prognosis. This case series was added to the series identified by a systematic literature review. This review included "Medline" via "PubMed", "EMBASE", and "Google scholar". All series were pooled for meta-analysis defining prognosis following steroidal treatment for AAT patients. RESULTS: The pooled analyses included 662 ears, out of which 250 underwent complete recovery of hearing (overall proportion = 0.2809, 95%confidence interval [CI] = 0.1611-0.4178). Any recovery was recorded for 477 ears (overall proportion = 0.7185, 95% CI = 0.5671-0.8493) and no recovery was documented for 185 ears (overall proportion = 0.2815, 95% CI = 0.1507-0.4329). CONCLUSION: The rate of overall recovery for AAT is around 70%, and around 30% for full recovery when steroids are initiated within the first 2 weeks following the insult.

Effectiveness of educational programs in hearing health: a systematic review and meta-analysis.

OBJECTIVE: To evaluate the effectiveness of hearing health education programs aimed at preventing noise-induced hearing loss (NIHL), of recreational and occupational origin, by means of a systematic review and meta-analysis. DESIGN: The search strategy was carried out in on five electronic databases, as well as referrals from experts. The risk of bias was judged, and the random effects meta-analysis was performed. The certainty of the evidence was assessed. STUDY SAMPLE: Effectiveness studies that used educational intervention in hearing health and prevention of NIHL were included. RESULTS: 42 studies were included. The Dangerous Decibels program was the only one that could be quantitatively analysed and showed improvement in the post-intervention period of up to one week [SMD = 0.60; CI95% = 0.38-0.82; I2 = 92.5%) and after eight weeks [SMD = 0.45; CI95% = 0.26-0.63; I2 = 81.6%) compared to the baseline. The certainty of evidence was judged as very low. CONCLUSIONS: The Dangerous Decibels program is effective after eight weeks of intervention. The other programs cannot be quantified. They still present uncertainty about their effectiveness. The level of certainty is still low for this assessment.

ERK1/2 Inhibition via the Oral Administration of Tizaterkib Alleviates Noise-Induced Hearing Loss While Tempering down the Immune Response.

Noise-induced hearing loss (NIHL) is a major cause of hearing impairment and is linked to dementia and mental health conditions, yet no FDA-approved drugs exist to prevent it. Downregulating the mitogen-activated protein kinase (MAPK) cellular pathway has emerged as a promising approach to attenuate NIHL, but the molecular targets and the mechanism of protection are not fully understood. Here, we tested specifically the role of the kinases ERK1/2 in noise otoprotection using a newly developed, highly specific ERK1/2 inhibitor, tizaterkib, in preclinical animal models. Tizaterkib is currently being tested in phase 1 clinical trials for cancer treatment and has high oral bioavailability and low predicted systemic toxicity in mice and humans. In this study, we performed dose-response measurements of tizaterkib's efficacy against permanent NIHL in adult FVB/NJ mice, and its minimum effective dose (0.5 mg/kg/bw), therapeutic index (>50), and window of opportunity (<48 h) were determined. The drug, administered orally twice daily for 3 days, 24 h after 2 h of 100 dB or 106 dB SPL noise exposure, at a dose equivalent to what is prescribed currently for humans in clinical trials, conferred an average protection of 20-25 dB SPL in both female and male mice. The drug shielded mice from the noise-induced synaptic damage which occurs following loud noise exposure. Equally interesting, tizaterkib was shown to decrease the number of CD45- and CD68-positive immune cells in the mouse cochlea following noise exposure. This study suggests that repurposing tizaterkib and the ERK1/2 kinases' inhibition could be a promising strategy for the treatment of NIHL.

Advancing noise management in aviation: Strategic approaches for preventing noise-induced hearing loss.

As urbanization and population growth escalate, the challenge of noise pollution intensifies, particularly within the aviation industry. This review examines current insights into noise-induced hearing loss (NIHL) in aviation, highlighting the risks to pilots, cabin crew, aircraft maintenance engineers, and ground staff from continuous exposure to high-level noise. It evaluates existing noise management and hearing conservation strategies, identifying key obstacles and exploring new technological solutions. While progress in developing protective devices and noise control technologies is evident, gaps in their widespread implementation persist. The study underscores the need for an integrated strategy combining regulatory compliance, technological advances, and targeted educational efforts. It advocates for global collaboration and policy development to safeguard the auditory health of aviation workers and proposes a strategic framework to enhance hearing conservation practices within the unique challenges of the aviation sector.

Quantification of suppressor effects on breech and action noise from AR-15 pattern firearms and its implications for the protection of human hearing.

Noise from firearms is well known to be harmful to human hearing. This problem has been addressed by various military units through the use of muzzle suppressors. However, as suppressor technology has advanced, shooters report hearing the mechanical action of gas-operated semi-automatic rifles (ArmaLite Rifle Model 15 style aka AR-15) as being louder than the suppressed muzzle noise. This study aims to evaluate if harmful noise is present in the shooter's ear, even when impulse noise emanating from the muzzle is suppressed. To characterize the impulse noise of the firearm action caused by the reciprocation of the bolt carrier group (BCG) and subsequent impact when it returns to battery (the forward locked position), the muzzle of a rifle was placed through a constructed plywood wall, and the noise of the action/breech was measured independently from the muzzle noise. This research finds that the impact of the BCG returning to battery (132 dBZ) has the potential to be harmful to the shooter's hearing even when the noise from the muzzle is effectively suppressed.

[Occupational diseases related to otorhinolaryngology]. / Berufskrankheiten mit Bezug zur HNO-Heilkunde.

In the German Ordinance on Occupational Diseases (BKV), there are currently 82 occupational diseases listed, of which 18 partially or completely fall within the field of ENT medicine due to the associated health disorders. Noise-induced hearing loss is usually the focus of attention for the ENT specialist, but it has long since ceased to be the only occupational disease. In order to help uncover possible causalities between occupational noxious substances and diseases, it is important that physicians report their own observations and new scientific findings regarding suspected cases to the German Social Accident Insurance, especially in situations where cancer may be linked to occupational influences.

Noise-Induced Hearing Loss and Use of Hearing Protection Awareness among Medical Students in Saudi Arabia: Mixed Qualitative and Quantitative Study.

BACKGROUND: Noise-Induced Hearing Loss (NIHL) is a prevalent occupational hazard among healthcare professionals, including medical students. Despite its detrimental effects, the awareness and utilization of hearing protection measures among medical students in Saudi Arabia remain understudied. OBJECTIVE: Is to determine the level of awareness and understanding of NIHL among medical students in Saudi Arabia, as well as their knowledge and usage of hearing protection measures and to identify potential barriers and facilitators for hearing protection utilization. METHODS: A mixed-methods approach was employed, involving a questionnaire survey and semi-structured interviews. The survey collected data on demographics, knowledge of NIHL, and hearing protection practices among medical students. Subsequently, a semi-structured interview was conducted to obtain in-depth insights into the students' experiences, attitudes, and beliefs regarding NIHL and the use of hearing protection. RESULTS: The level about NIHL was 59.32%. Better access to information is associated with increased odds of awareness (odds ratio=3.07, p=0.012). Having relatives with hearing loss increases the odds of awareness (odds ratio =2.49, p=0.034). Individuals with hearing loss or impairment have higher odds of awareness (odds ratio =2.27, p=0.046). Ear Pain, temporary hearing loss, tinnitus, or ringing in the ear: These factors are not significantly associated with awareness of noise-induced hearing loss (p>0.05). Using hearing aids is strongly associated with increased odds of awareness (odds ratio =3.94, p=0.006).The quantitative analysis provided statistical information on the prevalence rates and factors influencing hearing protection usage, while the qualitative analysis uncover nuanced perspectives and experiences. CONCLUSION: This research will contribute to the understanding of NIHL and hearing protection practices among medical students in Saudi Arabia. Improving hearing protection awareness and practices among medical students can ultimately reduce the incidence of NIHL and promote a healthier work environment within the healthcare sector.